Emergency Medicical Guidelines

March 27, 2018 | Author: Natalie Borisenko | Category: Emergency Medical Services, Emergency Department, Cardiac Arrest, Emergency Medical Technician, Medicine


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PREFACEFourth Edition Emergency Medical Guidelines PARTICIPATING AGENCIES INDIAN RIVER COUNTY EMS INDIAN RIVER SHORES PUBLIC SAFETY MARTIN COUNTY FIRE RESCUE SAINT LUCIE COUNTY FIRE DISTRICT STUART FIRE RESCUE TEQUESTA FIRE RESCUE ALL COUNTY AMBULANCE AMERICAN JETS COASTAL CARE TRANSPORTATION INDIAN RIVER COMMUNITY COLLEGE INDIAN RIVER MEMORIAL MEDICAL TRANSPORT SERVICE INTENSIVE AIR AMBULANCE LIFELINE MEDICAL SERVICES i EMERGENCY MEDICAL GUIDELINES This text book was created in its entirety with Adobe© PageMaker© and Adobe© Photoshop© in a Windows © environment. Research, preparation, compilation, editing and layout of this book took approximately three years and more than 2,000 man hours. No one agency alone could have produced a book of this calibre. Each agency made a unique contribution to this book without which it would not have been a success. The Development Team would like to recognize and thank each agency director for making the commitment of resources to see this project through. Without their faith and trust to let this Project find its own way, this book would not exist. As new scientific information becomes available through basic and clinical research, recommended treatments and drug therapies undergo changes. The Development Team has done everything possible to make this book accurate, up–to–date and in accord with accepted standards at the time of publication. However, the reader is advised always ii to check product information regarding dose, contraindications before administering any drug. Caution is especially urged when using new or infrequently ordered drugs. This book is published under the Sunshine Act of Florida and is protected by applicable laws. Copies of this book may be purchased from any participating agency (subject to availability). This book may be cited as a source or used in its entirety with the permission of the Participating Agencies. PREFACE Preface Imagine if you will, the public outcry that would ensue if a jumbo jet filled with passengers crashed every day in the United States. Regrettably, Americans no longer need to imagine disasters that result in the tragic loss of lives. However, each day, more people die of sudden cardiac arrest than would fill a Boeing 747. The most effective way to improve the odds of survival for sudden cardiac arrest is rapid defibrillation in the pre-hospital setting. As high quality Emergency Medical Services (EMS) developed during the 1970s, cardiac arrest survival rates increased from near nothing to about 20% in a few progressive cities. However, essentially no additional progress in survival from cardiac arrest has occurred since 1980. For children, the odds of survival remain abysmal. Less than 2% of children with pre-hospital cardiac arrest survive to leave the hospital. Trauma systems developed during the 1970s to address the inadequacy of care for victims of traffic crashes. EMS began to transport patients directly to regional trauma centers, often bypassing closer community hospitals. With the establishment of these regional trauma centers the odds of survival from motor vehicle crashes improved. This reduction in mortality from injury illustrates the value of having EMS professionals who understand how to use the emergency care resources available in each community. EMS provides out-of-hospital medical care to those with perceived urgent needs. It is a component of the overall health care system. EMS delivers care as part of a system intended to attenuate the morbidity and mortality associated with sudden illnesses and injury. The positive effects of EMS care are enhanced by linkages with other community health resources and integration within the health care system. Emergency medical service is regarded as including the full spectrum of emergency care from recognition of the emergency condition, requesting emergency medical aid, provision of pre-hospital care, through definitive care in the hospital. The vast majority of patients cared for by EMS, however, are not victims of cardiac arrest or major injury. They have illnesses or injuries that are not life threatening yet require access to medical care. This textbook is a unique approach to EMS protocols because it is a regional approach that unifies the prehospital care across boundaries, additionally it was promulgated based upon sound research and evidence based medical care thereby affording the patient the best possible approach to field medicine available. The time for major advancement in the science and practice of EMS is here. Emergency Medical Service providers must be able to deliver state of the art care based on sound scientific knowledge. A number of us, our families, or our friends will at some point turn to local EMS providers for assistance; and we expect that they will provide us with the best care possible. These guidelines take into account the complexity of emergency care in today’s environment. The emergency team is afforded great latitude in treating the patient; it is difficult if not impossible to define every medical condition into a set of rules and procedures. One thing is certain though: not all the methods that we utilize today will stay the same during your career. This project is a living breathing entity that will be revisited, re-researched and updated as new technologies, procedures and treatments become standard. You as the provider of care have an obligation to not only follow these guidelines but to seek out new information that will contribute to the amassed knowledge that represents this book; some of the best ideas come from practicing Paramedics, EMTs and educators who let us know what problems they face every day in the field. This will allow the development team to keep the guidelines on the leading edge of patient care. Our goal is a High Performance EMS system that provides the patient with care that is second to none!! -Joseph V. Ferrara iii EMERGENCY MEDICAL GUIDELINES RATIONALE OF EMERGENCY MEDICAL GUIDELINES FOURTH EDITION The philosophy of the Medical Directors is to treat patients to the fullest, appropriate extent within the medical standard of care for the community. This is accomplished by focusing on the goals set forth by the American College of Emergency Physicians, the American Heart Association and other guideline setting organizations. Paramedics have the discretion to alter any treatment guideline if it is deemed inappropriate. Justification must be made in the run report and reviewed by the Medical Director. All personnel will be subject to examination of case reports. Inquiries are conducted by the Medical Director, Supervisor, Training Officer or their designee at any time during or after care is rendered. The Procedural Guidelines , Treatment Guidelines with exceptions as noted in the relevant sections are hereby authorized for use by the Emergency Medical Technicians and Paramedics in accordance with Florida Statute 401. These guidelines are intended to provide a general approach to treatment of patients by the Emergency Medical Team. It is not intended that the Emergency Medical Team blindly apply these medical guidelines to each patient. It is intended that the Emergency Medical Team use their professional and clinical judgment to determine the best course of treatment for each patient. The treatments and procedures identified as Medic Discretion are generally appropriate actions to be provided by the Emergency Medical Team without prior physician orders. The treatments and procedures identified as Physician Consult are generally appropriate actions to be provided by the Emergency Medical Team after discussion with on–line medical control and direct physician orders received. On-line medical control will be provided by the Emergency Department Physician at the receiving facility, or by the Emergency Department Physician of the base hospital should communications be hindered. Early contact should be made to the Emergency Department Physician whenever doubt exists as to proper management of any patient. Physicians who wish to direct the Emergency Medical Team in the care of a patient should be referred to the on-line medical control physician for issuance of orders to the Team. The Medical Directors authorize the Team Paramedic responsible for controlled substances to take them to the scene of a call. All responsibility for these controlled substances remain with the Paramedic. iv PREFACE v D.D. SPECIAL THANKS TO: MARTIN COUNTY PROFESSIONAL FIREFIGHTERS AND PARAMEDICS IAFF LOCAL 2959 FOR HOSTING THE GUIDELINES DRAFTS ON THEIR WEBSITE KIT WORLEY FOR WEBSITE SUPPORT AND E-MAIL LIST SERVER vi . MATTICE M.D. D. M. P. DON TANABE. D.O. THOMAS MATESE D. ED. MARCH M.D.D.O. MARJORIE BOWERS.D.O. MAUREEN ZELINKA. LILLIAN I. ROBBINS M. PAUL F. GLENN TREMML M. DR.D. MICHAEL ADELBERG M.D. NICOSIA D.O. YVETTE WIRTA-CLARKE D.EMERGENCY MEDICAL GUIDELINES ACKNOWLEDGMENTS RESEARCH TEAM ALEX NATHANSON (TEAM COORDINATOR) PETER ALLEN MARK BENTZ KEN BRYAN JENNIFER CHAMBERS MARK CHAMPION JASON DAHL TONY DUDLEY CHUCK GORDILS CRYSTAL HAUBERT DAVID HOILMAN RICH HUNTER DAVE JACKSON LISA MCCARTY FRED NEFF STACEY NEFF BILL PETERS RICK SOSA GEORGE SUMNER KIT WORLEY CHRIS ZAMBELLO PROJECT COORDINATORS PRE-PRESS EDITING JAMES CHERRY (TEAM COORDINATOR) RALPH MORRISON (TEAM COORDINATOR) CINDIE BRANDT JENNIFER CHAMBERS JOSEPH COX EDWARD HILL DENNIS LIPOFSKY DONNIE LESKO FRED NEFF TERESA RAMSEY RUSTY RAMSEY ERIC WRIGHT JOSEPH FERRARA (EDITOR) MATT HIMES (PROJECT LEAD) CORY RICHTER (EDITOR) LAYOUT CORY RICHTER (TEAM COORDINATOR) CHUCK GORDILS RICH HUNTER RALPH MORRISON MOETAHAR PADELLAN GEORGE SUMNER CHRIS ZAMBELLO COVER DESIGN: RICHARD HUNTER REVIEWERS PETER ALLEN BLAKE BARTHOLOMEW RICK BELLOMY BRIAN BLIZZARD CINDIE BRANDT MARC DUCOTE VINCE FELICIONE MATT FENEX CHUCK GORDILS CHRYSTAL HAUBERT DAVE HOILMAN DAVE JACKSON LISA MCCARTY ALLEN MOORE DOUG MURPHY LORI RECCA JOEY RICHTER FREDDY RODRIGUEZ GARY ROTHE JOHN TAYLOR RICK VILLARS MARK WILSON KIT WORLEY CHRIS ZAMBELLO DAVID ZARKER CONTRIBUTING AUTHORS PETER ALLEN CINDIE BRANDT BRIAN BLIZZARD JASON DAHL MARC DUCOTE JOSEPH FERRARA CHRYSTAL HAUBERT DAVE HOILMAN DAVID HUTTON LISA MCCARTY CHRISTIAN MONTOYA ALEX NATHANSON CORY RICHTER RICK SOSA JOHN STIPO TODD STOLFI GEORGE SUMNER JOHN TAYLOR ROBERT TEARLE DAN WOUTERS DAVID ZARKER TECHNICAL ADVISORS J. CHI CHOU LIU. HOWARD M.D. M. M. TOMAS JACOME M. AVNER. MICHAEL J. ROGER J. PREFACE vii . EMERGENCY MEDICAL GUIDELINES viii . PREFACE ix . .................. E17 DO NOT RESUSCITATE ORDER (DNRO) ............................................................................ E33 SICKLE CELL ANEMIA ................................................................ E40 ATRIAL FLUTTER ........................................................................................................................................................................................................................ E7 ANAPHYLAXIS ............................................................................................................................................................................................................................... E25 RESTRAINTS ............................................................................................................... E3 ABDOMINAL PAIN .................................................................................................................................. E18 LATEX ALLERGY ........................... E19 OBSTETRICS/GYNECOLOGY ............................................................ E15 DIALYSIS ........................................................................................................................................................................... E38 ASYSTOLE ......................................................... E6 ALTERED LEVEL OF CONSCIOUSNESS/ALCOHOLISM .......................................................... E34 STROKE – “BRAIN ATTACK” ................................................................................................................................................................................................................... E41 CARDIAC TAMPONADE .................... E40 ATRIAL FIBRILATION ...................... E14 DIABETES MELLITUS ..................................Emergency Guidelines Contents Educational Guidelines................................................................................................................... E3 ABDOMINAL AORTIC ANEURYSMS ................................................................ E3 ALLERGIC REACTION ................................................................................ E2 GENERAL MEDICAL ....................................................................... E27 RAPID SEQUENCE INTUBATION (RSI) .......................................................................................................................................................................... E30 SEIZURES .................... E20 PAIN MANAGEMENT ......................................................................... E29 RENAL FAILURE ......................................................... E18 HYPERTENSION .................................................................... E1 INTRODUCTION .... E8 ASTHMA ....................... E41 ............................. E31 SEPSIS ......................................................................................................... E10 BLOODBORNE PATHOGENS ......................................................................................................................................................................................................................... E24 PSYCHIATRIC EMERGENCIES ................................... E38 ACUTE CORONARY SYNDROME ......... E11 CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) ............................................................................................................................................................................................................................................................................................................................................... E34 CARDIAC......................................................................... E37 CARDIAC ALERT ................................................................................................. E2 PATIENT PRIORITIZATION ........................................................... E13 COMBATIVE PATIENTS ................................................................................ .................................. E54 VENTRICULAR FIBRILLATION ........................................................................................................................................ E57 HAZARDOUS MATERIALS MANAGEMENT....... E75 WOUND CARE ............................................................ E51 PULMONARY EMBOLISM (PE) .................................... E65 DROWNING/NEAR DROWNING ............................................................................................................................................................................................. E50 PREMATURE VENTRICULAR CONTRACTIONS (PVC) .................................................................................................................. E48 PACEMAKER & AUTOMATIC INTERNAL CARDIAC DEFIBRILLATOR ................................................................................................................................................................................................................................................ E53 TORSADES DE POINTES (TDP)........................................................................................................................ E59 TOXICOLOGY ......................................................................... E51 PULSELESS ELECTRICAL ACTIVITY (PEA) ...... E56 WOLFF–PARKINSON–WHITE SYNDROME ................................................................................ E60 DESIGNER DRUGS .................................................................. E77 . E42 CESSATION OF EFFORTS ........................................ E69 SCUBA ....................................................................... E68 HEAT TRAUMA .............................. E58 ORGANOPHOSPHATE INSECTICIDES ...................................................................................................................................................................................................................... E67 FRACTURES ...... E73 SPIDERS ................. E64 CRUSH INJURY ................... E63 CHEST INJURY .................................................................................................................. E60 COCAINE TOXICITY ............ E68 HEAD INJURIES ............ E52 SINUS BRADICARDIA ...................................... E45 HEART TRANSPLANT PATIENTS ......................... E66 EYE INJURIES .................................................................................................................................................... E47 MYOCARDIAL INFARCTION .................................................................................. E62 TRAUMA................................................ E54 VENTRICULAR TACHYCARDIA (VT) ................................................................................................................................................................................................................................................................................................................................................................................................................... E69 SNAKE BITE .................................................................................................................................................... E43 CONGESTIVE HEART FAILURE ..................................................................................................................................................................... E58 N-METHYL CARBAMATE INSECTICIDES ....................................... E63 BURNS ........................................................................................ E49 PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA (PSVT) .................................................Emergency Guidelines CARDIOGENIC SHOCK ................................................................................................................................................. E74 TRAUMATIC BRAIN INJURY (TBI) .............................................................................................................................................................................................................................................................. E44 HEART BLOCK ....................................................... E61 POISONING/OVERDOSE .................................... E62 ABDOMINAL TRAUMA ............ ........................................................................................... P33 BONE INJECTION GUN (B....................................................................................................................................................................................................................................................................................................................................................................................... P9 LARYNGEAL MASK AIRWAY ............................................................................................................................... P17 CARDIAC................................................. P24 ZOLL M SERIES ..................... P9 ESOPHAGEAL OBTURATOR AIRWAY ................................................................................................................................................................................. P17 AUTOVENT 2000 . P3 CRICOTHYROTOMY ...............................................................................G..... P18 ALERTS — CARDIAC AND STROKE ................................... P10 NASOGASTRIC TUBE .................................................................................................... P15 VENTILATOR ................................................... P27 ZOLL PD 1400 PACEMAKER/DEFIBRILLATOR .................................... P18 MARQUETTE RESPONDER 1500 ..................................................................................................... P1 AIRWAY MANAGEMENT .............I....................................................... P34 DOUBLE LUMEN IV CATHETER ........................... P12 RETROGRADE INTUBATION ............................ P30 AUTOMATED EXTERNAL DEFIBRILLATOR ........... P28 PERICARDIOCENTESIS ........................................................................................................................ P19 PHYSIO CONTROL LIFEPAK 10 .................................................................. P14 SUCTION ..................................................................................................................... P33 AVAILABLE ROUTES OF ADMINISTRATION ............................................. P33 BURETTE ADMINISTRATION SET .............................. P2 CONTINUOUS POSITIVE AIRWAY PRESSURE (CPAP) .......................................................... P17 MINI–VENT ...................................................................................................................................................................................................................................................................................... P8 ESOPHAGEAL INTUBATION DETECTOR (EID) ............................. P36 .............................................................................................. P35 ENDOTRACHEAL MEDICATION ADMINISTRATION ......................... P21 LIFEPAK 12 ....................................................................................... P11 PULSE OXIMETRY .......................... P18 12 LEAD EKG .................................................................................................................... P30 MEDICATION AND FLUID ADMINISTRATION ........................... P11 PLEURAL DECOMPRESSION .............................. P29 TRANSCUTANEOUS PACING ................... P36 EPI-PEN AUTO INJECTOR ............................................................................................................. P6 END TIDAL CO2 DETECTOR .....................................................................................) ......................................................................................................................................................................... P2 ESOPHAGEAL TRACHEAL DOUBLE LUMEN AIRWAY (COMBITUBE©)....................... P13 RUSCH QUICKTRACH .Emergency Guidelines Procedural Guidelines ........................................................................... P4 ENDOTRACHEAL INTUBATION ...................................................................................................................................................... P35 DRAWING UP MEDICATIONS ............................................................................................................................................ P2 CAREVENT ........................................... ....................................... P61 SUSPECTED CHILD/OTHER ABUSE ........................................................................................................................................................................................................................................................... P53 SUBCUTANEOUS MEDICATION ADMINISTRATION ............................................ P61 RESPONDER INFLATABLE PEDIATRIC SEAT ................................. P59 PHLEBOTOMY ......................................... P62 IMMOBILIZATION ................................................. P52 RECTAL MEDICATION ADMINISTRATION ..................................................... P46 INTRAOSSEOUS INFUSIONS ......................................................................................... P59 PROPAQ ............................................................................................................... P41 IVAC 530 .......... P47 INTRAVENOUS CATHETER INSERTION ................................................. P52 SALINE LOCK ................................................................................................................ P62 TRAUMADEX .............................................................................................. P62 THERMOSCAN THERMOMETER ............................ P53 GENERAL ............................................................................................................................................... P40 INFUSION PUMP ................................................... P64 AMBU PERFIT ACE ............................................. P47 INTRAVENOUS MEDICATION ADMINISTRATION .............. P53 UMBILICAL VENOUS CATHETERIZATION ............................................................................................................................................................................................... P51 PIGGYBACK ............................ P50 NITROUS OXIDE ...............................................................................A................ P50 NITROGLYCERIN IV .. P45 INTRAMUSCULAR MEDICATION ADMINISTRATION ... P58 DOPPLER MEDISONIC .............. P39 INFUSA–PORTS .......................................................... 1 INTRAOSSEOUS INFUSION SYSTEM ............................................................................................................................................................................................. P56 COLIN BLOOD PRESSURE MONITOR .............................D......................................... P64 ..................................................................................................................... P64 CERVICAL IMMOBILIZATION DEVICE (C................. P57 DO NOT RESUSCITATE ORDER (DNRO) ................. P57 CRITICARE 506DX2 VITALCARE VITAL SIGNS MONITOR ...................................................................................................................................... P60 RADIO COMMUNICATIONS ..........................T......................................................................................... P48 MUCOSAL ATOMIZATION DEVICE (MAD) .....................................................I..................................................................................................... P58 MORGAN MEDI—FLOW® LENS ............................................) ............................................................................................................................................................ P55 BROSELOW PEDIATRIC EMERGENCY TAPE ................................................................................................................................... P58 FOLEY CATHETERIZATION ............................................................... P37 DRUG HANDLING ..........................S..... P44 IVAC MED SYSTEM 3 ..................Emergency Guidelines F............................................................... P49 NERVE AGENT AUTO INJECTORS ................................................................................................................................................................................. P48 NEEDLESS IV SYSTEMS ....................................................................................................................................................................................................... P55 BLOOD GLUCOSE LEVEL ................................................................................................................................................... P55 BLOOD ALCOHOL SAMPLING ..... ............................................ M7 HYPERTENSION .................................................... P74 LEVEL 1 RESPONSE ... P77 JUMP START PEDIATRIC TRIAGE ............................................................................................................... M11 SEDATION ..................................................................................... P69 PATIENT RESTRAINTS ... P64 KENDRICK EXTRICATION DEVICE (KED) ................................................... M14 SICKLE CELL ANEMIA .... M1 GENERAL TREATMENT PRECAUTIONS ..... M5 CHRONIC OBSTRUCTIVE PULMONARY DISEASE ............................................................................................................ P73 MULTIPLE CASUALTY INCIDENTS ................................................................................................................................................................... M9 PAIN MANAGEMENT ........................................ P71 SPIDER–TYPE PATIENT STRAP ....................................................................................................................................................................................................... M3 ALTERED LEVEL OF CONSCIOUSNESS ............. P72 STA-BLOCK HEAD IMMOBILZER ..................................................................................................... P66 MILLER BOARD ......................................................................................................... P68 NAJO PEDI–AIR–ALIGN BACKBOARD ................................................................................................................................................................................. P74 LEVEL 3 RESPONSE ............................................................................................................... M13 SEIZURES .......... M3 ABDOMINAL PAIN ...... P81 TRAUMATIC BRAIN INJURY ..................................................................... P74 LEVEL 2 RESPONSE ................................................................................................................................................................................. M9 OBSTETRICS/GYNECOLOGY ................................................................................................................................... P70 PEDIATRIC PATIENT IMMOBILIZATION ................................................................................ M2 MEDICAL ................................... M6 DIABETIC EMERGENCIES .......................................................... M6 DIALYSIS PROBLEMS ......................... P71 SPLINTING ..................................................................................................................................................................... M7 MEDICAL SHOCK SYNDROMES ........... P69 RIGID CERVICAL COLLAR ........................................................... M4 ASTHMA .... P75 INTERFACILITY TRANSPORTS ...... P79 SIMPLE TRIAGE AND RAPID TREATMENT (START) .................................................................. P65 LONG SPINE IMMOBILIZATION ......................................................................................... M15 STROKE .............................................................................................. M8 NAUSEA / VOMITING .................................................................................................................................................................................................................................................................................................................................................................................................... P82 Treatment Guidelines ......................................................... M3 ALLERGIC REACTIONS .................................................................................................................................................................................................................................................... M15 ................................................................. M10 RAPID SEQUENCE INTUBATION ...........................................................................................................................................Emergency Guidelines HALF BACK EXTRICATION/LIFT HARNESS ...................................................................................................................................................... ... T1 SNAKE BITE ...................................................... C6 PULSELESS ELECTRICAL ACTIVITY .......................................................................................................................................................................... T1 BROWN RECLUSE ............................... T10 COCAINE OVERDOSE ............................................... T8 OVERDOSE ................... C8 VENTRICULAR FIBRILLATION / PULSELESS V–TACH ............. T9 CARBON MONOXIDE .................................................................... C7 VENTRICULAR ECTOPY .................................... T10 ............................................................Emergency Guidelines CARDIAC.................................................................................................................................. C11 TRAUMA / ENVIRONMENTAL .................................................................................................................................. T6 SCUBA DIVING INJURIES ................................................................................. T2 BURNS .......................... T5 HYPOTHERMIA ................................................................................................................................. T8 SPECIFIC TOXICOLOGICAL EMERGENCIES .. T3 DROWNING/NEAR DROWNING ............................................... T4 HEAD INJURIES ......................................................... T5 HEAT TRAUMA ................................................... C1 BRADYCARDIA ............................................................................................................. T8 BENZODIAZEPINE OVERDOSE ............................................................ T9 TRICYCLIC ANTIDEPRESSANT OVERDOSE (TCA) .................................................................................................................................................. T6 TOXICOLOGY................................................................................................... T1 BLACK WIDOW .......................................................................................................................................................................................................................................... C1 ASYSTOLE ................................................................................................................................................................................................................................................................................................................ T4 FRACTURES .............................................................................................................................................................................................................................................................................................................................................................................................. C3 CHEST PAIN / MYOCARDIAL INFARCTION (SUSPECTED).......................................................................................... C4 CONGESTIVE HEART FAILURE/PULMONARY EDEMA ..... C2 CARDIOGENIC SHOCK ............... C9 VENTRICULAR TACHYCARDIA . T3 CRUSH INJURY .................................................................................................................................................................................................. C5 PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA ......................................................................................................................................................................................................................... T5 LOCAL ANESTHESIA ....................................................................................................................................................... T4 EYE INJURIES ................................................. C3 CARDIOVERSION / DEFIBRILLATION ....................................... T8 NARCOTIC OVERDOSE ............. C10 WIDE–COMPLEX TACHYCARDIA OF UNCERTAIN TYPE ............................................................................................................................................................................................................................................. T1 BITES AND STINGS ........................... T2 CHEST INJURY ... T1 MARINE INJURIES ......................................................................... T2 CONTRAINDICATIONS ........................................................ ....................................................................................................................... T11 GHB (GAMMA HYDROXYBUTYRATE) OVERDOSE ................................................................. APAP) ................................................................................................. D7 DEXAMETHASONE ................................................ D9 DOBUTAMINE ............................................................................................................................................................ D3 ADENOSINE .. T12 Drug Reference .............................................................................................................................................................................................................................................. D6 CALCIUM GLUCONATE ......................................... D2 (RECTAL TYLENOL) ............................................................................................................................................................. D6 (AS AN ANTIDOTE FOR POISONINGS) .................. T11 INHALED TOXINS ...................................................................................................................................................................................................... D10 (DOBUTREX) ................................................................................................................................................................ T12 ORGANOPHOSPHATE POISONING ........................................................ D4 AMIODARONE ............... D6 CALCIUM CHLORIDE .......................... D10 (ANZEMET) .......................................... D8 DILTIAZEM ..................................................................................................................................................................................................................... D10 DOPAMINE ............................................ D3 (ADENOCARD) ..................................................................................................................................................... D9 (CARDIZEM) ..............................................................................Emergency Guidelines ECSTASY (MCMA) OVERDOSE .................................................................................................. D2 ACETYLSALICYLIC ACID ... PACERONE) ............ D4 AMYL NITRATE ...... D7 (TAGAMET) ............................................................................................................................................................................................................................... D5 (AS A CARDIAC AGENT) .......................................... VENTOLIN) .................................................................................................................. D8 (VALIUM) .............................................. D9 (BENADRYL) .............................. D8 (DECADRON) ............................................ D1 ACETAMINOPHEN ........................................................................................................................................................................................................................... ASA) ................................................. D11 (INTROPIN) ..................................................................... D9 DIPHENHYDRAMINE ....................................................................................................................................................................................................................................... D3 ALBUTEROL ................................................................................................................................................................................................................................... D2 (TYLENOL*................................................................................................. D4 (PROVENTIL...................................................................................... D5 ATROPINE SULFATE ............................................. D10 DOLASETRON MESYLATE ...... D2 ACETAMINOPHEN SUPPOSITORIES ............... D5 ATROPINE SULFATE ...................................... D3 (ASPIRIN............................................................................................................................................................................................................................................... T11 TOXIC CHEMICAL EXPOSURE ..................................... D11 ........................................ D4 (CORDARONE.................... D8 DIAZEPAM ............................................................................................................................................... ................................................................................................................................................................................................................ D19 MAGNESIUM SULFATE .......................................000) . D12 ETOMIDATE ........................................................................... D13 (ROMAZICON) ............... D18 LIDOCAINE HCL TOPICAL ....................000 ................................... D20 MEHTYLPREDNISOLONE .......................................................................................... D19 (XYLOCAINE 2% JELLY) ............................................................................... D16 (ATROVENT) ..................................................... D19 LORAZEPAM .................................................................................................... D21 (MS) .................... D17 LIDOCAINE HCL .................................................................................................... D21 ........ D15 HYDROMORPHONE HCL ............................................................................................ D16 (DILAUDID) ............................................................. D13 (LASIX) ............................................................ D12 (1:10.................................................................................................................................................................................. D20 (SOLU-MEDROL) .......................................................................... D21 (VERSED) ...................................................................................................... D15 HEPARIN ..................................................................................... D14 GLUCOSE 50% ....................................................................................................................................................................................................................... D15 (GLUTOSE) ............................................................................................................................................................................................................................................................................................... D16 IPRATROPIUM ................................................................................................................................................................................................................................. D17 LABETALOL ... D18 LIDOCAINE HCL 2% WITH ............................................................ D14 GLUCOSE ORAL ...................................... D12 (AMIDATE.................................... D13 GLUCAGON . D11 EPINEPHRINE ...................................... D14 (DEXTROSE 50%) ............................................................................................................ D16 KETOROLAC ........................................................................................................................................................................................................................................ TRANDATE) . D14 (GLUCAGON) ..................... D17 (TORADOL) ................................................................................................................................................. D18 (XYLOCAINE) . D19 (ATIVAN) ........................................................................... D17 (NORMYDYNE.................................................................... D18 EPINEPHRINE 1:100.................................................................................Emergency Guidelines EPINEPHRINE ....................................................................................................................................................................... D20 MIDAZOLAM .............................................................................................................................................................. D21 MORPHINE SULFATE .................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................... HYPNOMIDATE) ..................................................................... D12 FLUMAZENIL ................................................................................................................................ D13 FUROSEMIDE .... D11 (1:1000) .............................................................................................................................................................................. ........................................................................................................................................................................................................ D23 (TRIDIL)......... D23 NITROGLYCERINE TOPICAL ................................................................................................................................... D25 (PITOCIN) ... D30 (NORCURON) ............................................................................................................................................................................... D25 PROCAINAMIDE ................................. D23 NITROGLYCERINE SL ........................................................................................................................................................................................................................................... D24 NITROUS OXIDE .................................................. D25 (NITRONOX) ........................................................... D22 NALOZONE ............................................ D28 (PRONTOCAINE) .... D26 (PHENERGAN) .......... D29 (PITRESSIN) ................................................................................................... D27 (DIPRIVAN) .................................................................................................................. D26 PROPOFOL ....................................................................................................................................................................................................... D27 SUCCINYLCHOLINE CHLORIDE ................................. D30 VERAPAMIL ................................................. D28 (ANECTINE........................................................................................................................................ D22 (NARCAN) .........................................Emergency Guidelines NALBUPHINE ....................................................... D27 SODIUM BICARBONATE ........................................... D26 (PRONESTYL) ........................................... D22 NITROGLYCERINE IV ....................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................................... D26 PROMETHAZINE ....... D29 (VITAMIN B-1) ......... D23 (NITROLINGUAL) (NITROBID) (NITROSTAT) ............................ D25 OXYTOCIN .. D29 VASOPRESSIN ................................................................. D24 NITROPRUSSIDE ................................................................................................................................................................................ D29 VECURONIUM BROMIDE ..................................................................... D28 TETRACAINE HCL......... QUELICIN) ....... D28 THIAMINE ..................................... D30 (ISOPTIN OR CALAN) .............................................................................................. D22 (NUBAIN) .............................................................................................................................................................................................................................................................................................................................................. D24 (NIPRIDE) .................................................. D30 ....................................................................................................................................................................................................................................................................................................................................................................................................................................................................... D24 (NITRO-BID) ....................................... ................................... H1 HAZARDOUS MATERIALS MEDICAL MANAGEMENT TREATMENT GUIDELINES .................................... AF1 HELICOPTER ACTIVATION CRITERIA ............ AE2 Appendix F ................ AND WONG-BAKER PAIN SCALE ...............................................................................................................................AG1 TASER INJURIES .............. A1 EDUCATIONAL SECTION .................................................................................................. AC1 Appendix D .................................................................................................................................................................................................................AG1 ....................................... AC1 TRAUMA TRANSPORT PROTOCOLS ................................................................................................. AD1 APGAR............... A2 AEROMEDICAL PROGRAM OPERATION .............................. AB1 GUIDE TO THE HOSPITALS IN THE OPERATING REGION ............... AA1 Appendix B .......................... A2 THE HISTORY OF AEROMEDICAL TRANSPORT ................ AE1 CINCINATTI STROKE SCALE ................................ H2 Appendix A ........................................................................ RULE OF NINE’S...................................................... A3 AIR TRANSPORT GENERAL INFORMATION ......................................................................................................AF1 Appendix G ......................................... A5 Haz-Mat Guidelines ................................................................................................................................................ AB1 Appendix C .................................. AE1 PREHISPITAL FIBRINOLYTIC CHECKLIST ......................................................................... AA1 ACLS QUICKIE ................................... AD1 Appendix E ...................Emergency Guidelines Aeromedical................................ E-1 2/15/06 . Clinicians priviledged to work within the scope of this protocol now have the opportunity for greater understanding of its content.EDUCATIONAL GUIDELINES Educational Guidelines The following section entitled “Educational Guidelines” focuses on pharmacological and emergent procedures specific to each protocol. Protocols 2005 is an extremely aggressive approach to pre–hospital emergency medicine. This new section is intended to provide a detailed explaination of the thought processes behind each treatment modality. Subsequent treatment received by your patient will be based upon a rapid. Cardiac or Stroke Alerts PRIORITY THREE—MINOR OR STABLE CONDITION Conditions considered minor are those which need attention but any delay in treatment will not result in immediate harm or permanent injury to the patient Minor conditions may include: 1. Cardiac dysrhythmias with diminished. Minor Fractures 2. calcium chloride. Minor Contusions 4. It is isotonic with the extracellular fluid. two–thirds of either of these solutions is lost to the interstitial space within one hour. because their administration causes an immediate expansion of the circulatory volume. one of your most important skills will be to obtain and interpret ECG rhythm strips. Falls Without Trauma 5. Three of the most commonly used solutions in prehospital care are lactated ringers solution. Circulation 2. D5W is a hypotonic glucose solution used to keep a vein open and to supply calories necessary for cellular metabolism. and sodium lactate in water. potassium chloride. Continuously monitor your patient and report appropriate information to the emergency department. Breathing. accurate interpretation. burn. Cervical Spine and/or Severe Head Injuries PRIORITY TWO—SERIOUS (SECONDARY) Serious conditions are potentially life–threatening or disabling problems which. remains with the on–line medical control physician. Normal Saline is an electrolyte solution of sodium chloride in water. In some cases. Active seizure activity 8.EMERGENCY MEDICAL GUIDELINES INTRODUCTION Monitor ECG: As a paramedic. due to movement of the electrolytes and water. glucose molecules rapidly diffuse across the vascular membrane with a resultant free water increase. rapid or irregular pulses 4. and 5% dextrose in water (D5W). etc. if left untreated. The ultimate authority for this decision. PATIENT PRIORITIZATION PRIORITY ONE—HIGHEST PRIORITY (IMMEDIATE/CRITICAL) Critical conditions are those which require immediate intervention involving the following: 1. pediatric. Open Chest or Abdominal Wounds 6. While it will have an initial effect of increasing the circulatory volume.Chest pain or Abdominal pain (Medical or Trauma) 5. however. Both lactated ringer’s solution and normal saline are used for fluid replacement. Disturbances of consciousness 2. Serious conditions which need prompt attention may include: 1. Minor Lacerations 3. Toxic Drug Overdose or Poisoning 7. Minor Burns REMEMBER: A patient’s condition is always subject to change and may occur rapidly. based on the needs of the patient and the availability of services. However. – means designating a facility that is not nearby. 0. Respiratory Arrest 3. IV: In the prehospital setting. and for the introduction of medications directly into the vascular space. Active hemorrhage 6. MCI Triage Priorities: Please refer to the START programs field operation guidelines E-2 2/15/06 . may result in a fatality or permanent disability. Respiratory distress 3. Lactated Ringer’s is an isotonic electrolyte solution of sodium chloride. Transport: Patients who are transported under the direction of an emergency medical service system should be taken whenever possible to the closest appropriate medical facility. the patient’s need for special services – trauma. Your patient’s condition should be the primary assessment tool in determining the priority category. the closest facility will be designated for stabilization of the patient while transfer is arranged. Cardiac Arrest (Trauma or Medical) 4. Penetrating injuries. The medical control physician should be the authority to designate that facility. Fractures or other trauma 9. Deforming injuries such as: Burns.9% sodium chloride (normal saline). intravenous therapy is geared toward electrolyte or fluid replacement. Massive Exsanguinating Hemorrhage 5. Airway. At other times. altered mental status. mottling. A 12-lead EKG is indicated for epigastric pain without evidence of gastrointestinal bleeding. A prolonged transport time may be an appropriate reason for request of pain medication and/or a nasogastric tube. The prognosis is guarded in patients who suffer rupture prehospital. differential diagnosis and is not appropriate to prolonged evaluation in the field. Isolated groin pain is a particularly insidious presentation. distended bowel. During physical examination. survival rate is good in the subset of patients who are not in severe shock and who receive timely. severe. ectopic pregnancy. and a high index of suspicion is necessary to make the diagnosis. and constant low back. but certain features of aortic aneurysm or dissection may be observed. but find it difficult to localize the pain. and mesenteric embolism or thrombosis. expert surgical intervention. or renal stone. abdominal. Patients at greatest risk for AAA are those who are older than 65 years and have peripheral atherosclerotic vascular disease. potentially life–threatening condition. Patients may experience unimpressive back. It is more ABDOMINAL PAIN Abdominal pain is a complex. This symptom may be present without any other associated findings. intestinal obstruction. the important surgical emergencies with pain as their outstanding symptom to keep in mind are appendicitis. which is composed of smooth muscle cells surrounded by elastin. On the other hand. as these should alert the clinician to the possibility of expansion with imminent rupture. Obese or elderly patients tend to tolerate pain better than others. and hypotension. vigorous fluid resuscitation as indicated and obtaining useful information concerning history in order to expedite treatment on ED arrival. of those who do. spleen injury. Prehospital care should consist of assuring airway management. flank. a leaking abdominal aneurysm. signs of hemorrhage. The 3 layers comprising the normal aorta are the intima. perforated peptic ulcer.EDUCATIONAL GUIDELINES commonly seen with a ruptured aneurysm. Most occur in association with advanced atherosclerosis. Rupture is believed to occur when the mechanical stress acting on the wall exceeds the strength of the wall tissue. media. However. It is important to note progressive symptoms. hysterical patients tend to exaggerate symptoms. At least 65% of patients with ruptured AAA die from sudden cardiovascular collapse before arriving at a hospital. resulting in a slow and continuous dilatation of the lumen of the vessel. More than 50% do not survive to the ED. intestinal obstruction perforated ulcer. The degeneration ultimately may lead to widening of the vessel lumen and loss of structural integrity. A history of smoking. AAAs are usually asymptomatic until they expand or rupture. ovarian cyst. gentle transport is indicated. ectopic pregnancy. general peritonitis from an unknown cause. GENERAL MEDICAL ABDOMINAL AORTIC ANEURYSMS Abdominal aortic aneurysm (AAA) is a relatively common. The Team should consider the possible etiologies of the pain: abdominal aneurysm in the elderly. perforated diverticulitis. is the rule for most patients with biliary tract disease. pancreatitis. Ruptured AAA is the 13th–leading cause of death in the US. AAA develops following degeneration of the media due to atherosclerotic changes. cardiac pain in epigastrium. Patients with a ruptured AAA may present in frank shock as evidenced by cyanosis. and proteoglycans. The clinician need not be afraid of properly palpating the abdomen because no evidence exists that aortic rupture can be precipitated by this maneuver. or groin pain for some time prior to rupture. rather than emergency care. gallbladder. mesenteric embolism or thrombosis. Establishing diagnosis in the field is usually difficult or impossible. or groin pain. This occurs with retroperitoneal expansion and pressure on either the right or left femoral nerve. flank. Expanding AAA causes sudden. It has a wide spectrum of presentations and should be considered in the differential diagnosis for a number of symptoms. survival rate drops by about 1% per minute. an AAA is even more difficult to palpate. recent trauma. vascular surgeons are unable to palpate a pulsatile mass while preparing the patient for surgery. E-3 2/15/06 . Use of pain medication is discouraged without physician consult. twisted ovarian cyst. Urgent. abdominal. and pain may be a less significant symptom to the patient. chronic obstructive pulmonary disease (COPD). and hypertension often is elicited. Textbook descriptions of abdominal pain have severe limitations. Infants and children may be unable to localize their discomfort and they have many diseases not seen in adults. and adventitia. In an obese abdomen. AAA is usually the result of degeneration in the media of the arterial wall. collagen. Structural and elastic properties of major arteries are most imparted by the media. Presence of a pulsatile abdominal mass is virtually diagnostic but is found in less than half of the cases. tachycardia. Prompt. because each individual reacts differently. Syncope may be the chief complaint. Even in 25% of patients known to have an aneurysm. gallbladder. or shoulder pain suggests an emetic perforation of the intra–abdominal esophagus. Vomiting results from either of 3 mechanisms: (1) severe irritation of local peritoneum or mesentery. Drug history should include details concerning drugs. both therapeutic and addictive. indicates an emergency.e. Family history of certain diseases (i. gallstones) may be helpful. Shock. aspirin) are highly irritating to the intestine and may lead to perforations and peritonitis.. . severe pain may herald serious diseases (i. esE-4 2/15/06 pecially if it is associated with shock. and testicular torsion in the affected testicle. jaundice. some measures may have been found to relieve it. A history of either esophageal reflux. gastroenteritis is a probable cause.e. bile duct... crampy pains followed by severe steady pain may mark the onset of strangulation. severe pain beginning in the mid– back and rapidly spreading to the abdomen is characteristic of a ruptured aortic aneurysm. The history must be detailed.e. In patients with acute intestinal obstruction. Appendicitis often is described as an ache. and other family members have just recovered from similar attacks. During the acute attack. and in many cases it will be sufficient to make the proper diagnosis. with peritonitis he will want to lie as quietly as possible.e. gallstone colic. constipation. or (3) absorbed toxin or drug stimulation of CNS centers controlling the vomiting reflex. If the symptoms include pain. perforated diverticulitis). or embolism). vomiting. Gallbladder pain often is felt beneath the right scapula. or recurrent attacks of mild intestinal obstruction from a benign tumor (i. a perforated peptic ulcer produces severe pain at the outset. In an older man. Abdominal pain in neonates. relief by antacids suggests peptic ulcer disease.e. or pancreas. Previous symptoms of ulcer disease..EMERGENCY MEDICAL GUIDELINES Diagnosis and therapy of a patient with severe abdominal pain must proceed simultaneously. Renal pain radiates to the region of the pubis or vagina. weight loss. intestine. acute pancreatitis. diarrhea. which later appears to subside but again increases in severity as peritonitis is established. hematuria.. Past history of preceding symptoms may help localize the site of the present problem. Are other symptoms associated with the pain? Symptoms that occurred immediately before the onset of the pain or in association with it are important. How severe is the pain? This is a very important guide to the importance of the complaint. K tablets. However. Epigastric pain associated with stomach. However. (2) obstruction of a muscular tube (i. biliary or renal colic is likely. Similar symptoms in a woman of childbearing age may be due to a ruptured ectopic pregnancy.. How is the pain described? A severe. or ureter). mild chronic discomfort localized to one area may point to an involved viscus that now is subject to a serious complication (i. Certain questions are always important. mucus. Left diaphragmatic irritation from blood or pus (due to a ruptured spleen or pancreatitis) can be felt in the region of the left shoulder. Recurrent attacks of severe colic suggest the possibility of gallstones. diarrhea.e. intestinal obstruction from atresia. the lower the site of the obstruction. Renal pain is felt over the corresponding kidney. sweating.e. and children has numerous causes not encountered in adults. Was the onset sudden? What was the patient doing when the pain started? A sudden pain severe enough to cause fainting suggests a perforated ulcer. or blood in the stool can help establish a diagnosis. Tearing pain is characteristic of a dissecting aneurysm. They include meconium peritonitis. carcinoid). free perforation of a viscus into the peritoneal cavity or rupture of an aortic aneurysm) or be more severe than seems warranted by the physical findings (i. duodenum. knife–like pain. or ruptured aneurysm. What gives the patient relief? If there have been previous attacks of somewhat similar pains. if the patient attempts to relieve the pain by walking the floor. or fainting can also accompany abdominal pain and furnish a rough guide to the severity of the pathologic process. i.. mesenteric arterial or venous thrombosis. the more delayed is the vomiting. careful diagnostic study. or diverticular disease are especially helpful.e. usually with appendicitis it is the initial site of pain before the pain shifts to the right lower quadrant. Vomiting is one of the most important. gastroenteritis is the probable diagnosis. Severe vomiting that precedes an intense epigastric. Vomiting usually occurs only 1 or 2 times/hour after the onset of pain with appendicitis. hematemesis. Does the pain radiate? Radiation often occurs along the distribution of the nerves of the same spinal segment (“referred pain”). Anticoagulants can increase the chances of bleeding. Some drugs (i. intestine. When it precedes pain and especially if it is followed shortly by diarrhea. How long did the attack last? If the pain stopped before the physical examination. stenosis. melena. Where is the pain? Location is a very important guide to the involved viscus. biliary colic is more likely. infants. Prednisone or immunosuppressives increase the chances of perforation of some portion of the gastrointestinal tract with relatively little response in the nature of pain or leukocytosis.. The cause is established by history and physical examination. Is the pain acute or chronic? Chronic complaints may be entirely functional or demand a long. pallor. left chest. perforated duodenal ulcer. Symptoms of intestinal obstruction usually have a less dramatic onset. kidney stones. If rose spots are present. The most common cause is radiculitis. and to orifices that could be the site of external hernias. level of consciousness. events that are associated with local pain and tenderness. The general physical examination must not be neglected. and degree of shock must be evaluated in severe cases. and distention should not receive nitrous oxide. pulse. Jaundice or evidence of bleeding in subcutaneous tissues is another diagnostic sign that may be present (i.9% Normal Saline – IV access is routinely established at a KVO rate. Promethazine (Phenergan) – Antiemetic/Analgesic. absent bowel sounds. (4) Pneumonia can lead to diffuse abdominal pain. Gastroenteritis is likely if family members or associates have had recent similar complaints. vomiting blood) or showing signs of impeding shock (postural hypotension) will require fluid resuscitation. Some relatively common diseases must be considered in the diffential diagnosis of acute abdominal pain. (1) Gastroenteritis: symptoms of colicky pain. volvulus of a gut with a common mesentery. which suggest the possibility of adhesions and intestinal obstruction. An ectopic pregnancy is life–threatening without emergency laparotomy. tabetic crises were a common cause of attacks of severe abdominal pain. complaints of burning pains are likely to remain unexplained. but the tenderness never becomes localized and the disease is self–limited. In the past. degree of distention and palpable masses are important. The center of attraction. Nasogastric Tube Insertion – Is indicated for the decompression of gastric distention and poisoning or overdose cases E-5 2/15/06 . Abdominal pain is one of the most difficult problems in the pre-hospital setting to diagnose and treat.e. This medication can concentrate in pockets of obstructed bowel and possibly lead to rupture. imperforate anus. This patient can deteriorate rapidly. however. Use of this pain medication is preferred in abdominal pain because it provides rapid relief and is easily reversible. The most troublesome problem that occurs in young women is pelvic inflammatory disease. (10) Patients with psychogenic somatoform disorders often complain of severe attacks of abdominal pain for which no organic cause can be found. (7) Anticoagulants or severe coughing can lead to a hematoma of the abdominal wall or rupture of the deep epigastric artery or vein. (9) Spinal or central nervous system disease can produce pain referred to the abdomen. is the abdomen. The sedative and analgesic properties of this medication may make diagnosis of abdominal pain difficult once the patient arrives at the emergency room. Dysmenorrhea may be trivial or disabling. Tenderness. (2) Inflammatory bowel disease: Crohn’s disease can mimic acute appendicitis. retroperitoneal bleeding from hemorrhagic pancreatitis or a bluish discoloration or frank ecchymosis of the costovertebral angles [Grey Turner’s sign} or around the umbilicus [Cullen’s sign}). (3) Herpes zoster: at times severe pain precedes the typical rash. In some instances symptoms are confined to the right lower quadrant so that there is great difficulty in determining whether the patient has pelvic inflammatory disease or appendicitis. Blood pressure. (11) Typhoid fever may. (6) Drug addicts may have severe colicky pains that suggest intestinal obstruction. (8) Sickle cell disease may be associated with attacks of severe abdominal pain.. patients who present with severe abdominal pain. uncontrolled vomiting. Intrauterine contraceptive devices may migrate into the peritoneal cavity and produce peritonitis and intestinal obstruction.EDUCATIONAL GUIDELINES web. Endometriosis is a common cause of pain. Therefore. Abdominal pain in women varies greatly in intensity. bloody stools. this disease must be considered. enterocolitis. Preferably it is treated with antibiotics. Tubo–ovarian abscesses require surgical treatment. High pitched peristalsis or borborygmi (bubbling in the bowels) in rushes suggest intestinal obstruction. this pain usually is chronic rather than acute. and others.e. of course. * Current research indicates the future of EMS leaning toward the use of a much higher concentration of normal saline as well as medications that allow for oxyhemoglobin enhancement. and diverticulitis can produce a similar syndrome (usually in the left lower quadrant). Severe pain combined with an absolutely silent abdomen is an indication for immediate exploration. Phenergan may be administered for prolonged. this can be confusing. Active peristalsis of normal pitch suggest a nonsurgical disease (i. Unless the patient has a peptic ulcer. (5) Acute myocardial infarction may be accompanied by diffuse abdominal pain. RATIONALE The abdominal cavity is the largest cavity in the body. vomiting and diarrhea may be accompanied by mild abdominal tenderness. Peristalsis is extremely important. particularly if the nerves in the right lower quadrant are involved in a patient whose appendix has not been removed. be accompanied by right lower pain. rebound tenderness. You will usually not be able to determine the cause in the field. constant reassessment and subsequent management are appropriate. but there is no localized abdominal tenderness.. Particular attention should be paid to operative scars. gastroenteritis). so its administration is given sparingly. This access allows for immediate delivery as needed. nausea. IV 0. The patient who exhibits active hemorrhage (upper or lower GI bleed. Nitrous Oxide (Nitronox) – Analgesic gas. It often can be controlled by hormones but in other cases may require operation. Your primary goal in dealing with a patient suffering an abdominal emergency consists of detection and stabilization. . heart. extravascular smooth muscle. They block the effects of histamine on GI tract smooth muscle. hay. this distressing condition responds well to immediate field treatment by the Team. Endocrine gland: Stimulation of catecholamine release from adrenal chromaffin cells also appears to be H1–receptor–mediated. Histamine H1 receptor antagonists (H1 blockers): The conventional antihistamines possess a substituted ethylamine side–chain (similar to that of histamine) linked to one or more cyclic groups. In man. urticaria (hives). marked hypertension.e. can produce circulatory shock. Antihistaminic effects of H1 blockers are noted only in the presence of increased histamine activity. sneezing. Early treatment is important. alcoholic beverages. In general. their relation to the environment and to the seasonal and situational variations. Symptomatic relief with drugs should not be neglected while the patient is being evaluated and specific control or treatment is being developed. or dust.e. The H1 blockers. Age of onset may be an important clue (i. at home. Other smooth muscle: In man. and (3) flare from a neuronal reflex mechanism producing a surrounding area of arteriolar vasodilation. infiltrative lung disease. In the cardiovascular system. various chemicals (including tissue irritants. and life stresses). thus inhibiting the wheal. H1 blockers effectively block histamine–induced increased capillary permeability and sensory nerve stimulation. and multiple drug therapies is preferred. Exocrine glands: Histamine increases salivary and bronchial gland secretions.. The Team should be prepared to treat the following: multiple cardiac arrythmias.EMERGENCY MEDICAL GUIDELINES when transport will be lengthy or delayed. Onset action usually occurs within 15 to 30 minutes. and gastrointestinal mucosa. (2) wheal due to local edema from increased capillary permeability. the highest concentrations are in skin. For advising the patient. with smaller amounts in the brain. sneezing. or those that appear after exposure to animals. The release of histamine from the mast–cell storage granules can be triggered by physical tissue disruption. causing (1) local erythema from vasodilation. tachycardia. Histamine is widely distributed in mammalian tissue. surface active agents. airway obstruction. appear to be mediated by two distinct receptors termed H1 and H2. histamine is a potent arteriol dilator that can cause extensive peripheral pooling of blood and hypotension. mild wheezing. or those that develop in specific environments (i. The similarity between the ethylamine moiety of histamine and the substituted ethylamine structure of the H1 blockers suggests that this molecular configuration is important in receptor interactions. itching. their clinical course. and exocrine glands. mild agitation.e. exercise. Histamine is present mainly in the intracellular granules of mast cells. Histamine also stimulates gastrointestinal motility. ALLERGIC REACTION Much more common than anaphylactic reaction. It also increases capillary permeability by distortion of the endothelial lining of the postcapillary venules. and polymers). and mucous secretion responses. Sensory nerve endings: Local instillation of histamine may produce intense itching. duration of action is usually 3 to 6 hours.. Review of the symptoms. impending anaphylaxis. tobacco smoke and other pollutants. combined with arteriolar and capillary dilation. which in man are exerted primarily on the cardiovascular system. E-6 2/15/06 . flare. cold air. correlating with specific pollen seasons). and most prominently by antigen–antibody interactions. H1 blockers appear to act by competitive inhibition. it is also helpful to investigate the effects of nonspecific contributory factors (i. Histamine also dilates cerebral vessels. severe contact dermatitis). childhood asthma is more likely to be allergic than asthma beginning after age 30). but in man the allergic reaction of the bronchial smooth muscle is not dependent primarily on histamine release and does not respond effectively to antihistamines alone. and the family history of similar problems should yield sufficient information to classify the disease as atopic. with widening of the gap between endothelial cells and exposure of basement membrane surfaces.. This accelerates loss of plasma and plasma proteins from the vascular space and. they do not significantly alter histamine production or metabolism. and prudent glucocorticoid use may be necessary when other measures are insufficient to manage chronic conditions. with peak effects attained in 1 hour. certain drugs. at work). but there is also an important extra–mast–cell pool in the gastric mucosa. and it is inappropriate to subject the patient to extensive skin testing unless reasonable clinical evidence exists for atopy. histamine may cause severe bronchoconstriction in susceptible individuals. early use of glucocorticoids is appropriate for potentially disabling conditions that are self–limited and/or relatively short duration (seasonal flares of asthma.e. Its actions. but some blockers act considerably longer. Also indicative are seasonal symptoms (i. Signs and symptoms include: localized redness and swelling. are usually well absorbed from the gastrointestinal tract. pruritus. The history is more valuable than tests in determining whether a patient is allergic. The “triple response” is mediated by local intracutaneous histamine release. serum sickness. The specific homeostatic function of histamine remains unclear. given orally or rectally. and other organs. However. which may be a factor in histamine headache. lungs. A clouded or depressed state of consciousness implies dysfunction of the cerebral hemispheres. in deep coma. Either inadequate blood flow or a chemical change may alter the electrical activity. wallet. Obtundation. trauma and underlying diseases should be asked. unconsciousness may last somewhat longer. words moans. Concussion and psychologic disturbances impair consciousness without detectable structural changes in the brain. with a convulsive seizure. cardiovascular disease (especially stroke). Impaired consciousness may be brief or prolonged. the upper brainstem. alcohol. Pharmacologic differences among them are most apparent in their sedative. ingestion of drugs. antiemetic. hypertension). focal lesions in supratentorial structures may extensively damage both hemispheres or may produce so much swelling that the hemispheres compress the diencephalic activating system and midbrain. convulsions. Look for data in the patient’s personal effects such as: medical alert tags. or both. Glascow Coma Scale Infant 4 3 2 1 Eye Opening spontaneously to speech to pain no response Best Verbal Response coos. Metabolic or infectious diseases may depress hemispheric and brainstem function by a change in blood composition or a direct toxic effect.EDUCATIONAL GUIDELINES theses agents are only partially effective in reversing histamine–induced vasodilation and hypotension. pons. Stupor is unresponsiveness from which the patient can be aroused only briefly and by vigorous. Police can help to find relatives or associates.e.. antiserotonin. Coma is unarousable unresponsiveness. drugs. alcohol. purse or pill containers. headache. and cranial trauma should be sought. Altered level of consciousness includes patients with decreased level of consciousness as well as an increased response such as the violent or irrational patient. In addition to blocking the effects of histamine. and medulla). midbrain. mation (the extensive network of nuclei and interconnecting fibers found throughout much of the diencephalon. and in concussion. The patient’s family or friends may provide a history. Impaired consciousness may also be due to reduced blood flow (as in syncope or infarction) or a change in electrical activity (as in epilepsy). Brief unconsciousness occurs with syncope. The Glascow Coma Scale is used to help determine a decrease in level of consciousness. Hypersomnia (excessively long or deep sleep from which the patient can be awakened only by energetic stimulation) and delirium and confusional states also are states of impaired consciousness. mild or profound. or other toxic substances. The patient's age may be significant: epilepsy and systemic infection are frequently responsible in those less than 40 years. and in their anticholinergic. reduced alertness. and diagnosis requires an orderly approach. is usually combined with hypersomnia. repeated stimulation. Initially. The patient may be wearing a tag or carrying a diagnostic card in his wallet. incontinence. Signs of hemorrhage. many antihistamines have other therapeutic uses. and local anesthetic properties. or poisons should be examined and saved (for chemical analysis and possible legal evidence). diabetes mellitus. infections. up to 24 hours.grunts incomprehensible no response no response Best Motor Response spontaneous obeys commands localizes pain localizes pain withdraws withdraws flexion flexion extension extension no response no response Child/Adult 4 3 2 1 5 4 3 2 1 6 5 4 3 2 1 5 4 3 2 1 6 5 4 3 2 1 The alert state with normal mentation requires an intact interaction between the cognitive functions of the cerebral hemispheres and the arousal mechanisms of the reticular for- 2/15/06 . Prolonged unconsciousness usually results from severe intracranial or metabolic disorders. heart disease. nephritis. The cause of unconsciousness often is not immediately evident. food or drug ingestion. causing brainstem damage. Observers or relatives should be questioned about the mode of onset or injury. Containers suspected of having held food. even primitive avoidance reflexes may be absent. and other CNS effects. Specific questions about abnormal motor movement.babbles obeys commands irritable cries confused cries to pain inapprop. Primary subtentorial (brainstem or cerebellar) lesions may compress or directly damage the reticular activating system anywhere between the level of the midpons and (by upward pressure) the diencephalon. metabolic disorders (diabetes E-7 ALTERED LEVEL OF CONSCIOUSNESS/ ALCOHOLISM Altered level of consciousness may occur from many sources. and previous illnesses (i. The airway must be patent and blood pressure supported before a detailed history or examination is undertaken. ANAPHYLAXIS The phrase anaphylaxis was first coined in 1902 when a second dose of sea anemone toxin caused a dogs death. A sensitizing antigen elicits an lgE antibody response in a susceptible individual.EMERGENCY MEDICAL GUIDELINES mellitus. but vitamin–free fluid intake over a period of several days or weeks (i. cyanosis or clubbing of the fingers and toes. Physical examination should note (1) temperature. cardiovascular. (5) ENT: escape of CSF or blood. (2) skin: color. and many develop a severe. (3) scalp: contusions or lacerations.e. due to this mechanism. Acute Wernicke's encephalopathy results from a failure to ingest thiamine. The term anaphylaxis refers to the physiologic events that follow.. vasodi- 2/15/06 . light–reactive with metabolic disorders. Acute Wernicke's disease is underdiagnosed and can be fatal. rigidity. stiff neck. Even suspected or borderline cases should receive parenteral thiamine. Severe cases show a striking elevation of peripheral pain threshold. acute reaction caused by the release of mediators from mast cells and basophiles. or metabolic. scarred or bitten tongue. or stuporous. (9) neurologic signs: paresis. hypoglycemia). (7) cardiovascular signs: apical rate and rhythm. With unconsciousness from a primary brainstem lesion. neurologic signs and symptoms first indicate involvement of one cerebral hemisphere. (4) eyes: pupil size and reaction to light. Then. or in women with hyperemesis gravidarum) can produce a similar deficiency. Continued carbohydrate ingestion gradually exhausts thiamine stores in critical areas of the thalamus and brainstem reticular formation. acetone. More than one organ system should be involved for the reaction to be considered anaphylaxis. the mammillary bodies and the dorsal gray matter of the brainstem. In addition to the partial ophthalmoplegia. oculocephalic reflex (“doll’s eye” response to head rotation). blood pressure in both arms. Typical examples of lgE-mediated anaphylaxis include the reactions to many drugs. reflexes. meaning without protection. hyper–or hypoventilation occurs with metabolic disease. breath odor (alcohol. correction of electrolyte abnormalities. confused. The neurologic appraisal provides the key to whether the disease is supratentorial. and initiation of general nutritional therapy including multivitamins. vestibular. because of enlargement of the mass and consequent shifts in brain tissues as a result of pressure changes. Characteristically in supratentorial mass lesions causing stupor or coma. paraldehyde. drowsy. fully developed cases should be treated as emergencies in the hospital under close supervision. clinical defects often appear in other cranial nerve functions. Delirium tremens often supervenes within a few days after beginning corrective treatment and abstinence from alcohol. sclerosis in peripheral vessels. subtentorial. insect stings. Symptoms and signs: Acutely ill patients develop nystagmus or partial ophthalE-8 moplegia and may become ataxic. ocular palsy. Treatment consists of immediately giving 50 to 100 mg thiamine IV before administering glucose–containing fluids. during oversights in postoperative care. The result causes acute abnormalities in the dorsal and medial thalamic nuclei. evidence of trauma or hypodermic injections (narcotics. The antigenspecific lgE antibodies then bind to mast cells and basophiles. The pupils are small and reactive to light with hypothalamic and pontine disease or narcotic poisoning. Most cases of Wernicke's encephalopathy have manifestations of nutritional deficiencies affecting other parts of the body as well. rashes. The physiologic responses to these mediators include smooth muscle spasm in the bronchi and gastrointestinal tract. character of the pulse. Anaphylaxis is a systemic. and gastrointestinal. and syncope). bitter almonds [cyanide]). (8) abdomen: spasm. respiratory. signs show progressive rostral–caudal deterioration indicating involvement first of the diencephalon and finally of the brainstem. fixed in midposition with midbrain damage or severe glutethimide overdosage. (6) respiratory pattern: hyperventilation. or diabetic or uremic retinitis. muscular twitching. fundic signs of papilledema. signs of cardiac decompensation. as can occur in dialysis patients. Subsequent exposure to the sensitizing antigen causes crosslinking of cell-bound lgE. The most common organs involved include the cutaneous. The most common precipitating condition is severe alcoholism. Breathing is Cheyne–Stokes (periodic) with hemispheric disease and irregularly irregular with pontomedullary disease. and normally reactive with hemispheric disease or psychogenic unresponsiveness.e. The term anaphylactic reaction usually refers to a type l hypersensitivity reaction with mast cell degranulation mediated by antigen binding of specific immunoglobulin E (lgE). postural hypotension. When mast cells and basophiles degranulate. convulsions. petechiae. insulin). pupillary and oculomotor signs are abnormal from the start. Confusion may be global or of the type characteristic of Korsakoff's psychosis (see below). delirium tremens) or hypoactivity (hypothermia.. resulting in mast cell (and/or basophile) degranulation. Autonomic dysfunction may appear either in the form of sympathetic hyperactivity (i. and other cranial nerve nuclei. and foods. The response was the opposite of prophylaxis and this was referred to as anaphylaxis. including the oculomotor. Cheyne–Stokes (periodic) breathing. Thiamine reverses these defects. dilated with anoxia or 3rd nerve compression. This should be followed by rehydration to restore blood volume. and uremia are more common after 40. corneal reflex. vascular sclerosis. histamine and newly generated leukotrienes and prostaglandins are released. sometimes fatal degree of autonomic insufficiency. The Wernicke–Korsakoff syndrome refers to the coexistence of Wernicke's encephalopathy and Korsakoff's psychosis. thereby treating flushing. urticaria. Diphenhydramine (Benedryl) and cimetidine (Tagamet) or ranitidine (Zantac) are an appropriate combination. hoarseness. The EpiPen automatic injector for adults delivers 0. Corticosteroids do not have an immediate effect on anaphylaxis but should be administered early to prevent a potential late-phase reaction (biphasic anaphylaxis). accompanied by pruritus and flushing. vasodilation. The oral route is less likely to cause a reaction. This can evolve rapidly into the following symptoms. Brochospasm that has not responded to subcutaneous epinephrine should be treated with inhaled beta2-adrenergic agonists. Cardiovascular . Laryngeal edema may present as stridor or severe air hunger. antagonizes effects of released mediators. Subcutaneous epinephrine should be administered into an unaffected extremity immediately.g. depending on the response. These physiologic events lead to the classic symptoms of anaphylaxis. symptoms usually occur within 2 hours.dizziness. hypotension. airway edema. conjunctiva pruritus.headache and seizure (very rare). Physicians sometimes are reluctant to administer epinephrine for fear of adverse effects. Alternate extremities when administering epinephrine. (e. Because hypotension is due to a dramatic shift of intravascular volume. evidence of respiratory failure mandates endotracheal intubation. epinephrine usually is well tolerated and is life saving. antagonizes the effects of the released mediators. Both an H1 and H2 blocker should be administered because studies have shown the combination to be superior to an H1 blocker alone in relieving the histaminemediated symptoms. Anaphylaxis is a medical emergency requiring immediate recognition and intervention. Adrenergic agonists . and abdominal cramping with nausea. In the acute setting. and the reaction usually is less severe. urticarial lesions.nasal congestion. Loss of voice may also be observed. and mucus hypersecretion may manifest as wheezing. and inhibits further release of mediators from mast cells and basophiles. pruritus. vasodilation. Anaphylaxis is a clinical diagnosis. palpitations. and hypoxic myocardial depression. and prevents further release of mediators. Cautious administration of cimetidine is recommended so as to not cause hypotension with rapid infusion. weakness. tracheotomy is required.Epinephrine maintains blood pressure. Position the patient supine. Epinephrine maintains the blood pressure. including fluids. and stimulation of sensory nerve endings. Neurologic . Hypotension often is the most difficult manifestation of anaphylaxis to treat. symptoms can be delayed in onset for several hours. rhinorrhea. Hypoxia can cause altered mental status. Severe angioedema of the tongue and lips may obstruct airflow. bronchospasm. the fundamental treatment intervention (after epinephrine) is aggressive intravenous fluid administration. stinger after bee sting). broken down by organ system: Cutaneous/ocular . the less likely an anaphylactic reaction will recur. flushing. Dopamine may also be required to maintain blood pressure. Intravenous access should be established. In rare cases. and albuterol. If the endotracheal tube cannot be passed because of severe laryngeal edema.. The first priority should be to assess the patient’s respiratory and cardiac status. Antihistamines . Hypotension (and resultant loss of consciousness) may be observed secondary to capillary leak. Symptoms usually begin within 5-30 minutes from the time the antigen is injected. Anaphylactic deaths correlate with delay in administration of epinephrine. chest pain. Hypotension and shock can result from intravascular volume loss.Block the effects of released histamines at the H1 receptor. increased vascular permeability.. Patients often initially describe a sense of impending doom.EDUCATIONAL GUIDELINES lation. and smooth muscle contraction in the bronchial tree and GI tract.urticaria. shortness of breath. The longer the interval between exposures. angioedema. syncope. stinger after bee sting). The source of the antigen should be removed whenever possible. such as albuterol. vitalize and administer supplemental oxygen as soon as possible. abdominal distention. Tachycardia is a compensatory measure for intravascular volume loss. vomiting.nausea. throat tightness. diarrhea. Respiratory . antihistamines. All other therapies are adjunctive. Increased permeability can result in a shift of 50% of vascular volume to the extravascular space in a matter of minutes. When the antigen is ingested. Gastrointestinal . cough. The source of the antigen should be removed if possible (e. RATIONALE The primary medication for acute anaphylaxis is epinephrine. corticosteroids. and myocardial dysfunction. though symptoms often can occur much faster. Antihistamine therapy should be considered adjunctive to epinephrine. Pay close attention to the airway and secure as needed. as with severe food allergy. both for administration of adjunctive medications and for intravenous fluids to maintain blood pressure if needed. The initial dose can be repeated as necessary. including flushing. Bronchospasm. and swelling. vomiting.3ml of E-9 2/15/06 . based on a history of acute exposure to a causative agent followed by the typical systemic manifestations. and diarrhea. cramps.g. However. vasodilation. weather. sub acute. The worst bronchospasm is usually about 4am.EMERGENCY MEDICAL GUIDELINES 1:1. and airway remodeling.g. sinusitis. One feature of asthma is the exaggerated response to numerous stimuli. profuse diaphoresis occurs. occurring within minutes of completing exercise. Approximately one half of all childhood asthmatics have a decreased or disappearance of symptoms by early adulthood. A detailed medical history should address if symptoms are due to asthma. and significant increases in humidity. airway inflammation. The mechanism of inflammation in asthma may be acute. The needle is delivered into the thigh automatically. Airflow obstruction can be caused by a variety of changes including acute bronchoconstriction. The nose is unable to condition the increased amount of air required for exercise. current medications and compliance (e. It can ob observed in any age based on level of underlying airway reactivity and the level of physical exertion. and nasal flaring. The inflammation also causes an associated increase in the existing bronchial responsiveness to a variety of stimuli. Pulse oximetry measurement is desirable in all patients with acute asthma to exclude hypoxemia. Asthma is the most common cause for hospitalization for children in the United States.. and the EpiPen Jr for children delivers 0. altered level of consciousness. particularly in athletes who breathe through their mouths. As the severity increases. air pollution. assess the severity of asthma and identify possible precipitating factors such as exposure to various allergens. breathlessness. In children. weather changes. heat loss from the airway. Some causes of acute asthma may be respiratory infections. assess supraclavicular and intercostal retractions. In susceptible individuals. 1:3 severe). The extent of reversibility of airway obstruction is based on structural changes in the airway due to longstanding inflammation. the patient increasingly assumes a hunched-over sitting position with the hands supporting the torso. The disease is believed to be mediated by either water loss from the airway. stridor. Specific historical factors are key in the assessment of acute asthma. Duration and precipitating factors are related to weather. In more severe cases. and the patient is willing to lie recumbent.3mg). and the presence of airway edema and mucus secretion also contributes to airflow obstruction and bronchial reactivity. 1:1 mild. Asthma incidence is increased in the very young and very E . chronic mucous plug formation. occupational exposure or medications. or a combination of both. wheezing. cyanosis. animal exposure. this inflammation causes recurrent episodes of wheezing.3ml of 1:2.g. old because of airway responsiveness and lower levels of lung function. or postnasal dripping during sleep. Two thirds of all asthma cases are diagnosed before the age of 18 years.000 epinephrine (0. The automatic injector is administered by taking off the cap and pushing the opposite end firmly into the upper lateral thigh.000 epinephrine (0. an inability to speak in complete sentences and wheezing. termed the tripod position. The pathophysiology of asthma is complex and involves 3 components. Common symptoms are cough. These episodes are usually associated with widespread but variable airflow obstruction that is often reversible either spontaneously or with treatment. last use of medications and the date of medication. In the most severe form of acute asthma. and chemical irritants.15mg). the patient assumes a sitting position. the patient may struggle for air and/or be bradypneic and be profusely diaphoretic.. particularly at night or in the early morning. shortness of breath with use of accessory muscles to breathe and sputum production. and the best airflow is at approximately 4pm.10 2/15/06 . Patients with mild acute asthma are able to lie flat. aspirin ingestion. The diaphoresis presents concomitantly with a rise in PCO2 and hypoventilation. intermittent airflow obstruction. dose of steroids). All patients with acute asthma should have oxy- ASTHMA The National Asthma Education and Prevention Program Expert Panel defines asthma in the following manner: Asthma is a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role. The diagnosis of asthma is made more often in children and young adults and is related to high levels of physical activity. The degree of airway hyper responsiveness generally correlates with the clinical severity of asthma. The hypoxemia of uncomplicated acute asthma is readily reversible by oxygen administration. The abnormal heat and water fluxes in the bronchial tree result in bronchoconstriction. exercise. or chronic. airway edema. If symptomatology becomes more severe. The upper airway is designed to keep inspired air at 100% humidity and body temperature at 37 degrees C. The patient should count to 10 before removing the pen to insure complete delivery of the medication. On physical examination the clinician may find the patient with accessory muscle use. need for medication. chest tightness and coughing. accessory muscle use. Inspiration-expiration ratio reveals prolongation of the expiratory phase (e. including cold and dry air. ED visits are decreased and mortality increased at night. support the likelihood of asthma such as with a family history. and bronchial hyper responsiveness. almost no breath sounds may be heard. possibly because of acid reflux. The patient should be instructed to obtain medical care immediately after injecting the EpiPen because additional doses of epinephrine and other therapy may be required. pleural fluid. CSF. influenza. OSHA 29 CFR 1910. In addition. Potentially infectious material is blood. or mouth – A cut with a sharp object covered with blood/OPIM Blood on intact skin is not an exposure! Bloodborne Pathogens cannot be transmitted by casual contact. sneezing. Glucocorticoids – The anti-inflammatory agent Methylprednisolne (Solu-Medrol) restores the beta2-agonist receptors in the bronchial smooth muscles and. any body fluid that is visibly contaminated with blood. gonorrhea. Ventolin) – When utilized together create a synergistic affect. Alpha-agonist effects increase peripheral vascular resistance and reverse peripheral vasodilatation. chlamydia. restore the response to beta2-agonists. Ipratropium . herpes simplex. HEPATITISA: Cause: Hepatitis A Virus Transmission: Fecal–Oral (enteric). peritoneal fluid. stool. saliva in dental procedures. amniotic fluid. scabies. tetnus. herpes zoster. semen. coughing. and vascular permeability. and has anti-secretory properties and inhibits secretions from glands lining the nasal mucosa and increases the duration of bronchodilation. urine. It has little effect on the heart rate. Glucocorticoids are indicated if response to the first or second beta2-agonist inhaler treatment is incomplete. and less than 92% signifies severe asthma. measles.EDUCATIONAL GUIDELINES gen saturation measured by pulse oximetry. This is the best treatment of choice if bronchospasm does not improve after 2-3 treatments with inhaled beta-2 agonists. thus increasing airflow and ventilation. rubella. sweat. vomitus. meningococcal meningitis. 92-97% constitutes moderate asthma. In controlled studies. vaginal secretions. it decreases inflammation. By reversing increased capillary permeability and suppressing activity. The mainstay of therapy for acute asthma in the pre-hospital setting is inhaled beta2-agonists. The following is intended to be utilized as a quick reference guide only! Please refer to your departmental Bloodborne Pathogens/Infection Control Program for more in–depth information on this topic. Ipratropium demonstrated the most consistent efficacy in children and smokers. Bronchodilators – Their primary action is to decrease muscle tone in both the small and large airways in the lungs. therefore. Albuterol (Proventil. Epinephrine .Ipratropium is chemically related to atropine. Infectious Diseases: Hepatitis A Virus (HAV) Hepatitis B Virus (HBV) Hepatitis C Virus (HCV) Hepatitis D Virus (HDV) Hepatitis E Virus (HEV) HIV/AIDS TB Other infectious diseases include chicken pox. Solu-Medrol – is used for treatment of inflammatory reaction. Ipratropium (Atrovent) and Albuterol (Proventil. diphtheria. synovial fluid. EXPOSURE DEFINITIONS: – A contaminated needlestick injury – Blood/OPIM in direct contact with the inner surface of the eye. Ventolin) – Is a bronchodilator utilized to reverse airway obstruction due to asthma. Oxygen saturation of 97% or above constitutes mild asthma. nose.11 2/15/06 BLOODBORNE PATHOGENS .1030 NFPA 1581 Ryan White CARE Act Needlestick Safety and Prevention Act RATIONALE The goals of therapy are to maintain Sa02 greater than 92% and treat dehydration if it is clinically apparent. and any unfixed human tissue or organs. In children. syphilis. or nasal secretetions unless they contain gross visible blood. mumps.(SQ administration or Epi-Pen)Patients who respond poorly or not at all to an inhaled beta-agonist usually respond to epinephrine subcutaneously. pericardial fluid. information may be obtained from the following documents. Beta-agonist activity of epinephrine produces bronchodilatation. systemic hypotension. food/waterborne Incubation: 15–50 days E . The onset of action of steroids is approximately 4 hours in children and 6 hours in adults. pertussis (whooping cough). pulse oximetry is used to grade severity of acute asthma. saliva. food or water. vomiting. nausea. hemoptysis. diarrhea Prevention: Universal Precautions Avoid touching mouth with contaminates Note: This virus is the chief cause of enteric NANB Hepatitis HIV/AIDS: Cause: Human Immunodeficiency Virus Transmission: Bloodborne.12 2/15/06 . fatigue. perinatal Incubation: 14 to 180 days Vaccine: No Signs/Symptoms: Jaundice. nausea. vomiting. vomiting Prevention: Universal Precautions Note: Hepatitis D requires HBV for replication HEPATITIS E: Cause: Hepatitis E Virus Transmission: Fecal–Oral (enteric) Vaccine: No Signs/Symptoms: Jaundice. breast milk Vaccine: No Signs/Symptoms: May not be apparent for years Loss of appetite Weight loss Fever Fatigue Night Sweats Skin rash or Lesions Diarrhea Swollen lymph nodes Decreased WBC’s S&S of Opportunistic infections Prevention: Universal Precautions TB: Cause: Mycobaterium Tuberculosis Transmission: Exposure to Airborne Particles Incubation: 4–12 weeks Vaccine: No Signs/Symptoms: Cough. chest pain. sexual contact. sexual contact Transmission: Vaccine: No Signs/Symptoms: Jaundice. fever hoarseness Prevention: Universal Precautions Fitted HEPA Mask Surgical or Oxygen mask for Patient Do not recirculate air. vomiting Prevention: Universal Precautions HEPATITIS D: Cause: Hepatitis D Virus Bloodborne. abdominal pain. vomiting Prevention: Vaccination Universal Precautions HEPATITIS C: Cause: Hepatitis C Virus Transmission: Bloodborne. sexual contact. fatigue. perinatal Incubation: 45 to 180 days Vaccine: Yes Signs/Symptoms: Jaundice. diarrhea Prevention: Universal Precautions Vaccination where contact with virus is likely Avoid touching mouth with contaminates HEPATITIS B: Cause: Hepatitis B Virus nausea. nausea.EMERGENCY MEDICAL GUIDELINES Vaccine: Yes Signs/Symptoms: Jaundice. OPIM. perinatal. nausea. fatigue. E . abdominal pain. fatigue. sexual contact. fatigue. abdominal pain. fatigue. abdominal pain. use exhaust vents Open windows Engineering and Work Practice Controls: Transmission: Bloodborne. abdominal pain. weight loss. Chronic bronchitis is defined in clinical terms and emphysema in terms of anatomic pathology. the small (peripheral) bronchioles. The respiratory bronchioles display a inflammatory process. Chronic bronchitis is defined clinically as the presence of a chronic productive cough for 3 months. measles.O. Currently COPD is the fourth leading cause of death in the U. lumen occlusion by mucous plugging. High Risk Factors: Homosexual and Bisexual Men Heterosexuals who have contact with infected persons Multiple sexual partners Infants of mother who are infected IV Drug Users Recipients of Blood or Blood Products N.I. This form is associated with cigarette smoking and is the most severe in the upper lobes. The cough is usually worse in the mornings and produces a small amount of colorless sputum. and dyspnea. CHRONIC BRONCHITIS Mucous gland enlargement is the histologic hallmark of chronic bronchitis. inflammation. This type is the most severe in the lower lung zones. These changes. diptheria. needleless devices.S. 95 Standard: It is MANDATORY that the N–95 fitted masks be used in the following situations: Known or suspected TB. drinking. bronchiolar abnormalities are most responsible for the deficit in lung function. disinfection with a 1:10 bleach solution. cause airflow limitation by allowing airway walls to deform and narrow the airway lumen. when emphysema is mild. handling contact lenses and lip balm are prohibited in the work areas where there is a reasonable potential for occupational exposure. particularly during exertion. The second type involves the entire alveolus distal to the terminal bronchiole. and may be partially reversible. The structural changes described in the airways include atrophy. rather than bronchiolar disease. COPD is defined as a disease state characterized by the presence of airflow obstruction due to chronic bronchitis or emphysema. eating. bronchoconstriction due to inflammation accounts for a limited amount of reversibility. combined with loss of supporting alveolar attachments. The third type is the least common form and involves distal airway structures. The first type is characterized by focal destruction limited to the respiratory bronchioles and the central portions of acinus’s. variable amounts of airway smooth muscle hyperplasia. intervals between acute exacerbations become shorter. cilia abnormalities. Breathlessness is the most significant. EMPHYSEMA Emphysema has 3 patterns. A productive cough or an acute chest illness is common.H. smoking. may be accompanied by airway hyper reactivity.EDUCATIONAL GUIDELINES Handwashing. cleanliness such as physical removal of dirt and debris. and sacs. In advanced E . Anorexia and weight loss often develop and suggest a worse prognosis. Wheezing may occur in some patients. Most patients with COPD have smoked at least 20 cigarettes per day for 20 or more years before the onset of the common symptoms of cough. during each of 2 consecutive years (other causes of cough being excluded). Although airflow obstruction in emphysema is virtually irreversible. With disease progression. The airflow obstruction generally is progressive.13 2/15/06 . and distortion due to fibrosis.S. PPE. accompanied by destruction of their walls and without obvious fibrosis. CHRONIC OBSTRUCTIVE PULMONARY DISEASE Both emphysematous destruction and small airway inflammation often are found in combination in individual patients. CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) / CHRONIC BRONCHITIS / EMPHYSEMA Chronic obstructive pulmonary disease (COPD) is a devastating disorder that causes exorbitant human suffering. is the mechanism of airflow limitation. and the lung parenchyma. smooth muscle hyperplasia. mumps. or patients who have a blood tinged productive cough. When emphysema is moderate or severe. Pathological changes in COPD occur in the large (central) airways. By contrast. alveolar ducts. and bronchial wall thickening. sputum. Respiratory rate increases proportional to disease severity. meningitis. sterilization with an autoclave or chemical sterilant. loss of elastic recoil. biohazard waste containers. chicken pox. Use of accessory respiratory muscles and paradoxical in drawing of lower intercostal spaces is evident. cyanosis and right heart failure may occur. Emphysema is defined as An abnormal permanent enlargement of the air spaces distal to the terminal bronchioles. Clenched fists 2. acrophobia (heights) or aviophobia (flying). g.14 2/15/06 . Thoracic exam reveals hyperinflation (barrel chest). accelerated decline. anti social personality. Albuterol is also a beta-agonist for bronchospasm refractory to epinephrine. Albuterol (Proventil. When administered concurrently with albuterol creates a synergistic effect. The predictors of mortality are aging. 1. Sitting on edge of seat. Ipratropium (Atrovent) . The following protocol is adopted to deal with this possibility. restore the response to beta2-agonists. E . e. Bronchodilators .In acute exacerbation. Speech pattern 1. Oxygen reduces mortality rates in patients with advanced COPD because of the favorable effects on pulmonary hemodynamics. b. Initiate preventative measures to reduce potentially combative patient’s anxiety. d. Recognize behavioral clues to potentially violent behavior. The onset of action of steroids is approximately 4 hours in children and 6 hours in adults.Chemically related to atropine. Ventolin) . Give honest answers to questions RATIONALE The goals of pharmacotherapy are to reduce morbidity and prevent complications. moderate to severe airflow obstruction.Recognize potential etiologies of combative behavior and carefully evaluate each patient prior to transport.is used for treatment of inflammatory reaction. History of psychotic or other psychiatric disturbances. By reversing increased capillary permeability and suppressing activity. organic brain syndrome. cyanosis. diffusely decreased breath sounds. Easily startled 5. The primary cause of COPD is exposure to tobacco smoke. Biting 3. Most patient will benefit from this treatment. 2. c. Seizure activity. Glucocorticoids . f. Overly animated 5.Severe claustrophobia. Tightening of jaw muscles 4. COMBATIVE PATIENTS The transport of combative and potentially combative patients can be a stressful and dangerous experience for Ground and Air Medical Crew members. OXYGEN . c. and overall poor functional capacity. Solu-Medrol . Reassure patient b. Acute psychotic crisis. The anti-inflammatory agent restores the beta2-agonist receptors in the bronchial smooth muscles and. or potential for seizure activity. Loud 3. continued smoking. elevated JVD and peripheral edema are observed. a. and wheezes frequently are heard on forced and unforced expiration. poor bronchodilator response. h. Beta Adrenergic Agonist & Antocholinergic Agent Combination .These agents act to decrease muscle tone in both small and large airways in the lungs. Rapid 2. and prolonged expiration. by increasing duration of bronchodilation by albuterol. severe hypoxemia. b. Excessive talking 7. development of cor pulmonale.EMERGENCY MEDICAL GUIDELINES disease.S.COPD commonly is associated with progressive hypoxemia. Hypoxia. threatening the safety of all EMS personnel. it decreases inflammation. a. when administered early in treatment modalities. a. Glucocorticoids are indicated if response to the first or second beta2agonist inhaler treatment is incomplete. Motor Activity 1. Smoking cessation continues to be the most important therapeutic intervention. or overdose. History of involvement in a violent situation. Disorientation in an elderly patient. Pacing 3. Acute exacerbation of COPD is 1 of the major reasons for hospitals admissions in the U.Head Injury or other central nervous system insult. Spitting 7. Alcohol or drug intoxication. Emotional lability 8. Has anti-secretory properties. Posture 1. therefore. Shrill 6. presence of hypercapnia. wheezing. Expressions of anger.(Alupent & Atrovent) Combines the effects of the rapid onset with prolonged action. carbon monoxide poisoning. Coarse crackles beginning with inspiration may be heard.Relaxes bronchial smooth muscle by action on beta 2-receptors with little effect on cardiac muscle contractility. steroids improve symptoms and lung functions over time. dementia. Abusive 4. thereby increasing ventilation and airflow. Excessive fidgeting 6. withdrawal. d. Strong consideration should be given to restraining all intubated patients. Look for potential etiologies and correct 1.. Do not yell at patient. Pharmacologic restraints may be used if physical restraints are not sufficient. Neuromuscular blocking agents (never give without prior sedation in a conscious patient unless its an emergency). Respiratory assistance and/or intubation may become necessary with sedative agents. Check distal extremities periodically (q 15 minute pulses). All pharmacologic agents that can cause respiratory depression. h. d. and land at the nearest appropriate airport. If a Medical Crew Member has any doubt regarding the safety of transporting a potentially combative patient by ground or in the air. a. 1. 1. Hypoxia. 2. Protect airway from aspiration. ventilator patient or cervical spine injury). Approach patient in a slow deliberate manner. Rayon webbing strapped across chest and legs. Antipsychotics: Haldol may be used for acute psychosis. declare an emergency if needed. Speak softly and calmly around patients.e. Sugars. Avoid compromising circulation by restraining too tightly. Restrain limbs at a comfortable angle. or if continued combativeness may interfere with deliverance of proper medical care or may cause further harm to the patient (i.. This also allows the medical crew to discuss patient’s condition without being overheard. c. May be combined with a sedative agent for better overall effect. i. must be documented on the (PCR) Patient Care Report. Respiratory status must be carefully monitored if these agents are used. a. the pilot should notify A. Excessive environmental stimulation. (Air Traffic Control). b. b. 3. 1. Use of mechanical or pharmacologic restraints. g. 4. b. 6. Frequently complications involve ketoacidosis and hypoglycemia. The complications of this disease are numerous. Diabetes Mellitus is characterized by decreased insulin secretion by the beta cells of the islets of Langerhans in the pancreas. e. Midazolam (Versed). the following steps should be taken. Law enforcement back up should be requested to assist in restraining after landing. 1. 5. En route considerations. c. If an unrestrained patient suddenly becomes combative in the air and cannot be controlled. (All 4 limbs) a. Do not use any padding under restraints as this may reduce efficiency. Vercuronium Bromide (Norcuron). Glucose. c– spine injury). DIABETES MELLITUS By far one of the most common emergencies you can expect to treat will involve diabetes. “Hard” extremity restraints.15 2/15/06 . c. The following physical restraints are authorized for use if (a) above does not work or apply.e. and is mandatory with all neuromuscular blockading agents. Morphine Sulfate. 3. (apply before transport if at all possible). (either for the patient or themselves) they should obtain the appropriate medical or law enforcement assistance and immediately notify the receiving facility physician of their concerns.EDUCATIONAL GUIDELINES c. 2. also called dextrose. Diazepam (Valium). also called carbohydrates. All pharmacologic agents are used by protocol only. a. or both. Be respectful of patients (small) personal space. b. Any patient whose physical activity will hinder the delivery of good patient care or cause further injury to him/herself should be restrained (i. 3. 2. 2. Safety must always take first priority in all transports.T. All combative patients will be transported by a two (2) person (minimum) medical crew. is a simple sugar required by the body to produce energy. Lorazepam (Ativan). Any unconscious patient who may awaken in flight should be restrained prophylactically. calm direction 4. These patients must be restrained at all times. are one of the three major food sources used by the E . Use earplugs to reduce noise stimulation to patient. Shock. Micellaneous considerations. If patient vomits turn patient on his/her side and suction as needed. Sedative agents. Respiratory status must be carefully monitored.C. All “criminal” patients who are accompanied by a law enforcement agent shall also be restrained with handcuffs if possible. c. Should a patient become combative. f. Give firm. organic brain syndrome or senile dementia / disorientation. However. usually begins later in life and tends to be associated with obesity. Type 1 diabetes. Without insulin. intravenous access. The rate at which glucose can enter the cell is dependent upon insulin levels. The glucose level at which an individual becomes symptomatic is highly variable. drinks alcohol. In its early stages. The mainstay for hypoglycemia is glucose. the patient may awaken and not desire transport. Insulin acts as a messenger. Type 11 diabetes can often be controlled without using insulin and by adjusting diet. Generally. Kussmaul respirations may also occur (deep. allowing glucose to enter the cell. Coma is not uncommon. oxygen. Hypoglycemia is an urgent medical emergency as a prolonged episode can result in permanent brain injury. lasting 12 to 24 hours. and malaise. warm skin and mucous membranes. This results in osmotic diuresis. Thiamine . is suffering from infection. Therefore. Glucose Supplement . When released by the pancreas. Dextrose is absorbed . it travels through the blood to tissues. vomiting.Vitamin B1. Persons not previously diagnosed as diabetic will occasionally present in ketoacidosis. When these start to accumulate classic findings of diabetic KETOACIDOSIS appear. hypoglycemia can develop quickly. and weakness. Ketoacidosis is often associated with infection or decreased insulin intake. or insulin dependent diabetes. and repeated blood glucose readings prior to and after administration of dextrose. harmful by-products such as ketones and acids are produced. The onset is slow. Ketoacidosis is often called DIABETIC COMA. It may aid in minimizing liver glycogen depletion and exert a protein sparing action. The patient may also experience a seizure or become comatose. Hypoglycemia can occur if a patient accidentally or intentionally takes too much insulin. he or she may display inappropriate anger or a variety of bizarre behaviors. Treatment should include ABC’s. has activity changes. eats an inadequate amount of food. rapid). In the early stages of hypoglycemia.This agent is used to restore the patient’s serum glucose levels. lies at the other end of the spectrum from diabetic ketoacidosis. Thiamine is indicated when giving E . overdoses. HYPOGLYCEMIA. If allowed to continue its progression.Carbohydrate.16 2/15/06 . It provides a source of carbohydrate calories. marked dehydration. Diabetic ketoacidosis is characterized by nausea. Deep respirations begin as the body tries to compensate for the metabolic acidosis as cellular glucose-depletion continues. The clinical signs and symptoms of hypoglycemia are many and varied. sometimes called INSULIN SHOCK. Diabetes mellitus results from inadequate amounts of circulating insulin. RATIONALE Treatment of hypoglycemia consists of correcting the glucose deficiency and directing further treatment to the underlying cause. This can result in serious brain damage or death. an unconscious patient or any patient with altered mental status. Type 11. Dextrose . urination. Once reaching its destination. transport for evaluation should always be encouraged to determine the underlying cause. The hyperglycemic patient ultimately needs insulin. Obtaining a blood sample for glucose check is performed in the case of infants and pediatrics as part of their baseline vital signs. or becomes dehydrated. The breath may have a sweet or acetone-like character. the patient may appear restless or impatient or complain of hunger. stored and utilized by tissues immediately. or noninsulin dependent diabetes. insulin combines with specific insulin receptors on the surface of the cell membrane. tachycardia. In contrast to diabetic ketoacidosis.EMERGENCY MEDICAL GUIDELINES body along with proteins and fats. Treatment by emergency personnel should be geared toward rehydration via fluid administration. Patients who have Type 1 diabetes must take insulin. Hypoglycemia occurs when insulin levels are excessive. When hypoglycemia is found and treated in the diabetic patient. the signs and symptoms include increased thirst. they begin to use other sources of energy. usually begins in the early years. Thiamine may also be appropriate if alcohol abuse is suspected. As cells become glucose-depleted. For the body to convert glucose to energy. The kidneys will excrete glucose in the urine taking water with it. the amount of glucose that can be transported into the cells is far too small to meet the body’s energy demands. In diabetes. sever metabolic acidosis occurs and coma ensues. a drop in insulin levels is accompanied by a steady accumulation of glucose in the blood. This is evident on examination by dry. the disease can be divided into two different categories. glucose must first be transported through the cell membrane. monitoring. An abnormal mental status is the most important. As the blood sugar falls lower. Physical findings may include diaphoresis and tachycardia. which in turn dehydrates the patient. excessive hunger. It can occur in patients who fail to take their insulin or who take an inadequate amount over an extended period. The most commonly seen abnormality is PVC’s. convulsions. Morphine is also useful for its vasodilating effects. normally excreted by the kidneys. you may be called upon to assist them. Massive hemorrhage can also occur with separation of arteriovenous fistulas. An arteriovenous shunt is a surgical connection between the arterial and venous systems. Complications may arise related to the venous access devices placed for chronic dialysis.EDUCATIONAL GUIDELINES intravenous dextrose to individuals with suspected or reported alcohol abuse. The site should not be used for routine IV access. Treatment of renal failure takes on of two forms: hemodialysis or peritoneal dialysis. Nitrates are effective by all routes. as measured by T waves on EKG.a function no longer adequately provided by the kidneys.Crystalloid. Exerts effects opposite of insulin on blood glucose. The internal fistula is located subcutaneous and will have a bruit that can be palpated. Useful when IV access is problematic. Pulmonary edema is frequent in renal failure and is usually due to volume overload. The best method to end the hemorrhage is by direct pressure and transport to the emergency department. Lactated Ringers should not be used because of its potassium content.9% Sodium Chloride . Consider pericardiocentesis if tamponade is suspected. Cardiac arrest may be due to hyperkalemia. Contact on line medical control for direction beyond immediate life threatening issues.17 2/15/06 . Glucagon . lethargy. to prevent sudden cardiac failure and second to allow carbohydrates to be adequately metabolized. such as proteins and fats.9% Normal Saline .These agents are used to reduce potassium levels. especially in the setting of pulse less electrical activity (PEA). IV Fluids 0. The two most common routes of access are external arteriovenous shunts or internal fistulae. Most medications used in pre-hospital care are used in the usual dosages. during or immediately after hemodialysis. SODIUM BICARBONATE . ELECTROLYTE SUPPLEMENTS . chest pain and dysrhythmias. the preferred regimen is small bolus doses (-200ml) with reevaluation for effect between doses. Complication of dialysis include hypotension. Antagonizes membrane effects of potassium. Another method for dialysis is via the peritoneum.It is utilized for fluid replacement because of its immediate expansion of the circulatory volume. or blood loss. and may even lapse into coma. E . An electrolyte solution of sodium chloride in water. Adjustments may need to be made in dosage or frequency of subsequent treatments to account for changes in metabolism and excretion secondary to renal disease. Consider pericardial tamponade. When used. Loop diuretics (Lasix) may be effective at promoting diuresis in patients with residual renal function. Dysrhythmias produced in response to dialysis can be caused by potassium intoxication. This process helps remove toxic substances from the bloodstream . RATIONALE In an immediately life-threatening emergency. Many people now have home dialysis units. Hemodialysis is a medical procedure whereby waste products. DIALYSIS Patients with chronic renal failure require dialysis to live.Redistributes extra cellular potassium into cells with 10-15 minutes. sepsis. treat hyperkalemia with IV calcium and bicarbonate. Patients with renal failure must undergo dialysis two to three times a week. Glucose Elevating Agent .These agents can act in the pancreas or the peripheral tissues to increase blood glucose levels. Vascular access must exist to dialyze the patient. Clotting of the shunt offistula can occur spontaneously. Hyperkalemia is the most common life-threatening emergency ion patients with ESRD. Hypotension due to dialysis is caused by dehydration. It can best be treated by hemodialysis. Its actions are two fold in vitamin depletion first. Elevates blood glucose levels by inhibiting glycogen synthesis and enhancing formation of glucose from noncarbohydrate sources. are removed by a machine. CALCIUM CHLORIDE .Pancreatic alpha cells of the islets of Langerhans produce this polypeptide hormone.Fastest acting drug to treat hyperkalemia (acts within Minutes). and disequilibrium syndrome. IV fluids should not be administered except for cases of frank shock. It can occur before. 0. Disequilibrium syndrome is characterized by cerebral symptoms in patients with severe renal failure. These patients may present with headache. Toxicity is potentially increased because of delayed excretion and higher blood levels. They may also develop from transient myocardial ischemia. personnel may use a hemodialysis access site for IV access with the precautions noted in procedures. The form must be accessible to EMS personnel. It occur in one percent or less of patients with hypertension. including the withdrawal or withholding of life–prolonging procedures. These include such things as pulmonary edema from left ventricular failure.Brady 3rd edition Paramedic Emergency Care. The original form should remain at all times in the patient’s home or with him when traveling.C. It states the kind of medical care an individual wants or does not want if unable to make his own decision regarding medical care. The form must have an effective date. or an incompetent adult through a health care surrogate who was previously chosen. Treatment should be directed at the primary problem. dissecting aortic aneurysm. The original pre–hospital DNRO should be located at the patient’s bedside table. 2/15/06 . or taped to the patient’s headE . Blood Pressures of systolic greater than 180 mm Hg/diastolic greater than 110 mm Hg require immediate intervention. Furthermore. It is important to note that in order to honor a DNRO it must be the properly completed original. A competent adult. The peak incidence in those aged 40-50 years. A patient’s signature is required in box “A” on side two of DOH form 1896 if the patient is competent. A properly executed DNRO must be signed by a physician who has determined that the patient is in a terminal condition or vegetative state with very little probability of recovery. because a DNRO serves as evidence that a physician has made a determination regarding the patient’s medical condition and that there is a mutual agreement regarding a course of treatment. Completion of this part of the form provides a convenient and rapid method for EMS personnel to determine that the form has been properly executed.. must occur in the presence of two subscribing witnesses who must also sign the form.S. An important point to remember in the management of the patient with any degree of BP elevation is to “treat the patient and not the number. you may encounter the form printed on white paper also. Patients with a true hypertensive emergency require careful titration of IV medications for good control and a smooth reduction of their BP. cardiovascular system. but not a living will. with the EMS Star of Life repeated on the bracelet. The signature of the patient on the DNRO form. In some cases a patient may be wearing a white DNRO bracelet. Physicians Desk Reference and E-Medicine Site A hypertensive emergency is a life-threatening elevation of blood pressure. hypertension often results from the primary problem. DO NOT RESUSCITATE ORDER (DNRO) Legislative authority for DNROs are provided for under chapter 765. The most common hypertensive emergency is a rapid unexplained rise in BP in a patient with chronic essential hypertension.104. A pre–hospital DNRO may be revoked at any time by the patient or designated health care surrogate pursuant to section 765. The DOH form 1896 is printed on yellow safety paper. and section 64–E. A living will may be executed by a perfectly healthy person or by one diagnosed with terminal condition. a copy of the form should be made available to the EMS provider to use when transporting the patient from his home to a health care facility. A hypertensive emergency is characterized by a rapid increase in diastolic blood pressure (usually >110 mmHg) accompanied by restlessness. However. EMS personnel may therefore honor a DNRO. has the right to be able to control decisions regarding medical care. and nausea and vomiting. Once the patient or surrogate or proxy or guardian has properly completed the DNRO form.18 HYPERTENSION SOURCE . Hypertension is a related factor in other emergencies. Both of these forms are acceptable provided they are properly completed. similar to a hospital bracelet. they should check the box stating “This DRNO has been properly completed” and sign on the designated line within the rectangular box located on the bottom half of side one of the DNRO form. Side one of the form must be signed by the patient’s attending physician. Florida Statutes “Health Care Advanced Directives”. if applicable. The three major organ systems affected by high BP are the CNS. or on the back of the patient’s bedroom door. The signature of the health care surrogate or court appointed guardian or proxy is required in box “B” on side two of the form if the patient is incapacitated or incompetent. confusion. usually when the hypertension is poorly controlled or untreated. blurred vision. there is a greater than 90% mortality rate with people who do not take control of acute hypertensive states. or a proxy or guardian. F. or the patient’s health care surrogate or proxy. nosebleed. toxemia of pregnancy.EMERGENCY MEDICAL GUIDELINES board or to the refrigerator door. In these cases. or guardian. and renal system. the copy is only for informational and charting purposes at the receiving facility.A. F. and cerebrovascular accident..” Hypertensive emergencies occur most commonly in middle-aged patients. The EMS Transportation Act (chapter 401) authorizes EMS personnel to honor a pre–hospital Do Not Resuscitate Order (DNRO) if the order is on a Department of Health Bureau of EMS (DOH) form and is presented to EMS personnel in a manner provided by DOH rule. banana.19 2/15/06 RATIONALE The BP should be lowered by up to 25% of the mean arterial pressure (MAP) over minutes to hours. and highly allergenic proteins. Latex allergy is increased in populations with chronic occupational exposure to latex. the prevalence of latex allergy is increased in persons with allergies to avocado. or nectarine. laryngospasm.Its use in hypertension is considered when the patient takes Lasix on a regular bases or is suffering with signs and symptoms of CHF. Latex is the milky fluid derived from the lactiferous cells of the rubber tree. Primarily inhibits the re-absorbption of sodium chloride Furosamide (Lasix) . The highest prevalence of latex allergy (20-68%) is found in patients with spina bifida or congenital urogenital abnormalities. It also contains a large variety of sugars. The third. Labetalol (Trandate) . The onset of labetalol is within 5 minutes with a target blood pressure of 160/90. which increases coronary blood flow. facturing process.Potent diuretic. Symptoms usually develop within 24-48 hours of cutaneous or mucous membrane exposure to latex in a sensitized person.Alpha and Beta-blocker. poorly regulated latex factories in tropical countries. Nitroglycerin . primarily as powdered. reduces incidence of myocardial infarctions and death. Patients with cerebral palsy. The administration of Lasix may avoid the administration necessity of more potent IV drugs. nonsterile examination gloves. blood pressure is reduced without reflex tachycardia. Patients with spina bifida also may have a genetic predisposition for latex sensitization. and peripheral edema. pulmonary edema. rhinitis. Cross-reacting antigens have been found between these fruits and latex. conjunctivitis. The incidence of minor and serious allergic reactions to latex began to rise rapidly among patients and health care workers. Protein content varies with harvest location and manu- . Type I allergy has been implicated clearly in intraoperative and intraprocedure anaphylaxis. Labetalol should only be administered with the patient in the supine position. or quadriplegia also appear to have increased risk of latex allergy. The pressure that was placed on manufacturing companies resulted in hundreds of new. and possibly inhalation of aerosolized particles with latex on their surfaces. Other patients with a history of multiple surgeries or other latex. decreasing cardiac workload. Symptoms generally begin within minutes of exposure. nucleic acids. peach. It is a result of mechanical disruption of the skin due to the rubbing of gloves and accounts for the majority of latex-induced local skin rashes. jugular vein distension. mental retardation. lipids. Symptomatic postural hypotension (incidence 58%) is likely to occur if the patient is tilted or allowed to assume the upright position with 3 hours of receiving labatalol. It may be used alone or in combination with other antihypertensive agents. peritoneal contact during surgery.EDUCATIONAL GUIDELINES Additional signs observed on exam may include seizure. and least common syndrome is immediate (Type I) hypersensitivity. chestnut. Labetelol should only be administered with the patient in a supine position. Latex allergy is present in 1-5% of the general population. Latex proteins vary in their allergenic potential. kiwi. BETA-BLOCKERS . Reinstitution of previously effective therapy in noncompliant patients may be all that is required. Finally. resulting in a typical contact dermititis. hypotension. Hypersensitivity symptoms may include: Pruritus of exposed skin and mucous membranes. including the HIV virus. and it can be fatal without emergent treatment. Lowers BP. coma. edema. More than 200 polypeptides have been isolated from latex. most serious. Because of alpha and beta blocking properties. Latex gloves were widely recommended to prevent transmission of blood-borne pathogens. and total peripheral resistance is decreased without significant alteration in cardiac output. The spectrum of clinical manifestations includes localized or generalized urticaria. ANTIHYPERTENSIVE AGENTS . Eight billion pairs of medical gloves were imported to the US in 1988. LATEX ALLERGY Allergy to natural rubber latex is increasingly common and serious in children and adults. and full-blown anaphylaxis. Latex exposure is associated with 3 clinical syndromes: The first syndrome is irritant dermatitis. Latex sensitazation can occur after skin or mucosal contact.Decreases coronary vasospasm.exposing procedures are also at increased risk relative to the general population. bronchospasm. hoarseness.These agents are used for exacerbations of hypertension. The second syndrome is a delayed (Type IV) hypersensitivity reaction. probably because of multiple medical procedures. LOOP DIURETICS . tearE . stupor. Also induces vessel dilation. papaya. It is found in 10-30% of health care workers.Potent agents with rapid onset. Common sources of latex exposure include but are not limited to tourniquets. most notably cytomegalo–. Medical procedures may cause reactions in sensitized providers or patients. Abortions may be spontaneous or induced. to a large number of women not having prenatal care.g. SPONTANEOUS ABORTION Abortion generally is defined as delivery or loss of the products of conception before the 20th week of pregnancy. Since in 60% of spontaneous abortions the fetus is either absent or grossly malformed. Early notification is key to their preparation. acute infection. For this discussion. Note the patient’s history of relevant allergies to medical devices or fruits. diabetes. Delivery between 20 and 38 weeks is considered pre–term birth. will be considered a Priority 2 patient. and the long bones of the limbs may perforate the uterus during evacuation. respiratory distress. and severe emotional shock. therefore all women six months or greater gestation will be transported in lateral position until delivery is imminent. and rubella viruses. Many viruses. and syringes. mucous membranes.EMERGENCY MEDICAL GUIDELINES ing. Prehospital providers should be aware of the risk of latex allergy in patients and providers. have been implicated as causes. Since a definitive placenta has begun to form with a more organized and larger blood supply. and in 25 to 60% it has chromosomal abnormalities incompatible with life. abdominal cramping. Major reactions in sensitized patients have been precipitated with latex medical equipment. the uterine cavity is obliterated and instrumentation is more likely to cause perforation. and shock. chronic nephritis. Latex-free resuscitation equipment must be available. especially crack. the size of a fetus at greater than 12 weeks of pregnancy makes it difficult to dilate the cervix enough to pass the fetus. spontaneous abortion may be a natural rejection of a maldeveloping fetus. but definitions vary. without prenatal care. About 85% of spontaneous abortions occur in the first trimester and tend to be related to fetal causes. hypothyroidism. Abortions per- RATIONALE Patients with known or suspected latex allergy who seek care for an unrelated medical condition or injury must be kept within a latex-safe environment to prevent serious complications. electrode pads. erythema. The complete suggested inventory list of supplies can be found on the following page. or airway (e. The receiving facility must be made aware of the need to completely avoid latex exposure to the patient during exams and procedures. or lacerated cervix. rhinitis. NPA. herpes–. ports. This distinction is made because more difficulties are encountered in treating late abortions. vomiting. It is important to note the number of pregnancies (gravida) and the number of live births (para) as part of the patient’s history. hypotension. The importance of uterine fibroids or retroversion and impaired corpus luteum function appears to have been overestimated. those occurring in the 2nd trimester usually have maternal causes. previous medical history of hypertension. and multidose vial tops. pre–existing heart disease or gravida 3 or greater. diabetes mellitus. Maternal factors that have been suggested as causes of spontaneous abortion include an incompetent. amputated. angioedema. 20 week of gestation. congenital or acquired anomalies of the uterine cavity. IV tubing. Search for and read Medical Alert-type bracelets. OPA. diarrhea. urticaria. or ET tubes). The National Institute for Occupational Safety and Health (NIOSH) recommends wherever feasible the selection of products and implementation of work practices that reduce the risk of allergic reactions. The cornerstones of treatment are epinephrine and H1 antihistamines..20 2/15/06 . 10 to 15% actually spontaneously abort. except they must be protected from further latex contact to avoid clinical deterioration. The history of latex allergy may be known or unknown. Systemic corticosteroids and H2 blockers may be useful. Spontaneous abortions occur without any instrumentation. A relationship to physical trauma has not been substantiated. An abortion is termed either early (before 12 week of pregnancy) or late (between 12 and 20 weeks). To rule out latex allergy that could worsen with further medical exposure. Further. OBSTETRICS/GYNECOLOGY Obstetrical emergencies are quite common in our area due E . See allergic reaction and or anaphylactic reaction rationales. After 12 weeks of pregnancy. Individuals may be exposed to latex through their skin. use of cocaine. bleeding is more likely. Any woman with known obstetrical problems. This includes all patients with spina bifida. Fetal bones have also begun to form. About 20 to 30% of women bleed or have cramping sometime during the first 20 weeks of pregnancy. nausea. review the patient’s history of activities/exposures immediately preceding any systemic allergic reaction. BP cuffs. catheters. Patients presenting with frank symptoms of Type I latex allergy are treated as any other patients with systemic allergic reactions. stethoscopes. which corresponds to a fetal weight of about 500 gm. Aortocaval compression syndrome can decrease cardiac output by 50%. is used as the limit for abortion. The Treasure Coast Guideline recommend providers carry a mobile container with complete latex free equipment. syncope. with symptoms and signs of infection and threatened or incomplete abortion—chills.. the abortion is incomplete. The patient is acutely ill. gastrointestinal tract lesions. shock. the uterus has contracted toward normal size. In ectopic pregnancy. Slightly greater than 50% of these deaths are stillbirths and the remainder occur in neonates up to the 28th day of life. with disseminated intravascular coagulation and progressive hypofibrinogenemia and possible massive bleeding when delivery finally occurs. 1/ 100 to 1/200 diagnosed pregnancies. Patients should be evaluated for unsuspected liver disease. in the cervix. The most common site of ectopic implantation is somewhere in a uterine tube. abruptio placentae. The incidence. ectopic pregnancy (10 to 25%).EDUCATIONAL GUIDELINES formed to save the pregnant woman’s life or health are referred to as therapeutic. the dead fetus syndrome may develop. In many cases (50%). If part of the products of conception is passed or if the membranes are ruptured. Interstitial (cornual) pregnancies have a somewhat longer course. hypothermia. inevitable. and the rupture is catastrophic. Critically ill patients may evidence bacterial shock (septic or endotoxic shock) with vasomotor collapse. Missed abortion occurs when the fetus has died but has been retained in utero 4 weeks or longer. Many pregnant women with morning sickness feel as though they are vomiting everything they ingest. ECTOPIC PREGNANCY Pregnancy in which implantation occurs outside the endometrium and endometrial cavity. oliguria or anuria. multiple Pregnancies. or after an abortion. it is estimated at 1/826. or present before conception. Risk factors can be categorized as inherent. but if they continue to gain weight and are not dehydrated. All pregnancies should be evaluated to determine whether there are or will be risk factors. After 6 weeks. and respiratory distress. hypotension. Hemorrhagic retinitis is a serious complication and indicates a grave prognosis: the mortality rate in such patients is 50%. ovary. dehydration. The usual signs include cramping and spotting. or occurring after conception. Intrauterine devices do not prevent ectopic pregnancies. Patients do not gain weight. Psychologic factors are prominent in this syndrome but do not lessen the danger. and antepartum. Untreated ectopic pregnancy is usually fatal. Physical examination HIGH RISK PREGNANCY Pregnancy in which the mother. Classifying pregnancies as high risk is an effective way to ensure extra attention to patients who need medical care the most. the abortion is complete. preeclampsia and eclampsia. Autopsies in such cases usually show severe necrosis in the central portion of the lobules or widespread fatty degeneration similar to that seen in starvation. and lower abdominal peritoneal irritation that may be lateralized. or induced abortion.e. and ketosis confirm that the vomiting is extensive.21 2/15/06 . i. and the cervix has closed. In these cases. In the USA. septic abortions were often associated with induced abortions performed by untrained persons using nonsterile techniques and were commonly called criminal abortions. Gradual hemorrhage from the tube causes pain and pressure. The symptoms are similar to those of threatened abortion. The incidence of septic abortion in the USA has fallen dramatically. Septic abortion develops when the contents of the uterus become infected before. pancreatitis. tubal implantation is caused by a previous tubal infection. is rising and is higher in nonwhites. kidney infection. If all of the products of conception are passed. Cornual pregnancies rupture between 12 and 16 weeks. In the USA before legalization of abortion. and intracranial lesions. but rapid hemorrhage results in hypotension or shock. Persistent hyperemesis gravidarum may be associated with serious liver damage. E . the condition is not hyperemesis gravidarum. spotting and cramping pain usually begin shortly after the first missed menstrual period. The incidence of high– risk pregnancy varies according to population. and peritonitis. incomplete. or complete. uterine tube. Weight loss. Perinatal mortality in the USA occurs in 17/1000 deliveries. since the uterine wall provides support and delays rupture. but much less rapidly than for maternal mortality in general. high temperature. shows signs of hemorrhage. Its likelihood increases with previous tubal disease. septicemia. or the abdominal or pelvic cavity. Spontaneous abortions may be threatened. Most perinatal deaths not directly due to congenital anomalies are associated with prematurity often accompanied by abnormal presentation. or newborn is or will be at increased risk for morbidity or mortality before or after delivery. intestinal obstruction. The dead fetus syndrome usually occurs only when the loss is in the 2nd trimester or later. fetus. The death rate for ectopic pregnancy has been falling. Inevitable abortion is intolerable pain or bleeding that threatens the woman’s well–being. Threatened abortion is any bleeding or cramping of the uterus in the first 20 weeks of pregnancy. or polyhydramnios. they usually lose weight. HYPEREMESIS GRAVIDARUM Malignant nausea and vomiting to the extent that the pregnant woman becomes dehydrated and acidotic. the uterus is usually asymmetric and somewhat tender on examination. during. placenta previa. since these conditions can cause vomiting. pedal edema or abdominal pain. 2/15/06 . During labor. intensity. If this condition is allowed to progress eclampsia will follow. patients who must be transferred for definitive care should have magnesium sulfate before transportation. In a first pregnancy. the amniotic and chorionic sac (the membranes) ruptures before labor begins. headache. This latent phase may be intermittent over several days or may last only a few hours. Patients with a blood pressure of 150/110 or with marked edema or albuminuria are considered to have severe preeclampsia. averaging 6 to 8 hours. and this therapy should probably be considered experimental. If the patient does not and if the fetus is at term. Labor usually begins within 2 weeks (before or after) of the estimated date of confinement. Eclampsia: Coma and/or convulsive seizures in the same time period. irritability. with irregular contractions of varying intensity that apparently ripen or soften the cervix. succeeding labors are shorter. usually in primigravidas and women with preexisting hypertension or vascular disease.EMERGENCY MEDICAL GUIDELINES PREGNANCY INDUCED HYPERTENSION Pregnancy induced hypertension is occurs when patients who are normotensive. In addition. Diagnosis of eclampsia or hypertension induced by pregnancy. A major complication of pre–eclampsia is abruptio placentae. visual pain. Keep in mind that during pregnancy the blood pressure will drop. without other etiology.22 eclampsic patient include: headache. The stimulus for labor is unknown. Magnesium sulfate should be administered before a visual pelvic exam of a patient with eclampsia accompanied by any of the warning signs due to the possible induction of a seizure in the patient. BUN and creatinine levels should also be obtained to rule out unsuspected kidney disease. Low– dose aspirin therapy has been tried as a preventive measure in high–risk patients. About 80 to 90% of patients with ruptured membranes go into labor spontaneously within 24 hours. she should contact her physician immediately. uric acid concentration. Signs of impending eclampsia in a severely pre– E . hyper– reflexia. labor is usually induced because of risk of infection. unresponsive edema. Both magnesium sulfate should be administered prophylactically if the patient is in labor. prothrombin time. epigastric pain. visual disturbances. and frequency. or albuminuria of greater than or = 1+ or whose blood pressure rises by 30 mm Hg systolic or 15 mm Hg diastolic (even though it does not reach levels above 140/90) must be considered to have preeclampsia. Criteria for Treatment: Headache. and amniotic fluid leaks through the cervix and vagina. Pre–eclampsia develops in 5% of pregnant women. Bloody show (a small amount of blood with mucous discharge from the cervix) may precede the onset of labor by as much as 72 hours. Circulating oxytocin secreted by the posterior pituitary gland may initiate labor. therefore 130/80 mmHg may be hypertensive for the patient. but no direct evidence supports this thesis. A latent phase. usually precedes actual labor. Any pregnant woman who develops a blood pressure of 140/90 mm Hg. edema of the face or hands. and partial thromboplastin time) should be obtained and any abnormalities corrected. protein in the urine and less frequently visual disturbances. All routine laboratory tests (CBC. Patients with eclampsia or severe preeclampsia should be transported rapidly but without the use of light or sirens due to the possibility of inducing a seizure. When a patient’s membranes rupture. contractions increase in duration. Eclampsia is defined as the occurrence of grand mal seizures with severe pre–eclampsia and may occur anywhere from the fifth month of pregnancy to the end of the first week after delivery. Pre–eclampsia will present with some or all of the following signs/symptoms: hypertension. hyperflexia all constitute a medical emergency. Systolic blood pressure greater than 140 mm Hg or a rise of 30 mm Hg above previous readings (prenatal) Diastolic blood pressure greater than 90 mm Hg or a rise of 15 mm Hg above previous readings (prenatal) NOTE: Blood pressures should be taken during resting state and not during contractions. or albuminuria. Delivery is the primary treatment for eclampsia. edema. develop a blood pressure of 140/90 mmHg or greater in pregnancy. electrolyte levels. apparently caused by vascular disease. abnormal weight gain. If untreated. Eclampsia develops in one out of two hundred pre–eclamptic patients and is usually fatal if untreated. the data on results are mixed. Occasionally. Pre–eclampsia is defined as development of hypertension with albuminuria or edema between the 20th week of pregnancy and the end of the first week postpartum. progressive contractions of the uterus that cause effacement and dilation of the uterine cervix. however. pre–eclampsia characteristically smolders for a variable length of time and suddenly progresses to eclampsia. NORMAL LABOR Labor consists of a series of rhythmic. urinalysis. The etiology of pre–eclampsia and eclampsia is unknown. labor usually lasts a maximum of 12 to 14 hours. since the disease process inevitably worsens at the time of delivery. Mild preeclampsia develops as borderline hypertension. One attempt at replacing the uterus may be made. which cuts off the supply of oxygenated blood from the placenta. Retroplacental bleeding occurs. infection. vacuum extractor. such as fibroids. Placenta previa occurs in one out of two hundred deliveries. Abruptio placentae develops in 0. para of greater than one. therefore blood loss may appear to be very small or could be massive. such as pregnancy induced hypertension. Administer high flow oxygen. painless vaginal bleeding begins late in pregnancy when the lower uterine segment begins to thin and lengthen and is followed by painless. Do not attempt to push to cord back into the vagina. Treat for shock and place in the shock position with the uterus displaced to the left. Possible sources of bleeding include uterine atony. if the loss is greater. In severe cases. place gloved hand into vagina with palm towards baby’s face. preexisting hypertension. 400 to 500 mL of blood is lost during delivery. Symptoms and signs depend on the degree of separation and blood loss. PROLAPSED CORD This condition refers to the situation in which the umbilical cord comes out of the vagina before the baby during delivery. LIMB PRESENTATION The presentation of an arm or leg through the vagina is an indication for immediate transport to the hospital. usually in multiparas or in patients with abnormalities of the uterus. The cause is unknown. Vaginal bleeding may be minimal. Preexisting conditions such as previous uterine surgeries can predispose a patient to this condition. Sudden. UTERINEINVERSION This conditions occurs when the uterus turns inside out after delivery. or it may encroach on the internal os (low implantation or marginal previa). from a few millimeters to complete detachment. UTERINERUPTURE This condition most often occurs at the onset of labor or can be caused by trauma. nausea or shock. signs of shock and hypotension. push the fundus with the palm of the hand toward the vagina.23 2/15/06 PROBLEMS WITH THE SECOND STAGE OF LABOR/THIRD TRIMESTER BLEEDING BREECH PRESENTATION The feet or buttocks present before the baby’s head. Place the mother in a knee– chest position or in a supine position the hips elevated and gently attempt to push the baby back up into the vagina to relieve pressure from the cord. Patients often report tearing sensation or constant area of specific pain. To replace the uterus. since the cord is compressed against the birth canal by the baby’s head. and maternal shock. Symptoms may include vaginal bleeding associated with pain.4 to 3. Form a “V” with the fingers on either side of the baby’s nose and push vaginal wall away until delivery of head is possible or until the receiving facility has taken over patient care. that inhibit normal implantation. This condition requires rotation of the fetus within the uterus prior to delivery and can not be handled in the field. Ordinarily. and possible use of forceps. Maintain a high buttocks position to prevent further presentation and transport immediately.5% of all deliveries. vaginal or cervical E . or an extremely short umbilical cord. Placenta previa frequently cannot be distinguished from abruptio placentae by clinical findings. Treat per the hypotension guideline. The baby is thereby in great danger of suffocation. Once the legs are clear. If head does not deliver within two or three minutes. Complete separation almost always results in death of the fetus. Separation can be either complete or partial. It is commonly caused by pulling on the umbilical cord while waiting on the placenta to deliver or from attempts to expel the placenta when the uterus is relaxed. correction of the problems if feasible.EDUCATIONAL GUIDELINES Various abnormalities of both 1st and 2nd stages of labor (problems of fetal distress. Noticeable contractions will cease and the uterus will be hard. Implantation of the placenta over or near the internal os of the cervix. Several factors may predispose a patient to this condition. PLACENTAPREVIA . Allow the buttocks and trunk of the baby to clear spontaneously. the reasons must be sought. the baby should be supported with hand and arm of the medic. All degrees of placental separation. Profound shock usually accompanies this condition. bright red bleeding. massive. or premature labor) require special investigation. PLACENTAABRUPTIO Placenta abruptio is premature separation of the placenta from the uterine wall. they include vaginal bleeding. and the blood may pass behind the membranes and through the cervix (external hemorrhage) or may be retained behind the placenta (concealed hemorrhage). bleeding disorders. evidence of fetal cardiac distress or death. if the attempt is unsuccessful cover the uterus with towels moistened in saline and transport the patient immediately. abdominal trauma. or cesarean section delivery by the delivering physician. The placenta may cover the internal os completely (total previa) or partially (partial previa). disproportions between fetus and maternal pelvis. Abruptio placentae may be confused with placenta previa. abnormal presentations. PROBLEMS WITH THE THIRD STAGE OF LABOR Maternal hemorrhage must be prevented during the 3rd stage. may occur. a tender and tightly contracted uterus. EMS clinicians must meet the patient’s needs for pain control with the judicious use of medications. The synergistic potential of benzodiazepines and narcotics or antiemetics is significant for respiratory depression. DEFINITION Analgesia is defined as a reduced state of awareness of painful stimuli and sensation. UNDERSTANDING THE PATIENT’S NEEDS Meeting the patient’s needs for pain control can improve patient care and satisfaction during an encounter with emergency pre-hospital clinicians. However. Paramedics must continue to monitor and assess patients during pain control and be prepared to intervene in the event of a complication. Proper pain medication can decrease heart rate. Elderly and pediatric patients in particular are at increased risk during analgesia. and the paramedic must be attuned to the need for pain management even in the patient who does not verbalize pain. Furthermore. The medications used for moderate to severe pain control carry the potential for respiratory depression. padding with pillows and blankets at the point of contact. Pre-medication vital signs. Analgesia is used to minimize pain. especially if traction is applied on the cord before the placenta is completely separated. including a reduction in normal activities. vasovagal episodes. Some patients perceive and verbalize pain differently. Opiates require careful titration to patient needs. or retained portions of the placenta. chronic pain patients are plagued by the unknowns associated with their pain and the long-term consequences of pain. including blood pressure. anxiety and blood pressure. with continued monitoring. work issues. traction and backboards can create tremendous discomfort for your patients. hear rate. When the placenta has dropped into the lower uterine segment and presents at the cervix. and to recognize patient or parental concerns related to treatment. hemorrhage will occur. Maintaining awareness of some patients’ drug-seeking behavior is also required in evaluating the need from pain control. interpretation and vocalization of pain vary considerably between patients. review of current medications and allergies. A brief history. family issues. Opiates are administered slowly and in small increments with adequate time for the sedative effects of the injected dose to be apparent before additional medication is given. The application of splints. patients have the right to pain control. to identify problems related to preexisting medical conditions such as the presence of any abdominal pain. PAIN MANAGEMENT Pain is the number one reason patients seek medical attention. SpO2. airway obstruction. ensure cooperation and comfort as well as reduce complications. the corpus may be depressed toward the pelvis to help push the placenta into the vagina. ice packs. If the uterus does not contract. In addition to the usual stresses of life. hypotension or a reaction to the medication(s) in use. hypoxemia. and mood disturbances or depression. since the primary mechanism for hemostasis within the uterus is contraction of myometrium. respiratory rate. ply acknowledging the patient’s pain and concerns. Maximize non-pharmacological methods of pain control prior to administering medications. Pain and anxiety are common side effects associated with both acute and chronic medical and trauma patients. as well as an assessment of cardiopulmonary status at the time of treatment are necessary to adequately provide for the safety of the patient. and simE . 2/15/06 . PREMEDICATION PATIENT ASSESSMENT All patients receiving intravenous pain medication require a rapid pre-medication evaluation to determine relative risk versus benefit. hypercarbia. POTENTIAL FOR COMPLICATIONS Complications can occur in the pre-hospital environment as a result of over-sedation. The use of pain medication requires continuous intravenous access until patient care is transferred to the emergency department.24 PAIN CONTROL Opiates administered intravenously provide primary analgesia. Unrelieved acute and or moderate to severe chronic pain and poor symptom control can lead to anxiety and irritability. EKG and temperature are documented. Patients who are currently taking sedative or opioids may also be at a greater risk for over-sedation. created by medications that allow patients to tolerate unpleasant situations while maintaining adequate respiratory function.EMERGENCY MEDICAL GUIDELINES lacerations. These methods can include transport in the position of comfort. loss of self-esteem. The paramedic must have good access to the intravenous line and medication port throughout on-scene time transport. Between 50% and 70% of patients with chronic pain have either secondary depression or anxiety. as well as a restricted social life. sleep deprivation. the uterus can be inverted if this procedure is done incorrectly. relationship issues. respiratory rate. a difficult airway. The perception. Paramedics are constantly challenged by having to move patients to stretchers from awkward positions. aspiration. hypoventilation. Comfort and compassion are mainstays of medical care and their importance cannot be overemphasized. Establishing pain levels will become the fourth vital sign. Monitoring the patient’s mental status is one of the most valuable indicators of the efforts of pain management. Determining the patient’s state of anxiety or pain prior to and after the administration of medication is critical. and the duration of action is about 20-60 minutes. patients should be assessed prior to administration of analgesics to establish a baseline of vital signs and level of mentation. The inherent limitations of and over-reliance on pulse oximetry as monitors of respiration have become evident with reports of unrecognized hypercarbia and delayed recognition of respiratory depression. which is primarily used to antagonize respiratory depression and central nervous system depression secondary to narcotic overdose. tion. vagal or anaphylactic reaction or diaphoresis. The increase in carbon dioxide levels does not stimulate an increase in respiratory rate. which include naturally occurring. but may mask impaired respiration or ventilation. particularly from the patient’s point of view. as well as outcome. Respiratory depression may occur when the pain is relieved and is no longer a stimulant. Patient observation and monitoring before. NARCOTIC ANTAGONISTS Narcotic Antagonists include naloxone hydrochloride (Narcan). ventilation and oxygenation until sedation is reversed or eliminated. Respiratory depression becomes significant when intervention is needed. PSYCHIATRIC EMERGENCIES Psychiatric emergencies stem from a wide range of disorders. Promoting patient comfort and reducing or eliminating pain are the responsibilities of all pre-hospital clinicians. in the intubated patient is an excellent monitor for adequacy of ventilation.EDUCATIONAL GUIDELINES Opiate and benzodiazepine antagonists. its use for purposes of detecting ventilatory depression and/or apnea has limitations. When dealing with a patient experiencing a psychiatric emergency. Monitoring of respiration. Sufficient time between doses is necessary in order to observe the effects of the agent and prevent and/or treat respiratory depression. Fixed doses of analgesic may not meet the individual patient’s needs in terms of pain management. and the patient may rely upon the less sensitive oxygen-driven. Symptoms of withdrawal include agitation. ventilation and oxygenation reduces the risk of negative outcomes associated with pain control. NARCOTICS Narcotics are divided into several classes. and drug and alcohol abuse. whether because of illness or pharmacological intervention.25 2/15/06 . Pulse oximeters do not detect apnea. are typically given supplemental oxygen and thus maintain adequate oxygenation despite inadequate ventilation. While the risk of adverse events is low. as well as any intervention taken by the paramedic. Onset of action is usually within 2 minutes. The paramedic must be prepared to immediately support the patient’s airway. The paramedic’s ability to use. along with any significant patient events such as nausea and vomiting. Keep these guidelines in mind: RESPIRATION MONITORING The primary cause of morbidity with pain control medications is drug-induced respiratory depression. interpret and act upon the data derived from the patient assessment and monitoring technology will help ensure a positive outcome for the patient. Opioids interfere with carbon dioxide chemoreceptors in the medulla by retention of carbon dioxide. including acute anxiety. Supplemental oxygen administration may reduce the risk of oxygen de-satura- GENERAL GUIDELINES To help the patient regain their sense of self–control. Repeat boluses may be required to maintain adequate blood levels until the opioid agonist is eliminated. The potency and duration of action between different classes varies widely. Anxiety relief via pain control using pharmacological agents are critical elements to improving patient comfort both mentally and physically. The patient record should document any clinical or technical problems during administration of medications. Capnography however. the Team’s priorities include providing for medical and psychiatric evaluation and managing aggression. respiratory distress. act E . while at the same time ensuring patient safety. hypertension. semi-synthetic opioids and synthetic opioids (nalbuphine). MONITORING Using additional personnel for monitoring does not replace continuous clinical evaluation and assessment prior to and during the administration of analgesic and antiemetics. Adverse reactions increase in frequency with the complexity of the patient’s illness or injury and the level of sedation. Hands-on monitoring should detect early signs of patient distress before compromises to vital functions occur. Patients at risk for respiratory depression. The paramedic must be diligent in recognizing early signs of distress and implement appropriate supportive or resuscitative measures. Opioids depress all phases of respiratory activity to some extent. such as naloxone and flumazenil respectively. depression. these medications do not instantaneously reverse the respiratory depression that may be produced in pain control. however. psychosis. sweating and irritability. respiration-regulation mechanism. While pulse oximetry is usually an excellent and noninvasive technology for monitoring oxygen saturation. during and after the administration minimizes complications. leading to significantly delayed recognition of hypercarbia. should be part of any sedation and pain medication array. This narcotic antagonist can precipitate acute withdrawal symptoms in opioid-dependant or addicted patients. Keep stance as relaxed and neutral as possible. tachycardia. call for help to subdue and restrain the patient. indifference. gastrointestinal complaints. Empathize with the patient about their situation and ask the patient for suggestion to help improve it. or death of loved ones increases the suicide risk. Remain calm and speak softly. who brought patient to hospital. and thought content (obsessive. or increased). remember that widowed. ask who or what he’s really angry with. If he’s unsure of their alternatives. normal. thought processes (normal. Agree with the real aspects of their anger (such as waiting a long line to see a doctor). not an impersonal target. as ordered. personal history of previous suicide attempts. intellect (slow. arrange for hospitalization and obtain psychiatric consultation. If patient complains vehemently. why patient wants help now. and monitor personal body language for signs of hostility. if possible. repetitive. fidgeting. or it can make the patient even more angry and violent. Provide suicide patient with psychologically and physically protective environment. giving the patient the Team’s undivided attention and maintaining eye contact. sense of impending danger. Perform a mental status examination. interpersonal relationships. DEALING WITH THE VIOLENT PATIENT The violent patient may take their anger out on the team. Review their complaints and restate what he’s said to try to identify their real concerns. listen carefully. Be aware of both verbal and nonverbal communication as facial expressions. Assure safety of patient and others by removing any items they could use to harm themselves or others. alcohol or drug abuse. Typical signs and symptoms include feelings of worthlessness. and establish rapport with the patient. in this situation. hopelessness. choking sensation. and that their behavior’s upsetting the team. Signs and symptoms of such an attack may include hyperactivity.26 DEALING WITH THE ACUTE PSYCHOTIC PATIENT Acute psychotic reaction. such as schizophrenic and paranoid episodes. provide emotional support and calmly direct the patient toward reality. Encourage the patient to express their concerns and to identify source of their anxiety. Keep in mind that suicidal thoughts represent an attempt to solve a problem. Try to involve their family or friends in this planning process. if a specific incident triggered it. mental or physical illness. DEALING WITH THE SUICIDAL PATIENT The suicidal patient typically has severe depression and low self–esteem and directs their anger inward. affect (flat. or confusion. or gestures can provoke a patient’s anger. and give medications. and history of past suicide attempt. insomnia and fatigue. Follow these guidelines to make sure the Team’s interactions are helpful and appropriate. and urinary frequency. as the primary caregiver. arrange for psychiatric consultation and/or hospital admission for observation. hyperventilation. Typical problems include job situation. and what patient expects from this visit. A patient with an organic problem (usually the result of metabolic or neurologic disorder) may be disoriented or confused and have recent. profuse sweating. sweaty palms. Obtain background information to help determine nature and severity of problem. did he choose a suicide method that was likely to succeed? When assessing for suicide potential. mental illness. and orientation to time. Assess patient’s anxiety level. Assist with diagnostic tests to help determine if an underlying physical condition is causing the psychiatric emergency. To decrease patients anxiety. decreased physical activity. in a nonthreatening way. phobic). Then assess their mood (their predominant emotion). normal or bright). Closely observe their body language. abstract thinking. memory (poor or good). Find out what events led to this condition. represent disorders of mood or thinking in which 2/15/06 . point out to the patient that their anger is only making it more difficult for the team and others to help the patient. debilitating physical illness. The Team’s response can calm the patient and help the patient cope. or hallucinatory). Try to find out what the patient thinks their problem is. financial problems. He may be demonstrating the behavior to obtain something he wants. sudden memory loss and decreased sensory perceptions. Is this a gesture—a way to manipulate others—or is it a real attempt at suicide? How upset or disturbed is the patient? If he attempted suicide. helplessness. sensation of chest pressure. preoccupied. but allow the patient some control of situation. inability to swallow.EMERGENCY MEDICAL GUIDELINES with decisiveness and compassion. association (normal. If their anger seems out of proportion to the situation. Help the patient set priorities. dry mouth. tone of voice. or loss of a loved one. Assess patient’s level of consciousness. Let the patient know that the Team members are people. delusionary. motor activity. tremors. and that a family history of suicide and a E . suicidal. compulsive. place and person. Keep these points in mind when dealing with a suicidal patient: Attempt to determine the patient’s suicide potential. or if he has no alternatives. Attempt to establish rapport with the patient to gain their trust and cooperation. divorced and single persons have a higher risk than married persons. Verbal abuse frequently precedes violent behavior. insight and judgment. loose or illogical). and determine if their judgment and insight are impaired by an acute anxiety attack. When in doubt. substance abuse. If the Team fears the patient may cause bodily harm. Speak to the patient firmly but calmly. confused. or access to their body. A patient having a schizophrenic episode typically has delusions. Move slowly and quietly. and well-being (ie. He typically believes that others are out to get him. Don’t try to convince the patient their delusions are wrong. sound clinical judgement. dignity.EDUCATIONAL GUIDELINES the patient loses contact with reality. Therefore. to protect patients and as part of approved protocol. If he’s violent or potentially violent. Restraints may be used in response to dangerous behavior. or catatonic behavior. Every effort should be made to utilize the least restrictive method of restraint. obsessive thoughts. place the patient in a quiet room. Documentation in the medical record should include clinical justification of the necessity for restraints and measures taken to protect the patient’s rights. but avoid validating their false beliefs. Their delusional system typically includes persecution feelings or excessive religious statements.27 2/15/06 . and disordered thinking. Give medications. Avoid closed doors or blocked doorways so that he doesn’t feel cornered. but also in which failure to use a restraint could result in injury to the patient or others. their use must be consistent with federal and state laws and most importantly. Use simple. Remain calm and authoritative. and place the patient in a hospital gown. observe for postural hypotension and pseudoparkinsonian effects. Obtain psychiatric consultation and arrange for hospital admission. let the patient stand near a door that’s slightly ajar. monitoring. Patients generally have a right to be free from restraints unless restraint is necessary to treat their medical symptoms or to prevent patients from harming themselves or others. let the patient verbalize distorted or illogical thinking. and interpersonal dealings deteriorate until they can no longer cope with the activities of daily life. When dealing with an acute psychotic patient. as ordered. before using restraints. affective responses. ALWAYS RESTRAINED If at any time a patient requires physical restraint. auditory hallucinations. poor associations. Speak to the patient firmly to assure the patient that the Team is in control of the environment. concrete language and brief sentences. RESTRAINTS Restraints are any physical or pharmacological means used ONCE RESTRAINED. and risk of physical and/or psychological injury resulting from restraints. Restraining a patient raises serious concerns. FOR A PATIENT WITH A SCHIZOPHRENIC REACTION: Determine if patient has been previously hospitalized and if he’s recently stopped taking major tranquilizers. such as infringement on patient autonomy. attention to patient’s needs). lines or tubes • Patients who are violent or could inflict potential harm to self or others due to an impaired psychological state • Allow assessment of disoriented and uncooperative patients or those under the influence of alcohol or drugs • Facilitate medically necessary procedures (ie. with false beliefs based on grossly exaggerated aspects of their life. and you should always consider whether alternatives to restraint are available. in addition to those described above. avoiding words or phrases that patient might misinterpret. and projective delusions. limits on freedom of movement. feelings of uniqueness or grandiosity. Instead. apply restraints. concrete expressions as the Team talks to the patient. and sit or stand on patient’s level to avoid appearance of power. A patient suffering from paranoia (a type of schizophrenia) may have the following signs and symptoms. reassessment. If possible. withdrawn. restlessness and agitation. the patient should remain restrained – in some manner – until delivE . bizarre gestures. as appropriate. Monitoring must be performed by direct observation of and interaction with the patient. combative. Their thought processes. Remove their clothing or any object that may conceal a weapon. and avoid arguing with the patient. if the Team gives phenothiazine. Examples of these situations include the following: • Patients with invasive catheters. FOR A PATIENT WHO’S PARANOID: Avoid any physical or psychological threats or challenges. gastric lavage) in uncooperative patients • Prevent elopement while patients are being evaluated and transported for potential suicidal or homicidal behavior • Protect disoriented patients from falls off stretchers and backboards • Patients with brain pathologies or injury • At the discretion of the flight crew to ensure flight safety • All prisoners Whenever restraints are employed. and use simple. activity. assaultive. Situations arise in which restraints are not only appropriate and necessary. clinicians must carefully weigh the benefits of the restraint against the risks of the restraint. claims of battery. Then intervene as follows: to restrict a patient’s movement. It should include a determination regarding the patient’s well-being as well as an on-going evaluation of the continued need for restraints upon arrival at the receiving facility. and kicking. • They can create injuries because they are not soft and padded. Restraint application is not a patient option. 2/15/06 . Patients may have injuries that result from being restrained. As soon as possible. lower. Personnel injuries can occur from violent behavior. Sedation could lead to drug interactions with adverse effects. more serious injuries can occur if restraints are inappropriately applied or the patient is not adequately monitored. Appearance of a team may convince a patient to permit application of restraints without resistance. For example. scratching. the following physical restraints are appropriate for the following situations: • Posey vests or sheet roles to prevent disoriented patients from climbing off stretchers. leather) to restrain violent patients • To ensure flight safety ALLOWANCE OF OPTIONS It is vitally important and therapeutic for all patients to be given as many options as possible. 4-point. In example “I need to make sure you’re safe and secure. The fact that restraint will occur does not change. spitting. upper. the patient should be given as many opportunities as possible to exercise some sense of control over the situation. • If not periodically cleaned and treated. This recognition of the need to allow options. A patient who vomits while in 4.EMERGENCY MEDICAL GUIDELINES ered to the emergency department. • They must be a non-locking variety to facilitate quick release. Do not allow the patient to bargain with you. compromising the patient’s ability to protect the airway. Pulse oximetry is helpful in measuring such patients. to restore a patient’s sense of selfcontrol. police. However. needles). USE OF LEATHER RESTRAINTS Leather restraints in the pre-hospital setting are obsolete and their use is strongly discouraged. or talk you into release of restraints. each team member is responsible for immobilizing one extremity. family and onlookers. firefighters. Uncooperative patients often provide inadequate histories. Once a clinician recognizes the need for restraint. At all times. E . Agencies currently utilizing leather restraints are encouraged to research and acquire soft. Most injuries are minor and include abrasions and bruises. Ideally. Be on the lookout for patients with concealed weapons or dangerous objects (ie. Oversedation could lead to loss of gag reflex. Side rails are not considered restraints by themselves. Patients who are being restrained after an overdose pose particular problems because the ingested substances often are unknown.(When was the last time you cleaned and treated your leather restraints?) • They are frightening to both patients. Would you prefer to be sitting up or lying down?” “Would you care for another blanket?” “Which arm would you prefer that I use for your IV?” The secret to offering patients options is this. STANDARDS When restraints are necessary. Giving patients choices and options helps them to begin regaining a sense of selfcontrol. does not change the fact that restraint is going to occur. full PPE will enhance personnel protection. disposable posey or Velcro type limb restraints as a superior alternative. practitoners must determine the most appropriate and least restrictive device that allows the patient to retain as much dignity as possible. a sense of normalcy. • They are bulky and slow to apply • They cannot be effectively anchored to afford a true medical restraint. • Soft wrist restraints to protect confused patients from extubating themselves • Limb restraints (ie. they become brittle and can break under stress. begin to allow patients as much control as you are comfortable with allowing. But. as long as it does not matter what the patient chooses. which presents increased possibility for allergic reactions. ems personnel) may be the best way to restrain a violent patient. Use caution whenever caring for patients in restraints. Emergency situations inflict an extremely frightening and threatening sense of loss of control upon the patients who experience them.28 COMPLICATIONS Complications from pharmacological sedation are more numerous than from physical restraints. Remember. restraint must be employed. however. offer them the option. A COOPERATIVE PATIENT WILL COOPERATE WITH RESTRAINTS. This team approach minimizes risk of injury to the patient and the crew. A team of several members working together (ie. such as biting. opposites. Although physical restraints generally are the first method employed when restraints are necessary. to improve the patient’s condition and encourage cooperation. soft.point restraints risks choking and aspiration. • They present a cross-contamination problem due to the material in which they are constructed. pharmacological restraints may be used as an alternative or adjunct to physical restraints. • Adult dose is 2-10mg IV. Can be given IV. just paralyzed. which commonly result in respiratory depression and loss of gag reflex.29 2/15/06 . 2. shivering may be prevented. Respiratory depression and impaired gag reflex are rare when used alone. exacerbation of glaucoma. respiratory and gag reflex. Appropriate use of restraints promotes patient and crew safety. and fetal damage.5mg over 60 years of age (may repeat once) initially over 2 minutes. They can hear and see everything going on around them. IM. ADVANTAGES OF CHEMICAL RESTRAINTS • Control violent behavior and patient agitation • May reduce need for physical restraints DISADVANTAGES OF CHEMICAL RESTRAINTS • May result in complications. Tachycardia 3. PRECAUTIONS • Patient dosing is very variable. When an airway cannot be secured by other means. • Adult dose is 1-4mg IV. Respiratory depression and loss of gag reflex usually do not result if recommended doses are used. More medication • may be administered if inadequate sedation results after initial dose. IO. Some signs of inadequate sedation or analgesia would be: 1. or intranasal titrated to effect • Onset of action is 5-10 minutes • Duration of action 4-8 hours • Adverse effects include exacerbation of glaucoma. neuromusclar blockade allows a patient to be more readily intubated. IM. Occasionally a patient may need to be given a muscle relaxant in order to prevent nerve damage during transport. • Onset of action is 1-5 minutes • Duration of action is 30-60 minutes Diazepam (Valium) is widely used for sedation. Midazolam (Versed) is commonly used for rapid sedation in emergency settings because of its rapid onset and brief duration of action. The intent of such medications is sedation for the duration contact until the patient arrives at the emergency department. Ventricular dysrhymias E . each situation in which use of restraints is considered must be evaluated carefully. Neuromuscular blockade is useful for a number of situations encountered in the prehospital setting. treatment of agitation secondary to alcohol withdrawal and treatment of seizures. but recently have become accepted for use in the prehospital setting for an aid in intubation.EDUCATIONAL GUIDELINES CHEMICAL RESTRAINTS Chemical restraints are any medications used for the purpose of restraining patients involuntarily to prevent them from harming themselves or personnel. Hypertension 2. Allowing 2 or more minutes to evaluate response. Lacrimation 4. Health care professionals can incur liability from inappropriate use of restraints and for failure to use restraints to protect a patient. CARE FOR THE PARALYZED PATIENT It is of paramount importance to remember a patient that has been given a paralytic is not unconscious. It has a high therapeutic-to-toxic ratio. Diaphoresis 5. In the past these medications have been reserved for use by anesthesiologists in the operating room. such as respiratory depression and loss of gag reflex • Limit mental status assessment and neurologic examination during sedation • Adverse effects include interactions with other s3edatives. and chest wall compliance may be increased through the use of muscle relaxants. or intranasal titrated to effect. Oxygen consumption is reduced. RAPID SEQUENCE INTUBATION (RSI) Rapid Sequence Induction (RSI). IO. • Adult IVP dose is 5mg under 60 years of age (may repeat once). IO. It will enable ventilation of patients who cannot be ventilated because of coughing or resisting ventilation attempts. IM or intranasal. • Onset of action is 1-5 minutes • Duration of action is 30-60 minutes Chemical restraints can be an effective adjunct or replacement for physical restraints. depression (especially when combined with other sedatives or narcotics). and paradoxical reactions. Monitor for respiratory depression and loss of gag reflex AGENTS Benzodiazepines Lorazepam (Ativan) is commonly used to sedate elderly patients and has a wide safety margin. Therefore adequate sedation and analgesia must be given. is the use of specialized medications to facilitate intubation and to provide for muscle relaxation. Duration of action is long. titrate slowly. cyanosis. There are many non–depolarizing agents in use today. and a variety of neuromuscular diseases. Signs and symptoms of renal failure are due to overt metabolic derangements resulting from inability of failed kidneys to regulate electrolyte. History and physical assessment may be lost when the patient is paralyzed. but the most commonly used one in the prehospital E .EMERGENCY MEDICAL GUIDELINES 6. closed head injuries. Succinycholine chloride is rapidly metabolized and normal neuromuscular transmission is restored in 5–10 minutes. Volume overload. Acetylcholine traverses the synaptic cleft and binds with receptors on the motor endplate causing a small endplate potential. It is important to remember these patients may also suffer from medical problems unrelated to their renal condition. An EKG may be helpful in diagnosis. depolarizing and non–depolarizing. With depolarizing neuromuscular blockade the medication binds to the acetylcholine receptors and creates a wave of depolarization that manifests itself as muscle fasciculation. PHYSIOLOGY OF NEUROMUSCULAR TRANSMISSION / BLOCKADE A wave of depolarization reaches the motor nerve terminal. starvation. Since paralyzed patients cannot swallow or cough. occurs when salt and water intake exceeds losses and excretion. electrolyte imbalances. There are no hemodynamic effects when used in clinical doses. carbon dioxide. The result of this increase in metabolism is excessive heat. Be sure to protect pressure points even during a short transport. or tachypnea. Increased pulmonary secretions. Whereas non–depolarizing muscle relaxants competitively antagonize acetylcholine and prevent depolarization of the muscle membrane. Severe hyperkalemia and cardiac arrest has been reported in patients with major burns. The condition is believed to be due to the decrease in calcium uptake by the sarcoplasmic reticulum resulting in increased intracellular calcium levels and the acceleration of aerobic and anaerobic cellular metabolic processes. and drugs are just a few of these factors. preexisting neuromuscular disease. setting is vecuronium bromide (Norcuron). No fasciculation is seen when non–depolarizing agents are used. Increased intragastric pressure with regurgitation may also occur. Medical direction via telemetry is always advised for treatment modalities other than immediate dialysis complications. Hyperkalemia is usually asymptomatic. This medication remains bound to the receptor and prevents subsequent binding of acetylcholine and neuromuscular blockade results. PARALYZED PATIENTS REQUIRE FULL VENTILATIONS. The most common cause of sudden death in patients with ESRD is hyperkalemia. Acidosis. and in patients with abnormally low pseudocholinesterase. If enough of these endplate potentials occur. both respiratory and metabolic. There are two types of muscle relaxants. Hypocalcemia is also potentially life threatening and re- COMMONLY USED MUSCLE RELAXANTS The most common depolarizing agent used today is succinycholine chloride (Anectine). Patients with ESRD commonly present with problems related to the metabolic complications of their renal disease or dialysis. It may also be due to diatary indiscretion. a common cardiovascular complication of renal failure. Beware not to cause joint dislocations when moving or handling the patients. There are a number of factors that may potentiate neuromuscular blockade. (potassium) this is often encountered in patients who have missed dialysis. This may be an important factor in patients with a changing neurologic status. fluid. One of the most life threatening side effects of neuromuscular blockade is Acute Malignant Hyperthermia. trauma. and acid-base balance. SEVERE RESPIRATORY AND METABOLIC ACIDOSIS. In the presence of calcium. Almost all major organ systems are affected by renal failure. the acetylcholine vesicles bind to the membrane and empty their contents into the synaptic cleft. Severely peaked T waves may be seen. be sure you keep the pharynx and trachea clear of secretions. Patient will present with unexplained tachycardia. Bronchospasm 7. pregnancy. Prolonged blockade (20–30 minutes) may occur in the presence of liver disease. they also are due to accumulation of toxic products of amino acid metabolism in the serum. Remember: MALIGNANT HYPERTHERMIA PRODUCES HYPOXEMIA. AND HYPERKALEMIA. RENAL FAILURE Chronic renal failure (CRF) requiring dialysis or transplantation is known as end stage renal disease (ESRD). and lactic acid. VENTILATOR DISCONNECTS OR MECHANICAL FAILURES CAN BE FATAL.30 2/15/06 . Vecuronium bromide has a duration of 30–60 minutes and generally requires redosing every 20–40 minutes. a wave of depolarization is set up in the muscle membrane. calcium is then released and muscle contraction occurs. This is a rapid rise in body temperature that can reach life a threatening level. Succinycholine chloride has also been associated with increased intracrainial pressure and increased intraoccular pressure. chloraquine. or a metabolic disease affecting the brain. Absence (petit mal) attacks occur in about 25% (4% alone. history of seizures. The seizures are transient in many of these conditions and do not recur once the illness ends. Auras (focal manifestations that immediately precede complex or generalized seizures) reflect where the seizure begins. However. intracranial hemorrhage. heat stroke).e. predominantly inherited neuronal abnormalities probably underlie most idiopathic cases. those beginning after age 25 are usually secondary to cerebral trauma. birth injury). or inappropriate behavior caused by abnormal excessive discharge of cerebral neurons. Generalized seizures usually affect both consciousness and motor function from the outset. convulsant drugs. but any recurrent seizure pattern may be termed epilepsy. In susceptible persons. cerebral edema (hypertensive encephalopathy. hypoxia. toxin. convulsive or toxic agents (camphor. pentylenetetrazol. Convulsive seizures result from a generalized disturbance in cerebral function. and cerebral infarct or hemorrhage. chronically recurring seizures (epilepsy) are perhaps 1/4 that frequent. Sometimes a focal lesion of one part of a hemisphere activates the entire cerebrum bilaterally so rapidly that it produces a generalized grand mal seizure before any focal sign appears. tetanus. CNS infections (meningitis. anesthesia. Unexplained. carbon monoxide poisoning. Epileptic seizures can be classified according to several different criteria. Partial seizures begin focally with a specific sensory. About 90% experience grand mal seizures. Seizures affect about 2% of the population. tumors. cocaine in nose. seizures may occasionally be precipitated by exogenous factors (sound. These include hyperpyrexia (acute infection. 21% with others). phenylketonuria). breath–holding). picro- . Psychomotor attacks occur in 18% (6% alone. 12% with others). developmental). neurosyphilis. motor activity. Most patients have only 1 type of seizure. or head injury. Epilepsy due to a microscopic scar in the brain resulting from birth trauma or other injury may be misclassified during life as idiopathic but show evidence of a causative lesion at autopsy or surgery for epilepsy. even the normal brain can discharge in a diffusely synchronous fashion and produce a seizure. Focal brain diseases can cause seizures at any age. or psychic aberration that reflects the affected part of the cerebral hemisphere where the seizure originates. cerebral hypoxia (Adams– Stokes syndrome. expanding brain lesions (neoplasm. the most common form of attacks. fever. eclampsia). lead. begin with loss of consciousness and motor control. and spread of the discharge to other portions of the cerebrum results in convulsive phenomena and loss of consciousness.. light. alcohol. which is the case in about 75% of young adults and a smaller percentage of children under age 3. encephalitis. drugs present at scene. Epilepsy is classed etiologically as symptomatic or idiopathic: Symptomatic implies that a probable cause has been identified that at times permits a specific course of therapy to eliminate that cause. or other organic brain disease. Acidosis may also be present as shortness of breath due to the work of breathing from compensatory hyperpnea. sensory phenomena. brief attacks of altered consciousness. hypoglycemia). or tranquilizers. carotid sinus hypersensitivity. motor. Convulsions may also occur as a withdrawal symptom after chronic use of alcohol. The seizure itself frequently has a genetic or metabolic cause. birth injuries. The Team should consider the following: alcoholic history. hypnotics. This may cause weakness and life-threatening dysrhythmias. convulsions may recur at intervals for years or indefinitely if there is a permanent lesion or scar in the CNS. hypoparathyroidism.31 2/15/06 SEIZURES The swift termination of seizure will protect patients from anoxic conditions conducive to brain injury.EDUCATIONAL GUIDELINES sults from loss of vitamin D and increased parathyroid hormone levels. and tonic or clonic jerking of all extremities. as a result of a focal or generalized disturbance of cortical function. E . anaphylaxis (foreign serum or drug allergy). falciparum malaria. the seizures are generalized from the outset. Epilepsy: A recurrent paroxysmal disorder of cerebral function characterized by sudden. about 30% have 2 or more types. in which case a diagnosis of epilepsy is made. rabies. In some instances. subdural hematoma in infancy). cysticercosis of the brain). brain defects (congenital. Seizures may be associated with a variety of cerebral or systemic disorders. cocaine). Convulsive seizures. brain abscess. idiopathic means that no obvious cause can be found. In primary generalized epilepsy. Given a sufficient stimulus (i. a small focus of dysfunctional tissue in the cerebrum discharges abnormally in response to endogenous or exogenous stimuli. Idiopathic epilepsy generally begins between ages 2 and 14. metabolic disturbances (hypoglycemia. beginning as a diffuse abnormal discharge affecting all cerebral cortical areas simultaneously. AIDS. cutaneous stimulation). Hysterical patients occasionally simulate convulsive attacks. Careful recording of appearance and duration are vital. Seizures before age 2 are usually related to developmental defects. toxoplasmosis. either alone (60%) or with other seizures (30%). cerebral trauma (skull fracture. tracks in arms. strychnine. with eye or muscle flutterings at a rate of three per second. Febrile seizures are the most common type of seizures observed in the pediatric group. such a patient occasionally may lash out at the person restricting his movement. rarely. Patients with temporal lobe epilepsy experience a higher incidence of interictal psychiatric disorders than does the normal population. trunk. the dysfunction may remain localized or may spread to other parts of the brain. Febrile seizures-A fever is the elevation of the body temperature above the normal temperature (0. The attacks are likely to occur several or many times a day. E . primarily generalized seizures manifested by a 10 to 30 second loss of consciousness. Brain damage is usually evident.e. The attack usually lasts 2 to 5 minutes. Mental confusion continues for another 1 or 2 minutes after the attack is apparently over.0 degree higher for rectal temperatures) for that person. The attacks may appear at any age. Infantile spasms (salaam seizures) are primarily generalized seizures characterized by sudden flexion of the arms. then clonic. often when the patient is sitting quietly. They are restricted to the first 3 years of life. or psychomotor focal phenomena without loss of consciousness. at times. The child falls or pitches to the ground. and extension of the legs. In most instances. Akinetic seizures are brief. The increased body temperature wards off infection by making the body a less hospitable environment for the invading organism. and tonic. with consequent loss of consciousness and generalized convulsive movements. physician consult should be made to discuss each patient’s condition.5-1. and head. Febrile seizures are usually be- . It may be preceded by a prodromal mood change. Pyrogens are any substances that cause fever. and utter unintelligible sounds. muscle soreness or. forward flexion of the trunk. Generalized seizures can be minor or major in their motor manifestations. The body develops a fever when pathogens enter and cause infection which in turn stimulates the production of pyrogens. particularly head injury. local) seizures begin with specific motor. the seizure continues with loss of consciousness. The patient at first may stagger. in which affected subjects act in a slow. low–grade astrocytomas). primarily generalized seizures seen in children and characterized by complete loss of muscle tone and consciousness. mesial temporal sclerosis. He does not understand what is said and may resist aid. Therefore. Further cooling may be inappropriate and are generally not recommended as these can drop the body’s core temperature too much. days. bewildered. but some studies show as many as 33% of patients with temporal lobe epilepsy having substantial psychologic difficulties. Absence (petit mal) attacks are brief. No satisfactory evidence suggests that premeditated or unprovoked aggression can ever be attributed to attacks of temporal lobe epilepsy. With that in mind oral administration may be inappropriate. and may be followed by a postictal state.EMERGENCY MEDICAL GUIDELINES Simple partial (focal. The cooling will induce shivering and additional heat production. They reset the hypothalamic thermostat to a higher level. headache. The patient suddenly stops any activity in which he is engaged and resumes it after the attack. followed by an outcry. or spread similarly from a corner of the mouth). often to be replaced by other forms of attacks. however. sensory. as may a patient in a postictal confused state after a generalized seizure. Complex partial seizures of temporal lobe origin are not characterized by unprovoked aggressive behavior. and sometimes confused state for hours or. producing a fever. focal motor or sensory phenomena. Altered mental status frequently accompanies fever. the patient has a 1 to 2 minute loss of contact with the surroundings. Tonic–clonic (grand mal) seizures occasionally begin with a partial “aura” of epigastric discomfort. or secondarily generalized (local cortical onset with subsequent bilateral spread).32 2/15/06 They are infrequent during exercise. In Jacksonian seizures (focal motor symptoms begin in one hand or foot and then “march” up the extremity. patients are normal. If restrained. Psychomotor attacks may develop at any age and are usually associated with structural pathology (i. Generalized seizures may be primarily generalized (bilateral cerebral cortical involvement at onset). Between seizures. Status psychomotor epilepsy may occur. fever is essentially a resetting of the hypothalamic thermostat. The attacks last only a few seconds but may be repeated many times a day. Urinary and fecal incontinence may occur. Metabolism is therefore increased. falling. Additional cooling may be obtained by removing all extra clothing and allowing the patient to lose heat to the environment by convection. The hypothalamic thermostat will rest to normal when pyrogen production stops or when pathogens end their attack on the body. Selection factors in evaluation make exact figures difficult to be sure of. In other words. with up to 10% showing symptoms of schizophrenia or depressive psychoses. and with or without loss of muscle tone. so that attacks carry the risk of serious trauma. Petit mal seizures are genetically determined and occur predominantly in children: they never begin after age 20. Complex partial (psychomotor) seizures are characterized by a variety of patterns of onset. The Physicians Desk Reference (PDR) does not specify a temperature for which an antipyretic (Tylenol) should be administered.. Isolated epileptic auras are simple partial seizures with a single sensory symptom (often olfactory) preceding a complex or generalized seizure. contractions of the muscles of the extremities. with deep sleep. perform automatic purposeless movements. Care is individualized to the patient. A family history of convulsions or neurologic disorders is significant. SEPSIS Sepsis is a bacterial infection of the bloodstream. upon arrival. Complex febrile seizures may indicate a more serious disease process.e. sensory. leading to a drop in blood pressure E . Depresses all levels of CNS. Meningitis is frequently associated with sepsis. Diazapam (Diastat.. About 70% of noninstitutionalized patients with epilepsy are mentally normal. Regardless of the clinical manifestations of generalized seizure. 20% show a slight reduction in intellect. and day care attendance. Interestingly. The history should include an eyewitness account of a typical attack and information on the frequency of seizures and the longest and shortest intervals between attacks. recur more than once in 24 h. abscess. when available. A history of prior trauma (i. particularly in an adult. or residual traumatic abnormalities. Valium) – Depresses all levels of CNS. In the US between 2% . family history of a febrile seizure in the first degree. high temperature. For other patients. a patient is actively seizing. with neuromuscular paralysis is needed. perinatal illness requiring hospitalization following delivery.EDUCATIONAL GUIDELINES nign but can cause considerable parental anxiety. Propofol (Diprivan) – Has general anesthetic properties when administered IV. This prevents the initiation and transmission of nerve impulses. In septic shock the rate rises to about 45%. These toxins cause peripheral vasodilatation. or toxic episodes (i. birth trauma). The presence of 2 of the following risk factors increase the probability of the first febrile seizure: family history. Partial continuous epilepsy is a form of rare focal (usually hand or face) motor seizures in which the attacks recur at intervals of a few seconds or minutes. Septic shock may develop due to the release of deadly toxins by the bacteria causing the infection. nasopharyngeal airway placement is sufficient for some patients. such as meningitis. relatively low fever at the time of seizure. Individualize doses and increases cautiously to avoid adverse effects. Patients with no risk factors have less than a 20 % chance of recurrence. Anesthetics – These agents stabilize the neuronal membrane so the neron is less permeable to ions. lasting from days to weeks at a time. Lorazepam. and brief duration between onset and initial seizure. motor.4% of children have febrile seizures by their fifth birthday. Focal cerebral symptoms and signs in association with seizures suggest brain tumor. or encephalitis. Patients with all 4 of the following risk factors have a greater than 70% chance of recurrence: young at the time of first febrile seizure. It usually occurs as a complication of an infection at another site such as pneumonia. rapid sequence induction. cranial injury producing unconsciousness. or are focal). The outlook is better when no brain lesion is demonstrable. Febrile seizures are divided into 2 types. Viral illnesses are the predominant cause of febrile seizures. infection (i. there is no data to support the theory that a rapid rise in temperature is a cause of the type of seizure. About one third of these patients have at least one recurrence. thereby producing the local anesthetic effects. or a urinary tract infection. meningitis. particularly if the seizures are stopped and the patient is awake. lidocaine toxicity may cause seizures. and 10% have a moderate to pronounced impairment. is thought to be the most effective and has a longer seizure half-life than diazepam.e. Lidocaine consistently terminates status epilepticus. aggressive supportive care and rapid termination of electrical seizure activity are the goals.. prompt administration of anticonvulsants may be necessary. Progressive mental deterioration is usually related to an accompanying neurologic disease that itself caused the seizures. For example. In status epilepticus. only rarely do seizures per se impair mental abilities. parental report of developmental delay. an ear infection. Lorazepam (Ativan) – Sedative hypnotic with short onset of effects and relatively long half-life. Fever and stiff neck accompanying convulsions of recent onset should suggest meningitis or subarachnoid hemorrhage. Most patients with epilepsy are normal between attacks. Grand mal status epilepticus may persist for hours or days and may be fatal. excessive alcohol or drug consumption and its relation to seizures) must be sought and evaluated. endotracheal intubation is necessary.. encephalitis. Grand mal seizures. It may occur spontaneously or result from too rapid withdrawal of anticonvulsants. but controlled studies are lacking. Benzodiazepines – These agents are employed commonly as the first drug for treatment of seizure. Furthermore. At times.e. simple febrile seizures (which are generalized and lasts <15 mins) and complex febrile seizures (which are prolonged.33 2/15/06 . although overuse of anticonvulsants can dull alertness. RATIONALE If. Growing anecdotal reports of the use in refractory status epilepticus have been promising. The mortality rate in sepsis is about 16-20%. always require a diagnostic search for an unsuspected focal lesion. cerebrovascular disease. or psychic seizures follow one another with no intervening periods of consciousness. pertussis). Sepsis can rapidly be fatal if not promptly identified and treated. Episodes of severe abdominal pain with vomiting may simulate severe abdominal disorders. Episodes of arthralgia with fever may occur. the spleen in adults is rarely palpable. nonspecific respiratory distress. The heart is usually enlarged. Long bone pain (i. especially if accompanied by fever. the incidence of the heterozygous S–C combination is much greater than that of the homozygous Hb C disease.e. Take them seriously! Sickle cell anemia is a chronic hemolytic anemia occurring almost exclusively in blacks and characterized by sickle– shaped red blood cells due to homozygous inheritance of Hb S.. retinal hemorrhages. More common is the aplastic crisis in both children and adults occurring when marrow red blood cell production slows during acute infections (especially viral). However. This decreases its electrical charge. Anemia is usually severe but highly variable E . but they are usually less frequent and less severe. The goal is to prevent the development of septic shock. or central nervous system involvement can. but the sickling trait (sicklemia) can be demonstrated in vitro. and other neurologic disturbances may result from occlusion of major intracranial vessels. but because of repeated infarctions and subsequent fibrosis. Hepatic. Hemiplegia.34 HEMOGLOBIN S–C DISEASE Since 10% of blacks carry the Hb S trait. and it moves more slowly toward the anode than Hb A on electrophoresis. STROKE – “BRAIN ATTACK” STROKE ALERT: Stroke as a medical emergency: “Brain Attack” In the past. with a prominent pulmonary conus. such painful crises are usually associated with back and joint pain. results in cellular adherence to endothelium and subsequent obstruction. Suspect sepsis in patients who become ill or who have been ill for several days. Homozygotes have sickle cell anemia (about 0. In addition to the previously mentioned findings. some patients even have normal Hb levels. of course. which appears due to an abnormal red blood cell membrane. Chronic punched–out ulcers about the ankles are a recurrent problem. Infections. irritability. and a septic necrosis of the femoral head are common. capillary refill greater than 2 seconds. In homozygotes. gross hematuria. pretibial) is a common clinical complaint. Anemia may be exacerbated in children by acute sequestration of sickled cells in the spleen. Keep in mind patients with sickle cell disorder have a high incidence of life threatening disorders and at a young age. Stained blood smears show target cells and a rare sickle cell. Patients may be poorly developed and often have a relatively short trunk with long extremities and a tower– shaped skull. Cholelithiasis is common. Priapism is a serious complication most commonly seen in the young adult. SICKLE CELL ANEMIA Vaso–occlusive crisis result from the occlusion of a vessel by masses of sickled red cells. each with its own symptomatology. patients with possible symptoms of ischemic 2/15/06 . Sepsis is a very serious condition that can deteriorate quickly. altered mental status. other signs and symptoms of sepsis include vomiting and diarrhea. Most symptoms are those of sickle cell anemia. Pain is the principle manifestation. most have mild jaundice with bilirubin levels of 2 to 4 mg/dL. tachycardia. especially in early childhood and are associated with a high mortality rate. The symptom complex varies with the occlusion. Initial management of the septic patient includes the standard primary and secondary assessment. also occur. “hand+foot” syndrome) is both common and typical. it forms a semisolid gel of rodlike tactoids that cause red blood cells to sickle at sites of low PO2. The vaso–occlusive lesion. cranial nerve palsies. which leads to occlusion and infarction.e. Distorted. and avascular necrosis of the femoral head is common. particularly pneumococcal. pulmonary. or shock. Septic shock may include a very ill appearance. inflexible red blood cells plug small arterioles and capillaries. in children severe pain in the hands and feet (i. valine is substituted for glutamic acid in the sixth amino acid of the beta–chain. are common.. and this represents the most common type of crisis. Hepatosplenomegaly is common in children. from patient to patient. heterozygotes (8 to 13% of blacks) are not anemic. hyperventilation and cool and clammy skin. clinical manifestations are due to both anemia and vaso–occlusive events resulting in tissue ischemia and infarction.3% of blacks in the USA). Deoxy–Hb S is much less soluble than deoxy–Hb A. Because sickled red blood cells are too fragile to withstand the mechanical trauma of circulation. Progressive decreases in lung and kidney function may be seen in older patients. Heart murmurs may simulate rheumatic or congenital heart disease. Many cases of anemia in patients with sicklemia may present undetected examples of the S–C combination.EMERGENCY MEDICAL GUIDELINES and decrease in tissue perfusion. In Hb S. The anemia in Hb S–C disease is like that of Hb C disease but milder. hemolysis occurs after they enter the circulation. It must be promptly recognized and treated appropriately. lethargy. response to stroke must change dramatically. Furthermore. including unilateral weakness or numbness. The National Stroke Association (NSA) is spear–heading an aggressive national campaign to educate members of the general public and health care community about the facts that stroke is a medical emergency and that delays in presentation may result in irreversible but preventable disability (“Time is Brain”). stroke is a nonspecific term encompassing a group of causes. vomiting. dysarthria. With the recent US FDA approval of tissue plasminogen activator (t–PA) for stroke. rapid transport of the victim to the receiving facility and prearrival notification of the receiving facility. the probability of a stroke is 72%. No historical feature distinguishes the two. and change in level of consciousness are more common in hemorrhagic strokes. The goals of the team management of patients with suspected stroke include rapid identification of the stroke. have altered mental status. t–PA must be administered within 3 hours of onset and the emerging neuroprotective therapies must also be given within a limited time frame. may be helpful) One arm does not move or arm drifts down compared with the other Have the patient say “You can’t teach an old dog new tricks” Patient uses correct words with no slurring Patient slurs words. facial droop. The team should be alert to the possibility of stroke in patients who have fallen. and expressive or receptive aphasia.EDUCATIONAL GUIDELINES Cincinnati Pre–Hospital Stroke Scale (CPSS) Facial Droop Normal Abnormal Arm Drift Normal Abnormal Abnormal Speech Normal Abnormal Have the patient show teeth or smile Both sides of face move normally One side of face does not move as well as the other side Patient closes eyes and holds both arms straight out for 10 seconds. The team should look for the most common signs of stroke. In response to these diagnostic challenges. Hemorrhagic strokes are caused by cerebral artery rupture with bleeding into the surface of the brain (subarachnoid) or bleeding in to the tissue of the brain (intracerebral). Today. and epidural or subdural trauma often resemble those of stroke. or is unable to speak Interpretation: If any of these 3 signs fall into the “Abnormal” category. Stroke is characterized by the sudden loss of circulation to an area of the brain. Ischemic strokes rarely lead to death within the first hour. and speech abnormalities. Both arms move the same or both arms do not move at all (Other findings. have had a seizure. your understanding of its pathophysiology. They are the result of complete occlusion of a cerebral artery caused by cerebral thrombosis or embolism. including thrombosis. Also called cerebrovascular accident. a brief stroke scale that can be used in the prehospital setting has now been developed (Cincinnati Prehospital Stroke Exam). The team should also remember that the signs and symptoms of hypoglycemia. brain abscess or tumor. The team members must be effectively trained in the recognition and treatment of stroke. clinical presentation. stroke were seldom regarded as high–priority cases because only supportive care was available once they entered the health care system. unilateral facial droop. Hemorrhagic strokes can be fatal at onset.35 2/15/06 . headache. support of vital functions. It includes a check for unilateral arm weakness. such as grip strength. are unresponsive or appear confused. and evaluation is essential. embolism. although nausea. Stroke is the third leading cause of death and disability in the US. Acute ischemic stroke refers to strokes caused by thrombosis or embolism and accounts for 75% of all strokes. EMS plays an important role in the initial evaluation and treatment of patients with acute ischemic stroke. or stroke syndrome. and hemorrhage. resulting in a corresponding loss of neurologic function. Although stroke often is considered a disease of the E . Strokes currently are classified as either hemorrhagic or ischemic. The team (EMS) plays a critical role in the prehospital management of stroke patients. uses wrong words. a “Stroke Alert” should be called and appropriate treatment regimens initiated. Therefore. If the medical history and physical findings suggest that a patient has had a stroke and the onset of signs and symptoms can be identified as having started within 3 hours. rapid recognition and transport within the pre–established three hour window is critical to the delivery of thrombolitics and the outcome. The Stroke Alert is based on answering “Yes” to three basic questions: 1. Management of the stroke patient can be remembered by use of the mnemonic of the 7 “D’s”: Detection Dispatch Delivery Door Data Decision Drug Delay may occur at any of these points of management. hyperthermia. EMS personnel will attempt to elicit any of 3 major physical findings suggestive of stroke: facial droop. intravenous fibrinolytic therapy should be considered for all patients presenting to the hospital within three hours of the onset of symptoms consistent with acute ischemic stroke. TIA’s precede nearly 30% of ischemic strokes. skilled and efficient at each point. Priority dispatch with prompt EMS response. the probability of a stroke is 72%. Pre–arrival notification (Stroke Alert) to the receiving facility shortens the time to definitive hospital–based evaluation and intervention for patients with stroke. Stroke should be considered in any patient presenting with an acute neurologic deficit or altered level of consciousness. arm drift. 2. ataxia. For these reasons. vital signs including blood glucose levels. Distinguishing stroke from stroke mimics. and 50% within the first year. Confirming the presence of a stroke. (The onset of symptoms is viewed as the beginning of the stroke and the eligibility for fibrinolytic therapy ends three hours from that time. 25% of strokes occur in persons younger than 65 years of age. and the estimated time of symptoms onset to the receiving hospital during encode before arrival.EMERGENCY MEDICAL GUIDELINES elderly. but accurate. temperature. one third of all TIA’s lead to ischemic stroke. With the availability of thrombolytic therapy for acute ischemic strokes in selected patients. Fibrinolytic therapy is cost–effective and results in sustained improvement in quality of life. aphasia. 2/15/06 . so response to and management of the stroke victim must be E . strokes go unrecognized by patients or their caregivers. Establishing a neurologic baseline should the patient’s condition improve or deteriorate. time in the field should be minimized and the patient prepared for immediate transport to a stroke center or hospital. The Treasure Coast Guidelines participants have selected the Cincinnati Pre–Hospital Stroke Scale (CPSS) as the mechanism to determine this information. If left untreated. Cincinnati Pre–Hospital Stroke Scale (CPSS) – Is quick and simplistic. Many strokes occur while patients are sleeping and are not discovered until the patient awakes.36 RATIONALE The goal of acute stroke management is rapid and efficient care. 3. The receiving facility should have a written plan to initiate therapy as quickly as possible by activation of the stroke teams and mobilization of necessary resources such as CT scan. If any of the 3 signs are abnormal. patients treated with fibrinolytic therapy are more likely to be discharged home and less likely to be discharged to a rehabilitative or chronic care facility. Occasionally.) EMS systems should communicate the results of the stroke scale or stroke screen. Patients with a decreased level of consciousness should be a assessed to ensure that they are able to protect their airway. Common symptoms of stroke include abrupt onset of hemiparesis. you must be able to perform a brief. Furthermore. neurologic examination on patients with suspected stroke syndromes. vertigo. The patient is at least 18 years of age 2. The goals of the neurologic examination include: 1. rapid transport and notification to the receiving facility are keys in accomplishing these goals. Strokes leave some patients too incapacitated to call for help. Assessment of the ABC’s. Signs and symptoms of a stroke are present based on the findings of the CPSS 3. the GCS. stroke recognition. These symptoms are more likely to occur in combination. The “Onset” of signs and symptoms has been within three hours. and/or hypertension. visual deficits. Once the diagnosis of stroke is suspected. Multiple factors contribute to delays in seeking care for symptoms of stroke. Fibrinolytic therapy offers the opportunity to limit neurological insult and improve outcome in ischemic stroke patients. and abnormal speech. EMS personnel can identify stroke patients with reasonable sensitivity and specificity. Care should be taken to accomplish any subsequent treatment rapidly. 20% occurring within the first month. and stroke scale evaluation should be performed urgently. atrial fibrillation. In the field it is important to be aware of the fact that patient use of beta blockers can sometimes alter the body’s normal response to certain medical conditions. Fibrinolytic therapy is not recommended for systolic blood pressures of > 185 mmHg. BGL Check and Dextrose 50% – Carbohydrates. Also included is a list of the more common drugs in each class the EMS providers will frequently find among their patients’ prescription.37 2/15/06 atenolol (Tenormin) Bisoprolol (Zebeta) labetalol (Normodyne) nadolol (Corgard) Propanolol (Inderal) timolol (Blocadren) Captopril (Capoten) Fosinopril (Monopril) Quinapril (Accupril) Spirapril (Renormax) Note: the generic names of all ACE Inhibitors ends in – pril Note: The generic names of all beta blockers end in – lol CARDIAC UNDERSTANDING ACE INHIBITORS. In stroke management. CALCIUM CHANNEL BLOCKERS AND DIGITALIS TOXICITY In this section. and migraine headaches. Beta blockers also have what is referred to as a membrane-stabilizing effect that. Therefore. hypovolemia would normally be expected to have a rapid heart rate. and oxygen consumption. after load and blood pressure. Propholactic administration is not indicated. ALL MEDICATIONIS GIVEN IN THE PRESENCE OF A STROKE MUST BE PHYSICIAN CONSULT. which has a shorter half–life. both can also aggravate ongoing neuronal ischemia. Administration of glucose in hypoglycemia produces profound and prompt movement. and tachyarrhythmias. angina. Rectal administration may be required in the stroke patient.) Labetalol (Trandate) – Antihypertensive. along with a brief explanation of how they work. decreased peripheral vascular resistance. is responsible for their antiarrhythmic capabilities. Reverses the effect of hypoglycemia. strict control of blood pressure is required to reduce potential for bleeding. Reduces fever by acting directly on hypothalamic heat–regulating centers. Recurrent seizures can worsen stroke and should be controlled. In candidates for fibrinolytic therapy. They are utilized to manage hypertension. Beta blocker use may modify this anticipated response by maintaining the heart rate in the normal range. Acetaminophen (Tylenol) – Antipyretic. some of the more commonly encountered classes of cardiac medications are listed.EDUCATIONAL GUIDELINES Oxygen – Low Flow unless hypoxic (Sa02<90%) or inability to protect airway requires oral tracheal intubation (OTI). Valium (Diazepam) or Ativan (Lorazepam) – Benzodiazepine/Anticonvulsant. THE FOLLOWING MEDICATIONS ARE NOT ROUTINELY GIVEN IN A STROKE: (These Medications are for the specific indications discussed. patients in the early stage of shock. thereby assisting in the relief of congestive heart failure and hypertension. For example. It is provided to help the reader feel more comfortable in handling cardiac medication problems that arise in the field. Dilacor) bepridil (Vascor) Felodipine (Plendil) E . in part. They are utilized for the treatment of hypertension. Zestril) Ramipril (Altace) BETABLOCKERS The overall effect is to decrease myocardial excitability. and inhibited coronary artery spasms. Lorazepam. lowering cerebral perfusion pressure below this can lead to worsening of the stroke causing underperfusion of the ischemic penumbra. Commonly Prescribed Calcium Channel Blockers Amlodipine (Norvasc) Diltiazem (Cardizem. cardiac workload. COMMONLYPRESCRIBED BETABLOCKERS Acebutolol (Sectral) betaxolol (Kerlone) carteolol (Cartrol) Metoprolol (Lopressor) penbutolol (Levatol) sotalol (Beatpace) CALCIUM CHANNEL BLOCKERS The effect is dilation and relaxation of cardiac and systemic arteries. ACE INHIBITORS Ace inhibitors relax blood vessels and help reduce blood pressure. The basic knowledge of thee . SVT. BETA BLOCKERS. Evidence suggests that mild brain hypothermia is neuroprotective. may be superior. Hyperthermia accelerates ischemic neuronal injury and can increase morbidity. Reserved for patients with markedly elevated blood pressures. Transport Position – Transporting the patient with the head at a 30° inclined angle may reduce blood pressure and reduce the need for more aggressive measures. atrial flutter. They also make it easier for the heart to pump. angina. common home medications helps in effective assessment and treatment. the target blood pressure is <185/110 or MAP > 130mmHG. or a diastolic blood pressure of > 110 mmHG. Not only can both hypoglycemia and hyperglycemia produce symptoms that closely mimic stroke. Commonly prescribed Ace Inhibitors Benazepril (Lotensin) Enalapril (Vasotec) Lisinopril (Prinivil. thus increasing the cardiac output. They are commonly prescribed for patients who have already been diagnosed with cardiovascular disease. these drugs work by inhibiting the hepatic enzyme that is essential to cholesterol synthesis. prehospital 12–lead ECGS and a chest pain check list lead to more rapid prehospital and hospital care. CARDIAC GLYCOSIDESAND DIGITALISTOXICITY Digitalis. it is the longest acting cardiac glycoside. the principal drug in the cardiac glycoside class. It is a potent and potentially toxic drug. It has also proved effective in the management of patients with atrial fibrillation and atrial flutter. vomiting. and drowsiness. The therapeutic index (therapeutic dose/toxic dose) is low. When given to patients in congestive heart failure. Visual disturbances (yellow vision). and hypercalcemia. Procardia) verapamil (Calan. due to atherosclerotic plaques. Digitalis and the related cardiac glycosides increase the force (inotropic effect) of the myocardial contraction. it significantly increases the stroke volume. or have other significant cardiac risk factors. Early reperfusion decreases infarct size and improves left ventricular function. and so on) nausea. To pre–notify the receiving facility so they can make sure their resources are ready for the patient. Isoptin) CHOLESTEROL – LOWERING AGENTS Also known as an antilipid agent. have had an MI. The plaques initially allow sufficient blood flow to match myocardial demand. with most benefit in the first few hours. which can be reduced by digitalis therapy. eating. is one of the oldest medications known to humans.EMERGENCY MEDICAL GUIDELINES isradipine (DynaCirc) nicardipine (Cardene) Nifedipine (Adalat. The acute coronary syndromes: “Time is Muscle” Current management of AMI contrasts dramatically with the expectant waiting and retrospective diagnosis of a decade ago. Angina that is reproduced by exercise. which has an underlying cause of an imbalance between supply and demand for myocardial oxygen. to a portion of the myocardium. In these patients rapid atrial rates produce accelerated ventricular rates. Myocardial ischemia most often develops as a result of reduced blood supply. Now the emergency triage and treatment of patients with acute coronary syndromes changes the immediate course of the AMI and alters long–term prognosis. PSVT with 2. The symptoms are due to myocardial ischemia. and. To classify patients as qualifying or non–qualifying for cardiac alert criteria. Early diagnosis and treatment of AMI significantly reduces mortality. including thrombolysis. The National Heart Attack Alert Program has published a series of important recommendations for the rapid identification and management of patients with AMI. and/or stress and is subse- 2/15/06 .Lowering Agents Cerivastatin (Baycol) colestipol (Colestid) gemfibrozil (Lopid) Cholestyramine (Questran) Fluvastatin (Mevacor) Pravacol CARDIAC ALERT PURPOSE OF PROGRAM: To help the team rapidly identify acute coronary syndrome patients with the appropriate assessment tools. Digitalis toxicity is potentiated in patients with hypokalemia. Digoxin (Lanoxin) it is the most commonly prescribed Ouabain has a rapid rate of onset and relatively short duration of effect Desanoside (Cedilanid – D) is the most rapidly acting digitalis preparation Cardiac Glycosides have profound effects on cardiac function and rhythm. a sense of urgency is mandatory. E . The team can significantly improve the door–to–needle time. For hundreds of years it had been used in the treatment of congestive heart failure. ECG. Because myocardial salvage is time–dependent. which can reopen blocked vessels. They are indicated to reduce total cholesterol and low-density lipids. risk factors. Almost any arrhythmia can be associated with digitalis toxicity. (LDL) Commonly Prescribed Cholesterol. thus slowing the heart rate. These include the following: Digitoxin. The “reperfusion ERA” has been ushered in by the recent formulation of thrombolytic agents that can dissolve acute coronary thrombosis and by the development of percutaneous transluminal coronary angioplasty (PTCA). Several digitalis preparations are available. It also decreases AV node conduction. This cardiac alert program is reflective of those recommendations. which means that the possibility of digitalis toxicity should always be considered in patients with this medication. 1 block. Signs of digitalis toxicity include cardiac arrhythmias (PVCs. hypomagnesemia. The interval between arrival of the patient at the ED and the delivery of a thrombolytic agent. headache. to a lesser extent. These areas of narrowing may become clinically significant and precipitate angina when myocardial demand increases.38 ACUTE CORONARY SYNDROME Initial diagnosis of acute coronary syndrome is based almost entirely on history. EDUCATIONAL GUIDELINES quently relieved with rest and without recent change in frequency or severity of activity necessary to produce symptoms is called chronic stable angina. Over time, the plaques may thicken and rupture, exposing a thrombogenic surface upon which platelets aggregate and thrombi form. The patient may note a change in symptoms of cardiac ischemia with a change in severity or of duration of symptoms. This condition is referred to as unstable angina. Other causes include arterial inflammation and secondary unstable angina. Arterial inflammation may be caused by or related to infection. Secondary unstable angina occurs when the precipitating cause is extrinsic to the coronary arterial bed, such as fever, tachycardia, thyrotoxicosis, hypotension, anemia, or hypoxemia. Most patients who experience secondary unstable angina have chronic stable angina. Irrespective of the cause of unstable angina, the result of persistent ischemia is myocardial infarction (MI). Angina becomes progressively more common, as does the underlying cardiac disease responsible, with increasing age. Typically, angina is a symptom of myocardial ischemia that appears in circumstances of increased oxygen demand. It usually is described as a sensation of chest pressure or heaviness that is reproduced by activities or conditions that increase myocardial oxygen demand. Not all patients experience chest pain. Some present with only neck, jaw, ear, arm, or epigastric discomfort. Other symptoms, such as shortness of breath or severe weakness, may represent anginal equivalent symptoms. Patients may complain of the following: palpitations, pain, which is usually described as pressure, squeezing, or a burning sensation across the precordium and may radiate to the neck, shoulder, jaw, back, upper abdomen, or either arm. Exertional dyspnea that resolves with pain or rest. Diaphoresis, nausea, and decreased exercise tolerance. Patients with diabetes and elderly patients are more likely to have atypical presentations and offer only vague complaints, such as weakness, lightheadedness, and nausea. Stable angina involves episodic pain lasting 5–15 minutes, provoked on exertion and relieved by rest or nitroglycerin. Unstable angina patients have increased risk for advance cardiac events, such as MI or death. Three clinically distinct forms exist, as follows: New–onset exertional angina, angina of increased frequency or duration or refractory to nitroglycerin, and angina at rest. Atherosclerotic plaque disease is the predominant cause. Coronary artery vasospasm is less common. Alternative causes of angina include ventricular hypertrophy due to hypertension, embolic occlusion of the coronary arteries, hypoxia, as in acute pulmonary disorders, cocaine and amphetamine use, underlying coronary artery disease, and inflammation of epicardial arteries. The immediate goal of emergency care is rapid identification of patients with AMI, and exclusion of alternative causes of nonischemic chest pain. RATIONALE The goals of treatment are to preserve patency of the coronary artery, augment blood flow through stenotic lesions, reduce myocardial oxygen demand thereby preventing major adverse cardiac events. All patients should receive antiplatelet agents, and patients with evidence of ongoing ischemia should receive aggressive medical intervention until signs of ischemia, as determined by symptoms and ECG resolve. Therapeutic benefit was seen for up to 12 hours but was the greatest when fibrinolytics were administered in the first 3 hours. Hence the cardiac alert criteria. Prehospital 12 lead ECG improves prehospital diagnosis, reduces hospital–based time to treatment, identifies patients requiring reperfusion, contributes to mortality reduction and facilitates triage to cardiac centers with interventional facilities. DRUG CATEGORY: Oxygen – Evidence suggests that breathing supplemental oxygen may limit the size of ischemic myocardial injury. DRUG CATEGORY: Anti-platelet agents – These inhibit cyclooxygenase, which in turn produces thromboxane A2, a potent platelet activator. Anti-platelet therapy has been shown to reduce mortality by reducing the risk of fatal strokes and fatal myocardial infarctions. Aspirin – Early administration of aspirin in patients with AMI may reduce cardiac mortality. After plaque rupture or erosion, a layer of platelets covers the surface of the plaque. Fibrinogen cross–links platelets, and the coagulation system is further activated by thrombin generation. At this stage the thrombus is platelet–rich. Therapy with antiplatelet agents is most effective at this time. Heparin – When Heparin is used in the presence of aspirin a reduction in mortality as well as a reduction in reinfarction has been seen. To reduce the incidence of increased intercrainial hemorrhage a lower dose of heparin is now recommended. DRUG CATEGORY: Nitrates – These agents oppose coronary artery spasm and reduce myocardial oxygen demand by reducing both preload and afterload. Nitroglycerin – (All forms) Causes relaxation of the vascular smooth muscle, causing a decrease in blood pressure. DRUG CATEGORY: Analgesics – These agents reduce pain, which decreases sympathetic stress, in addition to providing some preload reduction. Morphine Sulfate – Drug of choice (DOC) for narcotic analgesia because of its reliable and predictable effects, safety E - 39 2/15/06 EMERGENCY MEDICAL GUIDELINES profile, and ease of reversibility with naloxone. Morphine sulfate administered IV may be dosed in a number of ways and commonly titrated until desired effect is obtained. DRUG CATEGORY: Anticoagulants – These agents are used to prevent recurrence of clot after a spontaneous fibrinolysis Heparin – Augments activity of antithrombin and prevents conversion of fibrinogen to fibrin. Heparin does not actively dissolve but is able to inhibit further thrombogenesis. Parasympathetic influences during cardiopulmonary arrest have not been studied fully, and the clinical benefits of atropine have yet to be confirmed. High–dose epinephrine may improve the hemodynamics of CPR, thereby increasing the rate of return to spontaneous circulation; however, it has not been demonstrated to influence the final clinical outcome. Therefore, these doses no longer are recommended for children or adults. DRUG CATEGORY: Anticholinergic agents – The goal in using these agents is to improve conduction through the AV node by reducing vagal tone via receptor blockade. Atropine is a parasympatholytic agent used to eliminate vagal influence on the SA and AV nodes. Epinephrine (Adrenaline) Considered the single most useful drug in cardiac arrest. Used to increase coronary and cerebral blood flow during CPR. May enhance automaticity during asystole. Termination of efforts – A number of studies over the past decade observe consistantly that 1% of patients transported with continuing CPR survive to hospital discharge. It is now considered an unethical act to transport an arrest victim proven refractory to proper BLS and ACLS care. ASYSTOLE Asystole is cardiac standstill with no cardiac output and no ventricular depolarization; it eventually occurs in all dying patients. Asystole can be primary or secondary. Primary asystole occurs when the heart’s electrical system intrinsically fails to generate a ventricular depolarization. This may result from ischemia or from degeneration (i.e., sclerosis) of the sinoartial (SA) node or atrioventricular (AV) conducting system. Primary asystole usually is preceded by a bradydysrhythmia due to sinus arrest or complete heart block or both. It develops when cellular metabolic functions are no longer intact and an electrical impulse cannot be generated. Secondary asystole occurs when factors outside of the heart’s electrical system result in a failure to generate any electrical depolarization. In this case, the final common pathway is usually severe tissue hypoxia or acidosis. Asystole is associated with poor outcome regardless of its initial cause. Resuscitation is likely to be successful only if it is secondary to an event than can be corrected immediately. Prevalence of asystole as the presenting cardiac rhythm is lower in adults (25%–56%) than in children (90%–95%). Immediate diagnosis of asystole requires the recognition of full cardiac arrest and a confirmed flatline rhythm in 2 perpendicular leads. If the rhythm is truly asystole and has been present for more than several seconds, the patient will be unconscious and unresponsive. A few agonal breaths may be noted, but detectable heart sounds and palpable peripheral pulses are absent. Examples of common conditions that can result in secondary asystole include suffocation, near drowning, stroke, massive pulmonary embolus, hyperkalemia, hypothermia, and sedative–hypnotic or narcotic overdoses leading to respiratory failure. Hypothermia is a special circumstance, since asystole can be tolerated for a longer period of time under such conditions and can be reversed with rapid rewarming while cardiopulmonary resuscitation (CPR) is being performed. ATRIAL FIBRILATION Atrial fibrillation (AF) is a rhythm disturbance of the atria that results in irregular, chaotic, ventricular waveforms varying from bradyarrhythmia to tachyarrhythmia. Multiple re– entrant waveforms within the atria bombard the atrioventricular (AV) node, which becomes relatively refractive to conduction due to the frequency of upstream electrical activity. AF occurs in 3 distinct clinical circumstances: As a primary arrhythmia in the absence of identifiable structural heart disease. As a secondary arrhythmia in the absence of structural heart disease, but in the presence of a systemic abnormality that predisposes the individual to the arrhythmia. As a secondary arrhythmia associated with cardiac disease that affects the atria. Pertinent physical findings are limited to the cardiovascular system or, if embolization has occurred, the brain and/or peripheral vasculature. These include the following: Irregular pulse, with or without tachycardia, is described classically as the irregularly irregular rhythm. Hypotension and poor perfusion due to a decrease in atrial filling pressures and decrease in stroke volume. Signs of embolization, including transient ischemic attacks (TIAs) and cerebrovascular accidents (CVAs) may be identified. Congestive heart failure (CHF) Patients at the highest risk include those with long–standing hypertension, valvular heart disease (rheumatic), left ven- RATIONALE E - 40 2/15/06 EDUCATIONAL GUIDELINES tricular hypertrophy, coronary artery disease, or diabetes. CHF for any reason is a noted contributor to this disorder. Other causes may include: AMI, pulmonary embolism, cardiomyopathy, sick sinus syndrome, hyperthyroidism, ethanol use, cardiothoracic surgery, and use of over–the–counter herbs such (i.e., ephedra, ginseng) have been noted in some patients with new onset AF. When considering drug therapy for AF, remember the treatment caveat, “Electrical cardioversion is the preferred modality in the patient whose condition is unstable.” fibrillation (AF), which occurs in as many as 3% of certain populations. For the most part, morbidity and mortality are due to complications of rate (e.g., syncope, congestive heart failure – (CHF). In patients who suffer from flutter of the atria, the risk of embolic occurrences approaches that of atrial fibrillation (AF). A patient may present with a history of palpitations, fatigue or poor exercise tolerance, dyspnea, angina, or syncope. Pertinent physical findings are limited to the cardiovascular system. If embolization has occurred from intermittent AF, findings are related to brain and/or syncope. Tachycardia may or may not be present, depending on the degree of AV block that may be associated with the flutter activity. The rate may be regular or slightly irregular. Hypotension is possible but normal blood pressure is observed more commonly. CHF may be found and is usually be left ventricular dysfunction. Patients at the highest risk include those with long standing hypertension, valvular heart disease (rheumatic), left ventricular hypertrophy, coronary, coronary artery disease with or without depressed left ventricular function, or diabetes. Additionally, CHF for any reason is a noted contributor to this disorder. Additional causes include: postoperative revascularization, digitalis toxicity and pulmonary embolism. In cases of typical flutter, EKG reveals identically recurring regular saw tooth flutter waves. Flutter waves often are visualized best in leads II, III, AVF, or VI.. Flutter and fibrillation often coexist with alternating patterns (e.g., fib-flutter) in the same tracing. If the patient is unstable (e.g., hypotension, poor perfusion), synchronized cardioversion is commonly the initial treatment of choice. Cardioversion often requires low energies (<50J). If the electrical shock results in atrial fibrillation, shock at a higher energy level is used is used to restore normal sinus rhythm (NSR). To slow the ventricular response, dilitiazem may be the appropriate initial treatment. Adenosine produces transient AV block and can be used to reveal flutter waves. These drugs generally do not convert to NSR. If the flutter cannot be cardioverted, terminated by pacing, or slowed by the drugs mentioned, IV amiodarone has been shown to slow the ventricular rate and is considered as effective as digoxin. RATIONALE Rate control is the goal of medication in atrial flutter. When considering drug therapy for atrial flutter/fibrillation, electrical cardioversion is the preferred modality in the patient whose condition is unstable. Delivered energy should be syncronized with the QRS complex to reduce the possibility of inducing VF, which can occur when a shock “hits” the relative refractory portion of the cardiac cycle. Synchronized direct–current (DC) cardioversion is commonly the initial treatment of choice for the symptomatic patient. Cardioversion often requires low energeies. If the electrical shock results in atrial fibrillation, a second shock at a higher energy level is used to restore normal sinus rhythm (NSR). To slow the ventricular response, diltiazem is the appropriate initial treatment. Adenosine produces transient AV block and can be used to reveal flutter waves. This drug generally does not convert atrial flutter to NSR. DRUG CATEGORY: Calcium Channel Blocker – These agents reduce the rate of AV nodal conduction and control ventricular response. Diltiazem (Cardizem) is the DOC during depolarization. Inhibits calcium ion from entering slow channels or voltage– sensitive areas of vascular smooth muscle and myocardium. ATRIAL FLUTTER Atrial flutter is a rhythm disturbance of the atria that results in regular tachycardia ventricular waveforms. Atrial rates in atrial flutter are 240-400 beats per minutes. The QRS complexes are uniform in shape, but irregular in rate. P waves may have saw-tooth configurations. Multiple re-entrant or primarily generated (ectopic) atrial waveforms bombard the atrioventricular (AV) node. The most common form of atrial flutter involve a reentrant circuit that encircles the tricuspid annulus of the right atrium. Less commonly, atrial scars or atrial infarction may be the cause. Atrial flutter is less common than atrial CARDIAC TAMPONADE Pericarditis and cardiac tamponade are clinical problems involving the potential space surrounding the heart or pericardium. Pericarditis is one cause of fluid accumulation in this potential space; cardiac tamponade is the hemodynamic reE - 41 2/15/06 EMERGENCY MEDICAL GUIDELINES sult of the fluid accumulation. As the volume of pericardial fluid increases, the capacity of the atria and ventricles to fill is mechanically compromised, leading to reduced stroke volume and tamponade physiology. The pericardium (pericardial complex) consists of an outer fibrous layer and an inner serous layer. The fibrous pericardium is a flask–shaped, tough outer sac with attachments to the diaphragm, sternum, and costal cartilage. The serous layer is thin and is adjacent to the surface of the heart. The pericardium serves as a protective barrier from the spread of infection or inflammation from adjacent structures. The potential space produced by these layers contains approximately 20cc of fluid with electrolyte and protein profiles similar to plasma. Approximately 120cc of additional fluid can accumulate in the pericardium without an increase in pressure. Further fluid accumulation can result in marked increase in pericardial pressure, eliciting decreased cardiac output and hypotension (cardiac tamponade). The rapidity of fluid accumulation influences the hemodynamic effect. The early diagnosis of significant pericardial and cardiac injuries can prevent morbidity and enhance survival. Traumatic tamponade may present with acute dyspnea or altered mental status. Medical cardiac arrest patients may have a history of illness associated with the pericardium, particularly end–stage renal disease, severe infection, routine cardiac surgery and radiation therapy. Cardiac tamponade is influenced by volume and rate of accumulation. On physical exam a patient may present with jugular vein distention, hypotension, and muffled heart sounds (Beck’s triad). Hypotension and tachycardia without elevated jugular vein distension if associated hemorrhage is outside the pericardial sac. Pulses paradoxus is measured by careful auscultation with a blood pressure cuff. The first BP reading is recorded at the point when beats are audible during expiration and disappear with inspiration. The second reading is taken when each beat is audible during the respiratory cycle. A difference of more than 10 mm Hg defines pulses paradoxus. Cyanosis, varying degrees of consciousness may also be observed prior to cardiac arrest. Identification of any pericardial fluid in the setting of penetrating injury to the thorax or upper abdomen requires aggressive resuscitation. Hemopericardium is the most common feature of penetrating cardiac injuries. In acute massive hemopericardium, there is sufficient time for defibrillation to occur. The hemopericardium organizes and may partially clot, resulting in a pericardial hematoma. Potential causes of cardiac perforation include central line placement, pacemaker insertion, cardiac catheterization, and sternal bone marrow biopsies. A tamponade delay of hours to days has occurred secondary to catheter misplacement. E - 42 2/15/06 Cardiac arrest patients who present with traumatic injury or medical history as described require immediate treatment of the increase in pericardial pressure with pericardiocentesis. Removing as little as 30–50ml may produce dramatic hemodynamic improvement. The pericardium may have the potential of accumulating as much as 2,000 ml of fluid over time. For penetrating injuries, traumatic arrest, pulseless electrical activity (PEA), and asystole, the prognosis depends heavily upon the rapid identification of the potential for tamponade. CARDIOGENIC SHOCK Cardiogenic shock is characterized by a decreased pumping ability of the heart that causes a shock–like state with inadequate perfusion to the tissues. It most commonly occurs in association with, and as a direct result of, acute ischemic damage to the myocardium. The most common initiating event in cardiogenic shock is acute myocardial infarction (AMI). Dead myocardium does not contract, and once more than 40% of the myocardium is involved, cardiogenic shock may result. On a mechanical level, a marked decrease in contractility reduces the ejection fraction and cardiac output. These lead to increased ventricular filling pressures, cardiac chamber dilation, and ultimately, univentricular or biventricular failure that result in systemic hypotension and/or pulmonary edema. Mortality rates for medically treated patients with AMI and cardiogenic shock exceed 70%. Most patients with cardiogenic shock have an AMI and, therefore, present with the constellation of symptoms of acute cardiac ischemia (i.e., chest pain, shortness of breath, diaphoresis, nausea and vomiting). Patients experiencing cardiogenic shock also may present with pulmonary edema and presyncopal or syncopal symptoms. Physical exam often reveals that the patient is in the middle of an AMI. Patients are in frank distress, are profoundly diaphoretic, and have severe shortness of breath and chest pain. Neck examination may reveal jugular vein distention, which may be prominent. This finding is evidence of right ventricular failure. With increasing ventricular dysfunction, florid pulmonary edema and severe hypotension may develop. Auscultation of the chest may reveal varying degrees of congestive heart failure. Prehospital care is aimed at minimizing ischemia and shock. RATIONALE The goals of pharmacotherapy are to reduce morbidity and prevent complications. Early hemodynamic stabilization is beneficial and reduces mortality. DRUG CATEGORY: Vasopressors – These drugs aug- EDUCATIONAL GUIDELINES ment both coronary and cerebral blood flow present during the low–flow state associated with shock. Sympathomimetic amines with both alpha–adrenergic abd beta–adrenergic effects are indicated. Dopamine is the drug of choice to improve cardiac contractility. Dopamine (Intropin) stimulates both adrenergic and dopaminergic receptors. Hemodynamic effect is dependent on the dose. Lower doses predominantly stimulate dopaminergic receptors that in turn produce renal and meseneric vasodilation. Higher doses cause cardiac stimulation and renal vasodilation. reassess patient status. The responsible clinician should stop the resuscitative effort when he or she determines with a high degree of certainty that the arrest victim will not respond to further ACLS efforts. No reliable criteria are available to determine neurological outcome during cardiac arrest. TRAUMATIC CARDIAC ARREST Treatment of patients in cardiopulmonary arrest varies as to the mechanism of the injury and whether or not they exhibit any signs of life (pulse, respirations, or reflexes) on initial evaluation. Generally, trauma patients who are found with no signs of life in the field have suffered overwhelming cardiovascular or CNS injuries, which are not amenable to surgical treatment under any circumstances. The survival rate on these patients is essentially zero and attempts at resuscitation are futile. Patient’s suffering traumatic cardiopulmonary arrest after treatment has begun should be Diverted to the closest facility. Due to the rapid response from providers to scenes, many traumatic arrest patients are not yet in asystole, but present on exam to be in Pulseless Electrical Activity (PEA). In this case the provider should follow protocol and attempt to address all of the physiologic causes of PEA while enroute to the emergency department. These patients should also be diverted to the closest facility. CESSATION OF EFFORTS Patients in cardiac arrest exhibiting asystole have a dismal rate of survival – usually as low as 1 or 2 people out of 100 cardiac arrests. As with PEA, the only hope for resuscitation of a person in asystole is to identify and treat a reversible cause. The asystole protocol outlines an approach that focuses on “not starting” and “when to stop”. Field personnel will not be required to transport every victim of cardiac arrest to the hospital emergency department. However, transportation with continuing CPR and ALS interventions is justified if there are interventions available in the ED that cannot be performed in the field (such as central core re-warming equipment) or field interventions (such as tracheal intubation) that where unsuccessful in the field, or patient’s who do not have a valid state of Florida DNRO. For nontraumatic cardiac arrest solid evidence confirms that ACLS care in the ED offers no advantage over ACLS care in the field. Children are a special case. A pulse may be difficult to find without a Doppler. In any case, you should be especially aggressive in attempting to resuscitate children with no palpable pulse. Pregnant mothers and the newly born will also be conditions in which we will continue maximum efforts including transport. Likewise, it is inappropriate for personnel to apply routine “stopping rules” without thinking about their particular situation. Cessation of efforts in the pre-hospital setting, following system-specific criteria and under direct medical control will be standard practice in your EMS system. Healthcare professionals must understand the patient, the arrest features, and the system factors that have prognostic importance for resuscitation. These include time to CPR, time to defibrillation, pre-arrest state, and initial arrest rhythm. None of these factors alone or in combination is clearly predictive of outcome. The most important factor associated with poor outcome is time of resuscitation efforts. The chance of discharge from the hospital alive and neurologically intact diminishes as resuscitation time increase. Clinicians must constantly RATIONALE Not starting & Stopping Resuscitation One goal unique to CPR is the reversal of clinical death, an outcome achieved in only a minority of patients. However, the performance of CPR, may conflict with the patient’s own desires and requests or may not be in his or her best interest. Resuscitative efforts may be inappropriate if goals of patient care cannot be achieved. Each decision must be made for the individual, with compassion, based on ethical principles and available scientific information. Medical treatment is futile if its purpose cannot be achieved. The 2 major determinants of medical futility are length of life and quality of life. An intervention that cannot establish any increase in length or quality of life is futile. In resuscitation a qualitative definition of futility must include low chance of survival and low quality of life afterward. Key factors are the underlying disease before cardiac arrest and expected state of health after resuscitation. A careful balance of the patient’s prognosis for both length of life and quality of life will determine whether CPR is appropriate. CPR is inappropriate when survival is not expected or if the patient is expected to survive without the ability to communicate. The framework for decisions about futility can be best achieved by a social consensus. Discussion and debate among E - 43 2/15/06 that is when the patient is dead. CHF is the leading diagnosis among hospitalized patients older than 65 years. or “asystole. Long–term prognosis is variable. while left ventricular failure is secondary to reduced forward flow into the aorta and systemic circulation. it is recommended that all patients in cardiac arrest receive resuscitation unless: • The patient has a valid Florida DNRO order. Some examples are CPR for patients with signs of irreversible death. pulmonary edema. Albuterol has been shown to be successful in this setting. or decreased diastolic ventricular compliance.EMERGENCY MEDICAL GUIDELINES healthcare professionals and the public are encouraged so as to reach a consensus based on values of society. wheezing or rales may be heard on auscultation. It also recognizes that when people have died. decapitation. IV Nitroglycerin is the therapy of choice for afterload re- CONGESTIVE HEART FAILURE Congestive heart failure (CHF) is an imbalance in pump function in which the heart fails to maintain the circulation of blood adequately. develops when this imbalance causes an increase in lung fluid secondary to leakage from pulmonary capillaries into the interstitium and alveoli of the lung. Therefore. • Specific newly born conditions that may be set forth by your individual agency. A variety of cardiac diseases cause CHF and pulmonary edema. skin may be diaphoretic. DRUG CATEGORY: Nitrates – Reduce myocardial oxygen demand by lowering preload and afterload. nitrates. CPAP splints the airways open with positive pressure which will increase the surface area for gas exchange at the alveolar/capillary membrane and will reduce atelectasis from the “wash–out” affect of surfactant. such as rigor mortis. nating weak and strong pulse indicative of depressed left ventricle). Furthermore. The most common cause of heart failure is coronary artery disease. pulsus alternans (alterE . • No physiological benefit can be expected because the vital functions have deteriorated despite maximal therapy. Scientific evaluation has shown that there are no clear criteria to predict the futility of CPR accurately. and tachycardia are highly predictive of CHF. ongoing ischemia. and inotropic agents are indicated for the treatment of CHF and pulmonary edema. Steroids have been shown to worsen preexisting heart failure due to systemic sodium retention and volume expansion. treating both with the shotgun approach often is employed. dependent lividity. which is secondary to loss of left ventricular muscle. Backward failure is secondary to elevated systemic venous pressure. • Traumatic injury resulting in asystole. decapitation. The use of diuretics. and cardiac work while transiently enhancing cardiac function. a number of studies over the past decade observe consistently that < 1% of patients transported with continuing CPR survive to hospital discharge.” Therefore. gray. Healthcare workers are not obligated to provide treatment when there is scientific and social consensus that such treatment is ineffective. cold. • The patient has signs of irreversible death: rigor mortis. progressive symptoms. particularly as both may cause bronchospasm.44 2/15/06 . Some additional findings may include: tachypnea. which will inhibit sodium chloride reabsorption in the ascending loop of Henle. or dependent lividity. Former mainstays used to decrease preload such as alternating tournaquets and phelbotomy with removal of 500 cc of blood have been replaced with newer more promising therapies such as intravenous nitroglycerin. jugular venous distention. the heart monitor displays a flat line. analgesics. the new algorithm contains notes about what to do if asystole persists. and therefore it presents recommendations to follow for resuscitation. and cyanotic. Quantitative futility implies that survival is not expected after CPR under given circumstances. Furosemide (Lasix) Administration of this loop diuretic IV will allow for both superior potency and higher peak concentration. CHF can be categorized as forward or backward ventricular failure. use of accessory muscles of respiration. The most severe manifestation of CHF. The outcome should produce increased lung volume. and occasional hypertension. Continuous positive airway pressure (CPAP) ventilation therapy has demonstrated decreased need for intubation rates when utilized. or decomposition. decrease tachycardia. Mortality rates from 10% in patients with mild symptoms to 50% with advanced. The new ACLS asystole algorithm recognizes that some people in asystole can be resuscitated. hypertension. Because diffentiating CHF and asthma exacerbations is often difficult. hypokalemia. DRUG CATEGORY: Diuretics – First–line therapy generally includes a loop diuretic such as furosemide. Aerosolized beta–2–agonists. Findings such as peripheral edema. RATIONALE The goal of pharmacotherapy is to maintain adequate blood pressure and perfusion to essential organs. dysrhythmias. improve oxygenation and reduce the work of breathing. 45 2/15/06 HEART BLOCK First–degree heart block. unless the patient is symptomatic from a resulting E . DRUG CATEGORY: Analgesics – Morphine IV is an excellent adjunct in acute therapy. AMI. However. Also causes arterial dilation. Mobitz I AV block. A narrow QRS complex may be due to AV nodal or infranodal conduction delay. Electrophysiological studies have shown that first–degree heart block may be due to conduction delay in the AV node. including hypotension and altered mental status. Topical nitrate therapy is reasonable in a patient presenting with classic CHF. thereby slowing AV conduction. Second–degree heart block or second–degree atrioventricular (AV) block refers to a disorder of the cardiac conduction system in which some P waves fail to conduct to the ventricle and to generate a QRS complex. following are the most common causes of first–degree heart block: Intrinsic AV nodal disease. Symptomatic patients may have signs of hypoperfusion. ischemia. It can be caused by AMI. DRUG CATEGORY: Inotropic agents – In the hypotensive patient presenting with CHF. Cardiac stimulation and renal vasodilation are produced by higher doses. or a combination of the two. Mobitz I and Mobitz II. However. due to delayed absorption. Patients with first–degree heart block occasionally may progress to a higher–grade block. Doses >10 mcg cause vasoconstriction. Hemodynamic effects depend on the dose. or syncope.02 seconds. This occurs primarily in patients with AMI or myocarditis. beta– blockers. Lower produce renal and mesenteric vasodilation. electrolyte disturbances. and dysrhythmias. is a condition that results in prolongation of the PR interval on electrocardiogram (ECG) to > 0. vagal stimulation or enhanced vagal tone. Mobitz II AV block is characterized by sudden unexpected blocked P waves without variation or prolongation of the PR interval. in the His–Purkinje system is the most likely cause. and often accompanying bradycardia. is characterized by progressive prolongation of the PR interval causing progressive R–R interval shortening until a P wave fails to conduct to the ventricle. For these reasons. beta– blockers. Patients may have an irregular heart rate. however. with Mobitz II more likely to present with dizziness. AV nodal dysfunction accounts for the majority of cases. in the His–Purkinje system. in patients with more severe signs of heart failure or pulmonary edema. or toxicity relating to digitalis.EDUCATIONAL GUIDELINES duction. particularly inferior wall AMI. nitrospray’s onset is 1–3 minutes with a half–life of 5 minutes. Second–degree heart block requires no specific prehospital therapy. Patients with concomitant myocardial infarction (MI) may exhibit signs related to AMI. or calcium channel blockers. dopamine is reserved to be used with caution in patients whose blood pressure requires maintainance to continue the administeration of IV nitrates. or Wenckebach block. myocarditis. Patients may have symptoms of myocardial ischemia or myocarditis. SL and nitrospray are particularly useful in the patient who presents with acute pulmonary edema with a systolic blood pressure of at least 100 mm Hg. but the examination is otherwise generally unremarkable. Morbidity and mortality rates from heart disease appear to be unaffected by the presence of first–degree block. and drugs such as calcium channel blockers. Dopamine is a positive inotropic agent at 2–10 mcg that can lead to tachycardia. No specific therapy is required by the clinician. Mobitz II most commonly is caused by AMI (anterior or inferior). Mobitz I (Wenckebach) block is caused by conduction delay in the AV node in 72% of patients and by conduction delay in the His–Purkinje system in the other 28%. The . it may also be drug related. patients with concomitant AMI should receive appropriate therapy First–degree heart block is generally an incidental finding noted on ECG without any particular associated signs. which reduces systemic vascular resistance (SVR) and increases cardiac output. Patients may also have symptoms of myocardial ischemia or a history of organic heart disease. often with associated cardiovascular collapse. enhanced vagal tone. Mobitz II block carries a high risk of progression to complete heart block. which increases afterload. dopamine is the agent usually employed. and digitalis. which reduces preload. especially in the setting of an acute overdose. These drugs increase the refractory time of the AV node. its most important effect is venodilation. Both Mobitz I and Mobitz II blocks may present in the same way. or first–degree atrioventricular (AV) block. Similar to SL. In addition to being both an anxiolytic and an analgesic. IV nitroglycerin is preferred since it is easier to monitor hemodynamics and absorption. However. Oral nitrates. The PR interval is defined as the time from the initial deflection of the P wave from the baseline to the beginning of the QRS complex. particularly in the diaphoretic patient. lightheadedness. have little role in the acute presentations of CHF. Second–degree AV block comprises 2 types. Most are asymptomatic. often with accompanying hemodynamic instability. if acute MI is the underlying cause) but is likely to be ineffective unless the escape QRS complex is narrow. and death. which may be profound.e. Symptomatic patients will have signs of hypoperfusion. Valsalva. Transcutaneous pacing in the symptomatic patient is always appropriate. The ventricular escape mechanism may originate anywhere from the AV node to the bundle branch–Purkinje system. further slowing the heart rate. For example. Therefore. also referred to as third–degree atrioventricular (AV) block or complete heart. causing increased ventricular irritability and. atropine generally is ineffective. it’s presence is an indication for TCP. atropine should be tried first. Third–degree heart block may be congenital or acquired. Symptoms are more likely to be minimal in patients with narrow complex escape rhythms. metabolic disturbances and cardiomyopathies are some causes for this condition. oxygen administration. The physical examination will be notable for bradycardia. Patients with complete heart block frequently are hemodynamically unstable. thereby decreasing refractory time and speeding conduction through the AV node. blocks the effects of acetycholine at the AV node. The possibility of progression to higher degrees of block is always present and should be the primary concern. Careful monitoring is essential. Not all patients with AV dissociation have complete heart block. If clinicians are concerned about the use of atropine in higher–level blocks. because no AV conduction disorder is present. There is little to suggest that pacing will markedly change outcome. confusion. The goal is to improve conduction through the AV node by reducing vagal tone via atropine–induced receptor blockade. Block below the His bundle accounts for the majority o cases (approximately 61%). Third–degree heart block. and AV dissociation is complete. especially when the escape rhythm is wide and slow. or the bundle branch–Purkinje system. syncope. Acute inferior wall MI. Regularized atrial fibrillation is the classic sign of complete heart block due to digitalis toxicity. sudden death. This is effective only if the site of the block is the AV node. Follow standard advanced cardiac life support (ACLS) guidelines in Bradycardic patients. patients are profoundly symptomatic. patients with accelerated junctional rhythms that are faster than their native sinus rates have AV dissociation but not complete heart block. Similarly. or associated AMI symptoms. including the follow: Hypotension. If treatment is required. lethargy. In addition. Furthermore. This may lead to cardiovascular collapse. Atropine enhances sinus node automaticity. Atropine can be administered (cautiously. transcutaneous pacing with the symptomatic patient. Vagolysis leads to unopposed sympathetic stimulation. IV access and avoidance of maneuvers likely to increase vagal tone (i. E . The prognosis for patients who develop complete heart block is poor because of it’s usual association with extensive myocardial injury. DRUG CATEGORY: Anticholinergic – Drug therapy in second–degree heart block is aimed at vagolysis. and congestive heart failure. it carries a significant risk of progression to complete heart block. signs of acute myocardial infarction may be evident on examination. potentially. Insufficient doses may cause paradoxical effects. For patients with infranodal second–degree heart block. No P waves conduct to the ventricle. TCP may be necessary if atropine is not effective or if hemodynamically significant slowing is recurrent. These would include beta–blockers.. In patients with concomitant AMI.46 Prehospital treatment consists of rapid transport. Atropine is the only currently available agent. Because new onset Mobitz II patients have a propensity for progression to complete heart block. Third–degree heart block is caused by conduction block at the level of the AV node. is a disorder of the cardiac conduction system with complete absence of AV conduction. The rhythm is regularized because of the junctional escape rhythm. Drug therapy in third–degree heart block is aimed at 2/15/06 . altered mental status.EMERGENCY MEDICAL GUIDELINES bradycardia. When second–degree AV block of the Mobitz type 11 variety is associated with infarction. Symptoms may include the following: syncope. Atropine may in fact enhance the block or precipitate third degree AV block. ventricular tachycardia (VT)/ ventricular fibrillation (VF) when atropine is administered in suspected AMI. the His bundle. atropine is much less likely to be successful in Mobitz II block. second–degree AV block of the Mobitz 1 (Wenckebach) variety does not require therapy in the absence of hemodynamically significant slowing of the ventricular rate. remember that transcutaneous pacing (TCP)is a class 1 intervention and is ALWAYS appropriate. calcium channel blockers and digitalis glycorides. painful stimuli). Most commonly. RATIONALE First–degree AV block alone does not require treatment. The reestablishment of sequential atrioventricular contraction maybe of some value in these patients. Use caution in administering atropine to a patient with suspected AMI. Patients may have a prior history of organic heart disease or be on medications that affect AV nodal conduction. drug intoxication. because atropine has been reported to precipitate ventricular tachycardia or ventricular fibrillation in second–degree blocks. consider applying pacing pads to patients even if they are asymptomatic during prehospital care and transport. acts on dopaminergic receptors in renal and splanchnic vascular beds. most commonly. Fever may be low grade or absent. . myocardial ischemia in the denervated heart results in chest pain. In high doses (15–20mcg/kg/min). The one–year survival rate is approximately 85% in experienced centers. Symptoms associated with infection may be masked because of the immunosuppressant regimen. Moderately severe rejection may include hemodynamic compromise presenting with myocardial dysfunction. acts on alpha–adrenergic receptors to increase systemic vascular resistance and raise BP. because these conditions may have subtle presentations. alpha–adrenergic receptors are stimulated to a lesser degree. decreased heart sounds. The graft includes the sinus node so that a sinus rhythm is possible after transplantation. it can respond to cardiovascular influences by humoral mechanisms but not by sympathetic or parasympathetic nerve stimulation. The most common problems in the heart transplant recipient that may be observed are graft rejection. causing systemic vasoconstriction and increased BP. and the 5–year survival rate exceeds 65%. Graft rejection is controlled through an immunosuppressant regimen. The latter may lead to volume overload and hypertension. DRUG CATEGORY: Vagolytics – The goal is to improve conduction through the AV node by reducing vagal tone via muscarinic receptor blockade. and decreased exercise tolerance. and cardiac output. causing vasodilation in these beds. Chronic rejection involves progressive coronary artery stenosis over the course of years and terminates in myocardial ischemia with its attendant consequences. tachycardia. acts on beta–adrenergic receptors to increase heart rate and contractility. An ECG is indicated in all but minor complaints. Catecholamines have only a limited role. survival rate following transplantation exceeds that following medical therapy. Chances are good that the clinician will encounter patients who have undergone heart transplantation. and prednisone. The heart transplant recipient averages perhaps 1–2 rejection episodes per year. Insufficient doses may cause paradoxical effects. With advances in surgical technique and immunosuppression. cardiac contractility. Epinephrine stimulates beta–adrenergic receptors. however. survival rate following transplantation significantly exceeds that following medical therapy. azathioprine. Dopamine in low doses 2–5mcg/kg/min. further slowing the heart rate. infection. most rejection episodes are minor and are treated with steroids and adjustments in immunosuppressant dosages. Acute rejection is cell mediated and results in myocardial dysfunction in more severe cases. Because the transplanted heart is denervated. Acute rejection is not associated with specific physical findings. A major E . Acute cell–mediated rejection is most common in the first 3 months following transplant and decreases in frequency with time. The most common cause of death is infection. The donor heart is resected at the atria and. Atropine enhances sinus node automaticity and blocks effects of acetylcholine at the AV node. For patients with infranodal block. this therapy is ineffective. Vigilance must be maintained to detect rejection and infection. malaise. This is effective only if the site of the block is within the AV node. predominatly by increasing heart rate. and 4000 patients are awaiting transplantation. thereby decreasing refractory time and speeding conduction through the AV node. Approximately 2400 transplantations are performed annually. and signs of decreased peripheral perfusion such as distal cyanosis. Heart transplantation involves excision of the recipient’s heart above the atrioventricular valves and replacement with the donor heart. Patients with moderately severe to severe rejection may present with hypotension. and renal dysfunction. Mild rejection may have no physical findings and must be diagnosed by endomyocardial biopsy. Heart transplant recipients may present to the emergency worker with any complaint observed in the general population. A long–term immunosuppression usually is maintained with cyclosporine. fatigue. some patients need lifelong pacing. DRUG CATEGORY: Catecholamines – These agents improve hemodynamics by acting via beta–adrenergic receptor stimulation to increase the heart rate and contractility and via alpha–adrenergic receptor stimulation to increase systemic vascular resistance. Symptoms of mild rejection are nonspecific and may include low–grade fever. In mid–range doses (5–15mcg/kg/ min). In patients with advanced heart failure. is placed into the recipient at the level of the atria and at the base of the aorta and pulmonary artery.EDUCATIONAL GUIDELINES vagolysis.47 2/15/06 HEART TRANSPLANT PATIENTS Heart transplantation has become an accepted and definitive therapy for end–stage heart failure. Extremely rarely. with atropine being the only currently available agent. and acute rejection is the second most common cause. RATIONALE The main goal of treatment are rapid identification of candidates for thrombolysis.48 2/15/06 . which produces thromboxane A2. This usually results from plaque rupture with thrombus formation in a coronary vessel. but reperfusion within this period can salvage the myocardium and reduce morbidity and mortality. Prevents reaccumulation of clot after spontaneous fibrinolysis. Heparin augments activity of antithrombin lll and prevents conversion of fibrinogen to fibrin. usually across the anterior precordium. or percutaneous transluminal angioplasty and preservation of coronary artery patency and the myocardium. It usually indicates a large infarct and may be observed with right ventricular infarct. The left arm is affected more frequently than the right arm. syncope. promote pulmonary toilet. anxiety. normal or nonspecific findings do not exclude the possibility of AMI. or it may reflect elevated catecholamines do to anxiety or pain. Total occlusion of the vessel for more than 4–6 hours results in irreversible myocardial necrosis. Significant ST–segment changes in the ECG are indicative of a high probability for AMI however. which decreases sympathetic stress. high cholesterol and/or triglycerides. pressure. a potent platelet activator. intravenous volume loading of up to 1 to 2L is appropriate to achieve this objective. Morphine is the DOC for analgesia because of its reliable MYOCARDIAL INFARCTION Acute myocardial infarction (AMI) is the rapid development of myocardial necrosis caused by a critical imbalance between the oxygen supply and demand of the myocardium. resulting in an acute reduction of blood supply to a portion of the myocardium. neck. and have sedating properties. DRUG CATEGORY: Vasodilators – Opposes coronary artery spasm. Nitroglycerin causes relaxation of vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphate production. In the setting of AMI. There is an added mortality benefit when used in combination with thrombolytics. thrombus formation. be aggressive only if evidence of hypovolemia exists. which are beneficial for patients who experience chest discomfort resulting from a myocardial infarction. The most common cause of AMI is narrowing of the epicardial blood vessels due to plaque. and vascular death. fibrin accumulation. Type A personality. Early administration has been shown to reduce 35–day mortality rate by 23% compared to a placebo. poorly controlled hypertension. which augments coronary blood flow and reduces cardiac work by decreasing preload and afterload. back. The predominant cause of myocardial infarction is a rupture of an atherosclerotic plaque with subsequent spasm and clot formation. being male older than 70 years. topical administration is less desirable route because of unpredictable absorption and onset of clinical effects. coronary reperfusion via thrombolytic therapy. Pain may radiate to the jaw. arms. The result is a decrease in blood pressure. and varying degrees of vasospasm. This can result in partial or complete occlusion of the vessel and subsequent myocardial ischemia. Hypertension may precipitate AMI. The patient may also report nausea and/or abdominal pain often associated in inferior wall infarcts. Performing 12 lead V4R – RV dysfunction and acute infarction are very dependant on maintenance of RV filling pressures to maintain cardiac output. is described as tightness. Over– resuscitation can lead to worsening of right ventricular failure. or IV. patients once they arrive at the ED. a family history. The clinician may also observe diaphoresis and wheezing. Therefore. It is effective in the management of symptoms in AMI but may reduce the mortality rate only slightly. Aspirin is administered as soon as possible. Fluid resuscitation in patients presenting with hemodynamic compromise should be approached carefully. Hypotension indicates ventricular dysfunction due to ischemia. AMI is the leading cause of morbidity and mortality in the United States. Nitroglycerin can be administered sublingually by tablet or spray. DRUG CATEGORY: Antithrombotic agents – These agents prevent the formation of thrombus associated with myocardial infarction and inhibit platelet function by blocking cyclooxygenase and subsequent aggregation. fatal strokes. Does not actively lyse preformed clot. Antiplatelet therapy has been shown to reduce mortaility by reducing the risk of fatal myocardial infarctions. Plaque rupture with subsequent exposure of the basement membrane results in platelet aggregation. and sedentary lifestyle. lightheadedness. or squeezing. CHF. The risk factors associated with plaque formation include: age. topically. but it is able to inhibit further thrombogenesis after thrombolysis. Performing fibrinolytic screening in the prehospital setting is intended to speed up the administration of thrombolytic agents to eligible E . May provide some preload reduction. hemorrhage into the plaque. Analgesics ensure patient comfort. DRUG CATEGORY: Analgesics – Reduce pain. Chest pain.EMERGENCY MEDICAL GUIDELINES goal of the emergency worker is to evaluate for evidence of infection or rejection in patients who present with compatible symptoms. cough. Aspirin inhibits cyclooxygenase. smoking. and epigastrium. electric impulses are transmitted to the heart.e.49 2/15/06 . usually via the subclavian. For proper permanent pacer operation. commonly titrated until a desired effect is obtained. and improper amplitude or pulse width settings. and failure to sense correctly. If these potentials are too infrequent or absent. Alternately. Placing a magnet over a permanent pacemaker causes sensing to be inhibited by closing an internal read switch. In the demand mode. emergency workers must understand their common problems in order to manage them effectively. In the fixed–rate mode.. PACEMAKER & AUTOMATIC INTERNAL CARDIAC DEFIBRILLATOR Among the myriad of patients emergency workers evaluate daily are those with pacemakers and implantable cardioverter–defibrillators (ICD’s). the sensing circuit searches for an intrinsic depolarization potential. and a timing circuit. The application of a magnet can determine if the pacer’s battery needs to be replaced. With permanent systems. among other things. poor lead connection at the takeoff from the generator. with extra consideration given to treating metabolic abnormalities and potential myocardial infarction. An ICD is a specialized device designed to directly treat a cardiac tachydysrhythmia. a break in insulation. The battery most commonly used in permanent pacers is a lithium–iodide type and has a life span of 5–8 years. lead fracture. where pacing is initiated at a set rate. an elevated pacing threshold. a battery. however. This information is crucial when communicating with the cardiologist or ED about a pacer problem. safety profile. Signal amplitude is measured in electrical units of volts or milliamperes. Note that newer devices are a combination of ICD and pacemaker in one unit. The pulse generator is placed subcutaneously or submuscularly and connected to the leads. failure to capture. the device. Patients should carry a card with them providing information about their particular model. Pulse generators can be set to a fixed–rate (asynchronous) or demand (synchronous) mode. myocardial infarction at the tip. oversensing. a phenomenon seen when atrial output is sensed by a ventricular lead in a dual–chamber pacer). a pacing response is generated.EDUCATIONAL GUIDELINES and predictable effects. This may be due to battery failure. thereby stimulating myocardial contraction. If this is absent. hyperkalemia. lead dislodgement. usually around 10. acidosis. This temporarily “reprograms” the pacer into the asynchronous mode. Pacemaker energy output is dependent upon the signal RATIONALE Failure to capture occurs when either an atrial or a ventricular complex does not follow a pacing spike. Management of pacer capture complications is the same as for output complications. Pulse generators contain. may attempt to pace rapidly for a number of pulses. Major pacemaker complications include failure to output. Although numerous issues may arise with these devices. and ease of reversibility with naloxone. have an x– ray code that can be seen on a standard chest x–ray.. an output circuit. Various IV doses are used. These combination ICD/pacemakers are implanted in patients who require both devices. a sensing circuit. cardiac perforation. yet low enough to prolong battery life. an impulse is produced at a set rate and has no relationship to the patient’s intrinsic cardiac activity. certain drugs. This may be due to lead failure. They function by sensing intrinsic cardiac electric potentials. amplitude and pulse width. or cephalic vein. Most pacemaker generators. if so programmed. and advanced to the right ventricle and/or atrium. This mode carries a small but inherent danger of producing lethal dysrhythmias should the impulse coincide with the vulnerable period of the T wave. If a patient has a ventricular ICD and the device senses a ventricular rate that exceeds the programmed cut–off rate of the ICD.e. to attempt pace–termination of the ventricular tachycardia. endocardial leads are inserted into the venous system. metabolic abnormalities (i. the device performs cardioversion/defibrillation. signal amplitude and width are set high enough to reliably achieve capture of the myocardium. axillary. Failure to output occurs when no pacing spike is present despite an indication to pace. Pulse width is a measure of output duration and is measured in milliseconds. and “cross–talk” (i. alkalosis). Oversensing occur when a pacer incorrectly senses elecE . and a break in lead insulation. Permanent pacemakers are devices that provide electrical stimuli to cause cardiac contraction during periods when intrinsic cardiac electrical activity is inappropriately slow or absent. poor lead connection at the takeoff from the pacer. Pacing systems consist of a pulse generator and pacing leads. PSVT may start suddenly and last for seconds or days.. then to the bundle of His and the bundles branches. This should be considered if a patient presents in atrial fibrillation or if a patient has received multiple shocks in rapid succession without premonitory symptoms. Patients with WPW syndrome may be at risk for cardiac arrest if they develop AF or atrial flutter in the presence of a rapidly conducting accessory pathway. involves abnormalities in impulse formation and conduction pathways. and coexisting diseases. SVT occurs in all age groups. the duration of the PSVT. WPW). SVT may be classified as an atrial or atrioventricular tachyarrhythmia. a common clinical condition. one study found that one third of patients with SVT experienced syncope. It is helpful to characterize SVT by comparing the RP interval to the PR interval. A 12 lead ECG allows classification of the tachyarrhythmia. ineffective cardioversion/defibrillation. Atrioventricular reentrant tachycardia (AVRT) is the second most common form of PSVT. and treatment can be challenging. Inappropriate cardioversion is most frequent complication associated with ICD’s. Supraventricular tachycardia (SVT).50 2/15/06 . In fact. Incessant SVT can cause tachycardia–induced cardiomyopathy. This produces a short PR interval and a delta wave as seen in Wolff–Parkinson–White. infection. A final category of pacer failures is termed operative. required cardioversion. when present. magnet application.EMERGENCY MEDICAL GUIDELINES trical activity and is inhibited from correctly pacing. inhibit bradycardic pacing should the patient require it. AVRT is the result of 2 or more conducting pathways: the AV node and 1 or more bypass tracts. In a normal heart. The accessory pathways may conduct impulses anterogradely. and device deactivation. Patients may present with mild or severe cardiopulmonary complaints depending on their hemodynamic reserve as well as their heart rate. Chest discomfort may be secondary to rapid heart rate. In short RP tachycardias. This may be due to muscular activity. This includes malfunction due to mechanical factors. is any tachyarrhythmia that requires only atrial and/or atrioventricular (AV) nodal tissue for its initiation and maintenance. The most common cause of PSVT is AV nodal reentrant tachycardia (AVNRT). AVNRT is diagnosed in 50 –60% of patients who present with regular narrow QRS tachyarrhythmia. and venous thrombosis. however. or lead insulation breakage. P waves may not be visible. or had an episode of sudden death. pulmonary edema. Major ICD complications include operative failure. lead dislodgment. Treatment depends on the etiology. It usually is a narrow complex tachycardia that has a regular. Patients. and it may allow a precise diagnosis. ventricular preexcitation results. The heart rate is 120–150 bpm and typically is quite regular. 1 or more accessory pathways connect the atria and the ventricles. In short RP tachycardias. electromagnetic interference. If the magnet is left on for approximately 30 seconds. particularly oversensing of the diaphragm or pectoralis muscles. exceptions include atrial fibrillation (AF) and multifocal atrial tachycardia (MAT). In the absence of manifest preexcitation (i. skin erosion. In AVRT. the P wave is found within the QRS complex or shortly after the QRS complex. When impulses travel down the accessory pathway in an anterograde manner. Following termination of the tachycardia. an ECG should be obtained during sinus rhythm to screen for WPW syndrome. It does not however. Conduction begins at the sinus node. Extremely rapid ventricular rates during AF or atrial flutter can cause deterioration to ventricular fibrillation. the risk of sudden death with PSVT is extremely PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA (PSVT) Paroxysmal supraventricular tachycardia (PSVT) is episodic with an abrupt onset and termination. Depending on the site of origin of the dysrhythmia. It is important to note that AVNRT does not involve the ventricles as part of the reentry circuit. such as pneumothorax. Long RP tachycardias result when atrial activity precedes the QRS complex. progresses to the AV node. or myocardial infarction. studies have determined that the pathophysiology of SVT E . Management is similar to that for other types of failures. Undersensing occurs when a pacer incorrectly misses intrinsic depolarization and paces despite intrinsic activity. and it frequently subsides with the termination of the tachycardia. low battery states. This may be due to poor lead positioning. sensing and/or pacing failures. only a single route of conduction is present. lead dislodgement. hematoma. atrial activity occurs simultaneously with or shortly after ventricle excitation. pericarditis. myocardial ischemia. PSVT can result in heart failure. Aberrant conduction during SVT results in a wide complex tachycardia. the ICD is disabled and a continuous tone is generated. rapid rhythm. inappropriate cardioversion. retrogradely or both. Operative failures are identical to those found in regular pacemakers.e. and/or myocardial infarction secondary to increased heart rate in patients with poor left ventricle function. Use of a magnet over the ICD inhibits further shocks. Palpitations and dizziness are the most common symptoms reported by patients with SVT. they may be normal or abnormal depending on the mechanism of atrial depolarization. More than 90% of patients convert to sinus rhythm with adenosine 12mg. Lidocaine is the DOC in the setting of complex ectopy in the peri–MI period if the patient is symptomatic. As a result of its short half–life. With electrolyte imbalances. lidocaine shortens repolarization. DRUG CATAGORY: Calcium Channel Blocker – This drug decreases conduction velocity and prolongs the refractory period. even though about half have no clinical symptoms to suggest PE. correction of abnormalities is therapeutic. This. The net effect is to decrease firing of ectopic foci and allow a normal rhythm to reassert itself. platelets. Adenosine (Adenocard) is a first–line medical treatment for termination of PSVT. being second only to coronary artery disease as a cause E . In drug toxicity specific therapies are available. A good clinician actively seeks the diagnosis as soon as any suspicion of PE whatsoever is warranted. It also increases the refractory period via blockade of calcium influx.51 PREMATURE VENTRICULAR CONTRACTIONS (PVC) Therapy for complex ventricular ectopy depends on the setting and the underlying cause. Myocardial excitability is reduced by causing an increase in the threshold for excitation and inhibition of ectopic pacemaker activity. yet no firm evidence supports this practice. The belief that calf vein deep vein thrombosis (DVT) is only a minor threat is outdated and inaccurate. the diagnosis is missed far more often than it is made. It is effective in terminating both AVNRT and AVRT. because prompt diagnosis and treatment can dramatically reduce the mortality rate and morbidity of the disease. it is an often–fatal complication of underlying venous thrombosis. PE is the third most common cause of death in the US. It may be effective when Lidocaine has not achieved suppression. It is a short–acting agent that alters potassium conductance into cells and results in hyperpolarization of nodal cells. Unfortunately. Massive PE is one of the most common causes of unexpected death. Lidocaine suppresses ventricular arrhythmias predominatly by decreasing automaticity by reducing the slope of diastolic depolarization as seen in the QRS complex. Lidocaine seems to be more effective during AMI. Under pathological conditions. thetic properties may also help to suppress ventricular ectopy during an AMI. Furthermore. prevent complications. These arrhythmias depend on AV nodal conduction and therefore can be terminated by transiently blocking AV nodal conduction. Pulmonary thromboembolism is not a disease in and if itself. microthrombi (tiny aggregates of red cells. and reduce morbidity. in turn. 90% of tachycardia due to AVNRT or AVRT can be terminated with Adenosine. Thrombus in the popliteal segment of the femoral vein (the segment behind the knee) is the cause of PE in more than 60% of cases. The routine use of Lidocaine is no longer recommended. Under normal conditions. DRUG CATEGORY – Antiarrhythmics – These agents alter the electrophysiologic mechanisms responsible for PVC’s. and fibrin) are formed and lysed continually with the venous circulatory system. DRUG CATAGORY: Antiarrhythmic agents – These drugs can be used to treat or prevent arrhythmia. Studies suggest that nearly every patient with thrombus in the upper leg or thigh will have a PE if a sensitive enough test is done to look for it. one third of the cases of massive PE have their only identified source in the veins of the calf. stops the reentrant phenomenon. It increases the refractory period of the atria and the ventricles. because PE often causes only vague and nonspecific symptoms. The toxic–to–therapeutic balance is delicate. This increases the threshold to trigger an action potential and results in sinus slowing and blockage of AV conduction.EDUCATIONAL GUIDELINES low. Its local anes- 2/15/06 . Patients who are hemodynamically unstable should be resuscitated immediately with cardioversion. PE occurs when these clots break loose and embolize to block pulmonary blood vessels. The majority of the patients who present with PSVT have AVNRT or AVRT. RATIONALE The goals of pharmacotherapy are to correct arrhythmia. Rather. microthrombi may escape the normal fibrinolytic system to grow and propagate. Procainamide may also be used to treat PVC’s. adenosine is best administered in an antecubital vein as an IV bolus followed by a rapid saline infusion. DVT of the calf is a significant source of PE and often causes severe morbidity or death. Lidocaine stabilizes cell membranes and blunts action potential. This dynamic equilibrium ensures local hemostasis in response to injury without permitting uncontrolled propagation of clot. Diltiazem (Cardizem) Decreases conduction velocity in the AV node. PULMONARY EMBOLISM (PE) Pulmonary embolism (PE) is an extremely common and highly lethal condition that is a leading cause of death in all age groups. Current techniques allow us to demonstrate PE in 60–80% of these patients. In fact. high fever. acidosis). Patients may present with recordable aortic pressures and absent peripheral pulses from weak cardiac contractions or severe peripheral vascular disease. because IV fluids may worsen the patient’s condition. new onset of wheezing. and severe CHF. The initiation of ACLS may improve patient outcome if a reversible cause is identified and rapidly reversed. This event creates a vicious cycle. A spontaneous return of pulse is likely. In preload and afterload changes: severe hypovolemia. As long as no reliable method is available of making a clinical diagnosis of PE without diagnostic tests. and most of those who do have symptoms have an atypical presentation. or sodium bicarbonate administration. shoulder pain. Some common causes are: respiratory arrest. Further compromise of the inotropic state of cardiac muscle leads to inadequate mechanical activity. This form of electromechanical decoupling may be the final result of many factors. upper abdominal pain. massive pulmonary embolus) often result in PEA. prolonged immobilization. PEA is classified on the basis of etiology. and increasing vagal tone. rewarming. tension pneumothorax. PEA is most frequently the end result of a major cardiac insult and commonly is caused by respiratory failure with hypoxia. and this situation is exacerbated by worsening acidosis. For this reason. This may include chest decompression. Hypoxia secondary to respiratory failure is probably the most common cause of PEA. shortness of breath. Post–defibrillation PEA may be a marker for a better prognosis than if ventricular fibrillation continues. syncope. painful respiration. or underlying malignancy. productive cough. fibrinolytic therapy has been the standard of care for all patients with massive or unstable PE since the 1970’s. Symptoms that should provoke a suspicion of PE must include chest pain. syncope. Patients with PE often present with primary or isolated complaints of seizure. massive pulmonary embolus and sepsis may be the cause.e. These paE . In metabolic changes: hyperkalemia. hypothermia.. The most important thing that can be done in the prehospital setting is to transport the patient to a hospital. In the hospital. Many patients with PE are initially completely asymptomatic. dyspnea and chest pain. causing degeneration of the rhythm and subsequent death of the patient. PEA is caused by the inability of cardiac muscle to generate a sufficient force despite an electrical depolarization. back pain. The overall mortality rate is high in patients in whom PEA is the initial rhythm during cardiac arrest. digitalis. any new cardiac arrhythmia. The classic triad of signs and symptoms of PE are hemoptysis. The most important clinically identifiable risk markers for DVT and PE are a prior history of the same. because the diagnosis is unsuspected until autopsy in approximately 80% of cases. PEA is also referred to as electromechanical dissociation (EMD).52 RATIONALE The goals of pharmacotherapy are to reduce morbidity and 2/15/06 . hemoptysis. Most clinicians do not appreciate the extent of the problem. PEA is considered a rhythm of survival. The initial insult weakens cardiac contractions. Oxygen should always be started in the prehospital phase. calcium channel blockers). PULSELESS ELECTRICAL ACTIVITY (PEA) Pulseless electrical activity (PEA) is a clinical condition characterized by loss of palpable pulse in the presence of recordable cardiac electrical activity.e. occurring immediately after electrical cardioversion and in the absence of palpable pulse. This condition may result in PEA in as many as 60% of patients. or any of a host of other signs and symptoms. Fluid loading should be avoided unless the patient’s hemodynamic condition is deteriorating rapidly. abdominal pain. severe prolonged hypoxia. chest wall tenderness. Situations that cause sudden changes in preload or afterload (i. Reversible causes should be sought out and corrected immediately. cardiac tamponade. of sudden unexpected natural death at any age. volume infusion. new–onset atrial fibrillation. Post–defibrillation PEA is characterized by the presence of organized electrical activity. the clinician cannot know weather additional preload will help or hurt a heart that is failing already because of high outflow pressures from pulmonary vascular obstruction. True PEA is a condition in which cardiac contractions are absent in the presence of coordinated electrical activity. drug ingestion (TCA. Rapid initiation of advanced cardiac life support (ACLS) is paramount.. disseminated intravascular coagulation. and an IV line should be placed if it can be accomplished rapidly without delaying transport. PEA is always caused by a profound global cardiac insult (i. treating PE in a meaningful way in the field will remain difficult. cardiac rupture. recent surgery or pregnancy. hypoxia. even though electrical activity is present.EMERGENCY MEDICAL GUIDELINES tients are classified as having pseudo–PEA. massive myocardial infarction. pericardiocentesis. and cardiopulmonary resuscitation (CPR) should be continued for as long as 1 minute to allow for spontaneous recovery. or any other unexplained symptom referable to the thorax. PEA may result various etiologies and has a spectrum of manifestation. Without invasive testing or trial and surveillance. electrolyte disorders. Physiologic causes of increased vagal tone include bradycardia seen in athletes. bronchial smooth muscle relaxation. dyspnea. RATIONALE Drug treatment for sinus bradycardia usually is not indicated for asymptomatic patients. atropine and pacing usually are not recommended because of myocardial irritability. Epinephrine (Adrenalin) has alpha–agonist effects that include increased peripheral vascular resistance. Sick sinus syndrome occurs most commonly in elderly patients with concomitant cardiovascular disease and follows an unpredictable course. However. few patients actually become symptomatic until their heart rate drops to less than 50 beats/minute. causing an increase in cardiac output. although it may reveal the following signs: decreased level of consciousness. where available. Main therapeutic effects are cardiac stimulation. In symptomatic patients. systemic hypotension. isoproterenol was used quite commonly in patients with bradycardia. Routine administration is discouraged because it worsens intracellular and intracerebral acidosis and is not proven to benefit mortality. TCA. The pathophysiology of sinus bradycardia is dependant upon the underlying cause. which involves a dysfunction in the ability of the sinus mode to generate or transmit an action potential to the atria. in associated with sinus bradycardia. or alternating episodes of bradycardia and tachycardia. Identifying all possible causes and attempting to correct them is of the upmost importance to the survivibility of this rhythm. Although in the past. regular heart rate. Unstable patients may require immediate endotracheal intubation and transcutaneous pacing. or a long arrest interval in the intubated patient Routine use is not recommended. is the initial procedure of choice. This is followed by an investigation into the underlying cause of the bradycardia. but are not limited to. hypothyroidism. toxic or environmental exposure. DRUG CATEGORY: Anticholinergics — These agents are indicated when symptoms of hypoperfusion exist.EDUCATIONAL GUIDELINES prevent complications. IV atropine may provide temporary improvement in symptomatic patients. Pathologic causes include. Beta–agonist effects of epinephrine include bronchodilation. Cardiac auscultation and palpation of peripheral pulses reveal a slow. and increased intrac- 2/15/06 . infection. It works to increase heart rate through vagolytic effects. underlying electrlyte or acid–base disorders or hypoxia should be corrected. Sick sinus syndrome includes a variety of disorders and pathologic processes that are grouped within one loosely defined clinical syndrome. and positive inotropic effects. reversed peripheral vasodilation. DRUG CATEGORY: Alkalinizing agents – Useful in alkalinization of urine. Transcutaneous pacing. ranial pressure. Fluid Resusitation – Hypovolemia is the most common cause of electrical activity without measurable blood pressure. or in whom atropine therapy is contraindicated. hypoglycemia. Atropine is used for treatment of bradyarrhythmias. most ultimately require placement of a pacemaker. carotid hypersensitivity. chronotropic cardiac activity. DRUG CATEGORY: Anticholinergic agents – Improve conduction through the AV node by reducing vagal tone via muscarinic receptor blockade. and vascular permeability. DRUG CATEGORY: Inotropic agents – Increases the central aortic pressure and counter myocardial depression. pulmonary vascular congestion. The syndrome includes signs and symptoms related to cerebral hypoperfusion. In patients with hypothermia who have confirmed sinus bradycardia with a pulse. or phenobarbital overdose. Bradycardic TCP – May be beneficial early on because a healthy myocardium exists and only a temporarily disturbed cardiac conduction system stands between survival and death. This is the most common cause of symptomatic sinus bradycardia. atropine may aide patients transiently. although its use should be balanced by an appreciation of the increase in myocardial oxygen demand this agent causes. sinus arrest. peripheral edema. Other causes of sinus bradycardia are related to increased vagal tone. sleep apnea. They are thought to work centrally by suppressing conduction in the E . and dilation of skeletal muscle vasculature. Emergency care should first rapidly ensure the stability of the patient’s condition. Sodium Bicarbonate is used only when a patient is diagnosed with bicarbonate–responsive acidosis. Sinus bradycardia also may be caused by the sick sinus syndrome. Rewarming and supportive measures are the mainstays of therapy. hyperkalemia.53 SINUS BRADICARDIA Sinus bradycardia can be defined as a sinus rhythm with a resting heart rate of 60 beats/minute or less. Temporary pacing is recommended in symptomatic patients who are unresponsive or only temporarily responsive to atropine. In sick sinus syndrome. cyanosis. further appreciation of its substanial risks has deminished its role. drug effects. The physical examination is generally nonspecific. inferior wall MI. Through prompt recognition and fluid challenge. many causes of hypovolemia can be corrected. sinoatrial (SA) block. and poor perfusion. brain and myocardium are most susceptible. because it reminded the original authors of the torsade de pointes movement in ballet. The pre–hospital provider should institute immediate advanced cardiac life support (ACLS) protocol for VT. VF often occurs without forewarning. preexcitation syndromes. Sudden loss of cardiac output with subsequent tissue hypoperfusion creates global tissue ischemia. Atropine is used to increase heart rate through vagolytic effects. VT degenerates into VF. and is associated with sudden death due to either primary ventricular fibrillation or torsade that degenerates into ventricular fibrillation. The acquired conditions that predispose one to torsade either decrease the outward potassium current or interfere with the inward sodium and calcium currents. Because of the critical importance of early defibrillation.000 SCD cases in the US annually. Differentiating between these entities. palpitations.54 2/15/06 Ventricular fibrillation (VF) is a pulseless arrhythmia with irregular and chaotic electrical activity and ventricular contraction in which the heart immediately loses its ability to function as a pump. it generally should not be used in combination with another agent that prolongs the QT interval. therefore.000 sudden cardiac deaths occur per year. The ventricular rate can range from 150 beats per minute (bpm) to 250 bpm. VF usually develops secondary to an area of myocardial ischemia with a lowered fibrillation threshold. An often–described R–on–T extrasystole phenomenon may account for many VF cases. VF is the primary cause of sudden cardiac death (SCD). In the absence of ischemic heart disease. drive pacing may be necessary at a rate of up to 140 bpm to control the rhythm in a patient with torsade who is in extremis. Cardiovascular diseases cause 12 million deaths in the world each year and are the primary causes of death in the US. defibrillation. Untreated. Propagation to the whole myocardium implies that the initial fibrillation reached sufficient critical mass. such as amiodarone. OverE . thus. syncope and a possible increase in heart rate. Torsade usually occurs in bursts that are not sustained. In the US.EMERGENCY MEDICAL GUIDELINES vastibular cerebellar pathways. Torsade is defined as a polymorphous VT in which the morphology of the QRS complexes varies from beat to beat. dyspnea. VF can be initiated in ischemic heart disease when a premature ventricular contraction (PVC) overcomes a lowered fibrillation threshold. This was symbolically termed torsade de pointes. unconsciousness and wide and chaotic QRS complexes on the cardiac monitor. 300. Fibrillation is caused by simultaneous presence of abnormal irregular beats. Physical findings in VF reveal no pulse or respiration. The electrolyte disturbances that have been reported to precipitate torsade include hypokalemia and hypomagnesemia. or “twisting of the point” about the isoelectric axis. and early access to trained personnel capable of performing CPR. the rhythm strip usually shows the patient’s baseline QT prolongation. early activation of EMS. Other associated risk factors include a history of resuscitated arrest. The management of torsade with group lA antidysrhythmic drugs can have disastrous consequences. They may have an inhibitory effect on the parasympathetic nervous systerm. and chemotherapeutic agents. Although VF seldom is listed as the cause of death. and a family history of sudden death. VF is the major electrical mechanism for cardiac arrest. and systemic hypoxemia. is clinically important. presence of PVC’s or period of VT may occur immediately preceding acute cardiac arrest. often referred to as torsade. . and reentry. lithium. fatigue. The original report described regular variation of the morphology of the QRS vector from positive to negative and back again. congenital deafness. prehospital care is vital for arrests due to VF that occur outside the hospital. Since procainamide increases the likelihood of polymorphous VT developing. Magnesium sulfate is the first–line therapy in the treatment of torsade de pointes. TDP probably accounts for fewer than 5%. in general. quite different from those of garden variety VT. VF causes loss of oxygen to vital organ systems and brain death in minutes. it is thought to be responsible for more than 400. Ventricular tachycardia (VT) often precedes onset of VF in these cases. Other drugs that prolong the QT interval and have been implicated in cases of torsade include phenothiazines. Prolongation of the QT interval may be congenital. Interventions that impact survival and outcome of resuscitation include: early recognition of an arrest. VF has been described as the initial rhythm in almost 70% of out–of–hospital arrests. causing increase in cardiac output. VENTRICULAR FIBRILLATION TORSADES DE POINTES (TDP) Torsades de pointes (TDP). tricyclic antidepressants. The underlying etiology and management of torsade are. VF may occur secondary to antiarrhythmic drugs. Chest pain. is an uncommon variant of ventricular tachycardia (VT). prolonged QT syndromes. conduction disturbances creating abnormal electrical propagation of the action potential. and ACLS. the single most useful drug in cardiac arrest. Bystander CPR reportedly plays a significant role in prolonging the period (up to 12 min) in which VF may respond to a defibrillator. AEDs identify VF more rapidly than manual defibrillation techniques. Epinephrine is considered the most useful drug in cardiac arrest.. AICD effectively provides early defibrillation.EDUCATIONAL GUIDELINES Automated external defibrillators (AEDs) have revolutionized prehospital VF management because they have eliminated the need for rhythm–recognition training. forcing certain institutions and prehospital provider authorities to opt to ignore the ACLS updated recommendations pertaining to the use of Amiodarone. tive is to interfere with all reentrant arrhythmia and allow any intrinsic cardiac pacemakers to assume the role of primary pacemaker. Drug therapy may consist of sympathomimetics. prognosis is poor. In addition. Their use has resulted in increased survival rates and improved prognosis for patients in VF arrest. Lidocaine is the DOC for VF refractory to defibrillation and epinephrine.e. Post–defibrillation arrhythmias (mainly atrioventricular AV blocks) have been reported in up to 24% of patients. It is a Class 11B drug by ACLS criteria. Few survive when VF lasts more than 8 minutes without intervention. This means that fair to good evidence supports its use in humans. antiarrhythmics used successfully should be continued and control any hemodynamic instability. Prognosis for survivors of VF strongly depends on the time elapsed between onset and medical intervention. CPR may increase the number of patients in VF who benefit from defibrillation by response personnel. AEDs should not be used during emergency transport because patient movement creates the risk of inadvertent defibrillation. Early defibrillation often makes the difference between long–term disability and functional recovery. Controversy surrounds the issue of Lidocaine vs Amiodarone because providers have expressed reluctance to accept the recommendations. Biphasic waveform defibrillation shocks (repeated at < or = 200j) have equivalent or higher success for eventual termination of VF than monophasic defibrillators that increase the current (200. In post–resuscitative care. antiarrhythmics. Since it lasts longer than epinephrine. and require less time to achieve defibrillation. Amiodarone prolongs action potential and refracE . atropine. Vasopressin was recently considered equivalent to epinephrine. CPR–related injuries). They point out that while Amiodarone has been shown to improve the chance of a patient in VF to regain a pulse. by 4–6 minutes after onset of VF. The objec- 2/15/06 . AEDs identify VF more rapidly than manual defibrillation techniques.55 RATIONALE Automated external defibrillators (AEDs) have revolutionized VF management because they have eliminated the need for rhythm–recognition training. with fewer negative myocardial effects. Recent American Heart Association (AHA) and ACLS recommendations promote amiodarone as superior to the conventional use of Lidocaine. In refractory VF additional medications such as magnesium and/or procainamide may be effective (class IIb). The medication administration treatment goals are to electrically terminate VF so that an organized electrical rhythm follows and restores cardiac output. vasopressin is used only once in pulseless VT and VF. Lidocaine is a class 1B antiarrhythmic that increases electrical stimulation threshold of the ventricle. The incidence is related to the amount of energy used for defibrillation. However. Consenses exists to follow it with standard use of epinephrine after 5 minutes from the administration of vasopressin if no response/ return of spontaneous circulation. Their use has resulted in increased survival rates and improved prognoses for patients in VF arrest. and require less time to achieve defibrillation. 300. Always check for complication (i. aspiration pneumonia. and are 92–100% specific for VF. A shock is delivered to the heart to uniformly and simultaneously depolarize a critical mass of the excitable myocardium. and electrolytes. Electrical external defibrillation remains the most successful treatment of VF. Lack of response to standard defibrillation algorithms is challenging. are 92– 100% specific for VF. Success rates significantly decrease as the duration of ischemia increases. 360j) with successive escalating shocks. Automated implantable defibrillators (AICDs) are used for patients at high risk for recurrent VF. suppressing automaticity of conduction through the tissue. DRUG CATEGORY: Antiarrhythmics – Alter electrophysiologic mechanisms responsible for arrhythmia. Studies indicate patients with VF arrest who receive AICDs have improved long–term survival rates compared to those receiving only medications. Without intervention. the difficulty in drawing up and storing this medication and the cost of administration of amidodarone has been restrictive. and establish the need for emergent interventions. Amiodarone – May inhibit AV conduction and sinus node function. DRUG CATEGORY: Sympathomimetics/ Vasopressors – Augment both coronary and cerebral blood flow present during low flow states associated with CPR. the rate of survival out of the hospital is not increased in patients who receive Amiodarone. Post–resuscitation death and disability after successful resuscitation directly correlate with the amount of CNS damaged during the event. hypocalcemia. VT tends to deteriorate into unstable states and more malignant dysrhythmias. wide QRS complexes (>120ms). with varying QRS complexes). This degeneration also is the usual source of mortality in VT. VT generally has a favorable short–term outcome. VT may be monomorphic (typically regular rhythm originating from a single focus with identical QRS complexes) or polymorphic (may be irregular rhythm. characterized by a rate typically greater than 120 beats per minute and wide QRS complexes. Sodium bicarbonate is used only when the patient is diagnosed with bicarbonate–responsive acidosis. rales. its role in VF is limited due to the time it takes procainamide to reach therapeutic levels when administered IV. or altered level of consciousness. Magnesium sulfate. Long–term prognosis depends upon the underlying VENTRICULAR TACHYCARDIA (VT) Ventricular tachycardia (VT) is a tachydysrhythmia originating from a ventricular ectopic focus. Magnesium supplementation is used to treat torsades de pointes. Stable VT patients do not experience symptoms of hemodynamic decompensation. Unlike other dysrhythmias. rate greater than 100 beats per minute (usually 150–200). increased automaticity (which tends to favor ectopic foci). hypoxemia. hypokalemia. with breakdown of normal conduction patterns. and hypomagnesemia. and activation of re–entrant pathways in the ventricular conduction system. Myocardiac excitibility is reduced by an increase in threshold for excitation and inhibition of ectopic pacemaker activity. which should be sought and treated aggressively. a longer duration is considered VT. VT is generally a symptom of coronary artery disease (CAD) or structural heart disease. Magnesium sulfate acts as an antiarrhythmic agent. yet it often causes severe hemodynamic compromise and may deteriorate rapidly into ventricular fibrillation (VF). and sodium bicardbonate are used in VF secondary to other medications. or severe refractory VF. presence of atrioventricular (AV) dissociation. palpitations. VT is one of the most frequently observed dysrhythmias. yet the principal morbidity comes from its tendency to degenerate spontaneously into VF. Most patients present to the emergency worker with symptoms of either ischemic heart disease or hemodynamic compromise resulting from poor perfusion. However. or Phenobarbital overdose. anxiety and diaphoresis. If treated rapidly. Symptoms may include chest pain. It moderates nerve and muscle performance by regulating the action potential excitation threshold. hypotension and an altered mental status. known or suspected hypomagnesemia. Consider all patients with VT to have active myocardial ischemia. Nonsustained VT is defined as a run of tachycardia of less than 30 seconds duration. Physical findings usually reflect the degree of hemodynamic instability such as symptoms of CHF (dyspnea. or calcium channel blocker toxicity. Calcium chloride is also useful in the treatment of hyperkalemia. and calcium chloride is used to treat VF caused by hyperkalemia.56 2/15/06 . Arrhythmia may occur with or without either myocardial ischemia or infarction. dyspnea. several factors suggest VT including a E . A distinctive variant of VT is torsade de pointes. VT can produce congestive heart failure and hemodynamic compromise. indicating rate and stroke volume are not providing adequate cardiac output. Ventricular tachycardia may develop without hemodynamic deterioration. Deficiency in magnesium sulfate is associated with cardiac death and can precipitate refractory VF. type 1a antiarrhythmics and hypomagnesemia). tricyclic antidepressant. Unstable VT is characterized by symptoms of insufficient oxygen delivery such as chest pain. Electrolyte and sympathomimetics may increase the likelihood of VT in the susceptible heart. hyperkalemia. Patients with presistant or recurrent VF following antiarrhythmic administration should be assessed for underlying electrolyte abnormalities as a a cause for their refractory dysrhythmia. and fusion beats. However. DRUG CATEGORY: Electrolytes – Are considered therapeutic alternatives for refractory VF.e. No absolute ECG criteria exist for establishing the presence of VT. Sodium bicarbonate is used as an alkalinizing agent. hypotension. VT can be triggered by electrolyte deficiencies and the use of sympathomimetic agents (from relatively benign caffeine to more potent agents such as methamphetamine or cocaine) may stimulate VT in vulnerable hearts. and jugular vein distention). Routine use is not recommended.. VT usually is a consequence of structural heart disease. Procainamide increases the refractory period of the atria and ventricles. Among electrolyte abnormalities associated with VF are hyperkalemia. It typically occurs from drugs or conditions that prolong the QT interval (i. calcium chloride. with its unusual shifting–axis QRS complexes that appear as if the heart is rotating upon an axis.EMERGENCY MEDICAL GUIDELINES tory period in the myocardium and inhibits adrenergic stimulation. Emergency workers must determine if the VT is stable or unstable. Procainamide may be effective when lidocaine is not. failure to synchronize the shock with the patient’s QRS may precipitate VF. Both procainamide and amiodarone have vasodilatory effects which WOLFF–PARKINSON–WHITE SYNDROME Preexcitation is defined as. ECG is the diagnostic modality of choice for confirming that the patient’s tachycardia is VT. This arrhythmia will recur and seldom remains stable. but it is effective in treating hemodynamically unstable VT and VF. blood pressure monitoring for hypotension is critical. verapamil. acts as an antiarrhythmic. Lidocaine will more effectively suppress ventricular arrhythmias associated with acute myocardial ischemia and infarction once they occur. the whole or some part of the ventricular muscle is activated earlier by the impulse originating from the atrium than would be expected if the impulse reached the ventricles by way of the normal specific conduction system only. can destabilize hemodynamic status. Antiarrhythmic agents that have direct effects on accessory pathway conduction and reE . thereby answering the question – is the patient’s clinical presentation so severe that immediate electrical cardioversion is required or can the patient be managed adequately with pharmacological agents. Furthermore. although an electrolyte. The net effect is to decrease firing of ectopic foci to allow a normal rhythm to reassert itself. Although lidocaine can be administered rapidly with minimal effect on blood pressure. Emergency workers should be familiar with this syndrome and the proper treatment of its associated arrhythmias to avoid unnecessary morbidity and mortality. IV amiodarone may be better tolerated than procainamide. With this in mind. if in relation to atrial events. These agents alter the electrophysiologic mechanisms responsible for arrhythmia. there is the potential for extremely rapid ventricular responses during AF with degeneration to VF. monomorphic or polymorphic VT. Procainamide slows down phase 4 (diastolic) depolarization. it is a second choice. synchronized electrical cardioversion is always indicated. the clinician should never use more than 1 agent unless absolutely necessary. and antiarrhythmic therapy. If patients are clinically unstable. and possibly intravenous μ–blockers can cause a paradoxical increase in ventricular response rates in these patients with WPW. However. Unstable VT is treated with immediate synchronized cardioversion. Proarrhythmias (torsades de pointes)are serious tachyarrhythmias or bradyarrhythmias seemingly generated by antiarrhythmic agents. Of the various preexcitation syndromes. supplemental oxygen. In some patients a conduction pathway bypasses the AV node. Procainamide is contraindicated because of it’s QT prolongation potential. DRUG CATEGORY: Vasopressor – Augment both coronary and cerebral blood flow present during low flow states. This drug can also be expected to reach therapeutic levels slightly slower than Lidocaine. when an appropriate dose of a single antiarrhythmic medication fails to terminate an arrhythmia. during pharmacological interventions and after conversion to a regular rhythm. Such a conduction pathway is called an accessory bypass tract. Magnesium Sulfate is the DOC for torsades de pointes. DRUG CATEGORY: Antiarrhythmics – Mainstay treatments for clinically stable VT are antiarrhythmic drugs.57 2/15/06 . if this drug is selected by the clinician. Digitalis. magnesium sulfate. Procainamide is another antiarrhythmic agent known to effective in treating a broad variety of arrhythmias. Most patients respond to low levels of electrical energy. studies suggest that it is relatively ineffective for termination of VT and less effective against VT than IV procainamide. Polymorphic VT of the torsade de pointes type should be treated immediately because of the frequent transition to unstable VT. Other drugs are preferred over lidocaine in each VT scenario. ECG should be obtained before. In most patients. However. however torsades may be drug induced (proarrhythmic) or the result of an underlying magnesium deficiency. Lidocaine is appropriate for stable. Simultaneous 3–channel recordings and 12–lead tracings are more helpful than rhythm strips to analyze this dysrhythmia. Amiodarone has not been studied specifically for the termination of hemodynamically stable VT. Lidocaince may be utilized. In the stable VT setting. and slows intraventricular conduction. In these instances. In a few patients who have downward conduction through this pathway. turning to electrical cardioversion rather than a second antiarrhythmic medication is now exceptable. diltiazem. followed by expeditious airway management as needed. the most common is Wolff– Parkinson–White (WPW) syndrome. vascular access. DRUG CATEGORY: Electrolytes – This agent is considered a therapeutic alternatives for refractory VT. decreases automaticity. It can be used secondary to antiarrythmics and is reserved for treating the patient who presents with torsades de pointes. adenosine.EDUCATIONAL GUIDELINES cardiac disease. RATIONALE The primary objective is to establish whether a wide–complex tachycardia is stable or unstable. Pamelor Sinequan. Berkomine Norpramine. Rales are common. and hypotensive. Limbitrol Tofranil. VF may result. Consider any regular wide–complex tachycardia to be VT until proven otherwise. However. Janimine.. Generic Amitriptyline Imipramine Desipramine Nortriptyline Doxepin Protriptyline Maprotiline Trade Names Elavil. In addition. This slows the rate of impulse transmission through the accessory pathway and. Imavate. If the rate becomes too high. Death from WPW occurs secondary to the associated arrhythmias or from mistreatment of these arrhythmias with inappropriate medications. Men are affected 60–70% more than women. Atrial fibrillation (AF) in patients with WPW is very common and has an incidence of 11–38%. This is the anomaly seen in WPW. Presamine. irregular tachycardia on ECG. and in veterinary practice. Patients commonly present with heart rates in the 250 beat per minute range. Always treat arrhythmias associated with WPW with caution. The basic treatment principle in WPW AF is to prolong the anterograde refractory period of the accessory pathway relative to the AV node. however. dioxin). Typically. Triavil. In reality.e. calcium channel blockers. beta–blockers. allowing for much faster transmission of impulses and correspondingly higher rates. Patients may present with anything from mild chest discomfort or palpitations to severe cardiopulmonary distress or arrest. a stable patient initially may be treated E . the accessory pathway often has a much shorter anterograde refractory period. in the home. diaphoretic. thus. Therapy in the prehospital setting depends upon the patient’s degree of stability and the specific arrhythmia. an individual is protected from exceptionally high rates by the relatively long refractory period of the AV node. wide–complex. Accessory connections between the atrium and ventricle are the result of embryonic development of myocardial tissue bridging the fibrous tissue that separates the 2 chambers. Etrafon. the most common bypass tract is an accessory atrioventricular (AV) pathway. sympathetic discharge secondary to hypotension may lead to further shortening of the refractory period and subsequent increases in the ventricular rate. Pertofrane Aventyl. Although dozens of locations for bypass tracts can exist in preexcitation. otherwise healthy individuals. the ventricular rate. the rate of transmission through the accessory pathway likely would increase. This is best accomplished by temporarily prolonging the refractory period of the AV node with drugs such as adenosine. WPW has no specific examination features except for those that may accompany the arrhythmias. Adapin. in gardens. On physical examination. possibly causing the arrhythmia to deteriorate into VF. with a corresponding increase in ventricular rate. AF through an accessory pathway appears as a bizarre.58 HAZARDOUS MATERIALS MANAGEMENT ORGANOPHOSPHATE INSECTICIDES Organophosphates are used in agriculture. those affected are young. Curatin Vivactil Ludiomil The classic ECG morphology of WPW is described as a shortened PR interval. It also is the deadliest arrhythmia for these patients because of the possibility of deterioration into ventricular fibrillation Differential diagnosis includes ventricular tachycardia (VT). morphology depends directly upon the degree of preexcitation. This could have disastrous consequences. a widened QRS complex. as the high heart rate causes diastolic heart failure. the patient may be cool. and a delta wave. however. often associated with hypotension. Endep. If AF were treated in the conventional manner by drugs that prolong the refractory period of the AV node (i. In normal hearts. Patients with WPW have an excellent prognosis when treated with ablation of the accessory pathway. which is regular (unless it is torsade de pointes) or PSVT with aberrancy. Focus on breaking the cyclical transmission of impulses. In patients with WPW.EMERGENCY MEDICAL GUIDELINES fractoriness (such as Procainamide or amiodarone) are more likely to slow ventricular response during preexcited AF or atrial flutter as well as convert the arrhythmia to sinus rhythm. with adenosine. Sk–Pramine. with rates often in the 250 bpm or higher. All apparently share a common mechanism of cholinesterase inhibition and can 2/15/06 . as in narrow– complex tachycardias. has been misdiagnosed as alcohol intoxication. and sweating were less common. It is important to understand. and autonomic ganglia. as are a few reports of choreaform movements. vomiting. 80% of cases were transferred with the wrong preliminary diagnosis. however. skeletal nerve-muscle junctions. exposure to the same organophosphate by multiple routes or to multiple organophosphates by multiple routes can lead to serious additive toxicity. incoordination. lacrimation. memory loss. incoordination. within minutes to hours. They share with organophosphates the capacity to inhibit cholinesterase enzymes E . Other common presenting signs in children include flaccid muscle weakness. The result is a loss of available AChE so that the effector organ becomes overstimulated by the excess acetylcholine (ACh. The critical symptoms in management are the respiratory symptoms. depending on the method of contact. Increased pulmonary secretions coupled with respiratory failure are the usual causes of death from organophosphate poisoning. Likewise. depressed motor function. At sufficient dosage. Children will often present with a slightly different clinical picture than adults. high ACh concentrations cause sensory and behavioral disturbances. and excessive salivation. Seizures (22%-25%) and mental status changes including lethargy and coma (54%-96%) were common. The enzyme is critical to normal control of nerve impulse transmission from nerve fibers to smooth and skeletal muscle cells. followed by the gastrointestinal route and finally the dermal route. that there is a wide range of toxicity in these agents and wide variation in cutaneous absorption. 88% of the parents initially denied any exposure history. In one study. and confusion have been reported. and pulmonary edema. as well as within the central nervous system (CNS). and autonomic ganglia (nicotinic effects). muscular fasciculations. Toxic psychosis.EDUCATIONAL GUIDELINES cause similar symptoms. TOXICOLOGY Organophosphates poison insects and mammals primarily by phosphorylation of the acetylcholinesterase enzyme (AChE) at nerve endings. Muscle twitching. In a second study. the latter of which is manifested by sweating. bronchorrhea and bronchospasm may often impede efforts at adequate oxygenation of the patient. productive cough. weakness. At skeletal muscle junctions. and respiratory depression. glandular cells. manifested as confusion or bizarre behavior. and there usually is a secondary cardiovascular component. and rhinorrhea. and diarrhea all signal worsening of the poisoned state. producing tightness in the chest. Some critical proportion of the tissue enzyme mass must be inactivated by phosphorylation before symptoms and signs of poisoning become manifest. and respiratory depression. However. convulsions. At cholinergic nerve junctions with smooth muscle and gland cells. excess ACh may be excitatory (cause muscle twitching).59 2/15/06 . Exposure by inhalation results in the fastest appearance of toxic symptoms. SIGNS AND SYMPTOMS OF POISONING: Symptoms of acute organophosphate poisoning develop during or after exposure. only 2-3% of adults present with seizures. Anxiety and restlessness are prominent. Bronchospasm and bronchorrhea can occur. loss of enzyme function allows accumulation of ACh peripherally at cholinergic neuroeffector junctions (muscarinic effects). N-METHYL CARBAMATE INSECTICIDES N-Methyl carbamate insecticides are widely used in homes. but may also weaken or paralyze the cell by depolarizing the end-plate. The primary cause of death is respiratory failure. Exposure by inhalation results in the fastest appearance of toxic symptoms. this may be superseded by tachycardia and hypertension from nicotinic (sympathetic ganglia) stimulation. dizziness. followed Symptoms of acute organophosphate poisoning develop during or after exposure. and hypersecretion. The classic cardiovascular sign is bradycardia which can progress to sinus arrest. salivation. lacrimation. Psychiatric symptoms including depression. In comparison. All signs and symptoms are cholinergic in nature and affect muscarinic. the impulse-transmitting substance) in the nerve ending. Sufficient muscular fasciculations and weakness are often observed as to require respiratory support. tremor. abdominal cramps. and central nervous system receptors. as well as centrally. and agriculture. wheezing. respiratory arrest can occur suddenly. nausea. In the CNS. miosis. A life threatening severity of poisoning is signified by loss of consciousness. Miosis is often a helpful diagnostic sign and the patient may report blurred and/or dark vision. nicotinic. depending on the method of contact. Some of the most commonly reported early symptoms include headache. within minutes to hours. respectively. Because they share this mechanism. making specific identification and management quite important. Toxic myocardiopathy has been a prominent feature of some severe organophosphate poisonings. high ACh concentration causes muscle contraction and secretion. Recovery depends ultimately on generation of new enzyme in all critical tissues. incontinence. Some of the typical cholinergic signs of bradycardia. gardens. Ischemic chest pain / myocardial infarction – Risk of an AMI is increased by a factor of 24 during the first 60 minutes after cocaine use. (2) it accounts for the greater span between symptom producing and lethal doses than in most organophosphate compounds. Recent information indicates that children and adults differ in their clinical presentation. Unlike organophosphate poisoning. hyperactivity. although the latter tends to be the less toxic route. seizures. At skeletal muscle junctions. but may also weaken or paralyze the cell by depolarizing the end-plate. at skeletal muscle myoneural junctions and autonomic ganglia (nicotinic effects). and nicoE . respectively. Hyperthermia and physical restraint of the patient are exacerbating factors in persons who die from agitated delirium. Aggression. excess acetylcholine may be excitatory (cause muscle twitching). Respiratory depression combined with pulmonary edema is the usual cause of death from poisoning by N-methyl carbamate compounds. elevated acetylcholine concentrations may cause sensory and behavioral disturbances. salivation. the neuromediator substance. Manifests itself as bizarre and violent behavior. Above behavior is often followed by cardiopulmonary arrest. dizziness.60 TOXICOLOGY COCAINE TOXICITY Pharmacology – Cocaine stimulates the central nervous system primarily by blocking the reuptake of norepinephrine and secondarily by marked release of norepinephrine. and carbamates are more rapidly metabolized. N-methyl carbamates are absorbed by inhalation and ingestion and somewhat by skin penetration. Bradycardia and seizures are less common than in organophosphate poisonings. incoordination. and there is likely to be additive toxicity with simultaneous exposure to organophosphates. and sweating are commonly reported early symptoms. allowing accumulation of acetylcholine. PATHOPHYSIOLOGY Dysrhythmias – Tachdysrhythmias cause the most acute cocaine related nontraumatic deaths. and depressed motor function (rarely seizures). and in the brain (CNS effects). nausea. carbamate poisonings tend to be of shorter duration because the inhibition of nervous tissue AchE is reversible. as manifested by coma. the absence of them does not exclude the possibility of carbamate poisoning in the presence of CNS depression. bronchospasm. due to the somewhat different affinity for cholinesterases. as compared to organophosphates. and diarrhea are often prominent. even though the N-methyl carbamates do not penetrate the central nervous system very efficiently. combativeness. abdominal pain. and hypotonicity. tinic effects including hypertension and cardiorespiratory depression. However. vomiting. high acetylcholine concentration causes muscle contraction and secretion. TOXICOLOGY The N-methyl carbamate esters cause reversible carbamylation of the acetylcholinesterase enzyme.EMERGENCY MEDICAL GUIDELINES and therefore share similar symptomatology during acute and chronic exposures. and (3) it frequently invalidates the measurement of blood cholinesterase activity as a diagnostic index of poisoning. Neurological – Seizures Agitated Delirium – A common presentation in patients who die of cocaine overdoses. While children can still develop the classic muscarinic signs. unexpected strength. The primary manifestations of serious toxicity are central nervous system depression. and bronchorrhea with eventual pulmonary edema are other serious signs. This lability has several important consequences: (1) it tends to limit the duration of N-methyl carbamate poisonings. Physical Presentation Altered mental status New onset seizures Hypertension*** Tachycardia*** Chest pain 2/15/06 . SIGNS AND SYMPTOMS OF POISONING: As with organophosphate poisoning. At cholinergic nerve junctions with smooth muscle and gland cells. In the brain. Likewise. these poisonings are often somewhat easier to treat. Malaise. muscle twitching. Headache. Children are more likely than adults to present with the CNS symptoms above. Miosis with blurred vision. exposure can occur by several routes in the same individual due to multiple uses. and slurred speech are reported. extreme paranoia. Dyspnea. at parasympathetic neuroeffector junctions (muscarinic effects). the signs and symptoms are based on excessive cholinergic stimulation. The carbamyl-acetylcholinesterase combination dissociates more readily than the phosphoryl-acetylcholinesterase complex produced by organophosphate compounds. and incoherent shouting. incoordination. muscle weakness. capsules. frequently cocaine users will use Rohypnol to come down and it is used it enhance poor quality heroin. Drowsiness Deep sedation Respiratory distress Amnesia KETAMINE (Special K. swallowing. Flunitrazepam) Flunitrazepam (Rohypnol) is a prescription medication in other parts of the world. It is a benzodiazepine like Valium. Kay. They include: Volatile solvents Airplane glue Correction fluids Degreasers Gasoline Lighter fluid Paint thinners Spot removers Aerosols Air fresheners Cooking spray E . TOONIES) Nexus is another hallucinogenic amphetamine and produces similar effects SIGNS AND SYMPTOMS Anxiety Panic reactions ROHYPNOL (roofies. but is illegal in the United States. XTC. Jet) Ketamine is commonly sold at dance clubs for its hallucinogenic effects.61 2/15/06 . an overdose could result in coma or death. It is available in pill. SIGNS AND SYMPTOMS Seizure Hyperthermia Hypertension Hallucinations Agitation Irregular heartbeat Tachycardia Stroke Jaw clenching (the reason many “ravers” carry blow pops or pacifier) Muscle spasms Dilated pupils Sweaty NEXUS (STP.EDUCATIONAL GUIDELINES Myocardial ischemia / infarction Shortness of breath Epistaxis Psychiatric illness ***Note: Once considered classic presentations. especially in chronic users. SIGNS AND SYMPTOMS Low doses Lack of coordination Dizziness Pleasant or unpleasant hallucinations Nausea and vomiting Increased salivation Slurred speech Side to side or up and down eye movements Mood swings from quiet to violent High doses Stiff contorted muscles Sweating Hypertension Hyperthermia Amnesia Uncontrollable muscle and tongue movements Respiratory arrest DESIGNER DRUGS This informal classification of illicit drugs presents the team with somewhat unique patient presentations. Deaths are usually due to seizures or extremely high fever. the following provides some backround information on some of the more common “designer drugs” ECSTASY (MDMA. Ecstasy is a mind altering drug with “speed” effects and is commonly mixed with depressants. Since Ketamine is an anesthetic used to induce deep sleep for surgery. or injecting. rophies. SIGNS AND SYMPTOMS CNS depressant INHALANTS Many inhalants may be present at rave dances. or mixed with other “Designer Drugs” for snorting. roche. or powder form. ADAM. The normal dose is close to the toxic levels. but not always seen. Popular at “rave” dances as well as used in “date rape” cases. X) Ecstasy is a hallucinogenic amphetamine commonly bought in “rave” clubs. ruffies. but considered about 10 times stronger. ropies. Rohypnol is particularly dangerous when combined with other depressants such as alcohol. EMERGENCY MEDICAL GUIDELINES Asthma inhalers Deodorants Hair spray Spray paint Volatile Nitrates Amyl nitrate Butyl nitrate Isobutly nitrate IN SUDDEN SNIFFING DEATH SYNDROME (SSDS) AVOID THE USE OF EPINEPHRINE (if possible). MONITOR FLUIDS creased level of consciousness, administration of Sodium Bicarbonate 50 mEq followed by a Sodium Bicarbonate infusion of 1 amp in 500cc 0.9% NaCl to run at 50 cc/hr. Keeping the patient in an alkalotic state decreases the incidence of ventricular fibrillation. A 12 lead EKG should also be done enroute to the emergency room. COMMON TRICYCLIC ANTIDEPRESSANTS: SIGNS AND SYMPTOMS OF TCA OVERDOSE: CNS (early) CNS (late) confusion, agitation, hallucinations hyperactive reflexes, positive Babinski, rapid onset of coma, seizures GAMMA HYDROXY BUTYRATE (GHB, fall, scoop, liquid x, goop, Georgia Home Boy) This compound was initially used by body builders to stimulate muscle growth. In recent years it has become a popular recreational drug among dance clubs. GHB is synthesized from a chemical used to clean electrical circuit boards. It is available in both liquid powder forms. Often used in combination with other drugs, such as ecstasy, it is odorless and tasteless. GHB effects can be felt within 5 to 20 minutes after ingestion and the high lasts about 1.5 to 3 hours. Because it is odorless and tasteless it can be slipped into someone’s drink undetected. SIGNS AND SYMPTOMS CNS depression Nausea Respiratory depression Seizures Anticholinergic: flushing, dry mouth, dilated pupils Cardiovascular: QRS greater than 0.12 sec, bundle branch block, AV blocks, sinus tach, PVC’s, ventricular bigeminy, V– tach, V–fib, bradycardia, cardiac arrest, hypotension, pulmonary edema Worldwide, greater than 9 million natural and synthetic chemicals have been identified; fortunately, fewer than 3000 cause greater than 95% of accidental and deliberate poisonings. Identifying a poison and accurately assessing its potential toxicity are critical. Poisoning should be considered in the differential diagnosis of any unexplained symptoms or signs, especially in children less than 5. Similarly, in the young adult, any disparity between expected history and clinical findings should suggest poisoning. Recently, poisonings among the elderly (especially medication mix–ups), among hospitalized patients (drug errors), among workers exposed to occupational chemicals, and as a result of environmental pollution have been increasingly recognized. Often the type and speed of onset of the total clinical picture will confirm or refute a suspicion of poisoning. Occasionally, the absence of a specific finding will be as important as its presence. Any pertinent history should be secured and the person and premises inspected for traces of drugs; i.e., imprint identifications on solid medication forms, alcohol, etc, particularly for the unconscious patient. Specific antidotes: While not numerous, specific antidotes are remarkably effective; i.e., naloxone in opioid overdoses, atropine in organophosphate encounters, methylene blue for methemoglobinemia, acetylcysteine for acetaminophen, Digibind® for digoxin. A poison center should be contacted to determine if new specific antidotes have been developed, particularly for new drugs. Inhaled poison: The patient should be removed from the contaminated environment, his respiration supported, and other personnel protected from contamination. POISONING/OVERDOSE A relatively small percentage of the cases of poisoning and drug overdose are actually life–threatening situations when the Team arrives. Calm management of suspected poisonings include securing evidence from the scene and careful initial assessment of the patient. Suicidal patients should not be allowed to refuse care without law enforcement present to accept responsibility. Be alert for possible violent acts. Prompt consultation with the emergency room is appropriate. The Team should give special attention to neurological findings such as: level of consciousness., pupils, eye movement, gag reflex and response to pain. TRICYCLIC ANTIDEPRESSANTS (TCA) Tricyclic antidepressant overdose is probably the most common serious drug overdose encountered today. It represents an true medical emergency and is associated with approximately 20 % mortality rate. The tricyclic antidepressants remain a major cause of toxic death in the U.S. The standard of care for significant TCA overdoses includes a rapid assessment, aggressive airway management in the patient with deE - 62 2/15/06 EDUCATIONAL GUIDELINES Skin and eye contamination: Contaminated clothing (including shoes and socks) should be removed. The skin should be thoroughly washed and the eyes flushed with water. around visualization and palpation of all areas of the abdomen. This does not preclude that standard traumatic primary surveys should not be completed. In fact, this is just a small part of the overall assessment of any trauma patient. After the removal of all clothing in the region, the entire abdominal region needs to be visually assessed and manually palpated. Consideration should be given during clothing removal for the maintenance of legal evidence if it is needed (i.e., GSWs, stabbings, etc.). Following the standards put forth by BTLS International, the acronym “DCAP–BLS TIC” can be followed (deformity– contusion–abrasions–penetrations–burns–lacerations– swelling–tenderness–instability–crepitus). One also must remember that any signs of intra–abdominal trauma seen in the pre– hospital setting, typically indicates a significant underlying injury since abdominal injuries typically do not manifest themselves early. Abdominal distention or tenderness is considered to be an indication for immediate transport following a traumatic incident. Although auscultation and percussion of the abdomen are “nice” to complete during assessment, time should not be wasted in the pre–hospital setting since the benefits of such are minimal. Management of the abdominal trauma patient typically revolves around the standards impressed upon us throughout our careers, ABCs (Airway – Breathing – Circulation). After the maintenance of each of these has been achieved and assured, treatment of abdominal injuries can be addressed as part of the circulation assessment. Treatments should reflect a minimal on–scene time, as rapid transport of the patient to an awaiting OR is imperative. IVs should be considered en route to the ER and only run at a rate conducive to maintaining a systolic B/p of 90–100 mmHg. Other standard shock treatments should also be included during the transport. Since specific injury diagnosis is practically impossible in the pre–hospital setting, early recognition of a possible problem is the key to the proper management of the abdominal trauma victim. Rapid transport of all suspected abdominal injuries is imperative when you consider that no other area of the body is capable of readily hiding such large quantities of blood. Quick recognition and rapid treatments en route help to keep us “ahead of the game,” especially when considering that patients with serious intra–abdominal injuries can easily deteriorate rapidly and often without warning. TRAUMA ABDOMINAL TRAUMA Abdominal trauma is typically a difficult at best situation to assess especially in the pre–hospital setting. As with any traumatic incident, injury is delineated into two categories; blunt trauma and penetrating trauma. Penetrating trauma is obviously easy to recognize, as the integrity of the abdominal wall has been breeched. Blunt trauma on the other hand, can be subtle, which allows for the pre–hospital provider to possibly miss underlying injuries. Whether the mechanism of injury is blunt or penetrating, the two most life– threatening problems associated with abdominal trauma are hemorrhage and infection. The key to proper management of the abdominal trauma patient is rapid assessment and recognition, and proper shock management. Assessment of the traumatic abdomen causes us to remember our anatomy of the three regions within the abdomen; thoracic abdomen, true abdomen, and retroperitoneal abdomen. Each region houses both solid and hollow organs within which represent different injury patterns accordingly. The thoracic abdomen is considered to encompass all the organs which reside in the abdomen, yet are still protected anteriorly by the inferior portion of the rib cage (i.e. spleen, liver, gallbladder, stomach). Special consideration must be given, as rapid hemorrhage is very possible with injuries here. Even minor lacerations to liver or spleen can cause significant blood loss, resulting in a “shocky” patient. The true abdomen encompasses the large and small intestines, and the bladder. One also must incorporate the anatomy of the female patient since the true abdomen also holds the ovaries, uterus, and fallopian tubes. Injury to these organs typically cause infection, peritonitis, and occasionally shock (especially in females due to the vascularity of the uterus ). Finally, the retroperitoneal region lies posterior to both the thoracic and true abdomens. This region is the most difficult to assess due to its location anatomically. Organs located within this region include; kidneys, pancreas, abdominal aorta, and the inferior vena cava. Each of these present a large opportunity for massive hemorrhage with the possibility of no obvious changes to the region, so it is imperative that other signs and symptoms of shock are observed for. Proper assessment of the abdomen typically revolves BURNS Each year approximately 2 million people are burned in the United States resulting in approximately 12,000 deaths. As a result, many of the survivors of these incidents are unfortunately severely disabled and/or disfigured. Burns are classified by the cause, and, more importantly, severity, or degrees, E - 63 2/15/06 EMERGENCY MEDICAL GUIDELINES which depends upon the depth of the burn. Each burn creates a unique set of management problems while at the same time, each burn management case will follow the same treatment modalities. Burns are typically classified into one of the following causes: flame, electrical, chemical, radiation, steam, or scald. The skin, the largest organ in the human body, is the predominant reference made when talking about burns. However, its importance in temperature regulation, environmental protections, and other homeostatic functions is unsurpassed. Unfortunately, even though the skin is often the only place you actually see the effects of burns, it is the underlying structures, organs, and vessels which are the ultimate considerations treating a burn patient. The skin is divided into two layers: the epidermis, the thin outer layer seen on the surface, and the dermis, the thick connective tissue layer located just beneath the epidermis. Burns degrees are based upon the amount of tissue involvement as it pertains to the skin. First–degree burns typically involve just the outer regions of the epidermis and are commonly recognized by their red, painful skin, which usually heals within 3 to 6 days following the incident. Second– degree burns (commonly referred to as partial thickness burns) involve deeper regions of the skin including all of the epidermis and typically just the outer regions of the dermal layer. Second–degree burns are commonly seen as red, blistered skin that is very painful to touch and will typically heal within 2 to 4 weeks after the exposure. Finally, third–degree burns, which are considered the most dangerous. These are referred to as “full–thickness” burns due to the fact that all layers of the skin, including the underlying subcutaneous tissues and muscle layers are commonly involved in the burn–damaged area. Third–degree burns are commonly characterized by the white–gray, leathery, charred skin that is void of pain due to the complete destruction of the nerve endings located within that region of the skin. Third degree burns do not heal naturally due to the complete destruction of all the skin cells located within the area and long– term treatment typically includes skin grafts. Assessment of the burn patient encompasses the size and location of the affected area, as well as the cause of the burn itself, and, most importantly, the safety of the crew and patient. Scene safety must always be in the forefront of everyone’s thoughts when on any trauma call. Assessment of the burn patient follows the ABCs as we have all been taught, although special consideration must be made with regards to airway control. Inhalation burns, which account for more than half of all burn deaths, commonly cause E - 64 2/15/06 edema and swelling to the upper airways. This ultimately leads to the “closing off” of the airway. Early recognition of such a possibility must be considered and acted upon prior to the complete closure of the airway. Aggressive airway management will ultimately determine the viability of your patient. Determining the cause of the burn is also of great importance. Although flame exposure, chemical, and scald burns are easily recognizable on the surface, electrical burns may only manifest themselves as a small dot or circle on the skin, yet the damage created from the burn can be staggeringly more severe. One also must also consider the size of the affected area. The common “Rules of Nine” chart allows pre–hospital providers to approximate the percentage area affected by the burns, but this does not account for the possible areas affected when considering an electrical burn. One must believe that all areas between an entrance–burn and an exit–burn are also affected. This can drastically increase the size of your burn. One must also note the area affected by the burns. Face, hands, feet, genitals, and major joints are areas that require special attention by properly trained burn specialists. Special considerations for chemical burns are required, in such that even though you may have an easily recognizable outer burn area, you have to determine whether or not the skin has absorbed the chemical agent and is now possibly circulating it systemically. Management of the burn patient depends upon the cause and region of the burn. As a pre–hospital provider, you must realize that burn patients do not typically die rapidly from the burns themselves, rather, they die from the secondary conditions related to the burns (i.e. airway obstruction secondary to edema from an inhalation burn). Management should place the greatest emphasis on airway management and the removal of the patient from the source of the burn. Cooling of the burn site should be limited as to prevent the accidental causing of hypothermia or localized vasoconstriction. This would decrease the blood flow to an already damaged region. The long–term prognosis of the patient is increased when recognition for rapid transport is made. To minimize infection and other long–term considerations for the patient, pay attention to wound care. Remember, the most important thing you can do for your burn patient is airway management. CHEST INJURY Chest injury is often a deceptive diagnosis without the availability of X–rays. Any chest wall injury associated with difficulty breathing should be considered serious until proven otherwise. Chest injuries are the second leading cause of trauma related deaths each year. A thorough assessment is EDUCATIONAL GUIDELINES essential, as missed injuries can lead to impaired ventilation causing hypoxia, hypercarbia, and acidosis. The major types of chest injury are listed below. Rib Fractures, Flail chest, Pulmonary contusion Pneumothorax (open and closed), Tension Pneumothorax and hemothorax, Myocardial Contusion, Pericardial tamponade, Aortic, tracheal, and bronchial rupture, Traumatic asphyxia, Penetration and compromise of the diaphragm. The above can be caused by a variety of trauma: Motor Vehicle accidents, falls, sports injuries, crush injuries, stab wounds, and gunshot wounds. The goal in the treatment of these injuries is to maintain the patients ability to oxygenate blood passing through the lungs. Provide supplemental High Flow Oxygen, do a thorough assessment, and treat the injury following the appropriate procedural guideline. Chest injury may be penetrating or blunt. Penetrating injuries are caused by forces distributed over a small area as in gunshot wound, stabbing, or falls onto sharp objects. With penetrating trauma, any structure or organ in the chest cavity may be injured. With blunt trauma, the forces are distributed over a larger area, and many injuries occur from deceleration, bursting, and shearing forces. Conditions such as pneumothorax, pericardial tamponade, flail chest, pulmonary contusion, and aortic rupture should be suspected in blunt trauma or when the mechanism of injury involves rapid deceleration. Symptoms The symptoms of chest trauma include; shortness of breath, tachypnea, and chest pain. The pain is usually pleuritic, pain upon movement of the chest wall during respiration. The patient will usually try to splint the chest wall thereby limiting the movement during respiration. Conditions such as pneumothorax, and vascular injuries might not produce any symptoms initially. Repeat assessment is essential. Signs The evaluation of the chest should include observation, palpation, and auscultation. Signs to observe include, cyanosis, bruises, lacerations, puncture wounds, jugular vein distention, tracheal deviation, subcutaneous emphysema, and asymmetrical chest rise. The neck and chest should be palpated for the presence of tenderness, bony crepitus, subcutaneous emphysema, and an unstable chest segment. The chest should be auscultated for equal lung sounds, volume of inspiration, and diminished or absent breath sounds on one or both sides of the chest. Signs and Symptoms of Specific Injuries Rib Fractures: Pain on inspiration, local tenderness, bony crepitus. Flail Chest: Paradoxical Chest movement, pain, crepitus, hypoxia. Pulmonary Contusion: Usually seen with flail segment, pain, hypoventilation, hypoxia. Pneumothorax: Unequal lung sounds, difficulty breathing, tachypnea, pleuritic chest pain. Open Pneumothorax: Pain, difficulty breathing, bubbling sound as air moves in and out of the pleural space through the defect. Tension Pneumothorax: Pain, difficulty breathing, jugular vein distention, tracheal deviation, absent or diminished lung sounds, cyanosis, tachycardia, narrow pulse pressure. Hemothorax: Tachypnea, decreased breath sounds, dullness to percussion, clinical signs of Shock, difficulty breathing. Myocardial Contusion: May have no signs and symptoms other than chest pain from striking object. Arrhythmias are to be treated by ACLS protocol be alert to mechanism of injury. Pericardial Tamponade: Tachycardia, jugular vein distention, narrow pulse pressure, Pulsus Paridoxus (can be determined by noting the radial pulse diminish or even disappear with inspiration), muffled heart sounds. Aortic Rupture: Clinical signs of Shock, unequal pulses between the arms and the lower torso. (Radial and Femoral Pulses) Tracheal/Bronchial Rupture: Severe dyspnea, hemoptysis, subcutaneous emphysema. Traumatic Asphyxiation: Bluish discoloration to face and neck, jugular vein distention, conjunctival hemorrhage, difficulty breathing. Diaphragmatic Rupture: Difficult to diagnose, decreased breath sounds particularly over the left chest, sometimes bowel sounds may be heard in the left chest. If a considerable amount of abdominal contents is displaced into the chest, the abdomen may have a hollow or empty appearance. In summary serious injury to the chest can disrupt ventilation and also cause profound circulatory compromise. Maintaining the ABC’s as well as quick assessment and intervention for field treatable injuries (i.e.. Tension Pneumo, Pericardial Tamponade, Sucking Chest wound, Flail Chest) can be lifesaving. Interventions should be done enroute to the hospital if possible, as on scene times should be kept to a minimum for these trauma patients. E - 65 2/15/06 EMERGENCY MEDICAL GUIDELINES neck, and upper chest, but not below the nipple line. Associated injuries may require intubation and mechanical ventilation. All survivors in a large series were extricated within fifteen minutes of intrapment. Patient’s who survive for more than an hour will uniformly do well with 90+% chance of survival without sequelae or complications. CRUSH INJURY Crush injuries and their secondary metabolic complications are relatively uncommon, but are a significant form of trauma. The three major syndromes associated with crushing injuries are: Crush Syndrome Compartment Syndrome Traumatic Asphyxia These complex and often devastating injuries are among the most challenging types of trauma encountered by pre– hospital care providers. Early recognition and prompt therapy are essential to achieving a favorable outcome, whereas delays in diagnosis and treatment may result in permanent and severe disability. DROWNING/NEAR DROWNING Bystander CPR may be in progress. The Team should prepare for abdominal distention with vomiting. Focus on airway management and hyperventilation, with compressions if appropriate. A significant amount of drowning victims develop marked laryngospasm with airway occlusion. The Team should consider the following: head or spinal injury, aspiration of fluid, lung sounds, down time and water temperature. Near–drowning victims, because of aspiration or laryngospasm, usually sustain significant hypoxemia, with the consequent danger of respiratory failure and hypercapnia. Acute reflex laryngospasm may result in asphyxia without aspiration of water. Aspiration of fluid and particulate matter may cause chemical pneumonitis, damaging cells lining the alveoli, and may impair alveolar secretion of surfactant, resulting in patchy atelectasis. The perfusion of non–aerated, atelectatic areas of the lungs leads to intrapulmonary shunting of blood and aggravates hypoxemia; the more fluid aspirated, the greater the surfactant loss, atelectasis, and hypoxemia. Aspiration of large quantities of water may cause sizable areas of atelectasis, resulting in stiff noncompliant lungs and respiratory failure. Respiratory acidosis with hypercapnia and hypoxemia can occur. A concomitant metabolic acidosis may also result from tissue hypoxia. Hypoxemia and tissue hypoxia often result in pulmonary edema and even cerebral edema. The mammalian diving reflex in cold water allows survival after long periods of submersion. The diving reflex, first identified in seagoing mammals, slows the heartbeat and constricts the peripheral arteries, shunting oxygenated blood away from the extremities and the gut to the heart and brain. In cold water, the O2 needs of the tissues are reduced, extending the possible time of survival. Respiratory insufficiency is more critical than changes in electrolytes and blood volume, which vary in magnitude depending on the type and volume of aspirated fluid. Sea water may cause a mild elevation of sodium and Cl, but the levels are rarely life–threatening. By contrast, aspirating large quantities of fresh water can cause a sudden increase in blood volume, profound electrolyte imbalance, and hemolysis. Victims may succumb to the effects of these changes – asphyxia and possibly ventricular fibrillation – at the scene of the tragedy. Cardiac arrest, usually preceded by fibrillation, causes CRUSH SYNDROME: Following extrication, the patient frequently feels relatively little or no pain, and may have few physical complaints. Instead, emotional complaints dominate the history, as might be expected from a patient trapped or buried for hours. Multiple skin lacerations and tears are common when a direct pressure trauma occurs, such as when a car runs over an extremity. If crush syndrome develops and is untreated, Hypovolemic shock and hyperkalemia occur, followed by acidosis and acute renal failure secondary to myoglobin released from damaged tissue. COMPARTMENT SYNDROME: Compartment syndrome is caused by higher than normal pressure within a closed space, usually a muscle compartment. It occurs secondary to either a decrease in compartment size or an increase in compartment contents. The pathophysiology of compartment syndrome essentially results from too much volume in too little space leading to too much pressure. As perfusion is impaired, ischemia and tissue edema occur and are followed by more swelling. Tissue ischemia is followed by tissue necrosis. Muscle death may result in myoglobinuria, acidosis, and renal failure as well as amputation of the involved extremity, sepsis, or sepsis, or death. TRAUMATIC ASPHYXIA: Traumatic asphyxia, usually resulting from injuries that cause direct chest compression are rare. The exact pathology of this syndrome is unknown…one hypothesis is that blood forced out of the right atrium by the crushing force moves through the innominate and jugular veins toward the head. The clinical syndrome includes subjuctival and subcutaneous hemorrhages, bluish discoloration of the face, neck, and pronounced facial edema. Peleckiae is evident at the face, E - 66 2/15/06 EDUCATIONAL GUIDELINES many of the deaths attributed to drowning. However, current belief is that the pulmonary edema following near– drowning is a direct result of hypoxemia and analogous to pulmonary edema of high altitude, i.e., noncardiogenic pulmonary edema. Time should not be wasted in attempts to drain water from the lungs in a freshwater victim, because the hypotonic fluid passes rapidly into the circulation. Sea water, being hypertonic, draws plasma into the lung, and the Trendelenburg position may promote drainage. Hospitalization is mandatory for all victims. Resuscitation should continue during transport, regardless of the patient’s condition. Consciousness is not synonymous with recovery, since delayed death from hypoxia can occur. iris, cataract, dislocated lens, glaucoma, vitreous hemorrhage, orbital–floor fractures, retinal hemorrhage or detachment, and rupture of the eyeball may result. Emergency treatment may be needed before care by a specialist. It consists of alleviating pain and applying protective dressings. Traumatized lids should never be opened forcibly, since this could aggravate the injury. Rarely, after a laceration of the globe, the uninjured, contralateral eye becomes inflamed (sympathetic ophthalmia) and may lose vision to the point of blindness. Anterior chamber hemorrhage (traumatic hyphema) following blunt injury is potentially serious and requires attention by an ophthalmologist. It may be followed by recurrent bleeding, glaucoma, and blood–staining of the cornea. Although initially retinal detachment may be localized, without treatment the entire retina may detach. Rhegmatogenous detachment implies a break through and through in the retina and is seen more frequently in myopia, after cataract surgery, or following ocular trauma. Non– rhegmatogenous detachments can be produced by vitreoretinal traction (i.e. proliferative retinopathy of diabetes or sickle cell disease) or by transudation of fluid into the subretinal space (i.e., severe uveitis, especially in Vogt– Koyanagi–Harada disease, or primary or metastatic choroidal tumors). Retinal detachment is painless. Premonitory symptoms may include dark or irregular vitreous floaters, flashes of light, or blurred vision. As the detachment progresses, the patient notices a curtain or veil in the field of vision. If the macula is involved, central visual acuity fails drastically. Any patient with a suspected or established retinal detachment should be seen, on an urgent basis, by an ophthalmologist. Direct ophthalmoscopy may show retinal irregularities and a bullous retinal elevation with darkened blood vessels. Indirect ophthalmoscopy, including scleral depression, is necessary to detect peripheral breaks and detachment. If a vitreous hemorrhage obscures the fundus, especially in myopia, post–cataract extraction, or eye injury, retinal detachment should be suspected and ultrasonography performed. Subconjunctival hemorrhages may develop at any age, usually following minor trauma, straining, sneezing, or coughing; rarely, they occur spontaneously. They alarm the patient but are of no pathologic significance except when associated with blood dyscrasias, which is rare. They occur as gross extravasations of blood beneath the conjunctiva and are absorbed spontaneously, usually within two weeks with treatment. Vitreous hemorrhages, extravasations of blood into the vitreous, produce a black reflex on ophthalmoscopy. They may E - 67 2/15/06 EYE INJURIES The three principal types of eye injuries encountered by the Team are due to blunt and penetrating trauma, burns and foreign bodies (including chemicals). Chemical injury generally requires the fastest action to avoid permanent damage. Most of the field treatment of eye injuries involves only superficial care, since the majority of problems must be handled in the hospital by an opthamologist. Sudden loss of vision in one eye can be caused by thrombosis or occlusion of the retinal artery. Acute glaucoma produces pain, headache, nausea and haloes around the eye. Treatment is patching. Retinal detachment causes vision loss, flashing lights, and dark spots. Treatment is transport in supine position and patch both eyes. Trauma to the eye or adjacent structures requires meticulous examination to determine the extent of injury. Vision, range of extraocular motion, depth of anterior chamber, location of lid and conjunctival lacerations and of foreign bodies, and presence of anterior chamber or vitreous hemorrhage or cataract should be determined and recorded in detail for protection of patient, physician, and in industrial cases, employer. 1. Conjunctival and corneal foreign body injuries are the most common eye injuries. Seemingly minor trauma can be serious if ocular penetration is unrecognized or if secondary infection follows a corneal abrasion. 2. Intraoccular foreign body injuries require immediate emergency treatment, and the foreign body that has penetrated the eye must be removed by an ophthalmic surgeon. A patch and a metal shield are placed over the eye to avoid inadvertent pressure that could extrude ocular contents through the penetration site. The patient should not receive anything by mouth in preparation for urgent surgery. Trauma to the globe may severely damage internal structures. Hemorrhage into the anterior chamber, laceration of the EMERGENCY MEDICAL GUIDELINES occur in such conditions as diabetic retinopathy or hypertension or may result from trauma, retinal neovascularization, or retinal tears. Retinal hemorrhages are flame–shaped in the superficial nerve fiber layer, as in hypertension or venous occlusion, or round (dot and blot) in the deeper layers, as in diabetes mellitus or septic infarctions. Retinal hemorrhages are always significant, reflecting vascular disease that usually is systemic. Seeing floaters (spots) before one or both eyes is a frequent adult complaint. Floaters are usually most noticeable against a white homogeneous background and seem to move slowly. They result from contraction of the vitreous gel and its separation from the surface of the retina. Since the vitreous gel is denser where it attaches to the optic nerve, floaters are usually more apparent in this area. Though floaters usually are without significance, in a small number of patients they may indicate a tear in the retina. They are more prevalent in highly myopic and older persons, tending to become less noticeable with time. A minute vitreous hemorrhage may appear as a brown or red floater. Retinal detachments may be preceded by a shower of “sparks”or lightning flashes and may be accompanied by a shower of floaters. Only after the retina actually separates from its underlying structure (the retinal pigment epithelium) does a “curtain” of visual loss move across the visual field. Abnormal visual intolerance to light is common in lightly pigmented persons. Usually it is without significance and may be relieved by wearing dark glasses. It is an important, but nondiagnostic, symptom in keratitis, uveitis, acute glaucoma, and traumatic corneal epithelial abrasions. Ocular pain is important and, unless due to an obvious local cause such as a foreign body, acute lid infection, or injury, demands investigation (i.e., for uveitis, especially iridocyclitis, or glaucoma). Sinusitis occasionally causes referred eye pain. A blind spot in the field of vision is a negative scotoma. Frequently it is not noticed by the patient unless it involves central vision and interferes significantly with visual acuity. Negative scotomas noticed by the patient usually are due to hemorrhage or choroiditis. A scotoma found in the same visual field area in each eye is usually a quadrantic or hemianoptic defect resulting from a lesion in the optic pathways. A positive scotoma, perceived as a light spot or scintillating flashes, represents a response to abnormal stimulation of some portion of the visual system; i.e., as in the migraine syndrome. as simple injuries (splinting, elevation and ice). Treat long bone fractures, hip, pelvic or spinal injuries as major trauma. When the patient’s condition and time permits, the Team should establish IV and EKG monitoring prior to moving patient. The Team should consider the following: shock, assessment of painful areas, sensation and circulation tested before and after splinting and/or manipulation. Any complaint of paresthesia, weakness of motor function, diving or body surfing injuries should be treated as a spinal injury. Assess long bone fractures noting pulse and sensation. If a fractured limb is ischemic or cannot be stabilized because of deformity, apply gentle traction along the long axis of the limb to reduce and stabilize the fracture. Recheck and record neurovascular status after each movement of limb. Use of PASG is indicated for suspected pelvic fractures. HEAD INJURIES Significant head injuries, which have associated findings of disturbed consciousness, abnormal CNS exam, or significant signs of head and neck trauma, produce some of the most critical injuries attended. Assuming greater severity of injury is prudent. Treat every significant head injury as neck injury too. The Team should consider the following: CSF leaks, seizure activity, check mouth, drugs at scene, focal findings in neurological exam or Cheyne–Stokes respirations. Nasotracheal intubation is contraindicated with severe facial injuries. Head injury causes more deaths and disability than any other neurologic cause before age 50 and is the leading cause of death in men and boys less than 35 years old. Mortality in severe injury approaches 50% and is only little reduced by treatment. Damage results from skull penetration or from rapid brain acceleration or deceleration, which injures tissue at the point of impact, at its opposite pole (contrecoup), and also diffusely within the frontal and temporal lobes. Nerve tissue, blood vessels, and meninges are sheared, torn, and ruptured, resulting in neural disruption, intra– and extracerebral ischemia or hemorrhage, and cerebral edema. Hemorrhage or edema acts as an expanding intracranial lesion, causing focal neurologic deficits or increased intracranial swelling and pressure that can lead to fatal herniation of brain tissue through the tentorium or foramen magnum. Skull fractures may lacerate meningeal arteries or large venous sinuses, producing epidural or subdural hematoma. Fractures, especially at the skull base, can also lacerate the meninges, causing CSF leakage through the nose (rhinorrhea) or ear (otorrhea), or ingress of bacteria or air into the cranial vault. Infectious organisms may reach the meninges via cryptic fractures, especially when they involve the paranasal sinuses. Few head injuries occur in isolation, and most cases require simultaneous attention to other seriously traumatized parts of the body. FRACTURES The handling of fractures may dramatically alter prognosis of the injury. Minor or small bone fractures should be treated E - 68 2/15/06 Signs of primary brainstem injury (coma. red skin. and cocaine) increase susceptibility to heat illness. heat exhaustion and heat stroke. loss of oculovestibular reflexes. The worst form of severe head injury is that which causes near–complete damage to forebrain functions but spares the brainstem. Though stemming from the same cause. midposition or dilated and fixed pupils. Acute subdural or intracerebral hematomas are common in severe head injury and. The cerebral hemispheres and underlying diencephalon generally are more exposed and susceptible to the effects of non–penetrating trauma than is the brainstem.e. obesity. Age. producing decorticate rigidity (arms flexed and adducted.69 2/15/06 . fluctuating drowsiness or confusion. E . antihistamines. often following a lucid interval of relative neurologic normalcy. chronic subdural hematomas can cause enlarging head circumference. Temporal fracture lines suggest the diagnosis but may not be present. and respiratory irregularity may result from internal brain herniation and require immediate therapy. chronic alcoholism. sweating and flushed skin. because rapid brain compression and shifting can cause fatal or permanent neurologic deficits if not promptly evacuated. with seizures beginning as late as several years after trauma. Since severe head injuries frequently are accompanied by thoracic damage. hypoxia. but important. In infants. Few patients recover from the vegetative state when it lasts as long as 3 months after injury and almost none after 6 months. but not hemiplegia or decerebrate postural responses to noxious stimulation. These can occur from exposure or/and dehydration. later diagnosis can be difficult because of the time lapse between the injury and the onset of symptoms and signs. legs and often trunk extended). producing compression or distortion of the brainstem. or diffuse motor flaccidity) almost always imply severe injury and a poor prognosis. phenothiazines. Exposure to high ambient temperature may lead either to excessive fluid loss and hypovolemic shock (heat exhaustion) or to failure of heat loss mechanisms and dangerous hyperpyrexia (heatstroke). and mild to moderate hemiparesis are typical. or decerebrate rigidity (jaws clenched. neck retracted. lead to dehydration. decreased level of consciousness or coma. motor dysfunction. uni– or bilaterally dilated and unreactive pupils. hypotension. and many drugs (i. Chronic subdural hematoma may not produce symptoms until some weeks after trauma. heatstroke and heat exhaustion are sharply different. widening pulse pressure. Heat cramps are characterized by extreme cramping. sodium. numerous psychotropic drugs. hemiplegia. Prolonged exposure (greater than 2 to 3 weeks) and excessive sweating.. account for most fatal cases. Heat stroke is characterized by dry. suggesting hydrocephalus. Post traumatic epilepsy. Coma. Damage to the cervical spine can cause fatal respiratory paralysis or permanent quadriplegia from cord injury. especially if accompanied by vomiting or diarrhea. can last for many years. follows about 10% of severe closed head injuries and 40% of penetrating head wounds. Symptoms (increasing headache. together with severe brain edema. High ambient humidity. Heat exhaustion is characterized by confusion. they often are accompanied by severe surface wounds and by fractures located at the base of the skull or having depressed bone fragments. all limbs extended) is common. shock. particularly heatstroke. cool/moist skin. All 3 conditions can cause transtentorial herniation with signs of progressive rostral–caudal neurologic deterioration: deepening coma. More severe injuries may cause severe brain edema. and hypovolemia. nausea & vomiting. spastic hemiplegia with hyperreflexia. Increasing daily headache. extensor plantar responses may be present. and pupillary changes) may develop within minutes or hours after injury. sometimes produces a rising blood pressure coupled with a slowing of the pulse and respiration. and magnesium depletion. An epidural hematoma is less common than subdural hematoma. alcohol. anticholinergics. and the head injury may have been relatively trivial. and prolonged strenuous exertion with increased heat production by muscle increase the risk of heat illness. Survivors exist in a chronic vegetative state. Pupillary reactions and other signs of brainstem function are intact. the neurologic problems often are complicated by pulmonary edema (some of which is neurogenic).EDUCATIONAL GUIDELINES Concussion is characterized by transient posttraumatic loss of consciousness unaccompanied by gross structural lesions in the brain or leaving serious neurologic residua. the patient with concussion rarely is deeply unresponsive. deterioration of consciousness. Subdural hematomas are more common in alcoholics and patients over age 50. with assiduous nursing. fixation of the pupils to light. potassium. HEAT TRAUMA Exposure injuries include heat cramps. quadrispasticity. Cerebral contusion and lacerations constitute more severe injuries. even forgotten. Epidural hematomas most often have a temporal location (middle meningeal artery). by decreasing the cooling effect of sweating. Although diagnosis in early cases (2 to 4 weeks after trauma) may be suggested by a clinical course of delayed neurologic deterioration. which. Increased intracranial pressure. Although unconscious. Hemiplegia or other focal signs of cortical dysfunction are common. Depending on severity. and an unstable circulation. irregular breathing. or decerebrate rigidity. debility. decorticate rigidity. This occurs slowly and gradually if the diver ascends slowly and gradually. these disorders must be considered in any patient who recently has been exposed to a significant change in barometric pressure. Gas bubbles may lodge in many areas including the coronary arteries. If the diver has breathed compressed air underwater. and is experiencing any related symptoms. Patients should be placed on high–flow oxygen and have large– bore venous access with isotonic fluid infusion to maintain blood pressure and pulse. This will allow the hospital ample time to prepare specialized equipment and recall specialized personnel. As a result of the wide variety of presentations. stings. This can be vital in interpreting the cause of the inci- SCUBA DIVING INJURIES Scuba divers are susceptible to many types of injuries. – Continuous intravenous hydration to maintain adequate blood pressure. and should be treated as such until that assumption can be ruled out. Divers will often minimize the symptoms. as occurs in breath holding during rapid ascent. incidents of pneumothorax and pneumomediastinum as well as sinus squeeze and inner ear injuries can occur. These injuries range from minor traumas. Sprains and strains don’t get better with oxygen. The team must also be aware that often divers ignore symptoms or pass them off as muscle sprains or strains. from ear or mouth pain and headaches to major joint pain. decompression sickness (DCS). When at depth. This relief is short–lived and will return even worse when oxygen is removed. and death. bites. The team should always be stay alert to the possibilities of multiple injuries in the diver. ARTERIAL GAS EMBOLISM (AGE) Many of the following injuries have similar causes. and arterial gas embolism. lacerations. paralysis. some almost immediately. spinal cord or cerebral circulation. those injuries that are particular to the scuba diver and caused by increased pressure while underwater. neurologic deficit. Supine is the only currently acceptable transport position. Ninety–five percent of diving injuries present symptoms E . – Make every attempt to transport the divers gear with the patient.70 2/15/06 . Dive injuries do. Obtaining a blood glucose level and drawing Prothrombin time (PT). when nitrogen in a diver’s air tank dissolves in the diver’s fatty tissues or synovial fluids at depth. Onset is usually rapid. The purpose of this information is to familiarize the team with the pathophysiology and treatment of barotraumatic injuries. – Needle decompression of the chest is indicated for suspected tension pneumothorax. Gas embolism may present with symptoms similar to DCS or a stroke. As the diver ascends and the ambient pressure decreases air trapped in a flexible space will expand . Pathophysiology: Injuries caused by ambient pressure changes during ascent and descent are generally governed by Boyle’s and Henry’s Laws of physics. it expands with great force against the walls of that space (reverse squeeze). a diver is at a greater residual pressure. nitrogen will be released from those tissues as the diver ascends to a lower pressure environment. SOB or altered LOC the patient must be assumed to have experienced a barotraumatic injury. During rapid ascent. even in shallow water. – Consideration for relative hypothermia and passive re– warming is always appropriate for these patients who may be in shock. SCUBA Diving barotraumas can present with a variety of manifestations. either through breathholding or alveolar disfunction. and the nitrogen enters the bloodstream to the lungs and is exhaled. An arterial gas embolism occurs when air becomes trapped in the divers lungs. As the diver ascends. BAROTRAUMA Pre–hospital care should consist of assessing the ABC’s and correcting any immediate life–threatening conditions while maintaining adequate oxygenation and perfusion. ambient pressure decreases and the pressure within the lungs increases until an injury occurs within the lung itself and the gas is forced through the alveolar wall and into the bloodstream and surrounding tissues. bites or stings to a variety of barotraumatic injuries and even carbon monoxide poisoning. especially if they begin to go away with oxygen. nitrogen exits tissues rapidly and forms gas bubbles. allergic reactions and the like are treated like any other injury and are discussed elsewhere in these guidelines. Symptoms usually get progressively more painful though they will often be relieved with oxygen. coma. Below is a list of the most common barotraumatic injuries. End– tidal CO2 detection and sa02 monitoring are essential. The 3 major manifestations of barotraumas include sinus or middle ear effects. should the diver ascend rapidly. In addition. – Perform endotracheal intubation on a patient who has an unstable airway or has persistent hypoxia despite breathing 100% oxygen. activated partial thromoplastin time (aPTT) blue top blood tubes would be clinically helpful prior to hydration. either immediately or within a few minutes.EMERGENCY MEDICAL GUIDELINES within the first three hours. General trauma. 12 lead interpretation is appropriate in suspected AGE. The goal of treatment is early recognition of the possibility of a diving injury and prompt notification of emergency room. However. including but not limited to: pain. If air is trapped. anti–inflammatory medications. differentiating between them is not of great importance. A gas bubble forming in the back or joints can cause paresthesias (tingling). and analgesics. isotonic fluids. andomedications to alleviate and reverse the inflammatory process that is chiefly responsible for the progression of DCS. – Intravenous access with administration of isotonic fluids (normal saline or lactated ringers) to maintain urine output at 1–2ml/kg/hr. heart. Signs and symptoms that appear during or following a dive are pressure related until proven otherwise by a diagnostic or therapeutic recompression. Consultations: Consult a specialist at a recompression chamber for any patient with type 11 DCS or an unstable AGE. including high–flow oxygen. The primary medications in treatment of dysbaric injuries are oxygen.EDUCATIONAL GUIDELINES dent. Manifestations may include respiratory. both oral and nasal. peripheral nerve and/or CNS compromise. when a gas bubble forms in the arterial blood supply and travels to the brain. respirations. Type 1 is milder. – A complete list of recompression chambers is available from the Divers’ Alert Network (DAN) by phone 24 hours a day at (919) 684–8111 or (919) 684–4DAN (4326). Sinus squeeze – Patients generally present with complaints of facial or E .71 2/15/06 . Sinus & Middle ear squeeze – Symptomatic therapy with decongestants. A bubble forming in the circulatory system can lead to pulmonary or cerebral gas emboli. since the treatment of either requires recompression.e. “ This is considered normal output. decongestants. circulatory. Decompression sickness type II – All of the interventions for type 1 are appropriate for type II DCS. – Obtaining a small water sample to be transported with the patient can be advantageous in rapidly identifying the need for specific antibiotics and facilitating their administration. – The most appropriate management is to transfer to the nearest hyper baric chamber. Clinical History: Patients present with a history of diving. – Pain control should be instituted with non–steroidal anti– inflammatory drugs (NSAID’s) or narcotic analgesic medications. unstable blood pressure. A physical exam should be tailored to the patient’s history. and most commonly. Arterial gas embolism (AGE) is the most dangerous manifestation of type II DCS. DCS is classified into 2 types. DCS) DCS usually results from the formation of gas bubbles. This frequently is accomplished by air. Their US web site is http://www. DECOMPRESSION SICKNESS (BENDS. or paralysis. generally within 24 hours o£ the onset of symptoms. or neurologic status) require immediate recompression therapy in a hyper baric chamber. is indicated.diversalertnetwork. accounting for many disorders. Arterial gas embolism – These patients can have mild symptoms from a small embolism that may improve with the therapy for type 1 DCS. liberal intravenous hydration. and aspirin. which begins mildly and worsens over time and with movement. not life threatening. which can travel to any part of the body.org. – These patients need recompression therapy to resolve their symptoms. It occurs after a rapid ascent. DCS of the CNS is clinically similar to AGE. CNS cases treated with the protocol during transport were improved or asymptomatic upon arrival at the HBO chamber 72% of the time. – Patients with severe AGE (i. – The recompression chamber specialist must be contacted prior to transfer to determine chamber availability and the appropriateness of hyper baric oxygen (HBO) therapy. Aspirin may also be appropriate. The most common symptom is joint pain.. or lungs. neuropraxia. Type II DCS is serious and life threatening. Medical management techniques utilizing the triad of 100% oxygen. Decompression sickness type I – These patients should receive high–flow oxygen via a non–rebreather mask BVM. he or she is then classified as having type II DCS. Helicopter transport necessitates the pilot maintain altitude at less than 1000 feet. This is immediately life threatening and can occur even after ascent from relatively shallow depths. aggressive re–hydration. and characterized by pain in the joints and muscles and lymph node swelling. – If a patient’s medical condition continues to deteriorate. – These patients should also receive aspirin 324–650mg for anti–platelet effects as well as pain control. – An important issue to consider is time vs distance to the HBO chamber. and prior medical history. As with AGE the onset of symptoms is usually rapid. with the acceptance of Enriched Air Nitrox (EAN) as a breathing gas there is a greater chance of oxygen toxicity. pulmonary related problems. injuries or surgeries. – Pneumothorax – gas becomes trapped within the pleural space. decompression stop depth. and whether the pain worsened during the descent or ascent. lungs and great vessels. and length of stop. This occurs in the majority (70–85%) of patients. – They may have a history of previous diving ear injuries or a history of previous or current ear infection. nausea. tinnitus. It results in a narcotic effect on the diver which may greatly affect his/her judgement. or headache. or headache. Causes: The causes of DCS are related to predisposing medical or genetic factors. sinus surgeries. Altered level of consciousness at the surface is not Nitrogen Narcosis. They may complain of slowly progressing pain or numbness in their limbs or back. Other injuries similar to AGE & occurring on rapid ascent – Mediastinal emphysema – gas is forced into the media stinum – Pericardial emphysema – gas is forced into the pericardium and presents as pericardial tamponade. muscle. The danger is that the diver will do something foolish while under the effect of nitrogen narcosis and suffer a more serious injury. rapid ascent and or flying or traveling to high altitudes within 24 hours after diving. – Patients may present with shortness of breath (chokes). The increased partial pressure of O2 at depth combined with the increased percentage of O2 results in oxygen toxicity at shallower depths . resulting in an increased bottom time. – Other important information to gather includes any history of recent upper respiratory infections. ear pain.72 2/15/06 because they often present with altered mental status or in shock. Divers should be questioned as to the method of computing bottom and ascent times with safety stops. NITROGEN NARCOSIS (RAPTURE OF THE DEEP) Nitrogen Narcosis is caused by an over–saturation of nitrogen in the bloodstream through an unknown process. 32% and 36% O2 are common mixes. Decompression sickness type I patients often have a history of recent diving followed by a flight home. and shock. or back pain that worsens over time. – Essential history to ascertain includes time since dive ended. OXYGEN TOXICITY Oxygen toxicity has rarely been seen in the past when dealing with recreational divers diving within accepted limits (less than 130 ft). There is a trade–off here and that is increased risk of oxygen toxicity.EMERGENCY MEDICAL GUIDELINES oral pain. The dive profile consists of prior dives that day. As the diver ascends the trapped air expands. – Inquires should be made specifically about previous decompression ~ injuries. altered mental status. They also may complain of dizziness or weakness. Pain is reported in only about 30% of cases. severe headache. usually within minutes of surfacing. With the increase in oxygen the percentage of nitrogen decreases. These patients often die before reaching medical facilities. Pain may range from mild t9 severe (the bends). The shoulder is the most commonly affected joint. and suddenly screaming and losing consciousness. EAN is essentially air with an increased O2 percentage. Middle ear squeeze – Patients often have a history of sudden vertigo. allergies rhinitis. chest pain. MEDIASTINAL EMPHYSEMA Injury occurs similar to an AGE however the gas is forced into the mediastinum. However. This information should be recorded as part of the medical record. and to diver error. Decompression sickness type II – Type II usually presents sooner than type I. the dive profile. vertigo. Examples of diver errors include – multiple daily dives. sinus polyps. nausea. – Patients may have a history of previous decompression illness and multiple dives in the same day and frequently have not followed the dive tables closely. deafness. – Patients present with joint. compressing the heart. when the symptoms began. All signs and symptoms will disappear as the diver ascends to a shallower depth. poor adherence to the dive tables. bottom time. The pain worsens with motion but is always present. depth of dive. Arterial gas embolism (AGE) – AGE usually presents with a history of a diver ascending very rapidly. – Obtaining a history from these patients can be difficult E . breath holding (most common). often from fairly shallow depths. – Witnesses often report that divers experience a sudden or immediate loss of consciousness or collapse. Patients may rapidly deteriorate without emergent intervention. identification of this characteristic should be undertaken carefully. PNEUMOTHORAX Injury occurs similar to an AGE however the gas becomes trapped within the pleural space. usually around the neck and collarbones. it is believed to be somewhere between 50 and 100. children and infants being more vulnerable. The condition of the victim will seriously affect the outcome. and alert snake is deadlier. Depending on the mixture oxygen toxicity can occur in water between 90 and 100 ft. shy snake with a rather distinct pattern of red and black bands that are wider than the interspaced yellow rings. The early signs of a coral snake bite are slurred speech. This condition is similar to pericardial tamponade. The diver who is now at a normal ambient pressure will no longer be suffering from oxygen toxicity and may be treated accordingly. and so is its depth and the duration of the time of penetration of one or more fangs. There are three additional characteristics of pit vipers that aid in distinguishing them from harmless snakes. Hypertension. Palpation of the area can produce the effect of “Rice Crispies” under the skin. First. As the diver ascends the trapped air expands. Second. the treatment is fairly standard. quantity. the scales are arranged in double rows from the anal plate to the tip of the tail. restricting the pumping action of the heart. On a snake’s ventral side. Ideally this patient should be transported to an emergency room that has a recompression chamber on site. SNAKE BITE Although the annual mortality from venomous snakebites is unknown. scales are arranged in a single row from the anal plate to a point approximately a third of the distance away from the tip of the tail. either dead or alive. They need greater leverage to puncture the skin and a longer period to inject their venom. Copperhead (N. Each injury is treated according to the Diving Accident Guidelines (see treatment section) and the patient is monitored for complications. are whitish. If the snake is not available. Early transport and physician consult regarding the nature of the injury is critical. however the gas escapes under the skin. however the gas is forced into the pericardium. A thorough history should be taken including number of dives. Once on the surface this diver should be treated as any near–drowning/dive accident. cottonmouth or rattlesnake. The coral snake is a relatively small. diabetes. disturbed. it must be determined whether it is a pit viper or coral snake. As with AGE the onset of symptoms is usually rapid. and myalgia. Obviously. is important in order to determine whether it is harmless or venomous. The angle of bite is significant. a simple pneumothorax may become a tension pneumothorax as the air expands while ascending. the prudent team will keep close watch on the divers airway as a compromise is possible. In most harmless snakes. length and depth of dives and time on surface between dives. This has given rise to the following mnemonic rhyme: “Red on yellow. If the snake is venomous. as well as weakness and possible paralysis of respiratory muscles. A hungry. is shaped like an arrowhead. somewhat caudad. and quality of venom available. While there are a number of different injuries that can occur from breathing compressed gas at depth. Harmless snakes have oval or egg shaped heads.EDUCATIONAL GUIDELINES than before. FL. While certainly a cause for concern this injury is seldom life–threatening. Red on black. has a black snout with the previously described coloration of the body. venom lack—harmless snake. kill a fellow—coral snake. more precisely. Coral snake venom has a blocking action on acetylcholine receptor sites. The diver will experience a seizure and can obviously have a variety of complications depending on how the proximity of other divers and how quick they react. Most harmless snakes have round pupils. However. a reliable observer may have seen the snake well enough to identify it or describe it sufficiently. they have vertical pupils. The size of the victim is important. In venomous snakes. the eastern coral snake. The size and type of the snake govern the type.) Cottonmouth Coral Snakes Identification of the snake. SUBCUTANEOUS PNEUMOTHORAX Injury occurs similar to an AGE. whether it is a copperhead. seemingly loose scales called the anal plates. The condition of the snake is also important. and in the case of the former. Venomous snakes located in our area are: Pit Vipers Eastern Diamond Back Pygmy 2/15/06 . Frequently symptoms are not evident until 2–12 hours after the bite. dysphagia. a pit viper’s head is generally triangular in shape or.” The more plentiful species. Pericardiocentesis is the treatment of choice. If this occurs at depth. dilated pupils.73 PERICARDIAL EMPHYSEMA Injury occurs similar to an AGE. Death results from respiratory arrest secondary to CNS inhibition. A final distinction between pit vipers and harmless snakes lies in the pattern of plates on the snakes’ underside. although some venomous snakes also have round pupils. advanced E . Rarely three or four marks may be present. Loxosceles reclusa (sometimes called the brown recluse) and related species. Fortunately. It is safe to assume that the bite is venomous if one or two fang marks are present. Araneus species. such as peptic ulcers. and Phoneutria are not native to the USA but may be brought into the country on produce or other materials. NEUROTOXIC MANIFESTATIONS The effects of neurotoxins A and B on the central nervous system are manifested by dysphagia. fasciculation. Liocranoides and Chiracanthium. Pamphobeteus. manifested by weakness of the muscles. pain. Women who have endometriosis may bleed excessively and develop severe pain. or those on anticoagulant therapy. and tissue anoxia leading to necrosis. debility. Latrodectus mactans and related species. neurotoxic. Its enzyme activity is greater than that of Latrodectus venom. and pain predominate with pit viper bites. paralysis. and psychotic behavior. drop in hemoglobin. The lethal fraction appears to be a peptide that markedly affects neuromuscular transmission. Bothriocyrtum and Ummidia species. or coagulation disorders are aggravated by a venomous snakebite. Species that are dangerous include the widow spiders. Cupiennius. Tarantula venom contains approximately 12 proteins. all spiders are venomous. HEMOPATHIC MANIFESTATIONS Swelling. Drassodes. The incidence of spider bites in the USA is unknown. but the mechanism is not understood. A coral snake bite may present an atypical pattern. Steatoda grossa. Neoscona vertebrata. Absence of fang marks is presumptive of evidence of a harmless snakebite or an unsuccessful attempt by the pit viper without penetration. edema. the symptoms and signs are the only remaining criteria of severity. it is highly unlikely that the bite of one tarantula would produce a harmful cardiac effect in a human. Only a few spider venoms have been studied in any detail. and Argiope aurantia (orange argiope). lungs. because of impaired coagulation mechanisms. the tarantulas. Misumenoides aleatorius. Nevertheless. Individuals with bleeding tendencies. vomiting. but no fraction of Loxosceles venom has been isolated that produces the entire sequence of events that give rise to the unusual necrotic lesion characteristic of Loxosceles bites. Tarantulas native to the USA are not considered dangerous. the brown or violin spider. the trap–door spiders. and the comb–footed or false black widow. including swelling. however. Lycosa (wolf spider). the running or gnaphosid spiders. Fang marks separated by 15 mm or more indicate a bite by a very large snake. Fewer than 3 fatalities/year occur in the USA. diarrhea. Phoneutria and Cupiennius sallei. or with open wounds are susceptible to bleeding secondary to envenomation. the so–called banana spiders. the running spiders. Peucetia viridans. paresthesias. ecchymosis. Changes in red blood cells and their ability to transport oxygen may result in bleeding. and restlessness. peritoneum. rectum. The myoneural junction is also affected by neurotoxin B.74 2/15/06 . while those separated by less than 8 mm point to a smaller snake. Neurologic signs preE . which results in locomotor disturbances. Incidental penetration of fangs and injection of venom into a blood vessel is usually catastrophic. according to the number of fangs. Brown or violin spider venom consists of at least 10 or 12 proteins. There may be local bleeding from areas such as the endometrium or urinary tract or bleeding from pathological foci. The signs and symptoms are divided into hemopathic. and systemic manifestations. SYSTEMIC EFFECTS General systemic signs and symptoms of venomous snakebite include elevation or depression of the temperature. the orbweavers. The location of the bite is of great importance. edema. the fangs of most species are too short or fragile to penetrate the skin. Black widow venom consists chiefly of proteins. and vagina may occur owing to endothelial damage of small vessels and lymphatic channels. convulsions. extravasation of blood. a few of which are enzymatic. dominate with coral and cobra bites. greater than Phidippus species. and in very extreme cases. The pathogenesis of the bradycardia is obscure. at least 60 species in the USA have been implicated in bites on humans. usually in children. Polymorphonuclear leukocyte infiltration plays a major role in the poisoning. neurologic signs may also occur. While hemopathic and systemic signs. quickly examine the pattern of the snakebite on the victim. nausea. and bleeding from kidneys. Venomous snakebites on the head and trunk are from two to three times more dangerous than those on the extremities. If the offending snake cannot be identified. the green lynx spider. Women who are menstruating will bleed excessively after a pit viper bite. the jumping spiders. with active peptic ulcers. Cases of abortion in pregnant women who have been bitten by pit vipers have been reported. Renal failure from acute tubular necrosis of bilateral cortical necrosis has been reported SPIDERS With the exception of 2 small groups. and Heteropoda. After identifying whether the snake is venomous or harmless. Rheostica and Pamphobeteus species. Venomous bites on the upper extremities are more serious than those on the lower extremities.EMERGENCY MEDICAL GUIDELINES age. such as hemophilia. of which at least one affects cardiovascular function. the crab spider. bedbug. or hypoxemia. the central bleb becomes larger. understanding of the pathophysiology of TBI has increased remarkably. sweats. nausea. Emergency Medical Services (EMS) providers are often the first health care providers for patients with TBI. especially the head injured patient. Prehospital Treatment. particularly in areas where this species is not found. An estimated 1. ptosis. These guidelines cover three main areas: Assessment Triage. hours. erythema chronicum migrans. neurotrauma is a serious health problem that mandates continuing efforts in the areas of prevention and treatment. Early recognition of the initial signs and symptoms of TBI has a significant impact on the outcome of these patients. At present. pre–hospital assessment and treatment is the first critical link in providing appropriate care for individuals with severe brain injury. A bleb forms. EMS providers must aggressively assess and treat hypoxemia and hypotension.000 people are left with permanent neurological disabilities. Numerous reports of necrotic or gangrenous arachnidism attributed to Loxosceles reclusa. headache. and approximately 270. Every year. EMS providers have developed sophisticated systems for delivering emergency medical care to patients. etc. thrombocytopenia. these are often mistaken for spider bites. fills with blood. TBI treatment often begins in the field by EMS providers who have varied skills. sometimes numbing pain in the affected extremity. but some localized pain develops within an hour or so. The cost to society is more than $30 billion annually. malaise. and increased skin temperature over the affected area. Thus. chronic herpes simplex. Some cases of so–called brown recluse bites are misdiagnoses of epidermal necrolysis. death is a rare sequela. tick. TRAUMATIC BRAIN INJURY (TBI) Traumatic brain injury (TBI) is a leading cause of death and disability in children and adults in their most productive years. If possible capture and identify the offending animal. defined in these studies as a single observation of an SBP<90 mm Hg. weakness. Brown or violin spiders: A Loxosceles bite may cause little or no immediate pain.000 of the injured receive emergency department or other outpatient care. backgrounds. vomiting. The lesion may appear as a bull’s eye. hemolysis. and days. In addition to initial treatment. and biting fly bites. approximately 52. dizziness.75 2/15/06 . EMS providers must know about interventions aimed at minimizing secondary injury. eyelid edema. Associated manifestations may include restlessness. Over the past thirty years. Systemic symptoms and signs may develop. defined in these studies as apnea or cyanosis in the field E . Lyell’s syndrome. and by cramping pain and some muscular rigidity in the abdomen or the shoulders. All neurological damage does not occur at the moment of impact (primary injury). Specifically. and leaves an ulcer over which a black eschar forms and eventually sloughs. the precise definitions of hypotension and hypoxemia are unclear in these patients. and Hospital Transport Decisions. are probably caused by spiders other than Loxosceles or more probably by other arthropods.000 are admitted to the hospital. One central concept is now known. which may include muscle. ruptures. often surrounded by either an irregular ecchymotic area or a more target–like lesion. abilities result in a significant loss of productivity and income potential. back. salivation. Only in the past five to ten years has any attempt been made to evaluate the care provided to trauma victims in the field. TBI has a devastating effect on the lives of the injured individuals and their families due to the fact that dis- ASSESSMENT TRIAGE: OXYGENATIONAND BLOOD PRESSURE: Early post injury episodes of hypotension or hypoxemia greatly increase morbidity and mortality from severe head injury. This secondary brain injury can result in increased mortality and more disabling injuries. sweating. chills. respiratory distress. All recommendations in these guidelines are supported by the best available scientific evidence. Approximately 800.6 million head injuries occur every year in the United States. followed by a dull. Thus. They continue this care en route to the hospital. EMS providers must be familiar with the complex presentation of severe TBI patients.000 deaths occur from TBI. Some arthropod bites may give rise to bullous lesions that rupture and ulcerate. and kidney failure. During the past two decades. mite.EDUCATIONAL GUIDELINES Widow spiders: A Latrodectus bite usually gives rise to a sharp pinprick–like pain. skin rash and pruritus. ample Class II evidence exists regarding hypotension. and qualifications. leaving a large tissue defect. has lagged behind pre–hospital advancements in medical and general trauma management. The bite area becomes erythematous and ecchymotic and may itch. anxiety.000 to 90. The initial impetus for this development was the need to deliver such life–saving interventions as cardiac defibrillation. Treating trauma patients in the field. resembling those produced by the violin and certain other spiders. erythema nodosum. but rather evolves over the ensuing minutes. including nausea and vomiting. and an estimated 70. and chest. Far more common than spider bites are flea. Pain can be severe and involve the entire injured area. However. There may also be generalized pruritus. whereas bilaterally dilated and fixed pupils are consistent with brainstem injury. Inequality in pupil size of less than 1mm is common and has no pathologic significance. such as extensor posturing or pupillary asymmetry or nonreactivity. The pupil size and light reflex should be assessed and documented for each eye. Strong Class II evidence suggests that raising the blood pressure in hypotensive. The initial pupil examination. Fluid therapy is utilized to support cardiovascular performance in an effort to maintain adequate cerebral perfusion pressure and limit secondary brain injury. if the patient shows obvious signs of cerebral herniation. The evidence indicates that routine hyperventilation should not be performed. <80mmHg (age 6–12 years). In adult trauma. severe head injury patients improves outcome in proportion to the efficacy of the resuscitation. It is administered in quantities necessary to support blood pressure in the normal range. Abnormalities found in the pupil examination are helpful in generating a differential diagnosis and in directing diagnostic testing and therapeutic interventions. and 35 bpm for infants. 15–20 bpm for children. and <90mmHg (age 13–16 years) in pediatric severe TBI patients. Therefore. This hyperventilation may be performed as a temporizing measure until the patient arrives at the hospital when blood gas analysis will guide the ventilation rate. The GCS score should be measured preferably prior to administering sedative or paralytic agents. hypotension is usually defined as systolic blood pressure <90mm Hg. In children. GLASGOW COMA SCALE SCORE : Teasdale and Jennett developed the Glasgow Coma Scale in 1974 as an objective measure of the level of consciousness after head trauma. symmetry. therefore. PRE–HOSPITAL TREATMENT OF TBI AIRWAY. Perhaps even more important is maintaining cerebral perfusion pressure and delivering oxygen to the injured brain. the oxygen saturation should be maintained at a minimum of 90% or greater. and reactivity to light. Pupillary constriction to light is mediated through the parasympathetic nervous system via the third cranial nerve. hypoxemia. Inadequate fluid volumes or under–resuscitation can precipitate sudden hypotension and should be avoided. Dilation and fixation of one pupil signifies herniation. The evidence indicates that these values must be avoided. and 20 bpm for infants should be maintained. The GCS permits a repetitive and moderately reliable standardized method of reporting and recording ongoing neurologic evaluations. as well as lack of improvement or deterioration of GCS score of two points or more from the field to the emergency department. or rapidly corrected in severe head injury patients. hypotension is usually defined as SBP less than the fifth percentile for the age.EMERGENCY MEDICAL GUIDELINES or an arterial oxygen saturation <90%. PUPILS : Examining the pupils is a standard component of the neurologic examination that is particularly important in evaluating patients with traumatic brain injury. if possible. Hypotension produces a significant secondary brain injury that substantially worsens outcome. a respiratory rate of 10 breaths per minute (bpm) for adults. It has since become the most widely used clinical measure of the severity of traumatic brain injury (TBI). A single episode of hypotension has been shown to double mortality. Limited prehospital GCS data indicate that initial field GCS scores between 3 and 5. and the duration of pupillary dilaE . establishes the baseline against which all subsequent neurologic evaluations are compared. hyperventilate the patient at a rate of 20 bpm for adults. FLUID RESUSCITATION: The principle issue concerning pre–hospital fluid resuscitation with TBI centers around preventing and/or rapidly treating shock. The examination consists of assessing pupil size. the pupillary light reflex is an indirect measure of herniation or brainstem injury. hypotension. GCS scoring should occur after hypoxemia and hypotension are corrected and the patient has been resuscitated. and hypothermia are also associated with dilated pupil size and abnormal reactivity. A patent airway should be ensured and endotracheal intubation performed for patients with a GCS score less than 9 or those who are unable to maintain or protect their airway. or after these drugs have been metabolized. No studies prove the efficacy of mannitol in the pre–hospital setting. along with the GCS score. VENTILATION AND OXYGENATION: Class III evidence indicates that all severe TBI patients treated in the field should receive supplemental oxygen to maximize arterial oxygen saturation. <75mmHg (age 2–5 years). Specifically. After correction of hypoxemia or hypotension. have significant value as predictors of poor patient outcome. Pupils are generally round and roughly equal in diameter. However. Fluid resuscitation in patients with TBI should be administered to avoid hypotension and/or limit hypotension to the shortest duration possible. If pulse oximetry is available. The most common used resuscitation fluid for trauma patients in the prehospital setting is isotonic crystalloid solution.76 2/15/06 tion and fixation should also be documented. Destruction of the third nerve parasympathetic brainstem pathway results in a dilated pupil that is fixed to light. be defined as a SBP<65 mm Hg (age 0–1 year). 30 bpm for children. . Hypotension can. an unconscious TBI patient with a unilaterally dilated pupil or with bilaterally fixed and dilated pupils is presumed to have cerebral herniation and require emergent interventions to lower the ICP. If ventilatory assistance after endotracheal intubation is provided. making it necessary to resuscitate and stabilize the patient before assessing pupillary function. with the understanding that loss of the extremity distal to the tourniquet is likely. All other treatments should be performed following the appropriate guidelines. Inter–hospital transfers of these head injury patients are known to delay the time until neurosurgical consultation and intervention. Patient treatment/transport should not be delayed for wound care in life–threatening situations. When an integrated EMS and trauma system is in place and EMS agencies transport a patient directly fro the scene of the accident to an appropriate receiving facility (trauma center). HOSPITALTRANSPORT DECISIONS The management by EMS personnel of the head–injured patient prior to arrival at the hospital is influenced by a number of factors. This delay puts the patient at great risk for secondary insult to the brain.EDUCATIONAL GUIDELINES 0 SUMMARY Preservation of cerebral perfusion and oxygenation are the first priorities in managing patients with TBI. Sedation. Elevate– Hold extremity above the patient’s heart while applying direct pressure to the wound. Flush wounds with a generous amount of sterile water or saline only when bleeding is at a minimum. analgesia. Patients who exhibit signs of cerebral herniation during field management and transport should be initially treated with hyperventilation as defined. and the decision regarding choice of destination.77 2/15/06 . the patient is entered into a system of care that has been shown to improve overall patient outcome. The role of mannitol in treating herniation is yet to determined. including the mechanism of injury. Score 16 15 14 13 12 11 10 9 8 7 6 5 4 3 under 3 RESPIRATORYRATE: 10–24 15–35 greater than 35 less than 10 Interpretation 99% probability of survival 98% probability of survival 95% probability of survival 91% probability of survival 83% probability of survival 71% probability of survival 55% probability of survival 37% probability of survival 22% probability of survival 12% probability of survival 7% probability of survival 4% probability of survival 2% probability of survival 1% probability of survival 0% probability of survival 4 points 3 points 2 points 1 point TYPES OF WOUNDS\TREATMENT: E . betadine and scrubbing have been found to cause further injury and are therefore not recommended. TRAUMASCORE FOR SURVIVALPROBABILITY RESPIRATORY EFFORT: Normal Shallow or Retractive SYSTOLIC BLOOD PRESSURE: Greater than 90 70–90 50–69 less than 50 no carotid pulse CAPILLARY REFILL: Normal (less than 2 seconds) Delayed (more than 2 seconds) No capillary refill 14–15 11–13 8–10 5–7 3–4 0 points 1 point 0 points 4 points 3 points 2 points 1 point 0 points 2 points 1 point 0 points 5 points 4 points 3 points 2 points 1 point GLASGOW COMA SCALE SCORE: WOUND CARE All appropriate personal protective equipment should be used when treating patients. Hydrogen peroxide. and currently it is not recommended in these guidelines. Tourniquets– Only to be used in a last resort effort to control bleeding. (do not delay the control of bleeding to flush the wound). Pressure point– Apply pressure to the artery proximal to the wound. and neuromuscular blockade are important considerations during the transport of patients with TBI to minimize changes in ICP and to maximize safety during transport. the type and severity of injury. Bleeding control should be performed in the following order: Direct pressure– Apply sterile dressing with pressure directly over the wound. Once dressings have been applied do not remove due to potential for further bleeding. Hypoglycemia may mimic TBI and should be considered in all patients with altered mental status regardless of suspected etiology. or in a container with ice and water (if available). Puncture—A stab type wound from a knife or blunt object. Contusions—A severe bruise in which the skin is intact but there is swelling and possibly a hematoma in the area of the injury. (partially. Treatment: Control bleeding with proper technique. such as deformities. Gently cover the area with sterile gauze moistened with saline or sterile water. Evisceration—Open wound to the abdominal area where any organ or viscera protrude from the wound. The amputated part should be placed in a dry plastic bag . Avulsions—Involves the tearing loose of a flap of skin. Treatment: Apply ice packs to reduce the swelling. with injuries to tissues present. when appropriate). (do not wrap in moistened dressing).. therefore rapid assessment is necessary. and cardiac/respiratory disturbances. or may bleed very little.. requiring that these patients be monitored closely for deterioration in respiratory status. Never attempt to reinsert the organs or viscera. point of entry/exit (if applicable) and prepare to treat for shock. this can include gun shot wounds and impaled objects. Seal the bag . sterile dressing. Splint and treat per fracture guideline. Never use ice alone or dry ice. cover with a dry. or completely) Treatment: Control bleeding with proper technique. Fractures can commonly be found below contusions. Consider area of wound. Direct contact with freezing temperatures may cause tissue damage and should be avoided.78 2/15/06 Open chest wound— Usually a puncture type wound which is deep in nature. apply appropriate dressing (secure impaled objects. Amputations—Any injury that cuts off an appendage or projection of the body. Lacerations may produce severe bleeding. that can be clean or jagged. (clean with sterile water. The depth of the penetration depends on the force and the duration of the contact with the damaging surface. apply dry. Treatment: Control bleeding with proper technique. Maintain a high index of suspicion when dealing with gun shot wounds due to the potential for extensive internal injury. Note: Control bleeding. reasonable pressure across the entire stump. so the part will not lose moisture and place on cold packs. which may either remain hanging or be torn off altogether. reduced range of motion. Note: Chest injuries may require additional treatments including pleural decompression.. use occlusive dressings for sucking chest wounds) and maintain airway. Laceration— Is an incision type wound. sterile dressing. E . sterile dressing. Treatment: Control bleeding with proper technique. Treatment: Irrigate with a sterile solution (NaCL or water). Contusions generally result from a blunt blow. secure impaled objects with exception to airway obstruction. Treatment: Control bleeding with proper technique. cover the stump with damp sterile dressing and an elastic wrap that will apply uniform.EMERGENCY MEDICAL GUIDELINES Abrasions—Removal or destruction of the surface layers of the skin by friction. when appropriate. Treatment: Control bleeding with proper technique. or Saline. . otherwise irreversible damage will occur. Maintain a high index of suspicion for damage/injury to underlying tissues/organs. pain etc. pericardiocentesis. by proper technique. This type of injury often requires advanced airway techniques. underlying organs. deeper than the contusion itself. check for signs and symptoms of a fracture. replace avulsed portion to its natural position (if still partially attached) and bandage with dry. Note: Make sure to keep organs moistened. and is sometimes a “sucking” chest wound. and can range from the skin surface to the underlying tissues. 79 2/15/06 .EDUCATIONAL GUIDELINES E . PROCEDURAL GUIDELINES Procedural Guidelines 03/01/05 P-1 . Oxygen delivery systems and flow rates should conform to accepted ACLS guidelines.3–80 CONTINUOUS POSITIVE AIRWAY PRESSURE (CPAP) General: CPAP stands for Continuous Positive Airway Pressure and is very useful in keeping the smaller airways open. simply release the manual button and after a short pause (4–7 seconds) the ventilator will commence automatic cycling at the rate and volume selected on the indicator.6 13.5 18 21. The CPAP unit will supply approximately 130 liters of flow at an oxygen concentration (FiO2) of 30% (this can be increased to approx 50% with supplied supplemental oxygen tubing). it is an adjunct or in addition to them Indications: Pulmonary Edema Contraindications: Apnea Pneumothorax Gastric distention P-2 03/01/05 . It is important to remember that CPAP does not replace current treatment guidelines.3–110 1 O F F 2 200 20 12 3 4 5 6 300 400 600 15 15 12 13.7–40 40–60 53.6 20–30 7 800 12 28.3–20 26. If commencing automatic ventilations immediately. Application/Use Manual Ventilations Select the tidal volume/frequency of ventilation for the size of patient being resuscitated.8 1100 12 39. CAREVENT Unit can be used as either a manual or automatic ventilator. (Tidal volume= 10–15 mls/kg. Control Position Tidal Volume Vt (ml) Frequency (BPM) Automatic flowrate (LPM) Body Weight (kg) 73.EMERGENCY MEDICAL GUIDELINES Airway Management Airway management should conform to accepted ACLS guidelines. Rather. the Paramedic should choose the appropriate form and rate. Release the button when chest rise is adequate. Accordingly. see chart below) Depress the manual button and observe the rise of the patient’s chest. rotate the setting selector to t the setting appropriate for the size of the patient being ventilated and the ventilator will commence automatic cycling. Automatic Ventilation If you have been manually ventilating the patient. Provides “Demand Breathing” with automatic cycling shut off and re–start. administer CPAP Monitor and record SaO2 Continue to follow Treatment Guidelines for underlying cause (i. If rales present. kinked. attach 10.0 PEEP valve to mask Guidelines: Assess the patient (Vital signs and pre-oxygen SaO2) Administer Oxygen per protocol If wheezing present. Lasix. discontinue treatment and assist ventilations with BVM Setup: Connect flow generator to oxygen tank or oxygen outlet in Rescue Place filter on generator intake port Attach supply tubing to generator and to mask Explain procedure to patient Turn on oxygen supply and attach mask to patient using supplied straps After patient is accustomed to oxygen flow. This Device Is Not To Be Cleaned. Insure all necessary components and equipment are at hand Position the patient’s head in a neutral position Hyperventilate for at leased 30 seconds Lubricate tube for easier insertion Jaw–lift maneuver Insert COMBITUBE with curvature in same direction as natural curvature of pharynx 03/01/05 P-3 .PROCEDURAL GUIDELINES Severe facial injuries Hypotension secondary to trauma Asthma Altered LOC Precautions: Continuous monitoring of the patient is MANDATORY Watch for occlusion of the generator intake port Insure the supply tubing is not pinched.e. administer one (1) Nebulizer treatment. If no improvement. If severe difficulty in exhaling. administer CPAP treatment. NTG. or occluded Observe the patient to insure they can exhale. etc) ESOPHAGEAL TRACHEAL DOUBLE LUMEN AIRWAY (COMBITUBE©) Indications Cardiac arrest from any cause Respiratory arrest Unconscious patient with inadequate respirations and no gag reflex Contraindications Patient is under five (5) feet in height Patient is under sixteen (16) years of age Active gag reflex Patient has known or suspected esophageal disease Patient has ingested a caustic substance Procedure NOTE: The COMBITUBE Is Single Patient Use. ventilate through secondary (CLEAR TUBE) continue to ventilate through secondary tube (See Illustration D) To Replace COMBITUBE with an endotracheal tube Deflate the #1 cuff labeled 100 ml If the tube is not already in the trachea. redirect it or withdraw. Tracheal placement Breath sounds absent and epigastric sounds present. severe facial trauma. reoxygenate. Tube using currently accepted medical techniques Deflate the distal cuff #2 labeled 15 ml and remove carefully CRICOTHYROTOMY Indications Needle and surgical (scalpel) cricothyrotomy may be performed if more conventional techniques of controlling the airway are either unsuccessful or unobtainable as a result of edema. or other severe airway complication.EMERGENCY MEDICAL GUIDELINES Insert gently DO NOT FORCE tube Stop when BLACK rings on the tube are positioned between the patient’s teeth If tube does not advance easily. move the COMBITUBE to the left side of the mouth Intubate with an E. and reinsert (See Illustration A) To confirm tube placement Inflate pharyngeal cuff through line #1 (BLUE) with 100 ml of air and distal cuff through line #2 (WHITE) with 15 ml of air (See Illustration B) Ventilate through primary (BLUE TUBE) Tube placement is confirmed by auscultating breath sounds (high axillary & bilaterally) and auscultating over stomach Esophageal placement Breath sounds are present bilaterally with epigastric sounds absent continue to ventilate through primary (BLUE TUBE) (See Illustration C). Under this usage. severe oropharyngeal hemorrhage. Caution The following are common complications: hemorrhage at the insertion site subcutaneous emphysema aspiration of blood into the lungs perforation/laceration of the thyroid cartilage. anaphylaxis.T. Both procedures are temporary stabilizing techniques and are relatively easy to perform. Be careful as vomitus will frequently comeout of the clear tube with esophageal placement. locate cricothyroid membrane with the other Find the landmark by palpating the patients neck from the top P-4 03/01/05 . the clear tube may be used for the removal of gastric fluids or gas with the catheter provided in the airway kit. thyroid gland or esophagus laceration of carotid arteries or jugular veins MINI–TRACH II CRICOTHYROTOMY KIT Contraindications Children under 12 years of age Figure 1 Application/Use Patient should be placed supine (ensure cervical spine immobilization if trauma is suspected) Stabilize the larynx with one hand. inhalation injury. make a 1 cm midline vertical stab incision through the cricothyroid membrane into the airway Withdraw the scalpel ensuring the skin is pressed firmly against the larynx to prevent loss of alignment between the hole in the skin and the membrane Pass the introducer through the stab incision into the trachea Pass the 4. Once air is aspirated through the syringe. gently rotate the tube between your thumb and forefinger while advancing the tube Withdraw the introducer Attach the 15 mm adapter to the flange of the catheter Secure the flange to the neck using the neck tie that is supplied with the kit if needed. position the cutting edge caudally. Remove the needle pieces and advance the per trach until the tie down rests on the skin. and secure the trach.0 ET tube over the introducer and guide into the trachea until the flange of the tube rests against the skin some resistance may be noted when sliding the tube down the introducer if this occurs. check for breath sounds. NEEDLE CRICOTHYROTOMY Caution This procedure does not provide airway protection or elimination of carbon dioxide Procedure Patient should be placed supine (ensure cervical spine immobilization if trauma is suspected) Find the landmark by palpating the patient’s neck from the top (See Figure 1) the first prominence felt is the thyroid cartilage. the second prominence is the cricoid cartilage (See Figure 1) the space between the two is the cricothyroid membrane Cleanse the site using antiseptic swab Using the guarded scalpel. is the cricothyroid membrane 03/01/05 P-5 Figure 2 . suction the tube using the supplied catheter to remove excess blood or secretions suction should only be applied while withdrawing the catheter Ventilate with the highest available oxygen concentration Assess placement PER TRACH Application/Use Patient should be supine (ensure cervical spine immobilization if trauma is suspected) Hyperextend the patient’s head (unless trauma is suspected) Locate the cricothyroid membrane (See Figure 1) Prepare the site with a Betadine swab Perform a 1” horizontal incision on the skin over the cricothyroid membrane Insert a butterfly needle (with a syringe attached) into the cricothyroid membrane (angled slightly towards the feet). remove the syringe and advance the dialator (through the hub of the needle) as far as possible. characterized by a small depression.PROCEDURAL GUIDELINES the first prominence felt is the thyroid cartilage. Remove the dilator. the second prominence is the cricoid cartilage the space between the two. Squeeze the butterflies on the needle to split the needle. inflate the cuff. Ventilate with high flow oxygen. remove thumb from port allowing exhalation (See Figure 3) Figure 3 Pediatric For pediatric patients use the same procedure only use a 14–18 g catheter over needle SURGICAL (SCALPEL) CRICOTHYROTOMY Contraindications Children 12 and under Procedure Patient should be placed supine (ensure cervical spine immobilization if trauma is suspected) Stabilize larynx with one hand. is the cricothyroid membrane Cleanse the site using antiseptic swab Make a 2 cm horizontal incision with a scalpel through the membrane (See Figure 4) Insert handle of scalpel into incision and rotate 90 degrees to allow placement of a 5. characterized by a small depression. Lucie County uses hemostats to dilate the surgical opening instead of the scalpel handle. ENDOTRACHEAL INTUBATION EXTUBATION Indications Improper placement Occluded or damaged tube Procedure Ready suction unit Turn the patient’s head to one side if not contraindicated Deflate the cuff Remove the tube during exhalation (if applicable) Assess the airway P-6 03/01/05 .EMERGENCY MEDICAL GUIDELINES Stabilize larynx with one hand. removing needle and syringe Secure hub Attach oxygen tubing kit to the catheter Obstruct thumb port to insufflate the chest.0 mm ET Insert ET tube into the incision caudally and inflate cuff accordingly Ventilate with the highest available oxygen concentration Assess placement Figure 4 St. locate cricothyroid membrane with the other Cleanse the site using antiseptic swab Attach a 10 cc syringe to the needle of a 14 g catheter over needle set Insert needle through the cricothyroid membrane at a 45–60 degree angle caudally (See Figure 2) Apply negative pressure to syringe during insertion Entrance of air into syringe indicates placement in trachea Advance catheter over needle. locate cricothyroid membrane with the other Find the landmark by palpating the patient’s neck from the top (See Figure 1) the first prominence felt is the thyroid cartilage.0 to 6. the second prominence is the cricoid cartilage the space between the two. PROCEDURAL GUIDELINES NASOTRACHEAL INTUBATION Indications Any patient in need of intubation who cannot protect and maintain their own airway and who has spontaneous respirations Contraindications Apnea Airway obstruction caused by foreign body obstruction Severe head injury or possible basilar skull fracture Bleeding disorders Caution Nasal intubation prevents a patient from receiving thrombolytic therapy.5 mm smaller than that used for orotracheal intubation. this will usually be 0. lubricate the tube generously with Xylocaine jelly or a waterbased jelly Keeping the bevel next to the nostril. gently insert the tube into the biggest nostril. Anesthetize the nostrils and pharynx with topical anesthetic if time permits Pick up the tube and release the previously formed circle. If the tube is in the esophagus. forming a circle. confirm tube placement by auscultation of the epigastrium and lung fields. With gentle and even pressure. Once tube placement is confirmed. secure the tube and ventilate patient using an appropriately sized BVM OROTRACHEAL INTUBATION Indications Any patient in need of intubation who cannot protect and maintain their own airway Caution Do not use the teeth as a fulcrum Remove loose dentures Procedure Use universal precautions Select the appropriate size ET tube Insert appropriate size stylet Inflate and test cuff 03/01/05 P-7 . Listen down the tube for breath sounds and look for vapor condensation in the tube. This ensures anterior curvature of the tube making it easier to enter the trachea. epiglottis. Advancing the tube as the patient inhales will greatly enhance the chance of success When the 15 mm adapter is 1–2 cm from the nostril. withdraw it back until the tip is in the pharynx and advance it again on the patients inspiratory breath. inflate cuff. This consideration should be weighed when selecting the method of intubation Complications may include: bleeding from the nose nasal septal tear cranial perforation in basilar skull fractures injury to the pyriform sinus. advance the tube through the nostril into the pharynx. and vocal cords No stylet is used during this procedure Never force the tube at any time as soft tissue trauma may cause excessive bleeding and damage to the vocal cords may occur Application/Use Select appropriate sized endotracheal tube. Once selected insert the distal end of the tube into the 15 mm adapter. EMERGENCY MEDICAL GUIDELINES Deflate the cuff (leave syringe attached) Check laryngoscope light Preoxygenate the patient Place the patient in the sniffing position if not contraindicated Hold laryngoscope with the left hand Insert the laryngoscope blade in the mouth. Application/Use Expiration date should be checked prior to being placed in service. auscultate epigastric and lung sounds Note the depth of the tube Secure the tube with a restraint device Thomas ET Restraint Device END TIDAL CO2 DETECTOR Caution This device is unable to indicate right mainstem intubation and has been known to produce a “false positive” or “false negative” reading. Attach regulator to bag valve device and attempt to verify plug seal by squeezing bag without plug removal. (Depending on the percentage of CO2 detected. It is imperative that endotracheal tube placement be verified by alternate means.) Fluctuation of color strip during ventilation is normal. Documentation of verification is important especially in the incidence of a “false” reading. The device can accurately monitor for up to 2 hours. Remove plug and squeeze bag again to verify valve will function properly. verify placement by alternate means. Attempts to read prior to the 6th ventilation can lead to a false positive or negative reading. sweeping the tongue to the left Visualize the vocal cords Insert the ET tube Maintain visualization as tube is passed Remove the laryngoscope blade Inflate the cuff with air and remove the syringe Ventilate the patient observing chest rise. Compare color change on full expiration after the 6th ventilation. Regulator should be placed between the endotracheal tube and ventilator tubing to maintain the most accurate reading. Attach unit. P-8 03/01/05 . However. If using device in conjunction with an endotracheal tube. Plug should not be unsealed longer then 24 hrs. Variations in color range from light pink to bright yellow in the presence of CO2. which may dislodge the tube. (accuracy compromised) Verify initial color—should be dark purple. caution is necessary due to the weight of the unit. Use of CO2 regulator should be continued while utilizing a ventilator. as close as possible. Pediatric The Capno–Flo regulator may be used on pediatric as well as adult sized endotracheal tubes. to the expired air output and ventilate pt. helps prevent gastric distention and regurgitation. pulmonary edema. Indication To assist verification of placement of the endotracheal or Combitube into the trachea. tall Ingestion of caustic substances History of esophageal disease Alcoholism Conscious patient or patient with an intact gag reflex 03/01/05 P-9 . The advantages of an EOA are its relative ease of placement. Discard if an air leak is detected. Compress EID. does not require visualization of the chords. Warning Endotracheal tube obstruction. Contraindications Younger than 16 years old Less than 5 ft. Contraindications Children less than 5 years of age or less than 20kg (44) pounds. mainstem bronchus intubation. As the trachea is rigid. Procedure Perform leak test. Allow the bulb to self-inflate If air returns and fills the bulb rapidly (less than 5 seconds). Place a gloved finger over the end of the device and attempt to move air through. If location is in doubt re-intubate or support ventilation until you are prepared to attempt intubation again. ESOPHAGEAL OBTURATOR AIRWAY Indications The Esophageal Obturator Airway (EOA) is indicated for BLS airway control or in the event endotracheal intubation is not successful. The device is to be used in conjunction with all other means of establishing confirmation of placement. The endotracheal or combitube is likely in the trachea. Esophageal tissue will collapse around the EID. 7 in. severe bronchospastic or obstructive lung disease may lead to equivocal results due to decreased air available for aspiration. Carefully assess tube location clinically. If air slowly fills the bulb (5 to 30 seconds). morbid obesity. Direct larnyoscopy is always recommended in these situations. tall or 100 lbs More than 6 ft. attach to the endotracheal or combitube and release. use direct laryngoscopic visualization if a question still exists. Immediately after intubation. and before ventilating the patient with an automatic ventilator or BVM. The EID is not to be used on pregnant patients. and ventilates at the level of the pharynx/ epiglottis. The O-ring design assures leak proof connection with tubes.PROCEDURAL GUIDELINES ESOPHAGEAL INTUBATION DETECTOR (EID) Caution Ventilating the patient with an automatic ventilator or BVM prior to using this device may cause the esophagus to fill with air and therefore give unreliable results. This is indicative of esophageal intubation. Mask should appear spoon shaped without any wrinkles. Hold the LMA like a pen. with the index finger at the junction of the cuff and tube. Using one smooth movement. Procedure Assemble EOA gather all parts inflate mask (if necessary) test cuff snap mask to tube lubricate tube Position yourself at patient's head Preoxygenate patient for 1 minute Have suction prepared Flex patient's head slightly inferior Grasp jaw and pull anterior and inferior (See Figure 5) Insert tube until mask is fully seated on face Check location of tube listen for lung sounds look for chest rise listen for exhalation Inflate cuff 20–30 cc Detach syringe Recheck lung sounds Figure 5 LARYNGEAL MASK AIRWAY Indications The Laryngeal Mask Airway (LMA) is a device used to assist in securing an airway in a deeply unconscious patient when other methods of airway control have been unsuccessful. Never overinflate. Lubricate the posterior surface. Without holding the tube. Endotracheal intubation may still be accomplished after placement of an EOA.EMERGENCY MEDICAL GUIDELINES Severe facial trauma preventing mask seal Caution Complications accompanying the use of an EOA may include unintended endotracheal intubation. inflate the cuff with just enough air to obtain a seal.10 03/01/05 . assured vomiting on removal. press first against the palate. Press the tip of the cuff upward against the hard palate and flatten the cuff against it. Procedure Deflate the cuff completely. and advance the LMA into the hypopharynx until resistance is felt. and its dependence on a secure face–mask seal for adequate ventilation. then against the posterior pharyngeal wall. traumatization of the pharynx and esophagus. Figure 6 P . PROCEDURAL GUIDELINES NASOGASTRIC TUBE Indications Nasogastric tube insertion is indicated for decompression of gastric distention and in poisoning or overdose cases when transport will be lengthy or delayed Nasogastric tube insertion in poisoning or overdose is a Physician Consult modality Procedure Select proper size nasogastric tube Warm nasogastric tube in hand to increase pliability Explain the procedure to the patient if indicated Measure the nasogastric tube from the patient's epigastrium to their nose and mark it with tape (See Figure 6) Lubricate the nasogastric tube with a generous amount of lubricant Insert the nasogastric tube into the largest nare until the tube is inserted to the tape mark Confirm placement by auscultating over the epigastrium while injecting air Secure the nasogastric tube to the patient's nose with tape using the chevron style Figure 7 PLEURAL DECOMPRESSION Indications Figure 8 Tracheal shift towards the unaffected side of the chest Unequal breath sounds Jugular vein distention Increasing dyspnea Decreased lung sounds on the affected side Decreasing level of consciousness Decreasing oxygen saturation readings Procedure Primary –– midclavicular approach (See Figure 7) select site at the 2nd or 3rd intercostal space. The pleural chest drain kit accomplishes this via the Heimlich chest drain P . it is essential that an airtight one-way valve be utilized to prevent the condition from recurring.11 03/01/05 . midclavicular line cleanse the site with antiseptic swab insert a large bore over the needle catheter (14 gauge) just above the lower rib at a ninety degree angle advance the needle until the sound of escaping air is emitted advance the catheter and remove the needle apply appropriate one-way valve device secure catheter in place Alternate –– midaxillary approach (See Figure 8) select site at or around the 5th intercostal space at the midaxillary line cleanse the site with antiseptic swab insert a large bore over the needle catheter (14 gauge) just above the lower rib at a ninety degree angle advance the needle until the sound of escaping air is emitted advance the catheter and remove the needle apply appropriate one-way valve device secure catheter in place CHEST DRAIN KIT After performing a pleural decompression in the effort to relieve a tension pneumothorax. screw the Leur lock tubing onto the catheter. The pleural chest drain kit consists of: 14 g over the needle catheter Luer Lock tubing Heimlich valve Three foot suction tubing Indications Whenever pleural decompression is employed to relieve the signs and symptoms of a tension pneumothorax Figure 9 Application/Use Have the pleural chest drain kit assembled and ready for application prior to attempting pleural decompression Attach the Luer Lock tubing to the blue tip of the Heimlich valve.12 03/01/05 . or other respiratory distress PULSE OXIMETRY Indications All transported patients Procedure Select site Place SpO2 sensor on patient’s finger. or toe as indicated Observe pulse indicator for synchronization with pulse Record oxygen saturation prior to oxygen administration if possible Record oxygen saturation after oxygen administration a reading below 90% may call for aggressive oxygenation and /or ventilatory assistance Monitor for changes CAPNOGRAPHY(CO2): Indications All intubated patients Procedure Remove airway adapter from its package and inspect it Align the sensor over the adapter and between tabs P . The Heimlich valve is designed in a manner that allows air to pass out of it. while also preventing air from reentering the thoracic cavity and thereby effecting a simple pneumothorax. earlobe. keep tubing lower than insertion site for draining (See Figure 9) Upon successful pleural decompression and removal of the needle. Observe the Heimlich valve to determine if it is operating correctly (the internal flutter valve will pulsate and collapse along with the patient’s respiratory efforts). and tape in place to prevent accidental dislodging (correct valve operation is achieved when the arrow on the valve points away from the patient's chest) Attach the three foot suction tubing to the clear.EMERGENCY MEDICAL GUIDELINES valve. Secure the catheter in place with tape and gauze as needed Continuously monitor the patient during treatment and transport for the signs and symptoms of a recurring tension pneumothorax. thus preventing a tension pneumothorax. distal tip of the Heimlich valve and drain into appropriate container. 0 French black TFE catheter. Note: The black proximal positioning mark of the wire guide should be visible at the access site. Contraindications Ongoing coagulopathy Obsecure cricothyroid anatomy Infection of the cricothyroid membrane Mass (i.13 . antegrade over the wire guide via the mouth or nose and into the trachea until tenting is noted at the cricothyroid access site. Secure with a securing device and continuously monitor the end tidal CO2 indicator. advance the endotracheal tube over the catheter and into position below the level of the vocal cords. It is intended for use in situations where visualization of the vocal cords is not possible secondary to secretions. Remove the wire guide and catheter from the endotracheal tube and check the tube with the EID bulb auscultate lung sounds x 5. Advance the “J” end of the wire guide through the sheath and up the trachea in a cephalad direction.e. Free flow of air aspirated into syringe will confirm positioning.PROCEDURAL GUIDELINES Slide the sensor onto the airway adapter Gently push and twist the larger end of the adapter onto the ET tube Push the smaller end of the adapter onto the sensor circuitry Position the adapter so the sensor is on the top Printing Information: Manually prints real time strips as it is monitored Snap Shot prints the last 8 seconds Print Trends prints all trends that are enabled RETROGRADE INTUBATION COOK RETROGRADE INTUBATION SET Indications The Cook Retrograde Intubation Set has been designed to assist in the placement of an endotracheal tube during difficult or emergency airway access procedures. 03/01/05 P . Markings on the endotracheal tube should be in the range of 19cm to 23cm. Remove the sheath leaving the wire guide in place. This will insure enough wire guide is exposed orally or nasally for control of subsequent 11. Advance the 11. Remove the needle and syringe leaving the sheath in place.0 French TFE catheter introduction. With the TFE catheter in position.goiter) Procedure After standard prepping of the access site. blood and/or anatomic abnormalities. Note: Always maintain control and position of wire guide during advancement of the endotracheal tube. advance the 18 gauge sheath needle (attached to a 6cc disposable syringe) in a cephalad direction through the cricothyroid membrane and into the trachea. until the tip of the wire guide can be retrieved through the mouth or nose. 14 03/01/05 . SUCTION LAERDAL SUCTION UNIT (LSU) Indications: It is intended for intermittent operation to remove secretions. Step Four Remove the stopper. continue as in Step Five. it is possible to remove the stopper and carefully insert the needle further until entrance into the trachea is made. Secure the larynx laterally between the thumb and forefinger. (Note: Because of the sharp tip and conical shape of the needle. and connect the other end to the resuscitation bag or ventilation circuit. the needle is within the trachea*. secure the cannula with the neck tape. Step Three After puncturing the cricothyroid ligament. an incision of the skin with a scalpel is not necessary. Assure stable positioning of the neck region (place a pillow or piece of clothing under the patient’s shoulders) and hyperextend the neck (when applicable). After the stopper is removed. and lower vacuum levels are usually selected P . If air is present. This is the puncture site. Carefully remove the needle and syringe. blood or vomit from a patient’s airway to allow ventilation. Step One Place the patient in a supine position. be careful not to advance the device further with the needle still attached. check the entry of the needle into the trachea by aspirating air through the syringe. The opening of the trachea is achieved by dilating through the skin. and familiarize yourself with its contents. Step Two Firmly hold the device and puncture the cricothyroid ligament at a 90° angle. Step Five Hold the needle and syringe firmly and slide only the plastic cannula along the needle into the trachea until the flange rests on the neck. *Warning Should no aspiration of air be possible in Step Three because of an extremely thick neck. Now.EMERGENCY MEDICAL GUIDELINES RUSCH QUICKTRACH CRICHOTHYROTOMY DEVICE Istructions for Use Pre-Assembly: Open the package. The stopper reduces the risk of inserting the needle too deeply and causing damage to the rear wall of the trachea. Higher vacuum levels are generally selected for oropharyngeal suctioning. Find the cricothyroid ligament (in the midline between the thyroid cartilage and the cricoid cartilage). Next. apply the connecting tube to the 15mm connection. Once this is verified. This reduces the risk of bleeding as only the smallest necessary opening is made). remove the device. change the angle of insertion to 60° and advance the device forward into the trachea to the level of the stopper. As soon as LED 2 of the Battery Status Indicator comes on fully occlude the Suction Tubing. remaining battery capacity. The green LED bargraph has 3 functions: 1. During operation from internal battery. The test will start immediately.indicates which step of the test is currently in progress or which corresponding test result is being displayed. Before you press the TEST-button. If the indicator continues to be lit after three OFF/ON cycles and after replacing the battery with a fully charged battery.15 . Flashes slowly while the Automatic Power-save Function is activated. Replacing the Canister: 03/01/05 P . Note: Do not release the TEST-button until min. Test Button: This button allows you to run a user initiated Device Test program to identify whether the LSU operates satisfactory. 2. if the Device Test is interrupted and when the battery is discharged.indicates approx achieved battery capacity. 2. Contraindications: None known. Unit is turned off by turning knob to the far left setting (“0”). 3. is assembled correctly or if it needs service. If lit turn the LSU OFF. Press and hold the TEST-button while setting the Operating Knob to 500+ mmHg. Flashes rapidly during Device Test. and then ON again to check if the indication disappears. Battery Status Indicator: During operation from internal battery and during charging the displayed values must only be used as indications. 2 seconds after the Operating Knob has been set to 500+. During the Device Test. 3. Indicator lights: Power on indicator (circle with a colored in circle in it) This green LED has 3 functions: 1. Vacuum Indicator: Green LED bargraph indicates the actual vacuum level. If it stays off. Keep the tubing occluded until LED 1 comes on. During charging. External Power Indicator (circle with power cord in it) This green LED is continuously lit while external AC or DC power is connected. discontinue use. Is lit continuously when the LSU is switched ON.indicates approx.PROCEDURAL GUIDELINES for tracheal suctioning and the suctioning of children and infants. Operating knob: It is a combined ON/OFF switch and vacuum selector. Turn knob to desired vacuum amount. the LSU can be operated. make sure the Patient Suction Tubing is not occluded or bent. Failure Mode Indicator (circle with triangle and in it) The red LED is lit when a possible malfunction of the LSU has been detected. slide the holder into position and connect the tubing to the canister. disconnect the angled connector from the vacuum inlet on the lid. an orogastric tube should be placed to empty the newborn’s stomach since it may contain meconium that could later be regurgitated and aspirated PHARYNGEAL SUCTIONING Procedure Use universal precautions Inspect unit for proper function and parts Switch on suction and clamp the tubing to note if the pressure dial registers at least 300 mm/Hg Attach the suction tip to the tubing Open the patients mouth Insert the suction tip in to the mouth and apply suction on the way out Do not suction for more that 15 seconds Re–oxygenation should occur prior to repeated suctioning TRACHEAL SUCTIONING Procedure Prepare equipment Use universal precautions (should use sterile gloves) Hyperventilate the patient Grasp the suction catheter with the gloved hand Insert the suction catheter into the ET Tube without application of suction Apply suction during the withdrawal of the catheter P .EMERGENCY MEDICAL GUIDELINES To remove the Canister. To remove the battery. Replacing the Battery: Open the door. To insert battery. To release the Canister Holder. Withdraw the battery from the LSU. push and move it slightly to the left and then release. press down the Canister Holder Release Arm while sliding the Holder toward you. push it fully in and then to the right to lock it. Replace the canister in the holder. Close the battery door.16 03/01/05 . After inserting the battery. place the LSU on charge unless a fully charged battery is inserted MECONIUM SUCTIONING Caution When the infant's condition is unstable. it may not be possible to clear the trachea of all meconium before positive pressure ventilation must be initiated This intervention should not be delayed while the infant is dried Mechanical suction should be set no higher than 100 mm/Hg Figure 10 Procedure Visualize hypopharynx with a laryngoscope and remove any residual meconium with suctioning Intubate the trachea and suction the lower airway utilizing a meconium trap connected to the ET tube (See Figure 10) Repeat as necessary After initial stabilization is achieved. Remove the canister from the holder. Not recommended for use with patients less than 40 kg Normal BPM Adult 10 – 12 Should a mechanical problem develop or the patient appears to be experiencing difficulty while connected to the ventilator. and HIGH. and HIGH are equally divided according to tidal volumes from 0–500 or 1. Tidal volumes range from 0–500 ml for pediatric and 0–1. 03/01/05 P . During tidal volume tests it was found that almost maximum volumes were obtained in the LOW to MEDIUM range (See Figure 16). These are only approximates and are not exact volumes.250 ml for adults. If unsure of proper weight. CHILD. otherwise settings may not be accurate Application/Use Determine the volume setting for the patient. Contraindications This device should not be used for a patient less than 50 pounds body weight Application/Use Turn TIDALVOLUME control to 0 Turn MODE SELECTOR control to desired setting (ADULT. MEDIUM. If unsure of proper weight. use 8–10 ml per kg of ideal body weight or 5 ml per pound (70 kg = 700 ml). use 8–10 ml per kg of ideal body weight or 5 ml per pound (70 kg = 700 ml). disconnect and ventilate by other means Refer to manual for cleaning instructions and operating information MINI–VENT The volume indicator on the device is set for LOW. MEDIUM. Over ventilating a patient may have serious untoward effects.250 ml. It must not be assumed that the settings of LOW. it is preferable to go with lower volume.17 .PROCEDURAL GUIDELINES Remove the catheter Hyperventilate the patient Repeat as necessary VENTILATOR AUTOVENT 2000 Caution Serial number of patient valve and serial number of module must match. HYPERVENTILATE. it is preferable to go with lower volume. CPR) Connect the patient valve to the patient Slowly turn the TIDAL VOLUME control until the desired tidal volume is obtained Determine the volume setting for the patient. keep NPO. not remaining on scene to fulfill protocol requirements 12 LEAD EKG Indications All chest pain including blunt trauma to the chest Any cardiac dysrhythmias or irregularities Heart rate less than 50 BPM or greater than 150 BPM Epigastric pain unless evidence of GI bleeding Thoracic back pain without trauma Diaphoresis not explained by fever or environment Difficulty breathing P . unless ordered per treatment guidelinesor on-duty ER Physician Avoid IV glucose (give glucose only if BGL is lower than 50 mg/dl and with Physician Consult) Procedure If patient meets inclusion criteria. they are considered priority 2. and a stroke alert is called to dispatch and the hospital transporting to Treatment as specified by treatment guidelines Perform thrombolytic exclusion check sheet Transport should not be delayed CARDIAC ALERT CRITERIA: Patient exhibiting signs and symptoms consistent with an AMI ST segment elevation present on 12–lead EKG in 2 or more contiguous leads Patient is 18 years old or older Caution If QRS width is .EMERGENCY MEDICAL GUIDELINES Cardiac ALERTS — CARDIAC AND STROKE STROKE ALERT CRITERIA: Time of onset <5 hours Any abnormal finding on examination? Deficit not likely due to head trauma? Blood Glucose >50 Caution Prevent aspiration. Be prepared to correlate clinically Procedure If patient meets inclusion criteria. elevate the head 30 degrees Avoid treatment of HTN. they are considered priority 2 and a cardiac alert is called to dispatch Treatment as specified by guidelines Perform thrombolytic exclusion check sheet Emphasis is placed on expediting patient transport and performing treatments enroute to the hospital.18 03/01/05 . even if they excluded from thrombolytics.12 sec or greater do not read ST segment changes Be aware of multiple conditions which may result in non–AMI ST segment changes. upper arm or upper chest near the shoulder RL–right leg. upper arm or upper chest near the shoulder LA–left arm. Place electrodes as per diagram (See Figure 11) RA–right arm. midclavicular line V5–5th intercostal space between V4 and V6 V6–5th intercostal space midaxillary line V4R–5th intercostal space. Caution If both the multifunction pads and the patient cables are connected to the patient and either a lead or a defibrillation cable becomes disconnected. immediately to the right of the sternum V2–4th intercostal space. III or aVF. right midclavicular line Figure 11 MARQUETTE RESPONDER 1500 CAPABILITIES 3 Lead ECG monitoring Defibrillation Cardioversion Transcutaneous pacing Diagnostic / interpretive 12-lead ECG MONITORING Patients can be monitored using either the Multifunction pads or by using the three lead patient cables.19 . etc. the unit switches monitoring to the source that remains connected 03/01/05 P . Running a second 12 lead with the V4 lead in the V4R position could result in a false impression or diagnosis advisory from the 12 lead monitor analysis. shock. should be initiated prior to obtaining a 12 lead ECG Obtaining a 12 lead ECG should not delay transport of critically ill patients Procedure Clean area for electrode placement with antiseptic swabs Shave area if needed being careful not to cause lacerations The mid–clavicular line may be found by dropping an imaginary line from the middle of the clavicle down The mid–axillary line can be found by dropping an imaginary line from the armpit down Leads V4 through V6 must be in a straight line and this may not alys be in the intercostal space Run a V4R if ST changes seen in leads II. manually print V4R. immediately to the left of the sternum V3–placed between V2 and V4 V4–5th intercostal space. Move the V4 lead to the V4R position. acute pulmonary edema. upper leg or lower abdomen near the hip V1–4th intercostal space. upper leg or lower abdomen near the hip LL–left leg.PROCEDURAL GUIDELINES Syncope without seizure or obvious blood loss (near syncopes included) CHF/Pulmonary edema Tricyclic antidepressant overdose Caution Treatment of life threatening problems such as dysrhythmias. you may use the LEAD SELECT switch to select PADS. MENU SELECT 11. POWER LIGHT 10. EVENT MARK 2. When the unit has reached the selected charge the beeping will become rapid and continue to beep until the energy is delivered. ECG SIZE 7. the LEAD SELECT switch must be set to SYNC and you must press the SYNC button Once you press the SYNC button. SHOCK 5. II. please refer to the Operation Manual for more information DEFIBRILLATION Insure defibrillation pads are in place Select desired energy level on ENERGY SELECT 1 switch Press the white CHARGE 2 button The Marquette will indicate charging with an audible beep and the screen will state charging to XXX JOULES. PRINT 3. ENTER 12. ENERGYSELECTAND POWER 6. VOLUME 13. place switch in the ON/DISARM position the Marquette will enter a self test mode then indicate TEST OK turn the LEAD SELECTOR switch to the PADS position monitor will display ECG in Lead II only check expiration date on package pad position is anterior / anterior attach one pad to cable marked apex and the other pad to the cable marked sternum dry patient's chest peel off protective backing press the pads firmly onto the patient's chest in sternal / apex position monitor will display and print only in Lead II Using three lead patient cables turn power on and wait for the self test to be completed attach electrodes to patient cables using standard AHA code select the lead you wish to monitor ( I. CHARGE 4. adjust ECG SIZE and / or select a different lead) Select the proper energy level with the ENERGY SELECT 1 switch P . The screen will show READY XXX JOULES After assuring the patient is clear. SYNC 9.20 03/01/05 . The SYNC button will flash with each R wave detected and a marker will appear on each R wave on the display screen (if sync marker fails to appear. LCD DISPLAY CONTRAST SYNCHRONIZED CARDIOVERSION Caution In order to activate the synchronized cardioversion function.EMERGENCY MEDICAL GUIDELINES Application/Use Multifunction pads turn the power on with the select energy switch. LEAD SELECT 8. press the green SHOCK 3 button Controls and Indicators 1. or III while in synchronized mode Application/Use Connect both the three lead patient cables and the defibrillation cables to the patient as described in the monitoring section Select SYNC on the lead selector switch Press the SYNC button. LEAD I. II. or III ) the Marquette will display and / or print in the lead selected RECORDING SELECTED LEAD Paper pressing the button labeled PRINT starts the printer pressing the PRINT button a second time stops the printer Patient data card some Departments may use the optional patient data card to capture patient ECG information. M. 03/01/05 P . and OUTPUT parameters.PROCEDURAL GUIDELINES Press the white CHARGE 2 button When the unit is charged press and hold the green SHOCK 3 button until the energy is delivered Repeat as required PACING for The Marquette is capable of either fixed or demand pacing. and print the 12 lead ECG without any further action on the operators part. Do not move the LEAD SELECT from 12 lead position until you are completely finished with the 12 lead operation. or through a 3–lead patient cable. refer to TRANSCUTANEOUS PACING PROCEDURAL GUIDELINE Press START / STOP button to begin pacing Application/Use RUNNING A DIAGNOSTIC 12 LEAD ECG Connect the acquisition module to the A. RATE. Place both multifunction pads and patient monitoring electrodes on patient as previously described Press SETUP on the pacemaker control panel. disposable defibrillation electrodes. refer to 12 LEAD ECG PROCEDURAL GUIDELINE (SEE PAGE P-17) Then the message ACQUIRING DATA appears on the display screen. adjust the ECG SIZE and / or use the LEAD SELECT switch to select a different lead. avoid monitoring in environments with significant electrical interference as noise may corrupt the ECG signal. Caution Avoid contact with the conductive material Application/Use Paddles apply 1/4” — 1/2” of conductive gel over the entire surface of the paddles or use pre–jelled defibrillation pads and apply to the patient turn the monitor on by rotating POWER knob to any battery postion spare batteries are to be carried at all times. analyze. Set MODE. A marker will appear on the display screen on each R wave sensed. the LP 10 holds 3 batteries which are used individually until the power is depleted push LEAD SELECT to paddles postion assure that the gel is distributed evenly over the entire surface of the paddles place paddles on the patient's chest with approximately 25 pounds of pressure place APEX paddle on patient's lower left chest and STERNUM paddle on the sternum slightly to the right observe cardioscope for patient's rhythm Patient cable monitoring prepare the patient's skin surface. INPUT on the left side of the Marquette Turn the LEAD SELECT to 12 LEAD (12 with QRS image) Prepare the patient. If the marker does not appear. The default setting is demand pacing. PHYSIO CONTROL LIFEPAK 10 MONITORING ECG monitoring may be done through the external paddles. select START ANALYSIS and press ENTER The Marquette will automatically acquire.21 . prior to the application of the electrodes assure the electrodes have sufficient gel to conduct secure and support the patient cable whenever possible. recording continues until FREEZE is released CODE SUMMARY Application/Use Push CODE SUMMARY. If the power is turned off the code summary information will be retained for 5 minutes. the recorder will print a full report of the information stored in memory Printing of the CODE SUMMARY report can be interrupted by pushing the CODE SUMMARY button pushing the CHARGE button pushing the CHARGE button pushing the RECORD button running out of chart paper turning off the POWER The code summary report may be resumed by pushing CODE SUMMARY whenever the Lifepak 10 is on Critical events will be retained in memory whenever the Lifepak 10 is turned on. and numbers will scroll up under AVAILABLE ENERGY display until energy reaches pre–selected level at which time a charge tone will sound P . a ramping tone will be heard.22 03/01/05 .EMERGENCY MEDICAL GUIDELINES if the ECG is unreadable due to the size of the QRS complex the ECG SIZE may be adjusted attach the 6 pin cable plug to the right side panel attach lead wires to the electrodes apply the electrodes to the prepared sites turn on the POWER select the proper lead with the LEAD SELECT adjust the ECG Size push the QRS VOL until audible Push the ECG SIZE up or down until systole beeper coincides with every QRS complex Adjust the QRS VOL as desired CABLE PLACEMENT Application/Use White (right arm or right upper chest) Black (left arm or left upper chest) Red (left leg or left lower chest) RECORDING Application/Use Push RECORD Adjust ECG SIZE if necessary If FREEZE is selected while recording. After the 5 minutes the information will be erased DEFIBRILLATION Application/Use Apply conductive gel to paddles Turn the monitor on. O will be displayed under AVAILABLE ENERGY on status display Select energy to be delivered with ENERGY SELECT Push and release CHARGE button on APEX paddle. charge indicator will flash. If markers do not occur on the QRS complexes adjust ECG SIZE. adjacent indicator will illuminate Select desired pacing RATE (pacemaker powers up at a rate of 40 bpm) CURRENT level will begin at 0 mA 03/01/05 P . position electrodes on patient's chest Push PACER button. electrodes should be placed away from paddle sites and such that resultant will give a tall QRS complex Select LEAD with optimum QRS complex amplitude Push SYNC button. it is necessary to push SYNC again since it switches back to defibrillate mode after each synchronous discharge Thoroughly clean and store paddles in storage area after procedure PACING PROCEDURE Application/Use Rotate POWER control to a power source Connect ECG electrodes to patient cable and attach to patient For better adhesion. by looking and calling for “Clear!” Discharge the defibrillator by pushing both paddle DISCHARGE buttons simultaneously Observe patient and cardioscope to determine results To internally discharge an unwanted charge rotate ENERGY SELECT to another energy level Turn off monitor Thoroughly clean the paddles and store them in the storage area SYNCHRONIZED CARDIOVERSION Application/Use Rotate POWER to a power source Attach patient cable and ECG electrodes. change the lead or move the electrodes on the patient. clean and dry areas over which pacing electrodes will be placed Connect pacing cable to PACE connector at the right side of the LP 10 Connect the QUIK–PACE electrodes to pacing cable matching electrode color to connector color Peel off protective covering from electrode to expose conductive surface.PROCEDURAL GUIDELINES if the energy is changed after the charge has been initiated the energy will be discharged and the operator will have to re–initiate the charge by pushing the charge button Place the paddles firmly on the patient's chest in the same postion used for the QUICK LOOK procedure When the charge tones sound the defibrillator is ready for defibrillation Assure all personnel are clear from the patient as well as anything touching the patient. Push and hold paddle DISCHARGE buttons until discharge occurs with next QRS complex If rhythm does not convert and cardioversion is to be re–attempted. adjust ECG SIZE so that sync markers occur only on the QRS complex.23 . SYNC message on status display will blink off with each detected QRS complex Observe cardioscope. Prepare and postion the paddles on the patient's chest as described in the defibrillation procedure Select energy to be delivered with ENERGY SELECT Push the CHARGE button and wait for tone to sound indicating charge has completed. activate pacing by pushing START/STOP button. When low battery is indicated.EMERGENCY MEDICAL GUIDELINES Observe cardioscope. Option to display one or two additional waveforms Waveform display sweep speed: 25mm/sec for ECG and 12.9 in) high Resolution: 640 x 480 black and white LCD 640 x 480 amber and black EL display User selectable LCD contrast Displays a minimum of 4 seconds of ECG and alphanumerics for values. The pacing rate will maintain its pre–alarm setting. Inservice Mode: Provides simulated waveforms for demonstration purposes Low Battery Indication and Message: Low battery icon at top of display and low battery message in status area foreach battery. Setup Mode: Allows operator to customize the device. adjacent indicator light will go out If a pacing cable lead or QUIK–PACE electrode becomes detached during pacing. DISPLAY Size (active viewing area): LCD: 140.1mm (6. If this fails. Service Mode: Allows operator to execute device diagnostic tests and calibrations. When both batteries reach a low battery condition. the LEADS message will be displayed on the status display along with an audible alarm. Adjacent indicator will light and a positive going spike will be seen on the ECG display with each delivered pacing stimulus Increase current slowly while observing cardioscope for evidence of electrical pacing capture. device instructions or prompts.6mm (4.8mm (4. push START/STOP button again. Manual Mode: Provides normal operating capability for ALS users. When unit is sensing properly. however. If SENSE marker is not present on QRS or appears elsewhere.5mm/sec of CO2 P .24 03/01/05 .5 in) wide x 105. If intrinsic beats are not present skip this step. synchronous cardioversion and pacing.2 in) high EL: 165. LIFEPAK 12 GENERAL The LIFEPAK 12 defibrillator/monitor series has five main operating modes: Advisory Mode (SAS): Provides all features available except manual defibrillation. SENSE marker should appear on each QRS complex. there is a voice prompt toreplace battery. select another lead and readjust ECG SIZE. palpate patient's pulse or check blood pressure to assess perfusion Recorder will document pacing parameters. device autoswitches to second battery. each pacing stimulus will be marked with an arrow on the lower edge of ECG paper To terminate pacing. adjust ECG SIZE control for optimal sensing.8mm (5. the current will reset to 0 mA.5 in) wide x 123. Class 2 or 2.-” Heart symbol flashes for each QRS detection Continuous Patient Surveillance System (CPSS): In advisory mode while Shock Advisory System is not active. Snapshot . AVL.5. A 10-wire cable is used for 12-lead acquisition. 0. event and vital signs log. V3. CPSS monitors the patient. When the chest electrodes are removed. via paddles or Lead II ECG. external EIA/TIA modem. user test results and continuous ECG waveform records in internal memory.5. V4. II. AVR. V2.5. A 3-wire cable is used for 3-lead ECG monitoring. the 10-wire cable functions as a 4-wire cable. AVR. AVL and AVF acquired simultaneously (4-wire ECG cable) Leads I. Standard paddles or QUIK-COMBO pacing/defibrillation ECG electrodes or FAST-PATCH® disposable defibrillation/ECG electrodes are used for paddles lead monitoring. ECG ECG is monitored via several cable arrangements.0 fax MONITOR Voice Prompts: Used for selected warnings and alarms (configurable on/off). 2. for potentially shockable rhythms. Report Types: Three format types of CODE SUMMARY critical event record (short. II. III. AVF. 38400 and 57600 bps. vital signs log and vital signs graphs Vital Signs . EIA/TIA-RS232E compatible at 9600. V1. AVF. Lead Selection: Leads I. (3-wire ECG cable) Leads I. cellular modem or serial connection.25 cm/mV (fixed at 1 cm/mV for 12-lead) Heart Rate Display: 20 to 300 bpm digital display Out of range indication: Display symbol “. includes patient information. events (including waveforms and annotations). 19200. A 5-wire cable is used for 7-lead monitoring. III. 1. medium and long) Initial ECG (except short format) Automatic capture of vital signs measurements every 5 minutes 3-channel or 4-channel 12-lead ECG report Continuous waveform records (transfer only) Trend Summary . V1 (Labeled “C” on 5-wire ECG cable) Leads I. 1. V5 and V6 acquired simultaneously. The user can select and print reports and transfer the stored information via an internal modem through landline or mobile phones. 3. II.25 . 03/01/05 P . AVR.PROCEDURAL GUIDELINES DATA MANAGEMENT The device captures and stores patient data. Group III. (10-wire ECG cable) ECG Size: 4. 0. III. Supports EIA/TIA-602 compatible modems using Xon/ Xoff or RTS/CTS flow control at 9600 to 38400 bps. 2. II. III. AVL. includes patient information. includes patient information and 8 seconds of ECG captured at the time of transmission COMMUNICATIONS The device is capable of transferring data records by internal modem. 150. 5.2. Shock Ready Time: Using a fully charged battery at normal room temperature. 70. and 200 to 360 joules. ST shown in channels 2 or 3. P1. Energy output is limited to the available energy which results in delivery of 360 joules into 50 ohms. P . 20. EtCO2. RR. and 360 joules or user configurable sequence 100 to 200. 125. 70. 30. 3. 10. ST segment: After initial 12-lead ECG analysis. Note: ±5% accuracy applies when disposable therapy electrodes are attached. 4. 325. Output Energy (Biphasic): User configurable.0 in) or optional 100mm (3. VF/VT Alarm: Activates continuous CPSS monitoring in Manual Mode. sequence of three sequential shock levels ranging from 200. 7. 1. 150. 3. 175. 4. Reduced storage capacity with earlier versions. 100. SAS acquires ECG via therapy electrodes only. automatically selects and trends lead with the greatest ST displacement. Time scale: Auto. 300.9 in) Print Speed: 25mm/Sec +/. the device is ready to shock within 20 seconds if the initial rhythm finding is “Shock Advised. includes AMI statements. 200. 9. 6. typical Synchronous Cardioversion: Energy transfer begins within 60mS of the QRS peak ADVISORY Shock Advisory System (SAS) is an ECG analysis system that advises the operator if the algorithm detects a shockable or non-shockable ECG rhythm. 4 or 8 hours Duration: Up to 8 hours with -06 Memory PCB or later. 8. 100 to 300.26 03/01/05 . 30. 5. 20. 2.2) Delay: 8 seconds Autoprint: Waveform events print automatically (user configurable) Optional 50mm/sec timebase for 12-lead ECG reports MANUAL MODE Energy Select (Monophasic): 2. INTERPRETIVE ALGORITHMS 12-lead Interpretive algorithm: GE Medical 12SL.5. 30 minutes. ALARMS Quick Set: Activates alarms for all parameters. 4.5% (measured in accordance with AAMI EC-11. 100 to 360. 100. NIBP. 9. 225. SpO2(%). P2. PRINTER Prints continuous strip of the displayed patient information Paper Size: 50mm (2. 10. 200 to 300.EMERGENCY MEDICAL GUIDELINES SpO2 Measurement Range: 50 to 100% Trend Display: Choice of HR. sequence of 200/200/360 or 200/ 300/360 joules.” Output Energy (Edmark): User configurable. 300 and 360 joules or user configurable sequence 200/200/360 or 200/300/ 360 joules Energy Select (Biphasic): 2. 50. Charge Time: Charge time to 360J in less than 10seconds. 7. 8. 6. 250. Apnea alarm: Occurs when 30 seconds have elapsed since last detected respiration. 275. 50. 200. 15. If you’re unsure if rhythm is shockable. RL(green) 12L. Charge unit to desired energy level. press analyze button (if equipped).this monitor has a pulse ox built into it. 12L is then automatically ready for transmission. If it is shockable. III. The pads will still be sealed due to a double seal on the packaging. Use the anterior-posterior pad positioning for defib and pacing. Strips print out with leads II.27 . Cardioversion: Synch pad placement is the front pad goes on the 3rd intercostal space midclavicular and the posterior pad goes in the standard place. Recap 4 lead when finished. Contrast and volume buttons are on the lower left corner.push 12 lead button. Codemarker button. V1-V6 placement same as used now. do not take out until the ready light comes on. etc… Disposable probes can also be used (look like bandaids). LL(red). An alarm will sound reminding you to place the battery back in if you do. Keep the adult pads connected while in the case.Lists the commonly used procedures and drugs. When placing a battery in the charger. Paper: use the straight edge of the monitor to rip paper off. Print button marked Recorder. Pulse Ox.PROCEDURAL GUIDELINES ZOLL M SERIES MONITOR SELECTION AND GENERAL INFORMATION Lead Placement. then aquire. I. RA(white). Benefits by less skin effects and greater conversion rate. they will be listed on the summary printout. Defibrillator Biphasic waveform: Shocks at lower energy setting. To do 12L.plugs into 4 lead. Picks up minimal artifact from movement. Use the perforation on the paper when cutting for pasting. “shockable rhythm” will be displayed. 12 Leads are saved for a set time after unit is powered down. Energy settings: 03/01/05 P .LA(black). If these are pushed during a call. User needs to adjust the milliamps. temporarily withholds pacing. remember the patient must have the electrodes already attached in order to use lead I. 200j (progressive) Ped Synch Cardioversion for Atrial & Ventricular Tachys w/pulses: 1 j/kg. Pacer Unit is automatically set to 70 beats per minute. II. 2 j/kg (progressive) Adult Synch Cardioversion for Atrial & Ventricular Tachys w/pulses: 50j. 120j. 4:1 button: when pressed and held. 2 j/kg. III Apply conductive material to the patient or the paddles (multifunction electrodes are pre–gelled) Apply the paddles to the chest or attach the multifunction electrodes to the chest select the ENERGY LEVEL. 200j (progressive) Ped defib for V-fib & Pulseless VT: 1 j/kg. The settings that are being used will be remembered if switch is changed to defib or monitor. To access the pedi paddles push the PEDI button on the side of each paddle and slide the adult paddle forward. When replacing the adult paddles be sure the paddles lock into place. press the RECORDER ON–OFF button beside the monitor. may repeat at 2 j/kg (progressive). if 200 is not the desired level. by either depressing the UP/DOWN buttons located on the front of the panel or the sternum paddle charge the paddles by depressing the CHARGE button on the front panel or on the apex paddle discharge the defibrillator by holding both DISCHARGE buttons on the paddles or both buttons on the multifunction cable at the connection site P .28 03/01/05 Figure 12 . Application/Use Select DEFIB ON. 150j. Pacing will be delivered at ¼ the set ppm setting. ZOLL PD 1400 PACEMAKER/DEFIBRILLATOR MONITORING Application/Use Attach the patient electrodes to the patient and plug in the cable connector to the ECG INPUT Turn selector switch to the MONITOR ON position Press the LEAD button until the desired lead is displayed on the monitor Press the ECG SIZE button until the desired waveform size is displayed Adjust the systole beeper tone volume to the desired level Set HEART RATE ALARM by depressing the ALARM SET button and press the ALARM ON/OFF button Refer to the operator's manual to change the alarm limits To record the ECG tracing. 150j.EMERGENCY MEDICAL GUIDELINES Adult defib for V-fib & Pulseless VT: 120j. the recorder will continue to run until the button is pressed again Figure 11 DEFIBRILLATION Caution The pediatric paddles are built into the adult paddles (See Figure 12). 75j. this automatically sets the energy level to 200 joules Select the lead to use. (approx 1 every 4th beat). pneumothorax. or both. PERICARDIOCENTESIS Indications Emergency relief of cardiac tamponade on critically injured patients accompanied by severe hemodynamic impairment Contraindications Hemodynamically stable patients Caution Figure 13 This is a sterile procedure. Check the threshold periodically MCFR and SFR perform pericardiocentesis MULTI–FUNCTION ELECTRODES The multifunction electrodes allow for hands free defibrillation. pacing. This suppresses pacing unless the patient's rate drops below the set pacing rate. The pacing rate should be set at a level needed for adequate cardiac output.PROCEDURAL GUIDELINES repeat steps for each subsequent shock (the device is marked 1–2–3 for each step to be taken and the order of which it should be taken) PACING Application/Use Select MONITOR ON Set OUTPUT to 0 mA Apply pacer pads Connect pacer electrodes to the output cable Select PACER ON Set pacer RATE. The placement for the pre–gelled electrodes are anterior/posterior. The multifunction electrodes can only be used with a multi function cable. cardioversion.29 03/01/05 Figure 14 . observe the pacing artifact and confirm it is well positioned in diastole Increase output until capture STANDBY PACING Indications Indicated for patients in a bradycardic rhythm expected to drop below levels sufficient to maintain adequate cardiac output Application/Use Establish effective pacing Set the mA OUTPUT to 10% higher than the minimum mA output necessary to effect consistent capture Turn the pacing RATE below the patient's heart rate. and monitoring with a single pair of electrodes. use appropriate sterile technique Hazards cardiac arrhythmias including V–Fib and Asystole puncture or laceration of cardiac chambers or coronary arteries hemothorax. 14) P . injection of air into cardiac chambers if catheter is left open to air Procedure Place patient on 3–lead EKG monitoring if not already done Locate the entry site (between the xiphoid process and left costal margin) Prep the entrance site with antiseptic swabs and provide an aseptic area Place the 16 g intracardiac needle (3–4 inches in length) on a 30–50 cc syringe Consider sedation if patient is conscious Insert needle at 30–45 degree angle to the skin and advance toward left shoulder while aspirating continuously (See Figure 13. and qualified by Training in Advanced Cardiac Life Support. and is for the use on victims of sudden cardiac arrest. TRANSCUTANEOUS PACING Indications Symptomatic Bradycardia Pulseless Electrical Activity with bradycardia unresponsive to drug therapy Asystole Contraindications Traumatic asystole prior to fluid replacement and PASG application Overdrive pacing Figure 15 Caution Muscle twitch will make carotid pulse assessment difficult at best with output settings in excess of 100 mA. or radial pulses in these instances Procedure Leads applied.EMERGENCY MEDICAL GUIDELINES As the needle is advanced beneath the skin the tight pericardium may be felt. brachial. Contact of the needle against the epicardium my give a scratching sensation and the needle should be withdrawn slightly. assess femoral. monitor set to Lead II Pad placement anterior–posterior is preferred (See Figure 15) anterior–anterior should be used in spinal immobilization and when defibrillation is also being performed (See Figure 16) Perform pacer set up set RATE to 70 beats per minute set OUTPUT for symptomatic bradycardia set OUTPUT to minimum for asystole and bradycardic PEA set OUTPUT to maximum Initiate pacing Increase or decrease OUTPUT as needed to establish and maintain capture and pulses Figure 16 AUTOMATED EXTERNAL DEFIBRILLATOR The AED is for use by emergency care personnel specifically trained in the operation of the AED. Basic Life Support. Indications The AED is semi–automatic. on whom lack of circulation is indicated by: Unconsciousness Absence of breathing Absence of pulse Contraindications Consciousness Presence of breathing Presence of pulse Any condition incompatible with life P . or in other physician–authorized emergency medical response. Entry in to the pericardial space may produce a giving sensation.30 03/01/05 . and feel for air movement from the mouth or nose. If the hypothermic patient does not respond to three shocks. listen. IV access. ACLS providers should consider shocks delivered by the AED providers and incorporate that into the treatment of the patient. the ACLS providers should then move towards intubation. Cardiac Arrest Associated with Trauma Seldom responds to defibrillation Begin CPR if indicated Assess rhythm Initiate BLS interventions including: airway.PROCEDURAL GUIDELINES Conditions deemed environmentally unsafe Valid and verified DNRO present Patients less than 8 years old ( AHA) Patients weighing less than 25–30 kg. If no pulse is felt in 5–10 seconds then: 2 Rescuers – initiate CPR until AED is attached. If no spontaneous respirations follow. use head tilt / chin lift. and transport. Primary Survey: Verify unresponsiveness and then ABC’S.) (AHA) Caution Assure scene safety! Assess for hazards! Do not place pads directly over artificial pacemaker sites. If the ICD is in the process of shocking a patient. Traumatic. 03/01/05 P . Any medication including a NITRO–PATCH OR NITRO–PASTE should be removed from the patient prior to AED application. give 2 artificial ventilations. control of hemorrhage. After 1 minute of CPR you will be instructed to stop and let the AED analyze rhythm for 5–15 seconds. 1 Rescuer – attach AED then follow algorithm. If no breathing present. On Scene Trained Personnel and the arrival of ACLS Providers ACLS providers have authority of patient care over AED personnel. allow the ICD to complete its cycle for approximately 30–60 seconds before applying AED pads. and cervical spine immobilization. For example. Special Considerations Hypothermia Associated with Cardiac Arrest Defibrillation should not be withheld from the cold patient in ventricular fibrillation (core < 85 F). Breathing Look. Airway Open the airway. (55–66 lbs. stop defibrillation attempts. if the AED has delivered the first three shocks of a V–fib sequence. Defibrillate as indicated by AED Automatic Internal Cardiac Defibrillators (AICD) For patients with known ICD’S. Procedure Scene Survey. attach the AED and follow standard operating procedures. On arrival ask for a quick report from the AED providers concerning patient condition and performance of the AED. use jaw thrust method. use alternative site. and drug therapy. resume CPR and rewarming efforts. oxygenation.31 . proceed to pulse check. non–traumatic. Circulation Check for carotid pulse. continue to provide rescue ventilations and monitor the pulse. Operators can orient themselves best by understanding how each brand and model approaches the operational phase by referring to the training they received and the manufacturer’s recommendations. but no respirations. If the patient has a return of pulse and adequate respirations.32 03/01/05 . P . Apply pads per training instructions. energy levels. place in the recovery position and continue to monitor all vital signs until ACLS personnel arrive. Assess entire scene for life safety. PATIENT STABILIZATION: If at any time the patient develops a pulse. Follow algorithm prompts ARREST NOTIFICATION: Notify Dispatch if cardiac arrest in progress.EMERGENCY MEDICAL GUIDELINES Application/Use If the patient has met the AED criteria: Make sure the patient is not wet and in contact with water. rhythm display methods. Please refer to departmental procedure for retrieving the patient data after the AED has been used. Activate AED. Different brands and models of AEDs have a variety of features and controls that may differ in characteristics such as paper strip recorders. Radio transmission must be at least 6 feet away when AED is operating. and messages to the operator. 2. 3. Pediatrics below age 6 and in the elderly.5cm Procedure: 1. 4.G.1-2cm medially and 1-2cm distally to the tibial tuberosity. Choose either Adult or Pediatric B. Site Location: Adults. P . holding and pushing firmly on the rear part. at the selected site.G.red 18g Indications: Rapid infusion of fluids and drugs.7cm Pediatrics 3-6 yrs: 1cm – 1.) Adult.G. Triggering the B. is NOT adjustable) Infants 0-3 yrs: 0.5 – 0. Recommended Depth: Adults: 2. If pediatric.5cm (Adult B.I.PROCEDURAL GUIDELINES Medication and Fluid Administration AVAILABLE ROUTES OF ADMINISTRATION Endotracheal Inhalation Intramuscular Intranasally Intraosseous Intravenous Optic Oral Rectal Subcutaneous Sublingual Topical BONE INJECTION GUN (B. choose the desired depth by unscrewing the sleeve from the cylinder housing. can be done by pressing the rear part against the two handles of the housing or by pushing the rear part firmly against the injection site.G. Pull out the safety latch from the instrument by squeezing its two sides together.I. Tumor and fracture at insertion site. 5.I.blue 15g Pediatric.G. Contraindications: Skin infection.5cm Pediatrics 6-12 yrs: 1. Use a povidone iodine tincture to clean the selected site for injection.1-2cm medially and 1cm proximally to the tibial tuberosity. Position the front of the B.I.33 03/01/05 .I. then inject the fluid drug (bolus) or infusion. high pressure up to 300 mmHg to the infusion bag is recommended. Miscellaneous Information: The B. The burette is distinguished from other administration sets by the 150 cc chamber located within the tubing. Application/Use Choose appropriate fluid Close the upper roller clamp on the tubing and spike the IV bag Open the upper roller clamp and fill the burette to the desired level. Needle cannot be inserted next to a previous injection site. It should not be used when large fluid volumes are needed. It is especially useful when dealing with pediatric patients when fluid or medication administration is crucial.I. 9. close the upper roller clamp If applicable add medication to the chamber and gently invert to mix the drug with the fluid Squeeze the drip chamber and fill Open the lower roller clamp and allow the solution to fill the entire set Connect the solution set to the IV catheter and set desired rate Open lower roller clamp and verify proper flow rate Caution Prior to removing the cassette from the pump. Remove the B. The needle should be cleaned with an antiseptic solution everyday. the fluid will drain out through the other site. can be left in for up to 6 days.G. Connect the safety latch to the cannula. ensure that the lower roller clamp is closed to prevent bolusing the patient with fluid or medication Application/Use Choose appropriate fluid Close the upper roller clamp on the tubing and spike the IV bag Open the upper roller clamp and fill the burette to the desired level. it is recommended to start a slow flushing of the inserted needle with 1-5cc of Lidocaine over 1-2 minutes. Connect a syringe or infusion set to the needle. To maintain optimal flow. Only the needle cannula must remain in the bone.34 03/01/05 . Pull out the stylet trocar to separate it from the needle. 10. The chamber can be filled with the exact required amount of fluid or medication to prevent overdosing or bolusing with too much fluid.G.I. Flow Rates: Gravity fed: 10 – 20cc/min 300mmHg with pressure bag: 30 – 40cc/min Syringe: 60 – 100cc/min Shelf life is 3 years. BURETTE ADMINISTRATION SET The burette administration set is used when a medication needs to be mixed in 100 cc or less of fluid or any pediatric patient requiring IV therapy where fluid volume administered requires precise measurement. 7.EMERGENCY MEDICAL GUIDELINES 6. and separate the trocar needle from its housing. To reduce the pain in conscious patients. close the upper roller clamp P . 8. lumens are 20 g and 22 g (See Figure 17) Figure 17 Application/Use Flush the secondary access port with saline Cannulate the vein with the double lumen catheter the double lumen catheter is inserted as a standard IV catheter. Use of the double lumen catheter eliminates the need to establish a second IV site for medication administration.PROCEDURAL GUIDELINES If applicable add medication to the chamber and gently invert to mix the drug with the fluid Squeeze the drip chamber and fill to 1/3 full Invert the cassette with the flat side facing you Open lower roller clamp and allow solution to fill entire set Close the lower roller clamp and insert the cassette into the pump Connect the solution set to the IV catheter and set desired RATE on the Pump Open lower roller clamp and press OPR on pump DOUBLE LUMEN IV CATHETER This device is intended for use in the patient who requires multiple IV access. cloudiness. or particles.35 Figure 18 . assuring infiltration has not occurred. The infusion pump IV line should be connected to the secondary port. Pull back on the plunger of the syringe to withdraw the needed amount (dosage) of medication. The two lumen design prevents mixing of medications within the catheter. face ampule away and break off the top of the ampule neck along scored area. The second IV line may be attached either directly or by Luer–lock (this will avoid the need for needle insertion into the male adapter plug). refer to INTRAVENOUS CATHETER INSERTION PROCEDURAL GUIDELINE (SEE PAGE P-47) After removing the introducer needle. check expiration date Tap ampule with finger to move the solution down into the well Using a 4x4 gauze pad (See Figure 18). Break along the colored mark. Insert the needle into the ampule making sure the needle does not touch the rim of the ampule. the small 22g lumen of the secondary port will not restrict the positive pressure flow of the infusion pump as it might a gravity fed IV line DRAWING UP MEDICATIONS AMPULE Procedure Prepare a syringe of the appropriate volume with a needle Verify the name and concentration of the medication printed on the ampule. Indications Administration of IV nitroglycerin Preparation of the cardiac patient for thrombolytic therapy Caution Device is not intended for fluid resuscitation. 03/01/05 P . remove the male adapter plug from the second port by twisting. inspect the solution for discoloration. attach the IV line to the main port and flush. Some ampules have colored rings that mark the scored area of the ampule. and secure appropriately To attach the second IV line. hives. or particles. 2 cc of fluid in an infant Figure 20 EPI-PEN AUTO INJECTOR The EMT (or Paramedic) may administer prescribed Epinephrine via an auto-injector for patients who are exhibiting signs of respiratory distress associated with allergic reaction. assist patient in administering Epinephrine via auto-injector. cloudiness. Procedure Primary Assessment Assure auto-injector is prescribed for the patient (EPI-Pen for adult patient and EPI-Pen Jr. If patient is exhibiting signs of moderate to severe allergic reaction as described above. These signs include: dyspnea. drugs should be administered through an appropriate size suction catheter inserted through the endotracheal tube into the bronchial tree Resume ventilation Monitor the patient No more than 10 cc of fluid should be given endotracheally Endotracheal drug dosages should be 2—2. edema. check expiration date Hyperventilate the patient prior to drug administration Inject medication through the endotracheal tube medication port (See Figure 20) for endotracheal tubes without a medication port. inspect the solution for discoloration. cloudiness.36 03/01/05 . or particles. P . and inject the air inside the vial (See Figure 19) Invert the vial and draw out the needed solution (volume). inspect the solution for discoloration. and possible unstable vital signs. check expiration date and cloudiness or discoloration if possible.EMERGENCY MEDICAL GUIDELINES Expel any air present in the syringe and carefully recap the needle with appropriate technique (if it will not be used immediately) VIAL Procedure Prepare a syringe of the proper volume with a needle Verify the name and concentration of the medication printed on the vial. flushing of the skin. carefully withdraw the needle from the vial Expel any air present in the syringe and carefully recap the needle with appropriate technique (if it will not be used immediately) Figure 19 ENDOTRACHEAL MEDICATION ADMINISTRATION Procedure Verify the name and concentration of the medication.5 times the normal IV dose The drug should be diluted to 10 cc of fluid in an adult patient. wheezing. check expiration date Disinfect the rubber stopper of the vial using an antiseptic swab Draw air into the syringe of equal volume to solution to be withdrawn Insert the needle at an angle through the rubber stopper. for pediatric patient). 5 cc of fluid in a child. Remove auto-injector safety cap. Caution Do not use this product until you have been trained and evaluated for F. PRECAUTIONS For use with adult patients. Dispose of injector in biohazard container. either inclusions or exclusions.S. 1 Intraosseous Infusion System in patients with very severe osteoporosis has not been proven.0 mm. The F.S.S.T.A.A. 03/01/05 P . Check for midline sternotomy scars – the device may be less effective in patients with a previous midline sternotomy.A. Prepare insertion site with iodine and alcohol swabsprovided.S.T. CONTRAINDICATIONS None Known DESIGNATED INSERTION SITE The single designated site of insertion is the adult manubrium. Instructions for placement Administer local anaesthetic if the patient is conscious and alert.S.T. Record time. Adult patients are expected to have a manubrium thickness greater than 6. Insertion of the F. Check for fracture of the sternum or vascular injury which may compromise the integrity of the manubrium or its vascularization. Qualified professionals should determine any appropriate or necessary exceptions. midway between waist and knee. 1 INTRAOSSEOUS INFUSION SYSTEM WARNING Safety of the F.5 cm (5/8 inch) below (inferior to) to supra-sternal notch (sternal notch). 1 use.” Severe skin compromise such as trauma.0 mm into the manubrium. Indications The F. 1 Intraosseous Infusion system is designed to penetrate 6.PROCEDURAL GUIDELINES Select appropriate injection site. Maintain aseptic technique throughout the procedure. It is not intended to be used for more than 24 hours. Shoulder – fleshy portion of upper arm.T.S.1 Intraosseous Infusion System is intended for intraosseous infusion as an alternative to intravenous access to facilitate emergency resusitation through the use of drugs and fluids.T.37 . infection or burns over the infusion site may interfere with use of the device. Thigh – lateral portion of thigh.A. 1 Intraosseous Infusion System in sites other than the adult manubrium may result in ineffective infusion and may result in ineffective infusion and may result in overpenetration of the infusion tube with consequent serious injury to the patient. Hold in place until medication is fully injected (minimum of 10 seconds). Proper placement of the patch helps ensure insertion at the site. Reassess patient.A. to the criterion “For use with adult patients. Push auto-injector firmly against site until injector activates. F.A. Expose sternum.T. on the midline and 1. Take corrective action if error is greater than about 1 cm (3/8). P . Attach straight female connector on patch to purged source of fluid or drugs. exposing the infusion tube. Pressing straight along the introducer axis. Ensure that the introducer axis is perpendicular (90 degrees) to the skin at the insertion site. Advance the remover and turn it clockwise until it stops turning. Disconnect the infusion tube from the male connector. The remover is needed to eventually remove the infusion tube from the patient’s bone when intraosseous access is no longer required. to engage the threads in the proximal tip of the infusion tube. some users may find that a two-handed grip on the introducer allows better control during insertion of the infusion tube. and insert the remover into the infusion tube. push with firm and constant force until a distinct release is heard and felt. leg. Pull straight out on the remover to remove the infusion tube.) THIS PACKAGE MUST BE TRANSPORTED WITH THE PATIENT. Optional Steps: Verify placement by attaching syringe to straight female connector and withdrawing marrow into infusion tube. Secure top half of the patch to patient. Place dome over patch and press down firmly to engage Velcro fastening. NOTE: As the insertion force required in Step #5 can be considerable.38 03/01/05 . attach to IV bag. and the target zone should be over the patient’s midline. Locate sternal notch with index finger held perpendicular to manubrium.EMERGENCY MEDICAL GUIDELINES Remove top half of patch baking (labeled “Remove1”). Hold the infusion tube straight out from the patient (90 degrees to the patch) as the remover is being placed. Increase fluid flow rate by flushing system with 10 cc’s of saline. Dispose of the remover in a manner appropriate for contaminated sharps. Using index finger. Fluid can now flow to the site. etc. the notch in the patch should match the sternal notch. Ensure the entire bone probe cluster is within the target zone. Attach unopened sterile remover package to the patient (arm. Push the used bone probe cluster into the foam-filled sharps plug. If desired. take out the remover. Remove the patch. pull straight back to remove the introducer. with hand and elbow in line. remove the tubing protecting the threaded tip. infusion should be discontinued and an alternative vascular access method should be used. Verify location. NOTE: If fluid does not flow at all or if extravasation (leakage of fluid) occurs. Remove bottom half of patch backing. open the remover package. Attach right-angle female connector on patch to infusion tube. Press firmly to secure patch to patient. After release. align notch in patch with patient’s sternal notch. The introducer must remain perpendicular to the skin during insertion. place the original sharps cap over the sharps plug. Twist and pull back to remove sharps cap from introducer. REMOVAL OF THE DEVICE Remove the dome from the patch. Apply pressure after removing the patch and then dress the wound using aseptic technique. Maintaining aseptic technique. Verify target zone (circular hole in patch) is over patients midline. Place bone probe cluster in larget zone. inventory control officer. 1 may be used to administer drugs or fluids as boluses from a syringe. pressure cuffs. First Out (FIFO) stock method (stock is rotated so earliest expiring units are in front. Any item found below par level should be requisitioned in accordance with department policy. inventory clerk or other designated personnel in accordance with department policy.PROCEDURAL GUIDELINES NOTE: The F.A. inventory clerk or other designated personnel Shipping documents (packing slips) shall be handled in accordance with department policies. latest expiring units are in back) Rescue Vehicle The department paramedic and EMT on shift should conduct a physical inventory of the rescue vehicle every morning utilizing the par levels established by the department. The shipment shall be inspected and checked for the following by the inventory control officer. The appropriate stock should be pulled and issued to the crew by the inventory control officer. or the syringe/stopcock pumping method.S.T. Fluids have been infused into adult sternums through F. inventory clerk or other designated personnel. rather than by the intraosseous infusion system.S. inventory clerk or other designated personnel : breakage or damage accurate quantities (shipped vs.39 03/01/05 . backordered) accurate items (correct product shipped) expiration dates (drugs with less than one year left on expiration should be returned to supplier as “Expiration Unacceptable”) Inventory shall be placed in stock utilizing First In. 1 Intraosseous Infusion System at 30 ml/min using a one meter gravity drip (75 mmHg). or from fluid sources such as IV bags using gravity drip. DRUG HANDLING INVENTORY Central Supply All receiving/issuing of controlled substances from the controlled substance locker in the central supply shall be performed by the inventory control officer. The receipt/issue of controlled substance shall be logged on the controlled substance log and shall note the following: date and time of the transaction name/initials of employee/supplier receiving/issuing substance name/initials of designated person conducting transaction name of substance received/issued amount of substance received/issued expiration date of substance received/issued (in case of multiple units.T. the earliest expiring unit shall be listed) Receiving/issuing of medications shall be performed by the inventory control officer. Fluid flow rates during intraosseous infusion are typically determined by the pressure source and limited by the emissary veins of the bone. and at over 120 ml/min using a pressureized fluid source.A. SECURITY Access department personnel shall have access to IV fluids as necessary department paramedics. inventory clerk or other designated personnel shall have access to medications as necessary Controlled Substances access to the controlled substance locker shall be limited to the inventory control officer. inventory clerk or other designated personnel P . repeat twice (2). If it still will not run and the needle is properly placed. use aseptic technique and extra caution to avoid infection at the port site Procedure Attach Huber needle to IV setup and flush Identify Infusa–Port location Put on sterile gloves. 34). the port may be clotted and is not usable. Advance the needle into the port until it hits the solid template. Emergency Medical Guidelines and/or on–line medical control INFUSA–PORTS Indications IV access for necessary fluid or drug administration Figure 21 Contraindications Precautionary IV access Caution Do not use a saline lock with an Infusa–Port Do not force fluid into a port to flush it This is a sterile procedure. Apply an antibacterial ointment.EMERGENCY MEDICAL GUIDELINES the department paramedic on shift shall have access to the controlled substances maintained within the drug box on the apparatus Central Supply all IV fluids shall remain locked within the central stock area all medications shall remain locked within the locked central stock area all controlled substances (Morphine. If the IV will not run. open the IV line to flush the port (See Figure 33. Loop the tubing and secure the needle and the tubing to the patient. 400A The AVI Model 400A Volumetric Infusion Pump is indicated for use in venous pharmacological IV therapy to assure accurate. drugs and controlled substances shall be at the paramedic's discretion within the guidelines promulgated by the department medical director. continuous. Valium) shall remain locked within the controlled substance lock–box which shall remain within the locked apparatus when not in use USE Central Supply no IV fluids. The P . dress the area with 2x2 IV sponges using enough so the needle is resting on them. drugs or controlled substances should be used directly out of central supply for direct patient care Rescue Vehicle use of IV fluids. This step is absolutely necessary.Model 40 03/01/05 AVI 400A is equipped with a full range of comprehensive alarms to alert the . Cleanse the area with antiseptic swabs in a circular outward motion each time. non–pulsatile delivery. have the patient turn their head and/or shrug their shoulders. Figure 22 INFUSION PUMP AVI MODEL 400. Valium) shall remain double locked within the locked central stock area Rescue Vehicle all IV fluids shall remain within the locked apparatus when not in use all medications shall remain within the locked apparatus when not in use all controlled substances (Morphine. press STBY to silence the audio alarm Loosen the DOOR LOCK by turning the knob counterclockwise. turn the LOAD KNOB to its fully IN position. pump and/or cassette damage could result Attach the AVI administration set (with roller clamp closed) to the IV catheter Open the administration set's lower roller clamp Press RATE and enter the desired rate in mL/h using the NUMBER KEYS Press LIMIT and enter the desired VOLUME LIMIT in mL using the NUMBER KEYS Press CLEAR to return the VOLUME INFUSED display to zero Verify displayed settings and press OPR to begin the infusion To stop the infusion. Close the door. release the DOOR LATCH and open the door Install the AVI cassette in the pump with the flat side facing outward. Turn the DOOR LOCK clockwise until finger tight. the pump may be damaged if the upper clamp is closed when the LOAD KNOB is turned to its IN position Never push on the door when turning the LOAD KNOB to its IN position. unrestricted gravity flow will occur if the DOOR LATCH is released and the clamp is not closed Always verify infusion settings are correctly displayed prior to pressing OPR to avoid incorrect infusion Air Removal 03/01/05 P . When loading an administration set in an AVI pump be sure the set's upper clamp is open. Match the four small holes in the cassette with the four locating pins on the cassette housing. making sure the DOOR LATCH engages. With the set's lower roller clamp closed and the upper clamp open. the LOAD KNOB to its OUT position.41 . be certain the roller clamp on the standard IV set is also closed Application/Use Select appropriate IV set AVI Model 4220 Check valve IV Administration Set — used for standard IV medication administration AVI Model 290 Low Absorption IV Administration Set — used for Nitroglycerin IV administration only AVI Model 1230 Burette Administration Set — used for IV medication administration where the medication requires specific volume dilution in less than 250 mL of fluid Select appropriate fluid and follow instructions for specific IV set chosen AVI Model 4220 Check valve IV Administration Set AVI Model 290 Low Absorption IV Administration Set AVI Model 1230 Burette Administration Set Turn on the POWER SWITCH. either press STBY or move the pump's POWER SWITCH to the OFF/CHARGE position Always close the administration set's lower roller clamp before turning the LOAD KNOB either in or out. Indications The AVI Infusion Pump is indicated for use whenever a medication IV drip is established or precise delivery of fluids is required Caution If piggybacking AVI administration set into a standard IV set.PROCEDURAL GUIDELINES operator when a problem occurs. if applicable) and press OPR to restart the infusion Titration the AVI pump has the ability to titrate. without violating the integrity of the sterile fluid pathway. and turn the LOAD KNOB to its IN position open the set's lower roller clamp (and the check valve set's upper clamp. information from the previous program is still retained in memory. To clear memory. repeat procedure if all air is not expelled reinstall the cassette in the pump. and open the door Remove the cassette from the pump and hold it with the flat side facing you. This method forces the air through the upper tubing to the drip chamber and solution container. press the MAIN DISPLAY key (top right of front panel) to view the main display screen Powering Off While the pump automatically closes the dark blue slide clamp. away from the patient. Tilt the cassette so the upper chamber is slightly away from you. the non–insistent audio alarm sounds and the RATE display changes back to the original rate. the CHANGE PERSONALITY and NEW PATIENT soft keys will be showing If NEW PATIENT soft key is present. turn the LOAD KNOB to its OUT position. keeping each previous chamber depressed as you move upward along the cassette. If OPR is not pressed within 10 seconds of pressing CLEAR. press OPR to silence the alarm and repeat the correct titration procedure. If this occurs. press the NEW PATIENT soft key From the power on screen after self test. BAXTER COLLEAGUE INFUSION PUMP Powering On Turn power on by pressing the ON/OFF button When all self tests are complete. release the chambers and allow gravity to refill the cassette. Failure to close the proper clamp may cause piggyback solution to be flushed into the primary solution container.42 03/01/05 . press OPR to instantly begin infusing at the new rate When a new rate is entered as above. loosen the DOOR LOCK. press STBY close the administration set's lower roller clamp If removing air from a piggyback set and an AVI check valve administration set. tighten the DOOR LOCK. verify displayed rate within 10 seconds of pressing CLEAR. it is immediately displayed in the RATE display while the pump continues to infuse at the original rate. Gently squeeze each chamber in sequence from bottom to top. or change flow rates instantly without interrupting the administration of fluid press CLEAR while the pump is operating (do not press STBY first) enter the new rate using the NUMBER KEYS (it is not necessary to press RATE first). Air is removed from the AVI administration set in an upstream direction. always close the roller clamp before removing the tubing from the pump Press the ON/OFF key P . close the primary set's upper clamp before proceeding.EMERGENCY MEDICAL GUIDELINES The insistent audio alarm and the AIR and EMPTY BAG visual alarms are activated if air is detected in the upper cassette chamber. close and latch the door. release the DOOR LATCH. the loading mechanism automatically pulls in the dark blue slide clamp. This closes the dark blue slide clamp and opens the pump mechanism Remove the tubing from the pump Resetting the Manual Release Ensure there is no tubing or foreign objects in the tubing channel Turn the release tab clockwise to its stop and push the tab into its socket The DONE soft key is displayed when the manual tube release is reset. The automatic tube loading mechanism open. turning it out Rotate the tab counterclockwise to its stop. Verify that no solution is flowing (no drops falling in drip chamber and/or no flow from the end of the tubing) Attach the tubing to the patient access site Unloading the Tubing If the pump is running. grasp the tubing on both sides of the pump and remove the tubing from the pump. then closes and loads the tubing into the pumping mechanism After the tubing is loaded. the loading mechanism closes Ensure that the dark blue slide clamp occludes the tubing. Press the DONE soft key to clear the alarm The pump cannot be powered off until the manual tube release is reset Programming the Primary Rate When the main display screen is shown. press the RATE key. When the loading mechanism is open and STOPPED is displayed on the pump.PROCEDURAL GUIDELINES Loading the Tubing After turning the power on. press the OPEN key.43 . The display then changes to the programming screen and the rate field is highlighted Program the desired flow rate (in ml/hr) using the keypad Press the VOL key or use the arrow keys to highlight the volume field Program the desired volume to be infused After programming is complete. The mechanism closes automatically 60 seconds after the tubing is removed Manual Tube Release Use the Manual Tube Release ONLY when the automatic tube release is not functioning Close the roller clamp on the tubing Locate the manual tube release on the right side of the pump. Pull tubing taut and slide it all the way into and along the tubing channel When the pump detects the tubing. confirm that the tubing entering the pump on the left side is going to the solution container Open the roller clamp. as you face the panel Push and grasp the release tab. insert the dark blue slide clamp into the slot. verify the information before starting the pump Press START to being infusing 03/01/05 P . press the STOP key on the pump Close the roller clamp on the tubing Press the OPEN key The loading mechanism automatically closes the dark blue slide clamp and opens the tubing channel so you can remove the tubing Ensure that the tubing channel is completely open (arrow displayed on the pump display) When the mechanism is opened completely. If tubing is not loaded within 60 seconds. 44 03/01/05 . Press the UP arrow key next to the YES label for pump-assisted viewing of detected air. disconnect the tubing from the patient. verify all values and press the CONFIRM SETTINGS soft key Press the START key to begin the infusion Using the Volume-Time Function Press the appropriate programming key (Primary or Piggyback) From the programming screen. P . and flush the air from the tubing When the air has been removed. a FLUID DETECTED icon is displayed When the FLUID DETECTED icon is displayed. the alarm is reset. the advance air pop-up window is displayed. Visually inspect the air bubble. Enter the time period for the infusion in hours and/or minutes. press the STOP key or turn off the pump Changing the Flow Rate during Infusion Press the RATE key and enter the new value Press the START key to save the change and being infusing at the new rate Programming a Dose Based on Patient Weight On the primary screen. press the DOWN arrow key to manually purge the air. then press the CONFIRM SETTINGS soft key. then replace the tubing in the pump Press and hold the ADVANCE AIR key. press the CHANGE MODE soft key. When the pump detects fluid. the infusion may be restarted.EMERGENCY MEDICAL GUIDELINES Completing or Stopping the Infusion When the volume remaining reaches zero (0). If pump-assistance is not desired. The programming modes screen is then displayed Use the arrow keys and/or PAGE UP/PAGE DOWN soft keys to highlight the mg/ kg/min selection Press the SELECT soft key to display the programming screen Program each field listed When finished. The pump automatically calculates the flow rate Verify that the information is correct. The pump continuously pumps until the key is released. Press the Primary or Piggyback key then START IVAC 530 Notes Delivers at 45 psi and useful for intraosseous infusions Use vented tubing with glass NTG infusion bottles The pump does not detect infiltrations (monitor the site) Four hours of operation time on a fully charged battery The white drop indicator illuminates with each drop Close the drip clamp prior to opening the pump door. the pump automatically goes to KVO mode To exit this mode. then press the START key to being the infusion Air Alarm If the “air detected” alarm sounds. Remove the tubing from the pump and flush the air from the tubing. press the CHANGE MODE soft key Highlight either PRIMARY VOLUME-TIME or PIGGYBACK VOLUME-TIME then press the SELECT key Enter the volume to be infused Highlight TIME DURATION using the arrow keys. 45 . then snap in place. IVAC MED SYSTEM 3 Multi–Channel Infusion Pump Application/Use Priming the Administration Set use only IVAC 25 or 28 series Administration sets. be sure the roller clamp on the standard IV set is closed. press Enter when programming complete. C).(down) arrow. and ensure the tubing is not kinked. slide clamp must be flush with cassette. Start the infusion by pressing the red start button. Turn the machine on (green power button)and select the gtts/min setting. fill drip chamber to the fill line. verify flow of solution from the drip chamber. down arrow. use (up) arrow. Cassette Insertion turn instrument ON before inserting cassette. verify infusion status — INFUSING. to recall a setting before Enter is pressed. press Enter. or Fast (down) arrow to program new settings. Titration of Rate access desired channel by pressing channel key (A. B. three “beeps” indicate proper placement. change the rate by using the up arrow.e. FAULT. press the corresponding (up) or (down) arrow. press Recall.PROCEDURAL GUIDELINES Application/Use Prepare IV set with all air remove from the tubing and the drip chamber half full Place the drip sensor on the chamber above the fluid level Open the pump door. insert cassette at an upward angle. place tubing between the guide posts. SERVICE. or Fast (down) arrow. C). ensure tubing collar correctly seated. slowly prime set. Attach the tubing to an IV site (preferably a seperate site or twin–cath). ensure slide clamp is pulled out completely. Clearing the Volume Infused access desired channel by pressing channel key (A. 03/01/05 P . verify settings on Standard Display page. close regulating clamp. select Channel by pressing desired channel key (A. press Select until Volume Infused (VI) is highlighted. Instrument Quick Set–up verify instrument is turned on. press Select to move highlighted bar to choose setting to change. or C). If piggy–backing into a standard IV set. secure the latch. ALARM. B. press More Options. i. check vent position. STANDBY. Fast (up) arrow. press Clear to reset to zero. Fast (up) arrow. Rate. press START/STOP key to begin or stop infusion. STOPPED. tapping and inverting cassette and any Y sites to expel all air. KVO. to change direction of the “Fast” keys. Spike container. B. Volume Remaining or to clear Volume Infused. Close the door. stretch skin layer apart and flatten between fingers. return to the Standard Display page. press Clr Tot. press Enter. Pull back on the plunger to insure the needle has not entered an artery or vein by accident. primary and secondary press MORE OPTIONS until the Tot Vol softkey appears. Clearing the Total Volume Infused for all channels. press START/STOP key. Infusion status STOPPED on Channel page.46 03/01/05 . press Stndby softkey standby option is only available on Standard Display page. Clearing information from the standard display page when not in use the channel must be stopped and the cassette removed. 24). inspect the solution for discoloration. or particles. B. All values for each channel will clear and flash. check expiration date Disinfect the deltoid muscle using an antiseptic swab medication can also be given in the upper–outer quadrant of the buttocks Recheck the medication Using one hand. B. Holding the syringe in the other hand.e. when cassette is in a STOPPED channel. press any infusing channel key. indefinitely access desired channel by pressing channel key (A. there should be no blood return into the syringe Inject the medication Quickly remove the syringe and apply firm pressure over the injection site Properly dispose of the needle and monitor the patient for adverse reactions Figure 24 Pediatric Needle size should be 23–25 gauge and length 1 inch Recommended site is anterior thigh or upper–outer quadrant of the buttocks Figure 25 P . C). Total volume page appears. to clear the Status line highlighting. press START/STOP key. Infusion status STOPPED on Channel page. the information for the channel not in use will disappear from the Standard Display page after 2 minutes. Figure 23 INTRAMUSCULAR MEDICATION ADMINISTRATION Procedure Explain the procedure to the patient Verify the patient has no allergies to the medication Prepare a syringe of proper volume and attach a 21 gauge 1½ inch needle Verify the name and concentration of the medication. Stopping a channel temporarily access channel by pressing channel key (A. Status line for that channel must not be highlighted. i. the channel must not be selected. cloudiness. press Tot Vol. C). quickly insert the needle at a 90 degree angle in to the muscle (See Figure 23.EMERGENCY MEDICAL GUIDELINES press Enter. PROCEDURAL GUIDELINES INTRAOSSEOUS INFUSIONS Indications Multi system trauma with associated shock and/or severe hypovolemia Unresponsive and in need of immediate drug or fluid resuscitation due to: burns cardiac arrest anaphylaxis near–drowning status asthmaticus severe dehydration associated with vascular collapse and/or loss of consciousness Figure 25a Contraindications Fracture or crush injury to the same extremity Gross infection at the intended site of puncture Responsive patient (unless cardiac arrest is imminent) Caution No more than one insertion attempt per bone If the needle becomes obstructed. into the tibia using firm pressure and a boring motion until entering the medullary cavity which is noted by a lack of resistance. use the proximal tibia.47 Figure 28 . 25a). Choose appropriate site and cleanse with antiseptic swab Insert the intraosseous needle. Look for infiltration around the site or no flow of the intravenous fluid. Remove the stylet and attach a 3–way stopcock with 10 cc syringe to the needle and flush. remove the needle and apply firm pressure for a minimum of 10 minutes. caused by a pathogenic organism) Figure 26 Procedure There are two sites available for intraosseous infusion in the tibia. use the flat portion of the lower tibia approximately 2 cm above the medial malleolus (See Figure 26) due to the thickness of the proximal tibia compared to that of the distal tibia in that age group. If this is unsuccessful. which is located two finger widths below the tibia tuberosity on the anterior medial aspect of the leg (See Figure 25. The needle will feel firmly fixed in place. All fluids and medications may be administered via the intraosseous route. Children over seven years of age. If either of these two are present discontinue the procedure. directed slightly inferior to avoid the epiphyses (See Figure 27). attempt to clear by flushing with saline. Once placement is confirmed. insert a clean needle of a smaller diameter through the center of the original needle Use of sterile procedure should be documented on the run report due to rare but serious side affect of osteomyelitis (inflammation of the bone. open fluid administration set. especially the marrow. Secure the needle as you would an impaled object Figure 27 INTRAVENOUS CATHETER INSERTION Procedure Explain the procedure to the patient Assemble the equipment needed appropriate infusion set intravenous fluid select the catheter to be inserted antiseptic swab 03/01/05 P . Children under seven years old. reset the clamp to the proper flow rate MUCOSAL ATOMIZATION DEVICE (MAD) INTRANASAL DRUG DELIVERY The nasal route is an attractive method of drug delivery due to the rich vascular plexus that is present within the nasal cavity and the easy accessibility of this vascular bed. it can be drawn from the IV catheter using a 10cc syringe.48 03/01/05 . inspect the solution for discoloration. lower the catheter to approximately a 15 degree angle to enter the vein. A “pop” should be felt upon entering the vein. Because of this easily accessed vascular bed. The flow should be steady. Enter the vein from the side or from the top. enter the skin at a 30–45 degree angle (See Figure 28). and allow unimpeded flow of the IV solution. effective blood levels of the medication administered.EMERGENCY MEDICAL GUIDELINES tourniquet Apply tourniquet if appropriate Select a suitable vein Prepare the venipuncture site Scrub the area with antiseptic swab starting above the vein and wiping vigorously in widening circles Align the catheter. Note blood return in the catheter. inject the medication (See Figure 30) check the IV site for patency to prevent any medication infiltration Open the IV line clamp to flush any remaining medication from the IV line. If the fluid is unsteady in nature. nasal administration of medications is emerging as a promising method of delivering medications directly to the blood stream. prior to attaching IV fluid tubing Release the tourniquet Attach the IV tubing. Advance the catheter inside vein and withdraw the needle while holding the catheter steady. the catheter tip may be against the vein wall. take care not to jam the needle straight through and out the opposite side Pinch the tubing above the port to prevent back flow of medication into the IV bag (See Figure 29). P . or particles. check expiration date Disinfect the drug administration port of the IV line using an antiseptic swab Uncap the needle Recheck the medication Insert the needle in to the administration port. a bevel down technique may be used in pediatric patients or patients with fragile veins Slightly advance the catheter beyond this point to insure placement inside the lumen of the vein. With the bevel up. This method of delivery can eliminate the need for intravenous catheters while still achieving rapid. cloudiness. pull back slightly Figure 29 INTRAVENOUS MEDICATION ADMINISTRATION BOLUS Caution Beware of run away IV flow rate Figure 30 Procedure Verify the name and concentration of the medication. (A Venoject with adapter may also be used) If blood is required. After entering the skin. Ease and convenience: This method of drug administration is essentially painless. so all the medication is administered Reassess the patient and continue with treatment protocol NEEDLESS IV SYSTEMS Should be used when available. For many medications the rates of absorption and plasma concentrations are relatively comparable to that obtained by intravenous administration. Reduces the risk of accidental needle sticks. Due to direct absorption into the blood stream. CSF drug concentrations may exceed plasma concentrations.49 . Vial Access Cannula 03/01/05 P . Components Syringe Cannula For drawing and administering medications from an ampule. Due to the close proximity of the olfactory nasal mucosa to the central nervous system. allowing more drug to be bioavailable than if it were administered orally. more than that will just run out of the nose Indications Fast medication delivery for: Seizures Sedation Opiate overdose Hypoglycemia Intravenous access unobtainable or with a combative patient Contraindications Bloody nose Large volumes of mucous production Medications able to be given intranasally Ativan (Lorazepam) Glucagon Narcan (Naloxone) Versed (Midazolam) Procedure Draw desired amount of medication into a syringe with luer-lock tip Attach MAD nasal atomizer to syringe Place atomizer within nostril Briskly compress syringe to administer 1/2 of the volume as atomized spray Remove and repeat in other nostril. making this an attractive method of rapidly achieving adequate CSF drug concentrations for centrally acting medications.PROCEDURAL GUIDELINES Advantages The rich vascular plexus of the nasal cavity provides a direct route into the blood stream for medications that easily cross mucous membranes. Caution Do not give more than 2ml of medication. intravenous catheters or other invasive devices and it is immediately and readily available in all patients. gastrointestinal destruction and hepatic first pass metabolism (destruction of drugs by the liver enzymes) are avoided. does not require sterile technique. Blunt tipped. or death. These signs include: pinpoint pupils. These kits should be used as indicated in the “Hazmat” Section. emesis. Saline lock device (i. NERVE AGENT AUTO INJECTORS The Paramedic may administer the prescribed nerve agent antidotes via an auto-injector for rescuers or patients who are exhibiting signs of organophospate poisoning. The Nerve Agent Auto Injectors include the Mark I. Select appropriate injection site.EMERGENCY MEDICAL GUIDELINES For drawing and administering medications from a vial. midway between waist and knee. Atropen. Buttock – upper outer quadrant. salivation. coma. check expiration date.50 03/01/05 . and the CANA Kit.e. Ensure patient is exhibiting signs of organophosphate poisoning as described above. Record time. EMTs may self administer. gastrointestinal discomfort. Remove auto-injector safety cap. Re-adminster per dosing schedule in “Hazmat” Section NITROGLYCERIN IV Indications ST elevation in two or more contiguous leads of the 12 Lead EKG Continued chest pain partially relieved after 3 SL nitroglycerin when ST elevation is not present Congestive heart failure with moderate to severe dyspnea Hypertension with Physician Consult Contraindications Systolic blood pressure less than 100 mm/Hg Known allergy to nitrates Head trauma Hypovolemia P . defication. Only the Atropen is available in pediatric dosages. seizures. Drug Vial Adapter Used on multi–dose vials for syringe cannula usage. Dispose of injector in biohazard container. Reassess patient. lacrimation. Multi–access Port or MAP. pointed tip will remain in vial. Push auto-injector firmly against site until injector activates. Hold in place until medication is fully injected (minimum of 10 seconds). respiratory difficuty. Procedure Primary Assessment Verify the appropriate dosage auto-injector based on age and weight. urination. Heplock) Used for precautionary IV access Threaded Lock Cannula or Lever Lock Cannula Used to secure IV tubing to saline lock device or medication access port on compatible tubing. Thigh – lateral portion of thigh. Nitro is absorbed through the skin. Nitronox units that require a separate oxygen unit use a small Nitrous Oxide cylinder that is intended for single use. At the medic's discretion. Head injury Hypotension or shock COPD Acute PE Chest Trauma.51 . if mother is stable). a blending regulator and an Oxygen cylinder. This green zone indicates that the proper blending of Nitrous Oxide 50% with Oxygen is being maintained. 03/01/05 P . Contraindications Any altered level of consciousness (i. Some Nitronox units require a separate oxygen unit to connect the Nitronox unit. especially pneumothorax Nausea and vomiting Decompression sickness Air embolism Abdominal pain with distension or suspicion of obstruction Pregnancy (except during delivery. If this is not done a large bolus of Nitro will be administered to the patient with potentially disastrous results. The blending regulator gauge should indicate green. Utilize a double lumen catheter IV catheter or establish a second IV line. This will require that the Nitrous Oxide cylinder be changed after each use. Nitronox may be selfadministered by the patient. IV Nitro may be piggybacked as a last resort if no other IV site is available. When transferring patient to ER staff be sure to close the lower roller clamp on the IV tubing. turn on the Nitrous Oxide cylinder and the Oxygen cylinder. If this becomes necessary. The Oxygen cylinder may or may mot be part of the Nitronox unit. The use of PVC tubing does not alter the dose being received by the patient. alcohol intoxication or drug overdose).e. Indications Nitronox is indicated for pre-hospital relief of pain. use caution not to expose any unprotected skin to this medication NITROUS OXIDE NITRONOX Nitronox is a mixture of 50% Nitrous Oxide and 50% Oxygen Nitronox Equipment Nitronox units are comprised of a Nitrous Oxide cylinder. When turning the Nitronox unit on. piggyback the line at the lower hub of the regular tubing and use an 18 g needle advanced as much as possible through the lower hub. Patient is unstable to self-administer Nitronox. Procedure After the above contraindications have been excluded.PROCEDURAL GUIDELINES Caution Low absorption tubing does not have to be used in order to deliver accurate amounts of the medication. The pulse oximeter should also be used. inspect the solution for discoloration. identifying the medication and concentration Connect the administration set using aseptic technique Flush IV line and expel air Attach needle to IV line. check expiration date Draw up medication / assemble pre–filled syringe Clean the medication administration port on IV bottle/bag. Proper precautions should always be taken. discontinue Nitronox. PIGGYBACK Indication IV drug Therapy Contraindications Allergies to medication Infiltration at IV Site Procedure Prepare the necessary equipment Confirm that the patient is not allergic to medication Select the proper medication Verify the name and concentration of the medication. complications may develop. The patient may also be given Oxygen via nasal cannula @ 4-6 LPM to maintain oxygen therapy when the Nitronox is not being administered by the patient. with antiseptic swab Carefully add medication to bottle Mix the fluid by inverting the bottle several times Place label on bottle/bag.52 03/01/05 . Whenever Nitronox is administered to a patient. or particles. If the patient’s vital signs become unstable or the patient becomes symptomatic from the side effects. Nitronox should be considered a drug and as with any drug. the patient will be transported ALS. use luer–lock application when available Clean medication port with antiseptic swab and insert needle Secure needle Stop flow of primary line Set pump infusion rate Monitor patient for desired affect RECTAL MEDICATION ADMINISTRATION Indications For emergent medication administration when IV access is unobtainable in adults and children Procedure Place medication in a needleless syringe Attach the plastic catheter of a 14 gauge IV catheter on the end of the syringe Lubricate the catheter Insert catheter past anal sphincter Inject medication.EMERGENCY MEDICAL GUIDELINES All vitals signs are to be monitored frequently and documented. Patients will not be released to a BLS unit for transport. withdraw syringe P . cloudiness. but will probably not require fluids Hemodynamically stable patients complaining of: COPD dialysis problems hypertension post seizure other precautionary IV access Procedure Cannulate vein. inspect the solution for discoloration.53 . cloudiness. there should be no blood return Inject the medication Quickly withdraw the needle at the same angle it was inserted. gently grasp the skin over the injection site and pull it away from the underlying muscle (See Figure 47) Insert the needle into the subcutaneous tissue at a 45 degree angle to the skin (See Figure 48) Gently pull back on the plunger to verify an artery or vein has not been entered. or particles. apply firm pressure to the injection site Properly dispose of the syringe Monitor the patient for adverse reactions UMBILICAL VENOUS CATHETERIZATION Indications Asphyxiated newborn Hypovolemia Last resort for venous catheterization 03/01/05 P . check expiration date Disinfect the site using an antiseptic swab With one hand.PROCEDURAL GUIDELINES SALINE LOCK Indications Patients who need or require IV access. flush the saline lock with 1–2 cc of NaCl after the medication is given Figure 31 SUBCUTANEOUS MEDICATION ADMINISTRATION Procedure Figure 32 Explain the procedure to the patient Verify that the patient has no allergies to the medication Prepare a 1 cc syringe and attach a subcutaneous needle (short 25–30 g) Verify the name and concentration of the medication.9% NaCl to confirm placement in the vein and to flush the saline lock and catheter of blood Fluids may be piggybacked to the saline lock if needed If medications are administered via the saline lock. refer to INTRAVENOUS CATHETER INSERTION PROCEDURAL GUIDELINE (SEE PAGE P-47) Screw the saline lock onto the hub of the catheter Flush the saline lock with 2–3 cc of bacteriostatic 0. 5fr nasogastric tube) Appropriate infusion set Appropriate infusion fluid 3 Way stop cock (optional) Antiseptic swab Application/Use (see figure below) Prepare Equipment place newborn on a warm flat surface encircle the umbilical tape as close to the clamp and distal to the newborn. loose enough to control bleeding use aseptic technique to prepare site cut cord advance catheter into vein attach appropriate IV catheter set to catheter adjust umbilical tape to control bleeding.54 03/01/05 . may irritate the liver Reassessment of vascular site for patent access IV overload Procedure Obtain the proper equipment needed for procedure Umbilical tape or equivalent Scissors Select appropriate size catheter (14g IV catheter. but not to constrict vascular access suture (if jurisdiction allow) into position and tape onto the abdomen to secure line monitor IV flow rate to avoid overload P .EMERGENCY MEDICAL GUIDELINES Contraindications Non–Symptomatic newborn Other venous access available Caution Hypertension Thrombosis To far of a placement of the catheter. certified paramedic.1932(2)(f)(2) “Only a physician.PROCEDURAL GUIDELINES General BLOOD ALCOHOL SAMPLING Legal Interpretation FS Chapter 316. may withdraw blood for the purpose of determining the alcohol content thereof or the presence of chemical substances or controlled substances thererin…” Caution Drawing a blood alcohol sample SHOULD NOT DELAY TRANSPORT of the critical patient! Procedure The EMS run report shall contain the following information (if applicable) A blood alcohol kit was used Betadine (providone-iodine) solution (or hydrogen peroxide/acetone if allergic to iodine) was used for the skin preparation Name of the law enforcement officer requesting blood sample Time of draw If paramedic drawing samples is different from the one signing the report. that paramedic will sign under the above information All blood samples taken shall be surrendered to the requesting law enforcement officer The paramedic May be required to obtain multiple samples Shall obtain a minimum of two samples per person/per draw Shall render emergency medical service or treatment as necessary prior to the drawing of blood and alcohol samples Shall obtain alcohol samples only at the request of a law enforcement officer either in the field. …acting at the request of a law enforcement officer. upon arrival in the Emergency Department. or in the law enforcement facility 03/01/05 P .55 . and cardiac resuscitation within a respective weight class. P .EMERGENCY MEDICAL GUIDELINES BLOOD GLUCOSE LEVEL This procedure is used as a gauge for treatment. D50 use not considered in CVA unless reading less than 50mg/dl Indications Any change from the patients normal mental status Unconscious/unresponsive patients Stroke victims Alcoholic patients Seizure patients Patients with known diabetes. If patient's length falls at the extremes (upper or lower) of a respective color.56 03/01/05 . Measure from the top of the head to the soles of the feet. increased intracranial pressure. gently squeeze the finger to obtain a sufficient blood sample Touch the tip of the strip to the blood. the blood will be automatically be drawn into the test strip. with the multicolored side facing up. dispose of the device once used If necessary. Consider administration of D50 for any reading of 60 mg/dl or less. and insert into the meter Apply the blood sample to the white test area The meter will begin a count down and will show the results within 45 seconds the meter will show readings between 0–600 mg/dL if the results are above 600 mg/dl the meter will read HIGH Clean unit after each use BROSELOW PEDIATRIC EMERGENCY TAPE Application/Use Place the Broselow tape. Whichever color zone the bottoms of the child's feet align with will provide the appropriate size and type of airway equipment to be utilized. The blood glucose level will be shown after 60 seconds Once the blood is obtained remove and dispose of the strip and record the reading a reading of LO indicates a blood glucose level less than 40 mg/dl a reading of HI indicates a level above 500 mg/dl ONE TOUCH Application/Use Press the ON/OFF button to turn the meter on When the meter reads INSERT STRIP carefully remove a test strip from the package being careful not to touch the white test area. if the complaint warrants a glucose check GLUCOMETER ELITE Application/Use Insert the lancet into the glucolet pen Insert the test strip into the glucometer until an audible beep is heard Cleanse the finger with a antiseptic swab and allow to dry Perform a finger stick using a lancing device. next to the supine child with the red tip at the head. Immediately next to the color zones are the weight zones which provide the proper drug dosages for seizures. consider the next closest color category and follow clinical guidelines. As with the color / airway zones. overdose. Once the meter beeps remove the strip from the blood source. Procedure 1. Turn power on and allow unit to self–test Blood Pressure Select proper size cuff and secure onto patient’s arm Make sure that there are no kinks or other obstructions in the hose Press the NIBP Start /Stop button to take the reading. paralytics. 6.57 . On the opposite side of the tape are weight zones which. 4. Adjust the interval time 03/01/05 P . use the tape as a calculator by going directly to the respective weight / dosage zone. however. 2. defasciculating agents and induction agents COLIN BLOOD PRESSURE MONITOR Indications Continuous blood pressure monitoring Caution Unusual readings need to be confirmed with traditional procedures The machine will reinflate if the systolic pressure is high Application/Use Select the proper sized cuff Be sure the air line is without any kinks Turn the unit on and allow it perform its self–test Press the start button Adjust the interval times (5 to 10 min for stable patients) The alarm may be silenced by pressing the white alarm button The alarm limits may be adjusted CRITICARE 506DX2 VITALCARE VITAL SIGNS MONITOR Indications Automatic monitoring of Non–invasive Blood Pressure (NIBP) and Pulse Oximetry (SpO2) Temperature monitoring (oral and rectal) Caution Use only Criticare blood pressure cuffs for accurate readings Prolonged use of blood pressure cuffs and pulse oximetry probes can cause tissue damage. provide the appropriate calculations for infusions. 5. fluid volume expansion. 3. when measured against the supine child in the above described manner.PROCEDURAL GUIDELINES consult the weight / dosage zone that aligns with the bottom of the patient’s feet. If the actual weight of the patient is available. Periodically check patient. Place IVAC brand probe cover onto probe 3. Attempt to place sensor on the opposite extremity that the blood pressure cuff is on. Validate the form for completeness patient or surrogate’s signature properly executed physician’s signature properly executed Identify the patient photo identification (i.58 03/01/05 . 3.EMERGENCY MEDICAL GUIDELINES Pulse Oximetry 1. 4. distal pulses. Place the finger sensor on the patient’s finger with the LED’s positioned on the nail side. red for rectal) 2. 5. or substantially equivalent. DO NOT RESUSCITATE ORDER (DNRO) WHAT TO DO Get the original Florida Pre–hospital Do Not Resuscitate Order (DNRO). Temperature will start to be taken when probe makes contact with tissue. or witness Provide any care and comfort measures indicated Document information effective date of DNRO witness used for identification (if applicable) attending physician name of patient or surrogate who signed DNRO attach original (or validated copy) DNRO to run report DOPPLER MEDISONIC Indications Used for detecting very faint sounds (PEA. Eject probe cover by pushing on the colored end of the probe. Reading will automatically appear Temperature (if installed on machine) 1. Copies of the form are acceptable. usually associated P . bruits. 2. etc) Used in Obstetrics (fetal heart tones and stress detection during birth) Application/Use Sparingly apply ultrasound gel over the area to be assessed Place the doppler over the test site Press and hold the buttom until the audio is heard at a comfortable level Move the doppler in a circular motion until the desired sound is located FOLEY CATHETERIZATION Indications To relieve bladder distention and maintain urinary tract patency. Oct ‘93. Temperature is done when you hear an audible tone and either “F” or “C” will be displayed with the reading. Install the desired probe (blue for oral.e. DOH Form 1896. driver’s license). insert lens under upper eyelid. Have patient look down. repeat several times using a new cotton ball each time Insert lubricated catheter tip into urethra and ask patient to take a deep breath and exhale slowly Advance catheter until urine is noted and advance approx. Removal Have patient look up. Procedure Insertion Apply topical anesthetic to eye. the provider must be familiar with the aspects of this techniques prior to attempting this procedure Procedure Obtain catheter insertion kit Explain procedure to patient Open catheter insertion kit and place in an accessible location Put on sterile gloves using sterile technique Place drapes over perineal area Examine catheter and check to see if it is securely attached to drainage bag and attach syringe with sterile water to injection port Apply lubricant to catheter tip Cleanse urinary meatus using cotton soaked with antiseptic solution females—start above the meatus and wipe downward to the perineum. and drop lens in place. repeat several times using a new cotton ball each time males—cleanse in a circular motion from the meatus downward to the base of the glans.PROCEDURAL GUIDELINES with long patient transfers Caution This procedure requires the use of sterile technique. retract lower lid. 03/01/05 P . Have the patient look up. Slide lens out. 2–3cm further to ensure balloon is in the bladder Inject the sterile water into the port and pull gently on the catheter until resistance is met Place drainage bag below level of the bladder Tape catheter to inner thigh and make sure the system drains freely Measure and document amount of urine output MORGAN MEDI—FLOW® LENS Indication Anytime an eye injury needs to be irrigated. if available. Attach IV set or Morgan delivery set. Absorb outflow with towels or other cloth device. retract lower lid. Begin flow.59 . 60 03/01/05 . time. Inspect the needle. syringe. using the thumb to draw the skin taut. if the blood flow stops. one hand should hold the tube while the other pushes the tube onto the holder the tube should fill until the vacuum is exhausted and blood flow has ceased. determine if the plunger is being pulled back too hard and adjust accordingly once the venipuncture is complete. hold the tube at a slight angle so that the blood flows down the side of the tube to avoid breakage of the blood cells other methods a winged infusion set with a vacutainer is generally used on pediatric patients and patients with very small/ fragile veins Once the procedure has been completed be sure to remove the tourniquet.EMERGENCY MEDICAL GUIDELINES PHLEBOTOMY Procedure Assemble all equipment necessary for the procedure Explain the procedure to the patient Apply the tourniquet and visualize/palpate for a suitable vein Cleanse the venipuncture site using an antiseptic swab. If blood flow stops before an adequate amount of blood has been collected then pull back on the needle slightly once the tube has filled. the blood must be transferred to a tube (the top of the red top tube may be removed for filling) transfer the blood into a tube being certain not to force the blood into the tube (this could cause the tube to explode). Remember to cleanse the fingertip of the glove that is to used for palpating the site. pull the tube off the holder prior to exiting the vein to avoid developing a hematoma at the site syringe method this method should be used on patients with more difficult veins once venipuncture has been performed. date. and collector's initials All supplies should be disposed of properly ions chest trauma with dyspnea where inflation of the abdominal compartment will interfere with oxygenation distended abdomen (aortic aneurysm is possible exception) P . or evacuated tube before performing the procedure Perform the venipunture using one of the following methods: evacuated tube method grasp the patient's arm firmly. place a dressing on the site and label the tube with the patient's name. the vein is entered with the bevel of the needle upward. if blood does not readily flow into the tube change the tube. moving in a circular motion from the center of the site to the outer portion of the site. SUGGESTED ENCODE FORMAT Identify unit ID and paramedic/EMT name. and the team is encouraged to keep radio air time to less than 30 seconds for routine encodes. objective of communication (i. and to advise the hospital of the nature and seriousness of the patient’s problem so that they can be appropriately prepared for your arrival. Significant objective findings may need to take precedence over a detailed history.) History to include patient description (number. pertinent medications Objective findings of patient’s current condition. priority/level of care. level of consciousness. Describe the problem in enough detail to explain treatment initiated and rationale for request. sex).PROCEDURAL GUIDELINES PROPAQ CAPABILITIES: ECG monitoring Respirations Non–invasive Blood Pressure(NIBP) Pulse Oximetry (Nellcor) Mainstream CO2 OPERATION: Initial Power Up: Turn unit on by using on/off switch located on the right side panel Select patient mode (adult. etc. pertinent additinal symptoms. select: setup > more > change Unit is already set up for adult MONITOR ECG: Apply leads as in normal ECG Respirations: Respirations will automatically be recorded through the ECG NIBP: Place the proper sized cuff on the patient’s arm or thigh Auto or manual intervals may be set by: Pressing Auto/Man button Pressing Interval button to desired interval Pressing Start to initiate a measurement RADIO COMMUNICATIONS Standard rules for open air communications will be used. request for orders. notification. chief complaint. pertinent past history. requests Estimated time of arrival at ER 03/01/05 P . pertinent findings Treatment in progress and response to treatment. child.e.61 . age. infant) adult ³ 9 years old child = 45 weeks to 9 years infant = neonate to 44 weeks To change mode. EKG rhythm. vital signs. consultation. Open the Pedi-Seat. Make sure the pump is off before plugging into cigarette lighter. Turn the pump switch on and inflate for approximately 60 seconds (the sides will be firm and the bottom will be softer. unplug hose from seat and cap the seat valve. Some air will be released at this time. Secure Pedi-Seat to rescue. Do not put anything on the seat during inflation. Use the I-clip if securing with a lap-shoulder belt. (1) corrugated hose. notification of DOH is mandatory (per state law). Turn the pump switch on and deflate for approximately 60 seconds. Even though local authorities have been advised. unplug the hose and cap the seat valve. The kit contains one (1) pediatric seat. (1) I-clip. Should the team encounter a patient within one of these three groups whom they know or have reason to suspect has been abused or neglected. Caution Make sure the pump is switched off before plugging it into the cigarette lighter. they have both a legal and moral obligation to report same. Note: The Responder Inflatable Pediatric Seat is certified for use in motor vehicles and aircraft. To Inflate Connect one end of the corrugated hose to “inflate” on pump and the other end to the valve on the seat. Turn the pump switch off. the elderly and the disabled.EMERGENCY MEDICAL GUIDELINES RESPONDER INFLATABLE PEDIATRIC SEAT Indications Properly secure pediatric patients that weight between 20 and 40 pounds with a maximum height of 40 inches during transport to the Emergency Department. The following action shall be taken: Recognition of possible abuse or neglect Notify attending EDP and local law enforcement official Notify DOH Abuse Hotline 1–800–96–ABUSE Notify supervisor Complete written incident report (to be forwarded to DOH) Document notification steps on the completed run report Forward written incident report to administration as soon as possible Figure 33 Figure 34 P . SUSPECTED CHILD/OTHER ABUSE The State of Florida has strict concise laws regarding the reporting of suspected abuse and/or neglect of children. To Deflate Connect one end of hose to “deflate” on pump and the other end to the valve on seat. Suspected instances of abuse or neglect are to be reported. You will hear a “click” when properly attached. Turn the pump switch off. Ensure seat is properly cleaned with mild soap / disinfectant such as Cidex Fold the seat and store all components in carrying case. (1) 12volt DC pump.62 03/01/05 . Immediately reapply and maintain pressure at the source of the bleeding with a bandage or gauze Other information This is a single–patient. pull the ear pinna straight back. TraumaDEX will not interfere with would treatment at the ED. using a sterile bandage or gauze. single use product. When this is complete the display will show the temperature mode selected (i.PROCEDURAL GUIDELINES THERMOSCAN THERMOMETER Caution The Pro–2 should not be used on any patient's ear which exhibits symptoms of an acute or chronic inflammatory condition of the external ear canal Do not take a temperature on an ear that contains blood or purulent discharge Application/Use Make sure the thermometer is in the proper mode for the patient's age Install a cover on the probe by pressing the probe barrel straight down into the opened cover until you feel and see the cover seat securely. the button should be held down for one second If the patient is over one year of age or an adult the ear pinna should be pulled both up and back (See Figure 34). ORAL F) and the word READY If the patient is under one year of age. P . Identify the source of the bleeding. Procedure Tear open package and remove the cover.63 03/01/05 .e. the button should be held down for one second Eject the disposable probe cover by pressing the eject button TRAUMADEX INDICATIONS Temporary treatment of severe bleeding Contraindications Not for intravenous application and should never be injected into blood vessels. carefully but firmly to seal the ear canal and press the top button (See Figure 33). using a twisting and bending motion. then thoroughly cover the source and the wound bed with the TraumaDEX powder. and open fractures with exposed bone. Should not be used on sucking chest wounds. open brain injuries with exposed brain tissue. insert the probe. Can be easily washed away without disturbing the clot. this will automatially turn the unit on All display segments will momentarily be displayed. again removing any excess blood. Clean and remove excess blood from the wound site. Adjust the collar to appropriate size then push in the arrows and reengage the safety locks. when a neck injury is suspected Application/Use Apply a rigid cervical collar per guidelines Transfer the patient to a backboard using accepted technique Position approved device under the patient’s head and affix to the board (Ferno CID is attached to the board prior to patient transfer and is reusable) Position support blocks or side panels against the head on each side Ferno CID only.64 03/01/05 . disengage the safety locks and pull out the arrows. CERVICAL IMMOBILIZATION DEVICE (C.the angled side of the support blocks may be placed next to the patient’s head in cases where inline position cannot be maintained and the patient must be immobilized in position found Maintain neutral alignment of the head and neck and use straps provided to secure patient to the device Clean or dispose of the devices per department guidelines P .D. Simply pull the collar apart until the appropriate size is reached Reengage the safety locks by pushing down on the safety buttons If a smaller size is needed. disengage safety locks by pulling up on the safety buttons. Headbed II.I.EMERGENCY MEDICAL GUIDELINES Immobilization AMBU PERFIT ACE Collar Assembly Hold collar near tracheal opening with one hand and place the index finger on the foam side of the chin piece and the thumb on the plastic side of the chin piece Simply flip the chin piece from the back of the collar to the front of the collar This automatically forms the chin piece and places it in position of function Procedure for use Have one rescuer gently hold the head and neck in neutral alignment Second rescuer applies the collar to the patient Collar comes packaged to a Neckless Size 3. If a larger size is needed.) Approved devices: Ferno CID. Sta-Blocks Indications Used in conjunction with a rigid cervical collar to secure a patient’s head to a long spine board or similar device. leave loose Connect shoulder straps (color coded). This device will be employed when a patient has a suspected cervical/spinal injury and must be extricated from any position other than lying (where the patient could be log rolled directly onto a backboard) except as noted below Caution The device is applied quickly with very little time cost. sewer. short body immobilization board designed for suspected cervical/ spinal injuries during confined space extrication. repeat with other leg Disengage velcro from chin and forehead strap on head harness. grasp head harness by velcro flaps that attach harness to Half Back. etc.e. secure forehead strap (near eyebrows). remove head harness. connect (color coded) and tighten strap.65 . i. secure velcro flaps to Half Back. position top of head harness to patient’s head. construction area. pull padded section under leg. do not remove straps from pockets Insert Half Back behind patient Position sides under patient's arms Release padded leg straps to expose torso strap pockets Connect torso straps (color coded). place webbing portion (not padding) under patient's leg at knee. storage tank. work webbing back and forth under leg to the groin area. auto accident. adjust to bring sides of Half Back against patient's underarm Tighten torso straps Remove a leg strap from pocket. secure chin strap Release manual C–spine immobilization Extricate patient Place patient on backboard/Miller Board Loosen leg straps Secure patient on backboard/Miller Board Figure 35 03/01/05 P . but a patient with immediate life threatening injuries is extricated directly without employing the Half Back (at the discretion of the on–scene medical authority) Application/Use Manual C–spine immobilization C–collar applied Remove any eyeglasses and articles from shirt pocket(s) Open Half Back.PROCEDURAL GUIDELINES HALF BACK EXTRICATION/LIFT HARNESS Indications The LSP Half Back (See Figure 35) is a versatile. alcohol. but a patient with immediate life threatening injuries is extricated directly without employing the KED (at the discretion of the on–scene medical authority). ensuring it is all the way down to the seat Position side flaps under patient's armpits and around torso Fasten the mid torso strap Fasten the lower torso strap Position and fasten the groin straps Pad any space between the occiput and the upper portion of the KED Attach the forehead strap Attach the lower strap around the collar roller bandage (Kling) may be used in place of head straps as long as it secures the head in the same manner as the straps Fasten the upper torso strap Check all straps to ensure they are snug Loosen groin straps when placing patient supine for immobilization Figure 36 LONG SPINE IMMOBILIZATION Indications Any patient of an MVA. Caution The device is applied quickly with very little time cost. rescuer 3 at the hips.66 03/01/05 . backboard is place alongside the patient Rescuer 1 commands all movements Log roll placement rescuer 1 makes a preparatory count to three and the patient is gently log rolled up on the three count. rescuer 2 at the shoulders. neck. or where mechanism of injury suggests possible spinal injury Any trauma patient who complains of pain in the head. drugs. unconsciousness) Application/Use Manual C–spine immobilization C–collar applied Halfback/KED applied (if applicable) Position rescuer 1 at the head of patient (maintaining C–spine).EMERGENCY MEDICAL GUIDELINES KENDRICK EXTRICATION DEVICE (KED) Indications The KED (See Figure 36) device is employed when a patient has a suspected cervical/spinal injury and must be extricated from any position were the patient cannot be directly placed (log roll or standing) onto a backboard. Application/Use Establish manual cervical support Apply cervical collar Maintain in–line cervical support Move patient's torso forward as a unit Place the KED behind the patient.e. Rescuers 2 and 3 perform the roll while rescuer 1 maintains neutral C–spine alignment P . fall. or back Any trauma patient who may have injury to the spine but in whom evaluation is difficult due to altered mental status (i. 67 . The athlete wearing shoulder pads has his neck in a neutral position when lying supine with a helmet in place. Helmet Removal Important Points About Helmet removal Athletes wearing both helmets and shoulder pads (Football. motorcycle helmets often must be removed in the prehospital setting. Two are to be speed clipped to the pins by the patients's upper thighs and crisscrossed to the shoulders. releasing the air inflation system. Motorcycle helmets are often designed with a continuous solid face guard that limits airway access. After arrival at the emergency department the C-spine can be x-rayed with the helmet in place. there are four male straps with speed clips. Athletic helmet design will generally allow easy access once the face guard is removed. and then sliding the helmet off in the usual manner. In this case. Hockey and Rugby) are another special set of patients. On occasion. such as respiratory distress coupled with an inability to access the airway. Rescuers 2 and 3 perform the roll while rescuer 1 maintains neutral C–spine alignment Alternative placement techniques standing sliding placement with scoop–type device Double X Strapping there are four preconnected female straps attached to the long board. removing the cheek pads. Once the spine is evaluated. These helmets are not custom designed and frequently are poorly fitted to the patient. The removal technique is modified to accommodate the different designs. The above-mentioned helmets are custom fitted to the individual and are therefore more difficult to remove. Two are placed over the shoulders and onto the chest. or the shoulder pads must be cut away and removed. This occurs predominately with adolescents and nonprofessional athletes. Single X Strapping same as Double X Strapping except uses a single X strap method on the top and a single horizontal strap across the lower extremities Apply Cervical Immobilization Device Release manual C–spine immobilization. THESE TYPE HELMETS SHOULD NOT BE REMOVED IN THE PREHOSPITAL SETTING. In contrast. with the other two attached at mid chest (just under arm pit). patient is ready for transport Remember that the head is only immobilized after the body has been immobilized. The other two males will be speed clipped to the pins by the patient's ankles and crisscrossed to the females at mid chest (just under arm pit). the helmet must be removed and padding must be inserted under the head to keep the neck from hyperextending. Helmets used in different sports present different management problems for rescuers. the helmet can be removed by stabilizing the head and neck. Unless special circumstances exist.PROCEDURAL GUIDELINES the backboard is slid into place by Rescuer 3 (with one hand) or by additional personnel rescuer 1 makes a preparatory count to three and the patient is gently log rolled down on the three count. Their large size will usually produce significant neck flexion if left in place when the patient is placed on a backboard. Motorcycle accidents are usually associated with much more violent forces than are athletic injuries. The motorcycle helmet will make it 03/01/05 difficult to P . The face guard can easily be removed with a screwdriver or a pair of trauma scissors. face guard screws may be rusted and you will be unable to remove it in the normal fashion. MILLER BOARD Indications Any victim of trauma with obvious neurological deficit such as paralysis. place your hands on each side of the helmet. may obstruct access to the airway. and then up to remove. rescuer 2 at shoulders. this03/01/05 alignment is essential to providing proper T–spine immobilization. Your partner maintains steady immobilization of the neck during this procedure After removal of the helmet. Your partner then assumes the stabilization by placing one hand under the neck and the occiput and the other hand on the anterior neck with the thumb pressing on one angle of the mandible and the index and middle fingers pressing on the other angle of the mandible You now remove the hekmet by pulling out laterally on each side to clear the ears. weakness. not the head) If the patient is wearing glasses. rescuer 3 at the hips Rescuer 1 commands all movements Rescuer 1 makes a preparatory count to 3 and the patient is gently log rolled up on the three count.EMERGENCY MEDICAL GUIDELINES stabilize the neck in a neutral position. or paresthesia (numbness or tingling) Any victim of trauma with severe facial or head injuries Any victim of trauma to multiple systems Any victim of trauma in critical condition (priority one or two) or is unconscious Contraindications Patient weight greater than 250 pounds Children less than 65 pounds Caution Overtightening straps may obstruct chest expansion or inhibit respiratory effort Application/Use Manual C–spine immobilization C–collar applied Halfback / KED applied (if applicable) Open harness system and place board alongside the patient Position rescuer 1 at the head of patient (maintaining C–spine). Tilt full-face helmets back to clear the nose (tilt the helmet. remove them through the visual opening before removing the full-face helmet. The Miller Board is slid into place by Rescuer 3 (with one hand) or by additional personnel.68 . and immobilize the head and neck by holding the helmet and the patient’s neck Your partner positions himself to the side of the patient and removes the chin strap Chin straps can usually be removed easily without cutting them. Removing A Motorcycle Helmet From A Patient With A Possible Cervical Spine Injury Position yourself above or behind the patient. MOTORCYCLE HELMETS SHOULD BE REMOVED IN THE PREHOSPITAL SETTING. The shoulder pins of the board are aligned with the top of the patient's shoulders. P . and may hide injuries to the head or neck. Rescuers 2 and 3 perform the roll while rescuer 1 maintains neutral C–spine alignment. you again assume immobilization of the neck by grasping the head on either side with your fingers holding one angle of the jaw and the occiput Your partner now applies a suitable rigid extrication collar. secure chin strap Release manual C–spine Extricate patient. patient's hands may be placed inside or outside of strap based on patient consideration Thread and tighten the leg and ankle straps Disengage velcro from chin and forehead strap on head harness. Stiffneck Select. Procedure Sizing All approved devices rely on the same key dimension in sizing (figure 37. patient is ready for transport NAJO PEDI–AIR–ALIGN BACKBOARD Indications Infants and children needing c–spine immobilization Weight rating up to 100 pounds Strapping Technique Chest straps criss–cross across patient’s chest Remainder of straps go across the body Wrist restraints can be used if needed. Position shoulder straps based on anatomical considerations and the condition of the victims chest. Proper sizing is critical for good patient care. secure forehead strap (near eyebrows). RIGID CERVICAL COLLAR Approved devices: Stiffneck. Sure–Loc.PROCEDURAL GUIDELINES Rescuer 1 makes a preparatory count to three and the patient is gently log rolled down on the three count.38. improper sizing can cause hyperextension or lack of support. follow the color–coding down the patient’s left side of the board. Rescuers 2 and 3 perform the roll while Rescuer 1 maintains neutral C–spine alignment. position top of head harness to patient's head. follow the color-coding down the patient’s right side of the board. tighten the shoulder straps Thread and tighten the lower torso strap. If the top of the patient’s head starts in the green area. Thread both shoulder straps through their corresponding pins and leave loose.39) 03/01/05 Figure 37 P . and thread through the pin. secure velcro flaps to Miller Board.69 . excluding the arms. grasp head harness by velcro flaps that attach harness to Miller Board. Broselow Color Coding If the board is equipped with the Broselow Color Coding and the top of the patient’s head starts in the brown area. Place the chest strap loosely over the patient's chest. Caution These devices must always be used in conjunction with other immobilization adjuncts. All approved rigid cervical collars are designed to limit movement of the cervical spine in all patients in whom a cervical injury is suspected. WIZLoc and Philadelphia Indications Suspected cervical injury. Tighten the chest strap. the may cause further injury to the patient). Accordingly. Indications Patients with Endotracheal tubes/trachs Patients with Invasive Catheters.70 03/01/05 . lock the support in position Ensure that the chin piece stays in position during the application Clean or dispose of collars according to department guidelines Figure 39 PATIENT RESTRAINTS Restraints have the potential to produce serious consequences such as physical and psychological harm. lines and tubes Patients with Brain pathologies or injury P . Regular or Tall) Position the chin piece under the patient’s chin Slide the back portion of the collar behind the patient’s neck and loosely affix the hook and loop fastener strap to the collar Hold the bottom of the collar downward in contact with the patient’s chest Raise the mandibular support until contact is made with the chin (do not exert upward pressure on the chin. Stiffneck Select and Philadelphia While the patient’s head is being held in neutral alignment use finger width to visually measure the distance from the shoulder to the chin (key dimension) Use the finger measurement to select the collar size or adjustment that matches the key dimension Maintain neutral alignment of the head throughout application Position the chin piece by sliding the collar up the chest wall. loss of dignity. this may cause further injury to the patient). violation of an individual’s rights.EMERGENCY MEDICAL GUIDELINES The key dimension is the distance between the top of the patients shoulders where the collar will rest and the bottom plane of the patients chin (angle of the jaw) Stiffneck. physical activity or normal access to his or her body. not the foam padding WIZLoc Only–Pre adjust the occipital support based on visual inspection of the neck (Thick. Restraint is any method of physically restricting a person’s freedom of movement. Difficulty in positioning the chin piece may indicate the need for a shorter collar Slide the back portion of the collar behind the patients neck and affix the hook and loop fastener strap to the collar. soft roller bandage to cover and protect IV sites. lock the support in position Adjust the hook and loop fastener snug enough to maintain the chin piece in position Sure–Loc Only–Adjust the occipital support until contact is made with the patient’s occiput (do not exert upward pressure after contact with the occiput is made. Examples of alternative interventions may include but are not limited to utilization of adjustable stretcher restraint straps. Be sure the chin extends far enough onto the chin piece to cover the central fastener. the use of restraints will be limited to situations where other treatment interventions have clearly failed to address the patient’s presenting clinical needs and safety. and even death. the strap should be snug enough to maintain the chin piece in position Ensure that the chin piece stays in position during the application Figure 38 Sure–Loc and WIZLoc Maintain neutral alignment of the head throughout application The key dimension on the collar is the distance between sizing indicator and the lower rigid plastic band. or significant other. maintain proper body alignment.A. While continuing manual c–spine. of pediatric patients who fit within the height and weight guidelines specific to the brand of pediatric immobilizer used A. and release manual c– spine Device should be secured to either stretcher or bench seat. Caution Loss of pulses. Reassure the patient that this is not a punishment. but secure enough to assure effectiveness of device Apply according to the manufacturer’s instructions. prior to being initiated. or beside them if application is only for a backboard type use. prior to transportation Figure 41 Figure 42 03/01/05 P . the restraint should be applied to one arm and the opposite leg (two point restraint) or to all four extremities (four point restraint) you should be able to slip one finger between the restraint and the patient’s skin. and between 20–90 pounds LSP Pedi–Immobilizer (See Figure 42) infants and children up to 75 pounds Figure 40 Application/Use While applying gentile in–line manual C–spine . Tie with easily released hitches (Quick–release knots) out of patient’s reach. this should be adjusted to provide for patient comfort. When wrist restraints are used cocurrently with ankle restraints. apply the straps to the body and extremities Secure the head with the CID. Place the immobilizer behind the patient for extrication (if applicable). immobilize the patient's head and neck (cervical spine) with a cervical collar or similar device.PROCEDURAL GUIDELINES Patients who are violent or could inflict potential harm to self or others due to an impaired psychological state and/or substance abuse Contraindications The potential risks of restraints are believed to be offset by the potential benefits of a better patient outcome (such as the patient being safer from activities and behaviors that could cause physical harm and lead to a chance of increased morbidity) as well as being safer for crew members. Kinder (See Figure 40) infants and children up to 60 pounds Ferno Pedi–Pac (See Figure 41) patients 28–54 inches.71 . capillary refill and sensation can occur if restraints are overtightened Neurovascular exams shall be performed at 5 minute intervals during restraint Procedure Explain reason for restraint to the patient. a proper “log rolling” technique should be used. but a safety precaution. Do not release until immobilization is complete. Position patient to prevent aspiration and to allow visual contact. family. Select the appropriate restraint. Check pulses below the point of restraint to ensure circulation Check restraint integrity PEDIATRIC PATIENT IMMOBILIZATION Indications Spinal immobilization. supplied by the manufacturer. For this type of application. movement and/or sensation can occur if the splint is overtightened or overinflated Care should be taken to carefully assess circulation. capillary refill. and motor function after splinting VACUUM SPLINT Indications Any extremity fracture or injury Procedure Take C–Spine precaution as indicated by mechanism of injury Manually stabilize the extremity Expose the injury P .” transport should not be delayed to splint extremity fractures. When patient condition warrants “load and go. Close straps and evacuate air from splint. extremity fractures should be splinted prior to moving the patient. sensation and motor function Procedure Remove or cut away clothing to expose area of injury Control active bleeding Check distal pulses. discontinue air evacuation when splint is rigid Further immobilize as needed Reassess circulation. In the stable trauma patient. capillary refill. should be realigned along the long axis of the limb. sensation. Gross angulation of limbs that require alignment in order to stabilize.72 03/01/05 .EMERGENCY MEDICAL GUIDELINES SPIDER–TYPE PATIENT STRAP Procedure Lay strap over patient with V toward the head and feet and centered on body Open Velcro straps Secure top V strap over patient's shoulders and through backboard Secure center body straps through backboard openings: top strap over mid chest mid strap over pelvis lower strap over thighs above the knees Secure lower V strap around ankles and through the backboard Ensure all straps are snug before moving patient SPLINTING The decision to splint should be based upon patient condition. may be attempted (consider pain control) Open wounds should be dressed and bandaged Use the most appropriate splint to immobilize the joint above and below the fracture site Dislocations should be immobilized to prevent any further movement of the joint Check distal pulses. sensation/movement prior to splinting if distal pulses are absent in fractures or dislocations. sensation and movement prior to and after splinting. capillary refill. one attempt to place the injury into anatomical position. If there is a loss of circulation after splinting make one attempt to realign the injury and reassess. Caution Loss of pulses. POSITIONING THE STA-BLOK OCCIPITAL PAD Remove the occipital pad from the package and place pad under patient’s head while maintaining neutral alignment of the patient’s head and neck. sensation and motor response Choose appropriate size vacuum splint and form to injury. FOR EXTRA SUPPORT AS CHIN STRAP or FOR PATIENT WEARING HELMET Severe weather strap will also be used. discontinue air evacuation when splint is rigid Further immobilize as needed Reassess circulation. Center the pad at the patient’s temporal area. and motor function STA-BLOCK HEAD IMMOBILZER WARNING In cases of suspected spinal cord injury.73 . proper immobilization is only one part of the total immobilization. press down firmly on the occipital pad. pull the release liner to expose the adhesive backing material. sensation.PROCEDURAL GUIDELINES Assess circulation. The patient’s face and airway must be accessible at all times. around patient’s neck for extra stability. SECURING PATIENTS HEAD Take the soft white strap material and attach to the Sta-Blok support blocks with the hook. Make sure the strap goes over the forehead. in addition to the hook and loop strap. Because of its length. After removing the release liner. It is imperative that the patient be properly immobilized to prevent any movement of the spinal column. consider application of ice or cold pack to injury Close straps and evacuate air from splint. the severe weather strap is ideal for use with a patient wearing a motorcycle or football helmet. While holding the Sta-Blok occipital pad in place.POSITIONING SIDE SUPPORT BLOCKS Place side support blocks against the head just above the patient’s ears and press the hook down on the occipital pad. 03/01/05 P . OR Incident involving 10–20 persons COMMAND Incident Command established per Department SOG COMMUNICATIONS Request designation of staging area from Command Assign tactical channel Notify closest 2 hospitals.EMERGENCY MEDICAL GUIDELINES Multiple Casualty Incidents The Multiple Casualty Incident can be effectively managed if the appropriate command is established and necessary resources committed. The difficulty lies in recognizing the size of command structure and quantity of resources needed for small to medium size inidents. The triage system used with the MCI guideline is the START Method. The unit responses defined in the following MCI Level declarations are additional to the initially assigned ambulance. LEVEL 1 RESPONSE Defined as a single additional ambulance response. This guideline quantifies command structure size and function based on the number of medical units responding to a given incident and/or the number of persons involved.74 03/01/05 . request number of patients they can receive Notification of EMS and shift supervisor MEDICAL COMMAND Medical Command established by senior medical officer and reports directly to Incident Commander or Operations (if established) Management of patient area. treatment and transport officer roles Coordinates triage Establishes patient log P . This method will allow rapid triage to be performed in an efficient manner. This method will eliminate the possibility of too small a command structure for incoming units and will help avoid confusion. refrain from patient involvement until all patients triaged Medical command assumes triage. OR Incident involving 5–9 persons COMMAND Incident Command established per Department SOG COMMUNICATIONS Request designation of staging area from Command Assign tactical channel Notification only to local hospital Notification of EMS and shift supervisor TRIAGE Performed by senior medical officer or designee Triage tagging not performed Patient log not used TREATMENT Initiated at patient location Package per guidelines SUPPORT PERSONNEL One engine LEVEL 2 RESPONSE Defined as a two or three additional ambulance response. it may be appropriate to establish a triage area where patients are first moved from the incident site.e. request number of patients they can receive Notify additional hospitals as needed Notification of shift supervisor MEDICAL COMMAND Medical Command established by senior medical officer and reports directly to Incident Commander or Operations (if established) Assign Triage Officer to establish Triage group Identify areas to be used for treatment Identify ambulance transport staging area (coordinated with Incident Command) Assign Treatment Officer to establish Treatment area in pre–selected location (8 or more patients) Assign Transport Officer to establish Transport area in pre–selected location (8 or more patients) Assign Medical Communications Officer (as needed. colored tape may be substituted 03/01/05 P . OR Incident involving more than 20 persons COMMAND Incident Command established per Department SOG COMMUNICATIONS Request designation of staging area from Command Assign tactical channel Notify closest 3 hospitals.PROCEDURAL GUIDELINES Additional resources should be requested through Incident Command and given access and assignment instructions Assign resources to triaged patients based on priority TRIAGE Triage performed by designee of medical command Perform appropriate triage Note location of patient on tag (i. Transport Officer may double as Medical Communications in smaller incidents) TRIAGE Triage performed by Triage Officer and/or designee(s) when possible. triaged. then moved to appropriate treatment area All patients should be tagged with priority only for tracking Keep tally of total number of patients triaged and number assigned to each category Report patient numbers to Triage Officer at regular intervals Repeat triage sequence to monitor changes in condition If time and circumstances allow. patients are triaged where found and moved to appropriate treatment area. perform more detailed assessment and write information on the tag while the Treatment group continues to move patients out of the triage area Depending on the incident size and available number of tags. driver red vehicle) Triage results are reported to medical command SUPPORT PERSONNEL Two or three engines LEVEL 3 RESPONSE Defined as a four or greater ambulance response.75 . EMERGENCY MEDICAL GUIDELINES TREATMENT Establish patient treatment area after conferring with Medical Command regarding location Assemble Treatment group personnel into two subgroups. law enforcement) number of engines special needs (buses. if necessary.) P . one to perform basic packaging in triage area and then move patients to Green. Yellow or Red area Name of person providing treatment should be noted on triage tag TRANSPORT Establish loading zone after conferring with Medical Command regarding location. one Yellow and one Green patient per ambulance Do not assign more than one Red (priority 1) patient per ambulance As patients are queued for transport. give the transport control portion of the triage tags to the Medical Communications Officer and advise ambulance unit and destination Keep a unit ready for loading in the loading zone Do not allow patients to stack up in the loading zone MEDICAL COMMUNICATIONS OFFICER Record all patients and disposition in patient log Ensure all patients accounted for when loaded ambulance departs. medical. fire. Yellow or Red treatment areas and one to provide treatment within the treatment area so packaging groups may Treatment personnel should continue evacuating patients from the triage area fill out triage tag information as completely as possible noting patient. consider proximity to treatment area and ambulance approach and exit routes Make sure transport personnel stay with their vehicles Assign patients from treatment areas to ambulances for transport Determine patient destination through coordination with Medical Communications Officer Only two stretcher patients and one ambulatory patient (in front seat) per ambulance Attempt to assign one Red. heavy equipment. priority and brief description (chief complaint) of each patient's condition Transporting units should not communicate directly with the receiving hospital unless the condition of the patient deteriorates and Medical Control contact is necessary for the management of the patient SUPPORT PERSONNEL Must be scaled to the size and nature of the response Consider the following needs: number of personnel (command. delegate the loading of ambulatory patients on buses As patients are loaded. assessment and treatment information Uninjured victims should be kept in the Green treatment area until evaluated and released at the appropriate time by the Transport Officer (who must log all patients) or taken in a controlled manner away from the incident by the Transport Group A patient whose condition changes inside the treatment area should be moved to the appropriate Green. request another ambulance move into loading zone from ambulance staging area unit.76 03/01/05 . separate transport control portion of triage tag Triage tag remains with patient for transport Supervise the actual loading of patients. total number of patients. etc. neonates. and are essentially in a state of flux that is not likely to be resolved completely in the near or distant future.g. cath films or CD’s. H&P’s. lab work. The level of care to be provided is specified and appropriate to the patient’s condition to treat any reasonably foreseeable complication during transport. Either the attending physician. the Medical Director. Transfer papers (summary. x-rays. Ob Triage Guidelines The final decision with acceptance of an OB transport rests with the supervisor of MD. All medicated IV drips should be controlled by a battery-powered IV pump. If the patient has DNR orders. as change is a part of the nature of social legislation. and has a designated accepting physician. with the only possible exceptions being vitamin or electrolyte drips. whenever you have any doubt in your mind about the nature of a transport. The patient must be accepted at the receiving facility. e. current treatment. consults. or criticalcare. EMTALA Transfer Criteria EMTALA: EMERGENCY MEDICAL TREATMENT AND ACTIVE LABOR ACT All previous references to COBRA have been replaced by EMTALA. A specialty team member should accompany any patient whose needs exceed the scope and training of the transport personnel. This transfer is arranged as a physician to physician transfer. Procedure Transport caregivers must receive a thorough and complete summary of the patient’s condition. Patient ID must be verified. The patient (or surrogate) agrees to the transfer. or the Emergency Department Physician are authorized to arrange such transfers. If the hospital denies the request for additional personnel. All orders from the transferring (sending) physician are clearly specified in writing and are appropriate for the level of training of the attending personnel and equipment provided.77 . and other pertinent medical information. new definitions and interpretations of this act are in the process of determination. Although it has been designed to cover emergency transports. or direct verbal order from the doctor who is initiating the transfer. obstetrics. family. or personal physician desires The sending physician must be in compliance with EMTALA guidelines on patient transfers. These orders should be in writing.PROCEDURAL GUIDELINES INTERFACILITY TRANSPORTS Purpose A patient may be transferred to another hospital if: The patient. At the time of this writing. The only exception would be for a pediatric patient where the physician has determined that an IV would be detrimental to the patient. or supervisor should be contacted immediately. possible complications. Treatment orders should be given to the paramedic. if the trip is a transfer as defined by EMTALA.) should be given to the paramedic. etc. Transferring physician certifies the need/risk/benefits of transport. All Code Three transports must have at least one IV access before going enroute. Communications will verify acceptance of the patient by the receiving facility before the patient is moved. the original should always accompany the patient. Completion of the Physician’s Certificate of Transfer form accomplishes this purpose. 03/01/05 P . a supervisor. or the Medical Director should be consulted. once he or she is discharged. Nursing Notes. as well as catheter placement to avoid a bleed-out from a disruption of the system. Arterial Lines Procedure Make sure that the line remains open at all times by insuring that the pressure infuser has approximately 300mm Hg pressure on the bag at all times. Specialty Team Transports During specialty transports. the EMS Paramedic is nonetheless responsible for a full and complete Patient Care Report.EMERGENCY MEDICAL GUIDELINES Routine Interfacility Tranports Routine Interfacility transports by private providers characteristically do not destinate in the ER. Because the documentation of medical necessity for authorization (especially by Medicare) of interfacility transports is done post facto. laboratory results. Perfusionist. Special care must be given to insure that the balloon pump is moved with the patient in a manner so as to prevent any compromise of the electronic and pressure lines connecting the balloon pump to the patient. rather than interfacility transports. in most cases can only be justified by documentation of underlying conditions still present at the time of transport that support evidence that transport by other means is medically contraindicated. Periodically check the integrity of the tubing and all connections to the catheter. The EMS Team should assist within their level of training. including vital signs and an assessment consistent with state standards Balloon Pump for documentation. Every effort must be taken to ensure that the members of the team transfer the stretcher. or through dispatch as needed. If specific orders are not secured from the sending physician prior to transport. BLS transports. patient care is to be provided by the Specialty Transport Team. normal communications via Medcom for physician’s orders are not appropriate. Modern balloon pumps no longer mount to the bottom of the stretcher and are self-standing units with their own set of wheels. Monitor the patient’s hemodynamic and perfusion status. it is essential that copies of the History and Physicals. If the catheter should dislodge. Critical-Care Paramedic or Respiratory Therapist trained in balloon-pump operation should accompany the crew. Consultations.78 03/01/05 . An RN. Procedure All balloon pump transfers require additional manpower. Flush the line by squeezing the flush valve. ICD-9 Codes are generally more geared toward prehospital. The other alternative is to provide direct communications with the provider’s Medical Director for physician’s orders as needed. hold direct pressure and treat as an arterial bleed. patient. Although the Specialty Transport Team is directly responsible for the care of the patient. For this reason. P . and pump as a unit. Discharge Planner’s instructions and Interfacility Transfer Summary be included with the patient care report. arrangements should be made to contact the appropriate physician via cell phone. ) using mouth-to-mask/barrier technique. Respiratory and circulatory parameters remain unchanged. Infants who are developmentally unable to walk should be screened at the initial site (or at the secondary triage site for green patients if carried there by others). At a minimum.) must have their airway opened by conventional positional techniques. If spontaneous respirations resume.79 . Step 2B If upper airway opening does not trigger spontaneous respirations. One mask (with one-way valve) should be available on every potential first-in EMS unit. Appropriate intervention can then be determined based upon the resources available at the designated treatment site. pedal). brachial. If there is no peripheral pulse. children are somewhat less likely to have dangerous transmissible diseases and the number of children satisfying the criteria for a ventilatory trial will be relatively small. Crosscontamination is a minimal issue. secondary triage should consist of the RPM components of the JumpSTART algorithm. NOTE: Children with special health care needs are often chronically unable to ambulate.. the patient is tagged as deceased (black ribbon) and the triage officer moves on.e. although those with chronic respiratory problems may routinely have elevated respiratory rates. If the patient resumes spontaneous respirations. infants may be triaged to the minor category. If they satisfy all of the physiologic “delayed” criteria (i. using the JumpSTART algorithm. This is the pediatric “jumpstart”. the patient is tagged as immediate and the triage officer moves on without providing further ventilations. the rescuer palpates for a peripheral pulse (radial. If the ventilatory trial fails to trigger spontaneous respirations. A caregiver with knowledge of the children involved would be of invaluable assistance in this case. Also. Step 2A Nonambulatory pediatric patients are initially assessed for presence/absence of spontaneous breathing. where they will undergo secondary (more involved) triage. There is a trend favoring brief medical data cards to be stored in the driver’s area of buses and other vehicles routinely transporting children with special health care needs. Any patient with absolute apnea or intermittent apnea (periods of more than 10 sec. including (limited) BLS airway foreign body (FB) clearance only if there is an obvious FB. 03/01/05 P .) Ventilatory face shields such as those marketed for CPR classes and public use may also be used. The child may or may not still be breathing on arrival of other non-triage personnel. Neurological status may be difficult to judge due to lack of knowledge of a given patient’s baseline function. Be on the lookout for information about special needs children. Step 2C If there is a palpable peripheral pulse. the rescuer gives 5 breaths (about 15 sec.PROCEDURAL GUIDELINES JUMP START PEDIATRIC TRIAGE Step 1 All children who are able to walk are directed to the area designated for minor injuries. Any patient with spontaneous respirations is then assessed for respiratory rate (see Step 3). the child is classified as deceased. a red ribbon (immediate) is applied and the triage officer moves on. as this is already occurring because triage personnel do not change gloves between patients. fulfill no “immediate” criteria) and appear to have no significant external injury. (An adult mask may be used for a child if inverted. These children can be triaged similar to infants who are developmentally unable to walk. usually in the secondary triage stage. the patient is triaged in the delayed category (yellow ribbon). This has been substituted for capillary refill (CR) because of the variation in CR with body and environmental temperature and because it is a tactile technique more adaptable to poor environmental conditions. If there are no peripheral pulses. The rescuer now performs a rapid “AVPU” assessment. or responds appropriately to pain (localizes stimulus and withdraws or pushes it away). If there are palpable peripheral pulses. If the child does not respond to voice and responds inappropriately to pain (only makes a noise or moves in a nonlocalizing fashion). If the patient is alert. Assess perfusion by palpating peripheral pulses on an (apparently) uninjured limb. the rescuer assesses mental status (Step 5). has decorticate or decerebrate posturing. the patient is categorized as an immediate patient (red ribbon) and the triage officer moves on. responds to voice.80 03/01/05 . a red ribbon (immediate) is applied and the triage officer moves on. keeping in mind the apparent developmental stage of the child. If the respiratory rate is roughly 15-45 breaths/min proceed to Step 4 (assess perfusion). the patient is classified as immediate (red ribbon) and the triage officer moves on. Step 5 All patients at this point have “adequate” ABC’s.EMERGENCY MEDICAL GUIDELINES Step 3 All patients at this point have spontaneous respirations. If the respiratory rate is less than 15 (slower than one breath every 4 seconds) or faster than 45 or very irregular. or is truly unresponsive. P . Step 4 All patients at this point have been judged to have “adequate” respirations. C. dead patient Use the blue tags for contaminated patients in need of decontamination Move all walking wounded to the Green treatment area Begin by moving from patient to patient to assess the remaining victims Stop at each person for a quick assessment and tagging Each stop should not take more than 1 minute (Purpose at this point is to define and tag patients) Refer to the flow chart for methodology and corrective actions to be taken during triage NO INJURY OR COMPLAINTS DELAYED TRANSPORT UP TO THREE (3) HOURS No BREATHING? DEAD Yes CONTAMINATED? DECONTAMINATION RESPIRATION EFFORT? Inadequate <10 or >30 Adequate and <30 PERFUSION? Cap refill >2 sec or radial pulse absent CRITICAL/ IMMEDIATE TRANSPORT LOC? Unconscious or altered L.e.81 . can delay treatment and transport up to three hours Priority Four (Black Tg)–no care required. can delay treatment and transport up to one hour Priority Three (Green Tag)–delayed care. RMP): Respiration Perfusion Mental status The four levels of triage are identified by color codes: Priority One (Red Tag)–immediate care.O.PROCEDURAL GUIDELINES SIMPLE TRIAGE AND RAPID TREATMENT (START) The system is a method of triage that is proved to be very effective and is based on three observations(i. life threatening Priority Two (Yellow Tag)–urgent care. DELAYED TRANSPORT UP TO ONE (1) HOUR 03/01/05 P . in affected eye prn for pain.blunt or penetratingAdminister Tetracaine 1-2 gtts. Can be used with contact lens Control bleeding with gentle pressure over wound site Stabilize protruding foreign bodies with moist sterile dressings.EMERGENCY MEDICAL GUIDELINES TRAUMATIC BRAIN INJURY TRAUMA – Traumatic Brain Injury Complete trauma assessment per Trauma Guidelines Stabilize C-Spine and assure adequate airway Perform baseline Glascow Coma Scale (GCS) Treat per pre-hospital triage for TBI guideline Maintain an SAO2 > 90% Maintain a systolic BP of >100 mmHg Transport to most appropriate receiving facility by most appropriate means per Trauma Transport Protocol (TTP) Recover any avulsed tissue if possible (ear.82 03/01/05 . chemical burns) P . protect and cover both eyes if applicable Remove contact lenses if management of injury is complicated by their presence (ie. nose) and wrap in moist gauze Ocular Injury Treat specific ocular injury . braintrauma. 15) Trauma Center (GCS 9-13) Transport to: Trauma Center with TBI Resources* if available (GCS<9) First Priority: Asses. or open to pain Eyes do not open to pain Score GCS Verbal Says at least words Incomprehensible sounds or none Score GCS Motor Any motor response Localization or withdrawal Extensor or flaccid response Assess Pupils Any pupil response Pupils equal and reactive Pupils asymmetric or fixed and dilated Treatment Oxygenate Intubate (ventilate and oxygenate if intubation not available) Normoventilate Intubate (ventilate and oxygenate if intubation not available) Hyperventilate Transport Transport to: Emergency Room (GCS 14. prompt neurosurgical care and the ability to monitor intracranial pressure and treat intracranial hypertension as delineated in the Guidelines for the Management of Severe Head Injury (www. Moderate TBI Severe TBI (Comatose) Score GCS Eyes Eyes open. Stabilize Airway Breathing Circulation Ensure: Systolic blood pressure > 100mmHg and SaO2 > 90% *Trauma center with 24 hour scanning capabilities. Treat.83 .PROCEDURAL GUIDELINES TRIAGE FOR THE TRAUMATIC BRAIN INJURY PATIENT Mild. open to voice. 24 hour available operating room.org) 03/01/05 P . P . The decision for EMS personnel to follow these recommendations should be based upon discussion and approval by the EMS Division Chief and/or local Medical Control.84 03/01/05 .EMERGENCY MEDICAL GUIDELINES Treatment: Ventilation Rates (approximate) Normal Ventilation Breaths Per Minute Adults Children Infants 10 bpm 20 bpm 25 bpm Transport Decisions Hyperventilation Breaths Per Minute Adults Children Infants 20 bpm 30 bpm 35 bpm The recommended hospital destination may not always be possible given the variality of local resources and transport times. When undue pressure is applied d. 6. At a minimum. Tracheal “clicking” and “hold up” are positive signs that the introducer has entered the trachea. Contraindications for use: 1.85 . 4. 3. 5.PROCEDURAL GUIDELINES ENDOTRACHEAL TUBE INTRODUCER PURPOSE: TO FACILITATE DIFFICULT INTUBATIONS Indications for use: 1. auto vent ) Thomas lock Technique / procedure: 1. 6.e. ky jelly ) Means of ventilation ( bvm. 4. Difficult intubations If the laryngeal opening is not fully visible To control the direction of the endotracheal tube during insertion Short-bull neck Laryngeal edema ( i.0 or greater Gum elastic bougie Have suction available Lubrication ( sterile h2o. 7. 03/01/05 P . 6. Once the endotracheal tube passes beyond the teeth. Advance the introducer to a depth of approximately 25cm so that the distal tip lies at least 2-3cm beyond the glottic opening. continue to gently advance the introducer until “hold up” is felt. 5. Positioning past the carina c. Hyperoxygenate the pt 2. 2. 3. Appropriate level of universal precautions Laryngoscope with appropriate blade E. tube 6. burns. While holding the introducer securely and without removing the laryngoscope. anaphylaxis ) Anatomical abnormalities ( congenital / tumors ) Inability to position the pt due to entrapment or confined space etc. During blind intubation b. the tip of the epiglottis must be visible in order to direct the introducer into the glotic opening. If the tracheal clicking cannot be felt. Perform an optimal direct laryngoscopy 3. Pediatric pt’s under 14 y/o Precautions: 1.t. 2. Tactile confirmation of tracheal clicking will be felt as the distal tip of the introducer bumps against the tracheal rings. rotate the endotracheal tube 90* counter clockwise (1/4 turn to the left) so that the endotracheal tube lies in the mid trachea. Endotracheal tube is threaded over introducer without using a laryngoscope Equipment: 1. No tracheal clicking or hold up is indicative of esophageal placement. Soft tissue damage or bronchial rupture may occur: a. 4. advance the endotracheal tube over the proximal tip of the introducer. 5. 8. 7. EMERGENCY MEDICAL GUIDELINES 7. Confirm endotracheal intubation: · Esophageal detector device (self inflating bulb) · Chest auscultation along the mid-axillary lines and the epigastrium · End tidal c02 detection 10.86 03/01/05 . Holding the endotracheal tube securely. remove the introducer. Secure the pt’s head ( lsb. P . Advance the endotracheal tube to the proper depth so that the tip of the endotracheal tube lies in the mid-trachea. 9. 8. cid) *** do not clean or sterilize the introducer *** dispose of after each use . 87 .PROCEDURAL GUIDELINES 03/01/05 P . TREATMENT GUIDELINES Treatment Guidelines 10/7/2009 M-1 . 9% NaCl 250 cc/hr 41 gtts/min with 10 gtt set Fluid resuscitation (patients with signs of severe hypotension) rates shall be wide open rate M-2 10/7/2009 . Nitroglycerine will not be given to patients within 24 hours of PDE-5 inhibitors: sildenafil citrate (Viagra) vardenafil (Levitra) tadalafil (Cialis). 100mm/Hg systolic shall be the lower limit for medications that may cause hypotension The target blood pressure for maintaining hypotensive patients shall be 100mm/Hg systolic 180mm/Hg systolic or 110mm/Hg diastolic (with associated symptoms) shall be the hypertensive limits for consideration of treatment When administering nitrates. Physician consult should be obtained in the presence of suspected right ventricular infarct prior to continued administration of nitrates or morphine sulfate For other drugs. is contraindicated.. A Paramedic should attend all pediatric patients five (5) years or younger during transport.. These patients may be sensitive to nitrates. systolic blood pressure above 160mm/Hg or with a hypertensive or cardiac history Labetalol should be administered with caution to patients with heart rates less than 100 BPM Labetalol should be administered with caution to patients on Lasix When administering magnesium sulfate closely monitor the respiratory rate. All fluid boluses should be in 250cc increments allowing intervals for vital sign and lung sounds assessment Fluid hydration rates shall be 250cc/hr IV 0. use caution when administering to patients with wide QRS. Monitor blood pressures when. pulse above 120 BPM. A child restraint seat should be used when appropriate Fluids. Pediatrics.. short p–r interval or presence of a delta wave Albuterol (Proventil.5 mg may be given diluted in 3 cc saline nebulized in– line via ETT with BVM SLCFD paramedics must accompany all transported patients to hospital.. Other forms of nitroglycerine shall be discontinued when IV nitroglycerine is initiated Remove all forms of patient’s own nitroglycerine prior to treatment with nitroglycerine Concurrent use of PDE-5 inhibitors with nitrates.. Epinephrine should be administered with caution to patients over 60 years of age. in patients with right ventricular infarct.9% NaCl 250 cc/hr 62 gtts/min with 15 gtt set IV 0..EMERGENCY MEDICAL GUIDELINES GENERAL TREATMENT PRECAUTIONS Medical The following statements apply throughout the treatment guidelines If your agency does not utilize a specific treatment you are not responsible for its application..48 hours Administration of nitrates should be done with extreme caution.... if at all. blood pressure and reflexes Calcium channel blockers are contraindicated with history of Wolf Parkinson White syndrome. Ventolin) 2. either episodic or continuous. BLS Vitalize/Prioritize Oxygen/Airway ALS EKG monitor IV 0.5 mg IV (Max 25 mg.5mg IV PHYSICIAN CONSULT Nasogastric tube if indicated (prolonged transport time. BLS Vitalize/Prioritize Oxygen/Airway Identify the cause of the reaction.9% NaCl or LR KVO Nausea/Vomiting Promethazine (Phenergan) 6.9% NaCl infused over 15 minutes (50 gtts/ min 15gtt set) Methylprednisolone (Solu–Medrol) 125 mg IVP or dexamethasone (Decadron) 4mg IVP MCFR mixes Tagamet 300 mg in 100cc 0. pulse rate above 120.5mg or Dolasetron Mesylate (Anzemet) 0. and hemoptysis) Dilute Phenergan in 10cc NaCl before IV administration.25mg/kg IV not to exceed 12. Medical Pediatric Nausea/Vomiting Promethazine (Phenergan) 0. or hypertensive or cardiac history.9% NaCl run over 15 minutes. stinger from bee) Assist patient with personal EpiPen and/or personal albuterol inhaler PRN ALS EKG monitor IV 0. Rapid infusion of cimetidine (Tagamet) may cause hypotension and cardiac dysrhythmias. Ped 0. Epinephrine and albuterol should be administered 2 to 3 minutes apart. (100 gtts/min with a 15 gtt set) M-3 10/7/2009 .35mg/kg not to exceed 12. Remove source if possible (i.12.25 . systolic blood pressure above 160 mm Hg. Mild Reaction (itching and hives) Diphenhydramine (Benadryl) 25 mg IVP Cimetidine (Tagamet) 300 mg / 50 cc IV 0.e. distention.1mg/ kg over 30 seconds in place ofor Anzemet ALLERGIC REACTIONS CAUTION Epinephrine should be administered with caution to patients > 60 years of age.9% NaCl KVO Large bore IVs wide open for severe reactions until systolic BP of 100 mm Hg is maintained.TREATMENT GUIDELINES Medical ABDOMINAL PAIN CAUTION! Limit the use of phenergan in pediatrics with prolonged vomiting of unknown etiology. GI bleed.) or Dolasetron Mesylate (Anzemet) 12.5mg for children 2-16 years MCFR uses Ondansetron (Zofran) 4mg IV /IM over 30 seconds. Atrovent is CONTRAINDICATED in allergic reactions to peanut and soy products. Severe Reaction (Hypotension.e. titrate to resp. refer to SEDATION GUIDELINE (SEE PAGE M-13) M-4 10/7/2009 .2mg/kg to maximum dose 4mg Epinephrine 1:1. MCFR mixes Tagamet 300 mg in 100cc 0.0 mg Chemical sedation of the violent patient.1 mg/kg second dose (if needed) maximum cumulative dose of 2.000 0. Methylprednisolone (Solu–Medrol) 125 mg IVP or dexamethasone (Decadron) 4mg IVP SLCFD does not administer Tagament IM.5mg via mini–nebulizer or via diluted in 3 cc saline nebulized in–line via ETT with BVM .9% NaCl run over 15 minutes. diabetic. Ventolin) 2.repeat as needed Methylprednisolone (Solu–Medrol) 125 mg IVP or dexamethasone (Decadron) 4mg IVP Cimetidine (Tagamet) 300 mg / 50 cc IV 0. Alternate extremities Diphenhydramine (Benadryl) 50mg IVP CARDIAC ARREST IMMINENT epinephrine 1:10. and Solu–Medrol ETT with a BVM . refer to SEDATION GUIDELINE (SEE PAGE M-13) Physical restraint of the violent patient.9% NaCl KVO Blood glucose level >300 or <60 (<50 in newborn) refer to DIABETIC TREATMENT GUIDELINE (see page M6) Thiamine 100 mg IVP if alcohol abuse is suspected Naloxone (Narcan) 0. stroke. chest tightness. overdose.3 mg SQ repeated q 20 minutes to total of (3) doses.000 0. i.01 mg/kg initial dose then 0.3 mg ALTERED LEVEL OF CONSCIOUSNESS BLS Vitalize/Prioritize Oxygen/Airway Protect from injury / Restrain PRN Attempt to identify cause (i.000 0. anaphylatic shock) IV 0.000 0.3 mg SQ repeated q 20 minutes to total of (3) doses.9% NaCl infused over 15 minutes (refer to Drip Chart) Epinephrine 2–10μg/min or dopamine drip 5–10 μg/kg/min titrated to systolic BP of 100 mm/Hg Medical PEDIATRIC MCFR mixes Tagamet 300 mg in 100cc 0.5mg via mini–nebulizer or via Tagamet. (100 gtts/min with a 15 gtt set) Albuterol (Proventil.5 mg and Atrovent 0.9% NaCl infused over 15 minutes (50 gtts/ min 15 gtt set) Epinephrine 1:1. or edema) Albuterol (Proventil.e.25 mg/3 cc Diphenhydramine (Benadryl) 1 mg/kg Cimetidine (Tagamet) contraindicated under 16 years of age Methylprednisolone (Solu–Medrol) 2 mg/kg maximum dose 125 mg or dexamethasone (Decadron) 0.EMERGENCY MEDICAL GUIDELINES IM injection of Benadryl. wheezing. Alternate extremities. rate of 12 (Max 10 mg) Chemical sedation of the violent patient.000) May be given ETT if no IV access Albuterol (Proventil.01 mg/kg SQ (0. refer to PROCEDURAL GUIDELINE (SEE PAGE P-70) PEDIATRIC Apply appropriate pediatric immobilization device Naloxone (Narcan) 0. Ventolin) 2. Moderate Reaction (dyspnea.4–2 mg slow IVP or nasally. head injury.9% NaCl run over 15 minutes. Ventolin) 1.01 cc/kg) maximum single dose 0.5 mg and Atrovent 0.4mg to maintain airway.repeat as needed are appropriate when IV Diphenhydramine (Benadryl) 50 mg IVP access is unobtainable.3 mg IVP (instead of SQ 1:1. (100 gtts/min with a 15 gtt set) Cimetidine (Tagamet) 300 mg / 50 cc IV 0.9% NaCl fluid bolus as needed Epinephrine 1:1. and seizures) ALS Only administer Narcan in increments of 0. EKG monitor IV 0. refer to CHF/PE GUIDELINE (see page C-5) Intubate if no improvement or marked respiratory distress. BLS Vitalize/Prioritize Oxygen/Airway Assist patient with personal auto–inhaler ALS EKG Monitor IV 0. Abort continuous nebulized treatment if any of these signs are observed.5 mg.01 mg/kg (0. administer via mini–nebulizer May repeat Proventil after 10 minutes (Do not repeat Atrovent) Continuous nebulized albuterol treatment may be appropriate in severe distress Assess for secondary signs of cardiac failure: edema.9% NaCl 250 cc/hr (62 gtts/min with 15 gtt set) infusion Mix ipratropium (Atrovent) 0. or hypertension or cardiac history.5 mg with albuterol (Proventil) 2. PEDIATRIC 12 years of age and younger IV 0.3 mg SQ Repeat epinephrine 1:1000 0.9% NaCl KVO or saline lock (if stable) Mix ipratropium (Atrovent) 0. rales.2mg/kg maximum dose of 4mg CHRONIC OBSTRUCTIVE PULMONARY DISEASE CAUTION Continuous nebulized albuterol should be aborted in patients who are: > 60 years of age.9% NaCl over 3 minutes.25 mg via mini–nebulizer Methylprednisolone (Solu–Medrol) 2 mg/kg maximum dose of 125 mg IVP or dexamethasone (Decadron) 0.5 mg with albuterol (Proventil) 2.TREATMENT GUIDELINES ASTHMA CAUTION Epinephrine and albuterol should be administered with caution to patients over 60 years of age.9% NaCl or LR 2 cc/kg bolus Epinephrine 1:1. pulse above 120 BPM. Methylprednisolone (Solu–Medrol) 125 mg IVP over 2–3 minutes or dexamethsone (Decadron) 4mg IVP Epinephrine 1:1000 0. jugular vein distention. or with hypertension or cardiac history. up to 4-6 gm if severe distress Endotracheal albuterol (Proventil) and Atrovent if poor compliance with bag valve device (dilute albuterol and Atrovent in 3 cc of saline and inject into ETT or in– line nebulizer via ETT) Medical MCFR administers Magnesium Sulfate as 2 grams in 100cc over 10 min. systolic blood pressure above 160mm/Hg.000 0. and frothy sputum. BLS Vitalize/Prioritize Oxygen/Airway Low flow (2–4 LPM) to maintain SaO2 of 95% or higher concentrations until improved ALS EKG Monitor IV 0.01 cc/kg) SQ Albuterol (Proventil) 1. refer to RSI TREATMENT GUIDELINE (see page M-11) 10/7/2009 M-5 . systolic blood pressure above 160mm/Hg. pulse rates above 120 BPM.3 mg SQ 20 minutes after first dose in opposite extremity Magnesium Sulfate 2gm/10cc 0.5 mg and administer via mini–nebulizer May repeat Proventil after 10 minutes (Do not repeat Atrovent) Continuous nebulized albuterol treatment may be appropriate in severe distress. If BGL is less than 60 in pregnancy and/or stroke.9% NaCl Age: 1 month to 8 years Dextrose 25% 0. if blood pressure is less than 100mm systolic Thiamine 100 mg IVP or IM if alcohol abuse is suspected Dextrose 50% 25 gm IVP if blood glucose level is less than 60 mg/dl Repeat blood glucose within 15 minutes Repeat Dextrose 50% 25 gm IVP PRN Glucagon 1 mg IM or intranasally if no IV access Pediatric Age: birth to 1 month Dextrose 12.9% NaCl Age: 8 years and older Dextrose 50% 0.5 mg IM for children less than 20kg 1.0 mg IM for children more than 20kg M-6 10/7/2009 . BLS Medical Vitalize/Prioritize Oxygen/Airway Obtain blood glucose reading Assist with the administration of oral glucose when consciousness permits ALS EKG Monitor IV 0.9% NaCl KVO 250 cc/hr (62 gtts/min with 15 gtt set) infusion if blood glucose level > 300 mg/dl 250cc bolus.25 mg via mini–nebulizer Endotracheal albuterol (Proventil) and Atrovent if poor compliance with bag valve device (dilute albuterol and Atrovent in 3 cc of saline and inject into ETT or in–line nebulizer via ETT) Methylprednisolone (Solu–Medrol) 2 mg/kg over 2–3 minutes maximum dose of 125 mg IVP or dexamethasone (Decadron) 0.5% 0. repeat if necessary.5 cc of D50% and draw 37.5 cc of 0.EMERGENCY MEDICAL GUIDELINES Endotracheal albuterol (Proventil) and Atrovent if poor compliance with bag valve device (dilute albuterol and Atrovent in 3 cc of saline and inject into ETT or in–line nebulizer via ETT) Methylprednisolone (Solu–Medrol) 125 mg IVP over 2–3 minutes or dexamethasone (Decadron) 4mg IVP PEDIATRIC Albuterol (Proventil) 1. a physician consult should be obtained.5gm/kg Glucagon 0.5 gm/kg IVP slow Expel 25 cc of D50% and draw 25 cc of 0.2mg/kg maximum dose of 4mg DIABETIC EMERGENCIES CAUTION A physician consult should be obtained regarding treatment of low blood glucose levels Rescue Lieutenants and Flig associated with pregnancy and stroke.5 gm/kg IVP slow Expel 37. Patients who maintain a chronic hypertensive status may require a higher than normal systolic blood pressure to maintain cerebral perfusion. doubling each sequential dose until a BP of 140/90 or max of 300mg Discontinue all Nitrates prior to administering Labetalol. bronchial asthma. access dialysis port if applicable (critical pt’s only) Cautious incremental boluses of NaCl up to 250 cc. refer to DIABETIC EMERGENCIES TREATMENT GUIDELINE (SEE PAGE M-6) ACLS guideline Sodium Bicarbonate should be considered early in cardiac arrest Calcium Chloride 10% 10 cc IVP if ventricular tachycardia. This should be considered when administering treatment to lower blood pressure. or Greater than 110mm/Hg diastolic Nitroglycerin IV Initiate at 5-10μg/min IV infusion pump or dial-a-flow Increase 5-10μg/min q 5 minutes until desired response Labetalol (Trandate) 0. heart block (2nd and 3rd degree). epistaxis. visual disturbances. CHF. Medical BLS Vitalize/Prioritize Oxygen/Airway Confirm with two(2) sets of vital signs (right & left) Place the patient supine during drug administration Obtain additional blood pressures immediately prior to and at 5 and 10 minutes after drug administration ALS EKG monitor IV 0. reassess vital signs and lung sounds Blood glucose level. M-7 10/7/2009 . cardiogenic shock.TREATMENT GUIDELINES DIALYSIS PROBLEMS BLS Vitalize/Prioritize Oxygen/Airway ALS EKG Monitor IV 0. repeat as necessary if patient is in frank shock immediately post dialysis. Labetalol (Trandate) will decrease heart rate and should be used with extreme caution in patients with heart rates less than 100 BPM. ectopy or fibrillation are non–responsive to appropriate ACLS treatment (after lidocaine and/or sodium Flight Medics may administer bicarbonate) MCFR uses Amiodarone as the prefered antiarrhymic HYPERTENSION CAUTION Labetalol (Trandate) is contraindicated in acute coronary syndrome. sinus bradycardia.9% NaCl KVO or saline lock (if stable) Symptomatic (headache. Other forms of nitroglycerin should be discontinued when IV Nitro is initiated. nausea/vomiting) and blood pressure: Greater than 180mm/Hg systolic. and COPD when these conditions are acute.25 mg/kg IVP over 2 minutes (300 mg max dose) Target blood pressure (160/90) Repeat Labetalol after 10 minutes if BP remains > 180/110 IRSDPS uses Labetalol 20mg q10min.9% NaCl KVO or saline lock (if stable) If IV access is unobtainable. MCFR requires IV Nitro to be place on an IV pump only. Patients should be in supine position during and after the administration of Labetalol. 4mg Spray SL 1 inch of paste (may be administered concurrently with SL nitro) PEDIATRIC The safety of labetalol has not been established in children.25 . M-8 EKG Monitor IV 0.5mg IVP 10/7/2009 . refer to CHF/PE TREATMENT GUIDELINE (see page C-5) Chest Pain / Suspected Myocardial Infarction. refer to CHEST PAIN TREATMENT GUIDELINE (see page C-4) If fever is present and altered LOC. (48 hours for Cialis) Nitroglycerin 1 (one) 1/150gr SL Tab or 0. administer Children’s Acetaminophen Liquid 10mg/kg PO If altered LOC. Nitroglycerin is not indicated for use in children MEDICAL SHOCK SYNDROMES CARDIOGENIC SHOCK HYPOVOLEMIC SHOCK (MEDICALLY INDUCED) SEPTIC SHOCK BLS Vitalize/Prioritize Oxygen/Airway Trendelenberg positioning as tolerated by patient Body Temperature Medical ALS EKG Monitor IV 0.12.1mg/kg over 30 seconds in place of Phenergan or Anzemet NAUSEA / VOMITING Caution The use of Promethazine (Phenergan) should be used with caution in patients that are hypotensive BLS Vitalize/Prioritize Oxygen/Airway ALS Dilute Phenergan in 10cc NaCl before IV administration.9% NaCl Hypotensive (BP less than 100mm/Hg systolic) 250 cc bolus repeated as necessary to maintain systolic BP 100mmHg Dopamine 5–20 μg/kg/min titrated to effect Congestive Heart Failure / Pulmonary Edema.EMERGENCY MEDICAL GUIDELINES Hypertensive patients listed under “Caution” should receive nitroglycerin Nitroglycerin contraindicated if within 24 hours of sexual enhancing medication use. administer Acetaminophen Suppository 125mg MCFR uses Ondansetron (Zofran) 4mg IV/IM over 30 seconds Ped 0. administer Acetaminophen Suppository 325mg rectally MCFR does not carry Acetaminophen suppository PEDIATRIC Fluid bolus of 20 cc/kg repeated as necessary to maintain blood pressure Dopamine 2–20 μg/kg/min titrated to effect If fever is present.9% NaCl KVO Promethazine (Phenergan) 6.5 mg IV or Dolasetron Mesylate (Anzemet)12. GI bleed. apply trauma dressing to vaginal area PHYSICIAN CONSULT Post–Partum hemorrhage (post placenta delivery) Oxytocin (Pitocin) 20units/1000 cc 0.1mg/kg IV Nasogastric tube (prolonged transport time. Physician Consult for repeat Dolasetron Mesylate (Anzemet) Nasogastric tube (prolonged transport time.9% NaCl KVO large bore SEIZURES OR COMA (ECLAMPTIC) Magnesium Sulfate loading dose of 4 gm/100cc (piggyback) wide open Magnesium Sulfate drip 2gm/100cc at 100cc/hr (25 gtts/min with 15 gtt set) Utilize a Burette.1 mg IVP or nasally may repeat twice q5 minutes 10/7/2009 M-9 .9% NaCl over 15 minutes Magnesium Sulfate maintenance dose 2 gm/100cc at 100 cc/hr Seizures unresolved by magnesium sulfate (Eclamptic) Diazepam (Valium) 3-5 mg IV over 2 minutes May repeat to a total of 10 mg or Lorazepam (Ativan) 0. and hematemesis) IRCEMS gives Phenergan without consult. transport the patient in the left lateral recumbant position If perineal inspection reveals abnormal presentation (i.e. apply gentle perineal pressure Observe for meconium staining.TREATMENT GUIDELINES repeat Promethazine (Phenergan) to max 25mg IV if vomiting continues. place the patient in the knee-chest or left lateral recumbant position with immediate transport Delivery Slow. and hematemesis) over 30 seconds in place of Phenergan or Anzemet OBSTETRICS/GYNECOLOGY BLS Vitalize/Prioritize Oxygen/Airway (100% high flow for mother. buttocks.25 mg/kg IV not to exceed 12. hand or face).9% NaCl infused at 120–150 cc/hr (30 gtts/ min with 15gtt set) if extended transport time and/or distance Hypertensive disorder of pregnancy (Pre–eclamptic) using a burette or Volu–trol drip set: Magnesium Sulfate loading dose 4 gm/100cc IV 0. controlled delivery of the head. PEDIATRIC – PHYSICIAN CONSULT MCFR uses Ondansetron Promethazine (Phenergan) 0. Volu–trol administration set. blow by for neonate) Obtain BGL from mother Positioning If delivery is not in progress. foot. distention.5 . or IV pump SLCFD administers Mag. if present. GI bleed. stimulate and maintain body temperature Post–Partum Check APGAR at 1 and 5 minutes (Appendix D) Assess for post–partum hemorrhage Medical ALS EKG Monitor IV 0. vigorously suction oral pharynx during delivery and immediately after (intubation may be required) Double clamp cord 10–12 inches from abdomen Dry. FIRST/SECOND TRIMESTER BLEEDING Apply maternity or 5x9 pad to vaginal area If hypovolemic establish two large bore IV’s wide open using trauma tubing and pressure infusers to maintain systolic blood pressure of 100mm/Hg Post–Partum bleeding. Sulfate in Eclampsia 4gm diluted IVP over 3 minutes.35mg/kg IVP to max of 12.5mg seconds Ped 0. distention.5 mg or Dolasetron Mesylate (Zofran) 4mg IV/IM over 30 (Anzemet) 0. Dilute Phenergan in 10cc NaCl before IV administration.9% NaCl KVO or saline lock if stable Nitrous oxide for minor musculoskeletal pain May use either of the following medications: Dilaudid (hydromorphone hypochloride) 1-2mg slow IV or IM titrated to effect •may repeat to a total of 4mg •In elderly (65 years or older) 0.in patients 16 years old and older. head injury.1-0.1mg/kg in place of Phenergan or Anzemet MCFR Rescue Lieutenants and Flight Medics may administer Fentanyl 25-50 mcg IVP every 5 min.2mg/kg IVP.EMERGENCY MEDICAL GUIDELINES PAIN MANAGEMENT Caution Pain medications may produce respiratory depression Pain medications are not to be used in the presence of abdominal pain. SLCFD. IRSDPS & IRCEMS can use Nubain for pain management with the same dosage as Morphine.5mg IVP Medical MCFR first line drug for pain management is Dilaudid unless contraindicated.25 . myocardial infarction.2mg/kg IV or IM slowly Dilaudid’s safety and effectiveness in children has not been established 10/7/2009 .5mg IV or Dolasetron Mesylate (Anzemet) 12. fractures.25 .0. Ped 0. kidney stones. and burns BLS Vitalize/Prioritize Oxygen/Airway Monitor patient’s level of consciousness and respiratory status ALS EKG monitor IV 0. M . dislocations.5mg slow IV or IM titrated to effect •may repeat as tolerated Morphine or Nubain 1-5mg IV or IM titrated to effect •may repeat in small increments until desired effect is achieved Promethazine (Phenergan) (to be given with the selected pain medication) 6. MCFR uses Ondansetron (Zofran) 4mg IV/IM over 30 seconds.0. Patients under the age of 16 years old use Morphine 0.12.1 . or altered LOC Indications: Relief of moderate to severe pain associated with trauma.10 Pediatrics Morphine 0. TREATMENT GUIDELINES RAPID SEQUENCE INTUBATION This procedure is for patients requiring total airway control who may be fully or partially conscious. etc.11 . 0. Dolasetron Mesylate (Anzemet) 12.1mg minimum dose) Adults 1mg IVP • If bradycardia present or potential • MUST be given before any repeat doses of Anectine Lidocaine 1.5mg/kg Do not use if administering Etomidate Hydromorphone (Dilaudid) for pain control. Pre-oxygenation is REQUIRED for a minimum of 2 minutes before proceeding with paralysis.5mg IV titrated to effect • may repeat as tolerated Promethazine (Phenergan) or Dolasetron Mesylate (Anzemet) to be given with Dilaudid Adults: 6.. surgical airway.) MCFR requires a Rescue Lt. therefore it does not reduce pain Pre-medication Procedure O2 100% via mask or BVM. Two (2) paramedics must be in attendance with the patient before RSI can be performed and must accompany the patient to the hospital SLCFD requires a paramedic Lt. They need not IMPORTANT accompany patient to the A secondary airway device must be ready to use if endotracheal intubation cannot be ER. if needed 1-2mg IV titrated to effect • may repeat to a total of 4mg In elderly (65 yrs and older). or a Flight Medic to be present.5mg IV..5mg/kg not to exceed 6. Indications or Flight Medic presence Seizure/ convulsion disorder and accompaniment with Multi-system trauma patient to ER Head injury When other methods of airway control or treatments have failed or are either not possible or practical Contraindications It must be kept in mind that all contraindications are relative and risk must be weighed against possible benefits Digitalis toxicity Increased intracranial pressure Increased intraoccular pressure Known electrolyte imbalance Skeletal muscle myopathy Acute malignant hyperthermia MCFR uses a different Guideline for RSI.35mg/kg 10/7/2009 M .25-12.02mg/kg (0. The purpose is to cause a nitrogen washout in the lungs and create an oxygen reservoir. Refer to pages M 16 & 17 Medical Caution It is important to remember that neuromuscular blockade does not alter the patient’s level of consciousness.e.5mg IV Pediatrics: 0.0.25mg .25mg IM or Dolasetron Mesylate (Anzemet) 0. successfully performed (i. Atropine Pediatrics 16 years of age or less 0. LMA. This oxygen reservoir will allow approximately 3 to 4 minutes of apnea without hypoxemia in a normal patient. Combitube. 1mg/kg IV Onset in 2-4 minutes Duration of 20-40 minutes Side effects: hyperthermia Medical M .3mg/kg • Allow adequate time to assess the effectiveness of sedation SLCFD does not administer Etomidate under the age of 10yrs. peaked “T” waves • Constant monitoring of EKG • Administer calcium chloride 500mg slow IV Increased intracranial pressure Increased intraoccular pressure Sudden cardiac arrest in children with Duchenne’s muscular dystrophy (children usually undiagnosed) • Observe for peaked “T” waves • Administer calcium chloride 500mg IV • Administer sodium bicarbonate 1mEq/kg • Administer glucose per DIABETIC EMERGENCIES GUIDELINE (see page M-6) Vercuronium Bromide (Norcuron): indicated if transport time is > 15 minutes. PARALYTICS Procedure Succinycholine Chloride (Anectine) may be repeated in 2 minutes for desired effect Adult: 1. or the patient is still combative after sedation Adult and pediatric: 0.12 10/7/2009 .5mg/kg IV Pediatric and Infants: 2mg/kg IV Onset <1 minute Duration of approximately 4-6 minutes Caution Hyperthermia: presents as jaw spasm or general rigidity •Monitor body temperature •Cool as needed Hyperkalemia: presents as tall.5mg IV or IM titrated to effect.EMERGENCY MEDICAL GUIDELINES Etomidate (Amidate) 0.3mg/kg may repeat x1 If allowed may administer 20mg non-weight based Lidocaine is not used with Etomidate If Etomidate is contraindicated or unavailable Midazolam (Versed) • Adults over the age of 60yrs: 2. may repeat to a total of 5mg • Adults under the age of 60yrs: 5mg IV or IM titrated to effect may repeat to a total of 10mg • Pediatric dose: 0. patient becomes combative after the effects of the Anectine have worn off. Due to the short half life of Etomidate (6 min or less) administration must be carefully coordinated with the actual patient removal. of 4 mg Medical 0. Reassess every 5 minutes M-18 if a Rescue Consider further sedation or paralytic agent (see page M-12 for dosages) Lieutenant or Flight Medic Evaluate the need for effective neurological exam versus paralytic agent.6mg/kg IV / IM or nasally Lorazepam (Ativan) 0.5mg IV. OR refer to Guideline page MEtomidate (Amidate) 0. IM (if over 60yrs). Pediatric Diazepam (Valium) 0. Consider PAIN MANAGMENT GUIDELINE (see page M-10) • Look for increased BP.05mg/kg IVP (may repeat x1) during extended extrication to aid in ease and safety of extricating combative or uncooperative patients. IM (if over 60yrs). violent patient Caution Diazepam (Valium) may cause respiratory depression or compromise. IM (under 60 yrs). tearing.13 . or nasally (Diprivan) for sedation. Midazolam (Versed) • 2. or nasally • 5mg IV.5mg IV.1mg/kg IV / IM or nasally 10/7/2009 M . of 4 mg For intubation (also see RSI TREATMENT GUIDELINE.TREATMENT GUIDELINES SEDATION Indications Airway management (when RSI is not indicated or available) Cardioversion External pacing Altered level of consciousness.5 mg/kg IV / IM / PR no faster than 3mg/min Midazolam (Versed) 0.3-0. IM (under 60 yrs). or nasally OR Lorazepam (Ativan) 1mg IVP or nasally •may repeat as needed up to a max. page M-11) MCFR Rescue Lieutenants Midazolam (Versed) and Flight Medics may • 2. of 4 mg MCFR refer to Post Post Intubation Intubation Guideline page Re-evaluate the tube placement after movement or transfer of patient. ALS Anesthetic spray to posterior pharynx (for intubation) For combative patient and external pacing Diazepam (Valium) 5mg IV/IM •may repeat once after 5 minutes MCFR refer to Post Intubation Guideline page M-18 OR Lorazepam (Ativan) 1 mg IVP or nasally •may repeat as needed up to a max. evaluate physiological response to pain Etomidate (Amidate) 0. or nasally administer propofol • 5mg IV.2-0.05-0.3mg/kg IV MCFR Rescue Lieutenants OR and Flight Medics may Lorazepam (Ativan) 1 mg IVP or nasally administerEtomidate 0.3mg/kg IV For Cardioversion 17 for dosing.03• May repeat as needed up to a max. is present. refer to DIABETIC EMERGENCIES TREATMENT GUIDELINE (SEE PAGE M-6) prior to administration of diazepam (Valium) or lorazepam (Ativan) Diazepam (Valium) 3–5 mg IV/IM may repeat to a total of 10 mg may be administered rectally if no IV access OR Lorazepam (Ativan) 1mg IV. The Team should utilize appropriate personal protective equipment.1mg/kg IM. or nasally Febrile seizures If altered LOC. IV. Use of PO medications should be avoided in patients with decreased level of consciousness. nasally.EMERGENCY MEDICAL GUIDELINES SEIZURES Caution Refer to OBSTETRICS/GYNECOLOGY TREATMENT GUIDELINE (See Page M-9) for seizures associated with pregnancy Consider etiology of seizure for possible infectious disease isolation.5mg . or rectally may be repeated to a max of 4mg OR Versed 0. administer Acetaminophen suppository 125mg MCFR does not carry Acetaminophen suppository M .14 10/7/2009 . or rectally as first line drug Physician Consult diazepam (Valium) 3–5mg IV for doses greater than 10 mg lorazepam (Ativan) 0.1mg/kg IV or nasally Febrile seizures treat febrile seizures by cooling.5 mg/kg IV or rectal (no faster than 3 mg/min if IV) OR Lorazepam (Ativan) 0.1mg IV for doses greater than 4mg Pediatric Idiopathic (non–febrile) seizures Diazepam (Valium) 0. Use caution not to over cool a febrile patient to the point of shivering.5 mg/kg IV or rectal (no faster than 3 mg/min if IV) or Ativan 0.2-0.9% NaCl KVO Glucose level possible or suspected hypoglycemia.1mg/kg if seizures are continuous children’s Acetaminophen liquid 10 mg/kg PO when level of consciousness permits If altered LOC. administer acetaminophen suppository 325mg Medical MCFR uses Lorazepam (Ativan) 1mg IVP.2-0. Vitalize/Prioritize Oxygen/Airway Protect from injury Consider C-Spine precautions if suspected injury BLS ALS EKG monitor IV 0. (Use caution to avoid rapid temperature change. nasally.) consider Diazepam (Valium) 0. Medical BLS Vitalize/Prioritize Oxygen/Airway (Oxygen as per patient’s need) Evaluate for stroke alert Elevate patient’s head 30 degrees Do not delay transport ALS EKG Monitor IV 0.9% NaCl KVO or saline lock (if stable) Blood glucose level.TREATMENT GUIDELINES SICKLE CELL ANEMIA BLS Vitalize/Prioritize Oxygen/Airway (High flow) Emotional support ALS EKG monitor IV 0. refer to HYPERTENSION TREATMENT GUIDELINE (SEE PAGE M-7) Treat arrhythmias per appropriate Guideline Complete Stroke Alert check sheet If possible airway instability. refer to DIABETIC EMERGENCIES TREATMENT GUIDELINE (SEE PAGE M-6) Hypertension above 180 systolic or 110mm diastolic.35mg/kg IVP to max of 12. refer to PAIN MANAGEMENT TREATMENT GUIDELINE (See page M-10) Dilute Phenergan in 10cc NaCl before IV administration. Ped 0.15 . STROKE Caution All medications given in the presence of a Stroke must be Physician consult. refer to RSI TREATMENT GUIDELINE (see page M-11) MCFR refer to RSI Treatment Guideline page M-16 and M-17 10/7/2009 M .5mg Pain control.1mg/kg over 30 seconds in place of Phenergan or Anzemet Pediatric Promethazine (Phenergan) 0.25 mg/kg IV not to exceed 12. refer to PAIN MANAGEMENT TREATMENT GUIDELINE (See page M-10) MCFR uses Ondansetron (Zofran) 4mg IV/IM over 30 seconds.5 mg or Dolasetron Mesylate (Anzemet) 0.9% NaCl infusion 250 cc/hr Pain control. etc.) Indications Seizure/ convulsion disorder Multi-system trauma Head injury When other methods of airway control or treatments have failed or are either not possible or practical Contraindications Medical It must be kept in mind that all contraindications are relative and risk must be weighed against possible benefits Digitalis toxicity Increased intracranial pressure Increased intraoccular pressure Known electrolyte imbalance Skeletal muscle myopathy Acute malignant hyperthermia Caution Use extreme caution in pregnancy as Caution: opiates and Norcuron will cross the placental barrier. LMA.5mg/kg IVP Fentanyl .0mg IVP MUST Administer prior to second dose of Anectine If bradycardia present or potential Norcuron 0. The purpose is to cause a nitrogen washout in the lungs and create an oxygen reservoir. or Flight Medic presence and accompaniment with patient to ER This procedure is for patients requiring total airway control who may be fully or partially conscious.01mg/kg IVP for defasiculation (withhold in children <10 years old) Etomidate (Amidate) 0. Combitube.MUST be given slowly (Over 60 seconds) Adults < 60 years old 3 mcg/kg IVP Adults > 60 years old 1. This oxygen reservoir will allow approximately 3 to 4 minutes of apnea without hypoxemia in a normal patient.. Pre-oxygenation is REQUIRED for a minimum of 2 minutes before proceeding with paralysis.EMERGENCY MEDICAL GUIDELINES RAPID SEQUENCE INTUBATION (MCFR ONLY) MCFR requires a Rescue Lt.5 mcg/kg IVP Pediatrics 1-2 mcg/kg IVP Atropine All pediatrics < 10 years of age 0. The acronym “LOADS” is used to dictate proper administration L-Lidocaine O-Opioid A-Atropine D-Defasciculation S-Sedation Lidocaine 1.e. surgical airway.16 10/7/2009 .02mg/kg IVP (0..3mg/kg IVP (may be used with pediatrics) M . Two (2) paramedics must be in attendance with the patient before RSI can be performed and must accompany the patient to the hospital IMPORTANT A secondary airway device must be ready to use if endotracheal intubation cannot be successfully performed (i. Pre-medication Procedure O2 100% via mask or BVM.1mg minimum dose) Adults 1. 5mg/kg given as 40mgIVP every 10 secondsuntil desired level of sedation is reached with maximum single not to exceed 120mg (eldery 1-2 mg/kg given as 20mg every 10 seconds).TREATMENT GUIDELINES If Etomidate is contraindicated or unavailable Midazolam (Versed) Adults < the age of 60: 5mg/kg IVP or IM titrated to effect May repeat to a total of 10mg Adults > the age of 60: 2.17 .0mg/kg Caution Hyperthermia: presents as jaw spasm or general rigidity • Monitor body tempature • Cool as needed Hyperkalemia: presents as tall. 10/7/2009 M . Start at 25mcg/kg/min and increase 5-10mcg/kg/min until desired level of sedation is maintained.5mg IVP or IM titrated to effect May repeat to a total of 5mg Pediatric dose: 0. Use with extreme caution in the potentially hypotensive patient. • Observe for peaked “T” waves • Administer Calcium Chloride 500mg IVP • Administer sodium bicarbonate 1mEq/kg IVP • Administer glucose per Diabetic Emergency Guideline (page M-6) Diprivan (if available) may be used for sedation or intubation. The absolute contraindication is systolic BP of less than 100mm/hg.5mg/kg Pediatric 2. Loading dose (adults < 55) 2-2.1mg/kg Allow adequate time to assess the effectiveness PARALYTICS Succinycholine Chloride (Anectine) may repeat in 2 minutes Adult 1. Reassess blood pressure frequently and adjust Diprivan as needed. peaked “T” waves Medical • Constant monitoring of EKG • Administer Calcium Chloride 500mg slow IVP Increase ICP Increase IOP Sudden cardiac arrest in children with Duchenne’s muscular dystrophy. followed by a drip 25-120mcg/kg/min. EMERGENCY MEDICAL GUIDELINES POST INTUBATION MANAGEMENT Administer longer acting sedation for transport prior to Norcuron consideration Versed • Adults 0. This also includes medical patients with pain complaints prior to intubation i.1 mg/kg IVP (adults over 60 years old 0. Patients with traumatic injuries especially warrant re-evaluation for signs of pain.1 mg/kg IVP Assess for signs of pain and ensure systolic BP greater than 100mm/hg Fentanyl . M .1mg/kg IVP if the patient is unmamageable i. fighting the ET Tube and ventilator or becomes combative only after intubation. severe headache with a stroke. May repeat after 10 minutes Medical • Adults 2mcg/kg IVP (over 60 years old 1mcg/kg IVP) • Pediatrics 1-2mcg/kg IVP Vercuronium Bromide (Nurcuron) 0.e.18 10/7/2009 . Baseline neurological assessments must be determined prior to administering sedation and pain medications with the initiation of RSI and reported to the receiving physician accordingly.05 mg/kg IVP) • Pediatrics 0. Pain management is not to be withheld in the intubated head injured or stroke patient where signs of pain exist. sedation and pain management.MUST give slowly (over 60 seconds).e. 000 IVP/IO q 3–5 minutes Atropine 1. possibly helpful intubated and continued long arrest interval return of spontaneous circulation after long arrest interval not indicated. consider termination of resuscitative efforts by a physician.01mg/kg (0.0mg IVP/IO. probably helpful known preexisting bicarbonateresponsive acidosis overdose with tricyclic antidepressants to alkanize urine in overdoses acceptable.000 IV/IO. Vasopressin 40u IV push is first line for MCFR Physician Consult Consider termination of efforts after 10 minutes of treatment with no change Pediatric Refer to Broselow/Pediatric Resuscitation Tape Epinephrine Epinephrine repeated every 3–5 minutes 0.1cc/kg) Epinephrine 1:1. refer to AED GUIDELINE (see page P-30) CPR (5 cycles or aproximately 2 minutes of CPR between interventions) ALS Intubate EKG monitor IV 0.0mg 1:10.000 ET IRCEMS does not use termination guidelines SLCFD considers termination of efforts after 20 minutes of treatment with no change C-1 10/7/2009 . repeated every 3–5 minutes up to a total of 3mg (0.1mg/kg (0.CARDIAC GUIDELINES Cardiac ASYSTOLE Caution Ask and verify DNR Orders (Must see original) or other acceptable form refer to page E-18 for information on DNRO Sodium bicarbonate 1 mEq/kg definitely helpful known preexisting hyperkalemia acceptable. or 0. Consider interval since arrest.04mg/kg) Consider possible causes: 6H 6T Hypovolemia (volume infusion) Hypoxia (ventilation) Hypothermia.0mg IVP the shorter atropine dosing interval (3 min) is possibly helpful in cardiac arrest Cardiac Patient remains in asystole if patient remains in asystole or other agonal rhythm after successful intubation and initial medications and no reversible causes are indentified.9% NaCl Confirm asystole in more than one lead Vasopressin 40u IVP to replace first or second dose of Epi or Epinephrine 1. refer to HYPOTHERMIA TREATMENT GUIDELINE (SEE page T-5) Hydrogen Ion (acidosis) (sodium bicarbonate) Hyper/Hypokalemia (consider calcium chloride or sodium bicarbonate) Hypoglycemia Tamponade (pericardiocentesis) Tension pneumothorax (needle decompression) Thrombosis–Coronary (ACS) Thrombosis–Pulmonary (embolism) Toxins Trauma Calcium Chloride 10mg/kg IVP if patient on calcium channel blocker or history of renal failure Atropine 1.03– 0.1cc/kg) Epinephrine 1:10. may be harmful hypoxic lactic acidosis BLS Consider TERMINATION GUIDELINE ( See page E-43) Vitalize/Prioritize Secure airway with appropriate adjunct Application of AED. 02mg/kg minimum dose 0. trans-cutaneous pacing is recommended.02mg/kg minimum dose 0.03–0.1mg maximum single dose 0.1mg maximum single dose 0. It has been suggested that atropine should be used with caution in atrioventricular (AV) block at the His-Pukinje level (type II AV block and new thirddegree block with wide QRS complexes) (acceptable.04mg/kg.03-0.1cc/kg) epinephrine 1:10.01mg/kg (0.000 IV or IO 0.5mg.2% solution expel 25cc of sodium bicarbonate 8. possibly helpful).9% NaCl BRADYCARDIA Caution Patients with 2nd degree type II or 3rd degree block should recieve TCP as first treatment BLS Serious symptoms chest pain shortness of breath decreased level of consciousness Cardiac Cardiac Serious signs hypotension shock pulmonary congestion congestive heart failure acute myocardial infarction Vitalize/Prioritize Oxygen/Airway Observe closely ALS EKG monitor IV 0.8 yrs) may repeat after 3–5 minutes maximum cumulative dose 0.20 ug/kg/min Transcutaneous pacing profound symptomatic bradycardia refractory to BLS and ALS anterior–posterior position is preferred.04mg/ kg) Transcutaneous pacing pt severely symptomatic or delay in drug administration consider pacing before atropine use discretion for transthoracic versus A/P placement sedation.5mg for a child (1-8 yrs).000 ET Dopamine (Intropin) 5 . 1.0mg for adolescent (8-16 yrs) may repeat after 3–5 minutes maximum cumulative dose 0.03–0. if heart rate <60 with poor perfusion start CPR if Atropine ineffective Atropine 0. repeated as necessary every 3–5 minutes up to a total of 3mg (0. Third-degree heart block never treat third-degree heart block plus ventricular escape beats with lidocaine Pediatric * Give atropine first for bradycardia due to suspected elevated vagal tone or primary AV block.1mg/kg (0. but anterior–anterior is acceptable provided the negative (–) pad is placed near the apex of the heart Epinephrine drip is appropriate with Atropine and TCP if the patient appears to be in a prearrest state C-2 10/7/2009 .9% NaCl Consider transcutaneous pacing Serious signs or symptoms: Atropine 0.04mg/kg Epinephrine repeated every 3–5 minutes 0.04mg/kg Sodium Bicarbonate 1 mEq/kg infant (1 yr) or younger use 4.EMERGENCY MEDICAL GUIDELINES Atropine 0.4% and draw 25cc of 0. Use the shorter dosing interval (3 minutes) in severe clinical conditions. refer to SEDATION TREATMENT GUIDELINE (SEE PAGE M-13) Dopamine (Intropin) 5–20 μg/kg per minute Epinephrine 2–10 μg/min Atropine atropine should be given in repeat dose every 3-5 minutes up to total of 0.5mg for child (1 .03–0.1cc/kg) epinephrine 1:1. go immediately to unsynchronized shocks ALS IV access established per primary Treatment Guideline Premedicate whenever possible. see SEDATION TREATMENT GUIDELINE (See Page M-13) Synchronized cardioversion/Defibrillation See Appendix A for specific Joule Settings.9% NaCl KVO Hypotensive (blood pressure less than 100 mm/Hg systolic) 250cc fluid bolus. refer to CHEST PAIN / MYOCARDIAL INFARCTION (SUSPECTED) (See Page C-4) Cardiac Pediatric Dopamine (Intropin) 5–20 μg/kg per minute CARDIOVERSION / DEFIBRILLATION BLS Vitalize/Prioritize Oxygen/Airway Check oxygen saturation Ready suction device Delays in synchronization if delays in synchronization occur or clinical conditions are critical. refer to CONGESTIVE HEART FAILURE/ PULMONARY EDEMA (See Page C-5) Chest pain / suspected myocardial infarction. III.000cc frequently check blood pressure and lung sounds Congestive heart failure / pulmonary edema.CARDIAC GUIDELINES CARDIOGENIC SHOCK BLS Vitalize/Prioritize Oxygen/Airway Trendelenburg position ALS EKG monitor 12 Lead EKG V4R should be manually evaluated if any ST elevation in leads II. repeat as necessary. or aVF IV 0. to maintain systolic of 100 mm/Hg contraindicated if lung sounds indicate pulmonary edema Dopamine (Intropin) 5–20 μg/kg per minute titrated to BP of 100mm/Hg systolic Evidence of right ventricular infarct (ST elevation in lead V4R) treat hypotension with cautious fluid bolus up to 2. 10/7/2009 C-3 . 5mg slow IVP titrated to effect. head trauma. Other forms of nitroglycerine should be discontinued when IV Nitro is initiated BLS Vitalize/Prioritize Oxygen/Airway ALS EKG monitor 12 Lead EKG V4R should be manually evaluated if any ST elevation in leads II.0.5mg IVP Dilaudid (hydromorphone hypochloride) 1-2mg slow IVP titrated to effect may repeat to a total of 4mg. MCFR drug of choice for pain relief is Dilaudid unless contraindicated MCFR uses Ondansetron (Zofran) 4mg IV/IM over 30 seconds. refer to VENTRICULAR ECTOPY TREATMENT GUIDELINE (See Page C-8) ACLS guideline Cardiac Cardiac Cardiac MCFR does not use double IV catheters.9% NaCl KVO double lumen IV catheter is preferred for the MI patient Hypotensive (blood pressure less than 100 mm systolic). dose 10 mg and Promethazine (Phenergan) 12. bleeding ulcers. or aVF Evaluate for Cardiac Alert IV 0.e. may repeat as tolerated Promethazine (Phenergan) 12. surgical procedure.4mg spray SL (may administer 1 SL prior to 12 lead or IV access) may repeat at five minute intervals to a total of three (3) 1 inch paste (may be administered concurrently with SL nitroglycerine) 5–10 μg/min IV infusion pump. stroke. gastrointestinal bleeding. These patients may be sensitive to nitrates. Two (2) separate IV lines must be established Cardiac Enzyme Field Test Kit used by SFR Dilute Phenergan in 10cc before IV administration. III. draw green top tube Nitroglycerine (contraindicated if sexual enhancing medications were taken within past 24 hours [i.5 mg IVP or Dolasetron Mesylate (Anzemet) 12. increased 5–10 μg/min every 3–5 minutes until pain is relieved or 100 mmHg systolic blood pressure is maintained if either of the following two conditions exist: ST elevation in any two contiguous leads of 12 lead ECG (it is not necessary to administer 3 SL nitro prior to initiating IV nitro). Levitra. or pain partially but not completely relieved by 3 nitroglycerine SL Aspirin 324–325mg chewable (4 pediatric chewable aspirin) Pain relief (one of the following) Morphine Sulfate in 2 mg increments IVP until desired effect max. Viagra] and within 48 hours for Cialis) contraindicated if blood pressure less than 100 mmHg systolic 1/150gr or 0.1mg/kg over 30 seconds in place of Phenergan or Anzemet C-4 10/7/2009 . In elderly (65 years and older) 0.5mg IVP Ventricular ectopy. Ped 0.5mg IVP or Dolasetron Mesylate (Anzemet) 12.EMERGENCY MEDICAL GUIDELINES CHEST PAIN / MYOCARDIAL INFARCTION(SUSPECTED) Contraindications Aspirin or aspirin based products are contraindicated in children 16 years of age or younger due to Reye’s syndrome allergy Heparin is contraindicated if recent bleeding.25 . transient ischemic attack (TIA) or history of bleeding tendencies Caution Physician consult should be obtained in the presence of suspected right ventricular infarct prior to continued administration of nitrates or morphine. refer to CARDIOGENIC SHOCK TREATMENT GUIDELINE (See Page C-3) Perform cardiac enzymes using Field Test Kit. administer IV nitroglycerine as soon as possible 1/150 gr SL may administer 1 SL prior to 12 lead or IV access may repeat after five minutes to a total of three (3) 1 inch paste (may be administered concurrently with SL nitroglycerine) Nitroglycerine 5-10 μg/min IV Infusion Pump increase 5-10 μg/min every 3–5 minutes maintain at least 100 mmHg systolic blood pressure Furosemide (Lasix) 0. Physician consult should be obtained in the presence of suspected right ventricular infarct prior to continued administration of nitrates or morphine. dose 10 mg and Promethazine (Phenergan) 12.e.5–1.1–0. Cardiac BLS Vitalize/Prioritize Oxygen/Airway (high flow) Body temperature ALS EKG monitor 12 Lead EKG V4R should be manually evaluated if any ST elevation in leads II. III. consider respiratory distress etiology of infection (pneumonia) rather than CHF Administration of nitrates should be done with caution in patients with right ventricular infarct. maximum single dose 4mg 10/7/2009 .1mg/kg over 30 seconds in plave of Phenergan or Anzemet C-5 Pediatric Furosemide (Lasix) 1. consult EDP before administering furosemide or nitroglycerine.000 units) IV in suspected acute MI draw blue top blood tube for prothrombin time and partial thromboplastin time (PT.5mg IVP contraindicated if blood pressure less than 100 mmHg systolic IRCEMS uses up to 100mg of Lasix Dilute Phenergan in 10cc before IV administration.0mg/kg IVP not to exceed 80mg Dopamine (Intropin) 5–20 μg/kg per minute titrated as needed for hypotension Morphine Sulfate in 2 mg increments IVP until desired effect max. MCFR uses Ondansetron (Zofran) 4mg IVP/IM over 30 seconds.CARDIAC GUIDELINES Physician Consult Nitroglycerine IV if pain unaffected by 3 nitroglycerine SL contraindicated if blood pressure less than 100 mmHg systolic initiate at 5–10 μg/min IV Infusion Pump increase 5–10 μg/min every 3–5 minutes until pain is relieved or 100 mmHg systolic blood pressure is maintained Heparin 60 units/kg (max. PTT) prior to administration of Heparin IRCEMS does not need orders for Ntg Drip MCFR does not carry Heparin CONGESTIVE HEART FAILURE/PULMONARY EDEMA Caution If patient is febrile. Levitra.5 mg IVP or Dolasetron Mesylate (Anzemet) 12. or aVF Consider using CPAP early Intubate if marked (extraordinarily severe) respiratory distress sedation for conscious patients. Viagra] and within 48 hours for Cialis) contraindicated if blood pressure less than 100 mm systolic moderate to severe distress.2mg/kg IVP slowly.9% NaCl KVO Nitroglycerine (Contraindicated if sexual enhancing medications were taken within past 24 hours [i. These patients may be sensitive to nitrates. refer to RSI TREATMENT GUIDELINE (See Page M-11) IV 0.0mg/kg IVP slowly over 1–2 minutes Morphine Sulfate 0.4. Ped 0. 35mg/kg IVP over 2 minutes. The max first dose is 25 mg with a max second dose of 35 mg. consider synchronized cardioversion if rhythm does not convert and / or patient becomes unstable Irregular Rhythm (A-Fib. over 5 minutes.) after 1–2 minutes. MAT {multifocal atrial tachycardia}) > 130 symptomatic Diltiazem (Cardizem) 0.1 mg/kg IVP rapid push maximum single dose 6 mg second dose 0. low blood pressure. EKG monitor 12 Lead EKG V4R should be manually evaluated if any ST elevation in leads II.9% NaCl KVO Unstable. MCFR administers Cardizem by IV infusion only. shortness of breath.25mg/kg IV over 2 minutes may repeat. if necessary. followed by a rapid fluid bolus. congestive heart failure. Lifeline uses Verapamil 2nd line.2 mg/kg IVP rapid push maximum single dose 12 mg third dose 0. shock.35mg/kg IVP over 2 minutes. A-Flutter. pulmonary congestion. with serious signs or symptoms ventricular rate greater than 150 beats per minute may give brief trial of medications (see STABLE OR BORDERLINE below) refer to CARDIOVERSION TREATMENT GUIDELINE (See Page C-3) immediate cardioversion seldom needed for rates less than 150 beats per minute (see SERIOUS SIGNS OR SYMPTOMS at left) Regular Rhythm further treatment not recommended if patient stable vagal maneuvers Adenosine Phosphate (Adenocard) 6mg IVP over 1–3 seconds (As rapid as possible in the most proximal IV port. decreased level of consciousness. if necessary.EMERGENCY MEDICAL GUIDELINES NARROW COMPLEX TACHYCARDIA BLS Vitalize/Prioritize Oxygen/Airway ALS Serious signs or symptoms chest pain. acute myocardial infarction unstable condition must be related to the tachycardia Vagal maneuvers carotid sinus pressure is contraindicated in patients with carotid bruits avoid ice water immersion in patients with ischemic heart disease IRCEMS uses Adenocard 12mg for each dose. or aVF IV 0. 15 minutes after first dose. 15 minutes after first dose. may repeat once Diltiazem (Cardizem) 0. 0.25mg/kg IV over 2 minutes may repeat. 12mg IVP over 1–3 seconds. 0.2 mg/kg IVP rapid push maximum single dose 12 mg C-6 10/7/2009 . III. synchronized cardioversion if rhythm does not convert Wide QRS complex refer to WIDE–COMPLEX TACHYCARDIA TREATMENT GUIDELINE (See Page C-10) Cardiac Pediatric Adenosine (Adenocard) 0. 04mg/kg) Sodium Bicarbonate 1 mEq/kg IVP Calcium Chloride 10mg/kg IVP if patient on calcium channel blocker or history of renal failure Glucagon 1-5mg IVP for β –blocker overdose Sodium Bicarbonate 1mEq/kg definitely helpful in known preexisting hyperkalemia acceptable.1cc/kg) 1:10.01mg/kg epinephrine (0.000 IVP or IO. possibly helpful intubated and continued long arrest interval return of spontaneous circulation after long arrest interval not indicated. refer to HYPOTHERMIA TREATMENT GUIDELINE (See Page T-5) Hydrogen Ion (acidosis) (sodium bicarbonate) Hyper/Hypokalemia (consider calcium chloride or sodium bicarbonate) Hypoglycemia Tamponade (pericardiocentesis) Tension pneumothorax (needle decompression) Thrombosis–Coronary (ACS) Thrombosis–Pulmonary (embolism) Toxins blockers Trauma Vasopressin 40u IVP to replace 1st or 2nd dose of Epi or Epinephrine 1.000 ET Sodium Bicarbonate 1 mEq/kg infant (1 yr) or younger use 4. may be harmful hypoxic lactic acidosis Atropine 1.1cc/kg) 1:1.0mg IVP the shorter atropine dosing interval (3 min) is possibly helpful in cardiac arrest Cardiac Vasopressin 40u IV push is first line for MCFR SFR uses Vasopressin in place of Epi in PEA Pediatric Epinephrine Epinephrine repeated every 3–5 minutes 0.9% NaCl Consider possible causes: 6H 6T Hypovolemia (volume infusion) Hypoxia (ventilation) Hypothermia.1mg/kg epinephrine (0.4% and draw 25cc of 0. repeated every 3–5 minutes up to a total of 3mg (0. probably helpful in known preexisting bicarbonateresponsive acidosis overdose with tricyclic antidepressants to alkanize urine in overdoses acceptable.0mg IVP.2% solution expel 25cc of sodium bicarbonate 8.9% NaCl 10/7/2009 C-7 . or 0.0mg 1:10. refer to AED G UIDELINE (see page P-30) CPR (5 cycles or aproximately 2 minutes of CPR between interventions) ALS EKG monitor Intubate IV 0.000 IVP/IO q 3–5 minutes Absolute or relative bradycardia give Atropine 1.CARDIAC GUIDELINES PULSELESS ELECTRICAL ACTIVITY BLS Vitalize/Prioritize Oxygen/Airway Application of AED. 4) 17 mg/kg is reached (12 mg/kg for patients with cardiac or renal dysfunction) maintenance infusion 1–4 mg/min Cardiac Cardiac MCFR uses Amiodarone as the preferred antiarrhymic MCFR does not carry Procainamide (Pronestyl) C-8 10/7/2009 . 3) QRS is widened by 50% of its original width or.1mg/min Lidocaine 0.5–0.9% NaCl KVO Determine need for acute suppressive therapy (use only 1 antiarrhythmic) suspected MI or acute chest pain with one or more of the following: multiformed PVCs couplets runs of VT Amiodarone 150mg IV over 10 minutes. AHA recognizes that mixing two or more antiarrythmics can cause ectopy. unconsciousness. congestive heart failure. the maintenance dose should be decreased by 50% in the presence of jaundice. or aVF IV 0. JVD. or in patients older than 70 years of age.EMERGENCY MEDICAL GUIDELINES VENTRICULAR ECTOPY Caution Although the loading dose of lidocaine does not need to be reduced. circulatory shock. acute MI. may repeat once Maintenance drip.75 mg/kg IVP repeated every 5–10 minutes to cumulative total of 3 mg/kg maintenance infusion 2–4 mg/min Procainamide (Pronestyl) 20mg/min IV drip until: 1) ectopy suppressed or. BLS Vitalize/Prioritize Oxygen/Airway ALS EKG monitor 12 Lead EKG V4R should be manually evaluated if any ST elevation in leads II. III. 2) hypotension ensues or. 01mg/kg Epinephrine (0. heart rate and rhythm Rhythm change without spontaneous circulation PEA. support airway. refer to PULSELESS ELECTRICAL ACTIVITY TREATMENT GUIDELINE (See Page C-7) asystole. MCFR uses Amiodarone as the preferred antiarrhymic Pediatric Defibrillate with a single shock (refer to Appendix A for Joule settings) Epinephrine Epinephrine repeated every 3–5 minutes 0. overdose with tricyclic antidepressants. the maintenance dose should be decreased by 50% in the presence of jaundice.1cc/kg) 1:10.0.000 ET Amiodarone 5mg/kg IVP my be repeated up to max 300mg Maintenance drip refer to Broselow for dose Lidocaine 1mg/kg IVP or IO.0mg IVP every 3-5 minutes defibrillate (refer to Appendix A for Joule settings) administer medications of probable benefit in persistent or recurrent VF/VT Amiodarone 300mg IVP repeated at 150mg IVP in 5 minutes Maintenance drip of 1mg/min after conversion Lidocaine 1.2% solution expel 25cc of sodium bicarbonate 8. possibly helpful intubated and continued long arrest interval return of spontaneous circulation after long arrest interval not indicated. circulatory shock.75 mg/kg every 3–5 minutes to a cumulative total of 3mg/kg Magnesium Sulfate 1–2 g IVP in torsades de pointes or suspected hypomagnesemic state or severe refractory VF defibrillate (refer to Appendix A for Joule settings) Sodium Bicarbonate 1 mEq/kg Cardiac or Vasopressin 40u IV push is first choice for MCFR AHA recommends: Avoid mixing antiarrhymics if possible. refer to HYPOTHERMIA TREATMENT GUIDELINE (See Page T-5) Persistent or recurrent VF/VT intubate IV 0. breathing provide medications appropriate for blood pressure.4% and draw 25cc of 0. congestive heart failure. probably helpful known preexisting bicarbonate-responsive acidosis.000 IVP or IO. may be harmful hypoxic lactic acidosis BLS Vitalize/Prioritize Oxygen/Airway Perform CPR until defibrillator attached.9% NaCl KVO Vasopressin 40u IVP to replace 1st or 2nd dose of Epi Epinephrine 1.1cc/kg) 1:1. to alkanize urine in overdoses acceptable.5 .1mg/kg Epinephrine (0. repeated every 3–5 minutes to a total of 3mg/kg Magnesium Sulfate 25 to 50 mg/kg max 2 gm IVP in torsades de pointes or suspected hypomagnesemic state or severe refractory VF Sodium Bicarbonate 1 mEq/kg infant (1 yr) or younger use 4.5mg/kg IVP repeated at 0. refer to ASYSTOLE TREATMENT GUIDELINE (See Page C-1) Hypothermic.9% NaCl MCFR uses Amiodarone as the preferred antiarrhymic 10/7/2009 C-9 . refer to AED GUIDELINE (see page P-30) CPR (5 cycles or aproximately 2 minutes of CPR between interventions) Fluid bolus after drug administration be prepared to administer a 20-30cc bolus of IV fluid and elevate the arm after each IV medication ALS Defibrillate with single shock For specific Joule settings refer to APPENDIX A Resume CPR immediately (give 5 cycles or aproximately 2 minutes of CPR) Return of spontaneous circulation assess vital signs. or 0. unconsciousness or in patients older than 70 years old. continue through arrest Application of AED. acute MI. Sodium Bicarbonate 1 mEq/kg definitely helpful known preexisting hyperkalemia acceptable. JVD.CARDIAC GUIDELINES VENTRICULAR FIBRILLATION / PULSELESS V–TACH Caution Although the loading dose of Lidocaine does not need to be reduced in the pulseless patient. 10 10/7/2009 .2 mg/kg IVP rapid push maximum single dose 12 mg third dose 0. congestive heart failure. with serious signs or symptoms ventricular rate greater than 150 beats per minute (monomorphic VT) may give brief trial of medications (see STABLE OR BORDERLINE below) refer to CARDIOVERSION TREATMENT GUIDELINE (See Page C-3) immediate cardioversion seldom needed for rates less than 150 beats per minute (see SERIOUS SIGNS OR SYMPTOMS at left) ventricular rate greater than 150 beats per minute (polymorphic VT) consider sedation refer to APPENDIX A for cardioversion settings Regular Rhythm (V-Tach or Uncertain) Amiodarone 150mg IV over 10 minutes repeated as needed to max of 2. pulmonary congestion. or aVF IV 0. low blood pressure. shock.2 mg/kg IVP rapid push maximum single dose 12 mg Amiodarone 5mg/kg IV over 20 . decreased level of consciousness.5–0. go to CARDIOVERSION/DEFIBRILLATION TREATMENT GUIDELINE (See Page C-3) Irregular Rhythm (Polymorphic V-Tach) Unstable .75mg/kg IVP repeated every 5–10 minutes to cumulative total of 3mg/kg Magnesium Sulfate 1-2g IV diluted in 10cc over 2 minutes for Torsades de Pointe Serious signs or symptoms chest pain.2g in 24 hrs Lidocaine 0. sinus tachycardia may actually be present C .5–0. may repeat once consider synchronized cardioversion or defibrillation if patient becomes unstable.1 mg/kg IVP rapid push maximum single dose 6 mg second dose 0.Defibrillate refer to CARDIOVERSION/DEFIBRILLATION TREATMENT GUIDELINE (See Page C-3) Amiodarone 150mg IV over 10 minutes repeated as needed to max of 2.60 minutes Synchronized cardioversion go to CARDIOVERSION/DEFIBRILLATION TREATMENT GUIDELINE (See Page C-3) if conversion to sinus rhythm does not occur after two attempts. shortness of breath.75mg/kg IVP repeated every 5–10 minutes to cumulative total of 3mg/kg SVT with Aberrancy Adenosine Phosphate (Adenocard) 6 mg IVP over 1–3 seconds after 1–2 minutes. 12 mg IVP over 1–3 seconds.EMERGENCY MEDICAL GUIDELINES WIDE–COMPLEX TACHYCARDIA If there is any doubt whether monomorphic or polymorphic VT is existant in the unstable patient. cardiovert refer to CARDIOVERSION/DEFIBRILLATION TREATMENT GUIDELINE (See Page C-3) BLS Vitalize/Prioritize Oxygen/Airway ALS EKG monitor 12 Lead EKG V4R should be manually evaluated if any ST elevation in leads II. acute myocardial infarction unstable condition must be related to the tachycardia Cardiac Lidocaine use lower doses and longer intervals for: patients older than 70 years liver failure heart failure smaller body size bradycardias conduction disturbances (particularly blocks) Maintenance drip initiate maintenance drip of drug that converts rhythm MCFR uses Amiodarone as the preferred antiarrhymic IRCEMS uses 12mg doses of Adenosine only Adenosine is used for diagnostic reasons after Lidocaine Pediatric Adenosine (Adenocard) 0.9% NaCl KVO Unstable.2g in 24 hrs Maintenance drip of 1mg/min Lidocaine 0. the diagnosis of SVT should be reconsidered. III. sea water. page M10) MARINE INJURIES BLS Prioritize/Vitalize Irrigate area with 0.9% NaCl KVO Pain control (see Pain Management Treatment Guideline.3 mg/kg IV no faster than 3 mg/min or lorazepam (Ativan) 0.9% NaCl KVO in large vein Diazepam (Valium) 5 mg IVP to max of 10mg or Lorazepam (Ativan) 1mg IVP or nasally may be repeated to a max of 4mg Pain control (see Pain Management Treatment Guideline. do not try to grab it or more poison will be released) Apply hot packs to relieve pain 10/7/2009 T-1 .1mg/kg IV Rationalization: Benzodiazepines (Valium/Ativan) potentiate the effects of GABA (gamma-amino butyrate) which will facilitate inhibitory GABA neurotransmission and other inhibitory transmitters. page M10) Physician Consult Calcium chloride 10% (request dosage) Pediatric Calcium chloride 10% (request dosage) Diazepam (Valium) 0.9% NaCl. BROWN RECLUSE BLS Prioritize/Vitalize Oxygen/Airway ALS EKG monitor IV 0. blocking the pain. vinegar or ammonia Jellyfish or Man-of-war stings Apply meat tenderizer paste Remove barbs or tentacles if visible (scrape off.TRAUMA AND ENVIRONMENTAL GUIDELINES Trauma / Environmental Evaluate all trauma patients for Trauma Alert Criteria BITES AND STINGS Trauma/Environmental BLACK WIDOW BLS Prioritize/Vitalize Oxygen/Airway ALS EKG monitor IV 0. please refer to Allergic Reaction Treatment Guideline (see page M-3) ALS EKG monitor IV 0. refer to Pain Management Treatment Guideline. page M10) Trauma/Environmental SNAKE BITE CONTRAINDICATIONS The use of ice.EMERGENCY MEDICAL GUIDELINES Observe for shock or allergic reaction. physician consult is indicated prior to removing the tourniquet. if patient has had loss of consciousness. Let the physician decide whether or not it should be removed. BURNS Caution Burn patients are at high risk of developing hypothermia. bring to ED for identification ALS EKG Monitor IV 0. (see Appendix D. sterile burn sheet for 2nd and 3rd degree burns Use Rule of Nines to determine percentage of body surface area involved in burn. refer to Allergic Reaction Treatment Guideline (see page M-3) Refer to apropriate guideline for arrhythmias Physician Consult Pain control. Observe closely for any signs of shivering BLS Prioritize/Vitalize Oxygen/Airway High flow for inhalation burn (strongly consider advanced airway control) Remove or cool heat source if present (i. Caution If a tourniquet is applied prior to arrival.9% NaCl KVO Pain control (see Pain Management Treatment Guideline. undelayed transport If snake is DEAD.9% NaCl KVO Allergic reaction or anaphylaxis. tar. ( see page M-10) Rationale: may potentiate the toxin SLCFD uses Kool-A-Burn for 1st. page AD-1) Consider a Trauma Alert for 2nd and 3rd degree burns greater than 15% BSA Electrical and chemical burns Spinal immobilization on electrical burns. clothing) Cool compress dressing on minor burns with sterile saline (1st degree only) (do not apply ice directly to burns) Dry. or pain from trauma T-2 10/7/2009 . BLS Prioritize/Vitalize Oxygen/Airway Mark initial edematous area Keep patient calm Rapid.e. fall. if allergic reaction. tourniquet or constricting bands is contraindicated. 2nd and 3rd degree burns less than 15% BSA. page M-10) Pediatric Bolus 20 cc/kg. or abdomen should be removed immediately Indications Compression in excess of 60 minutes Involvement of large muscle mass Absent pulse / capillary return in distal limb Weak. two (2) lines if major burns If hypotensive (blood pressure less than 100 mm systolic).9% NaCl 1000cc bolus then 250-500cc/hr infusion Sodium Bicarbonate 50mEq IVP Pain control. neck. refer to Pain Management Treatment Guideline (see page M-10) 10/7/2009 T-3 . rapid pulse Usually absence of pain in affected region Onset of shock The activation of specialized teams (i. then 250 cc/hr infusion Pain control (see Pain Management Treatment Guideline.e. 250 cc bolus. repeat as necessary. stabilize and seal around it ALS EKG monitor 12 Lead EKG if time allows IV 0. BLS Vitalize / Prioritize Oxygen / Airway ALS EKG monitor IV large bore 0.TRAUMA AND ENVIRONMENTAL GUIDELINES ALS EKG monitor IV 0. page M-10) SLCFD requires two or more of the following to perform Pleural Decompression: *Altered LOC or unconscious *Respiratory distress and/or cyanosis * Loss of radial pulse or hypotension Trauma/Environmental CHEST INJURY BLS Vitalize/Prioritize Oxygen/Airway (high flow) reevaluate oxygenation Spinal immobilization if indicated Repeat chest exams Consider the following treatments leave any penetrating object. seal on three (3) sides (observe for signs of tension pneumothorax) pericardiocentesis refer to PERICARDIOCENTESIS GUIDELINE (See Page P-29) Refer to apropriate guideline for arrhythmias CRUSH INJURY Caution Compressive force to the head. Technical Rescue and HAZMAT) should be considered early. chest.9% NaCl set as needed Consider the following treatments tension pneumothorax refer to PLEURAL DECOMPRESSION GUIDELINE (See Page P-11) dress open chest wounds. then 20 cc/kg hr Pain control (see Pain Management Treatment Guideline.9% NaCl. drugs may be given endotracheally or intraosseous EYE INJURIES BLS Vitalize/Prioritize Oxygen/Airway Toxic chemical/burns remove any contacts flush eyes with 0. then 250 cc/hr ACLS guideline Physician Consult sodium bicarbonate 1 mEq/kg IVP for near drowning MCFR and SFR carry the Morgan Lens Pediatric Do not delay transport for multiple IV attempts. BLS Vitalize/Prioritize Oxygen/Airway Spinal immobilization if indicated ALS EKG monitor IV 0. DROWNING/NEAR DROWNING Trauma/Environmental Caution Consider the possibility the drowning may be secondary to some other trauma MCFR consider CPAP if lungs sound “wet” and no history of barotrauma.9% NaCl 40cc/kg bolus (max 1000cc) Sodium Bicarbonate 1mEq/kg IVP Above treatments should be done concurently with extrication. minimum of 20 minutes for acids and alkalines use Morgan Eye Lens. refer to SPLINTING PROCEDURAL GUIDELINE (See Page P-72) Dress open wounds with sterile dressings T-4 10/7/2009 .EMERGENCY MEDICAL GUIDELINES Pediatric IV 0.9% NaCl KVO if hypotensive (blood pressure less than 100 mm systolic) run wide open until blood pressure is 100 mm systolic.9% NaCl. if available Trauma stabilize any penetrating objects apply sterile dressing to both eyes ALS Toxic chemical/burns tetracaine 1–2 gtts in the affected eye(s) prior to flushing FRACTURES BLS Vitalize/Prioritize Oxygen/Airway Spinal immobilization if indicated Immobilize. page M-10) line. then 250 cc/hr Passive Rewarming Methods include removing wet clothes. hot water bottles.9% NaCl 250 cc/hr infusion (if lungs clear) when patient’s condition permits.8 °F) •passive rewarming •active external rewarming moderate hypothermia.2–96. long bone or pelvic fracture administer 250 cc bolus.9% NaCl KVO 250 cc bolus if blood pressure less than 100 mm systolic HEAT TRAUMA Caution Do not over cool to the point of shivering BLS Vitalize/Prioritize Oxygen/Airway Cool patient ALS EKG monitor IV 0. repeat as necessary. HYPOTHERMIA Caution Certain brands of thermometers may not read as low as the temperatures listed in this section. pelvic or open fractures EKG monitor IV 0. 34–36 °C (93.2 °F) 10/7/2009 T-5 . long bone.0–93. radiant heat sources. and warming beds. heating pads. hot packs BLS Determine patient priority Remove wet garments Protect against heat loss and wind chill (blankets) Maintain horizontal position Avoid rough movement and excess activity Core temperature: mild hypothermia. 30–34 °C (86.9% NaCl 250 cc bolus. Active external warming Methods include electric or charcoal warming devices. repeat as necessary Pain control (see Pain Management Treatment Guideline. page M-10) HEAD INJURIES Trauma/Environmental BLS Vitalize/Prioritize Oxygen/Airway Spinal immobilization Transport with backboard elevated 30 degree head–up position ALS EKG monitor IV 0. covering with blankets or sheets and turning the heat on in the vehicle.TRAUMA AND ENVIRONMENTAL GUIDELINES ALS ALS transport is indicated for any multiple. establish IV access prior to moving patient if multiple. refer to Ventricular Fibrillation Treatment Guideline. Helicopter transport necessitates the pilot maintaining altitude at less than 1000 feet. Mary’s Medical Center SCUBA DIVING INJURIES Do not use Nitrous Oxide in SCUBA injuries CAUTION The following are CONTRAINDICATED – CPAP. but at longer intervals • Repeat defibrillation for VF/VT as core temperature rises Notification of receiving facility early to place rewarming equipment on standby Trauma/Environmental MCFR does not use this procedure.9% NaCL KVO Cardiac arrest VF/VT initial treatment. LOCAL ANESTHESIA Indications Anesthetize insertion area for sternal IO BLS Vitalize/Prioritize Oxygen/Airway Circulatory support as necessary ALS EKG monitor Lidocaine 1% with Epinephrine 1:100.EMERGENCY MEDICAL GUIDELINES •passive rewarming •active external rewarming of core areas Severe hypothermia. Trendelenburg positioning. (see page C-9) CPR Intubate Core temperature less than 30 °C (86. the site is anesthetized Hyperbaric Facilities: St.000 10cc Create wheel with approximately 5cc SQ in area to be injected Allow for the initial effect of SQ Lido/Epi. BLS Vitalize/Prioritize Oxygen/Airway (High flow) via non-rebreather mask or BVM T-6 10/7/2009 . then administer remainder of solution onto the periosteum / bone cortex and surrounding tissues After 90 seconds. and massage of the affected joints.0 °F) • Continue CPR • Withhold IV medications • Limit shocks for VF/VT to 3 maximum • Transport Core temperature greater than 30 C (86 °F) • Continue CPR • Give IV medications as indicated.0 F) Vitalize/Prioritize Oxygen/Airway ALS EKG monitor IV 0. less than 30 C (86. Contact St. This will initiate recall of the hyperbaric diving medicine specialists to the receiving facility. and water sample from scene Treat for associated hypothermia with passive re-warming PRN Obtain a thorough clinical history of the event For Professional consultation contact: DAN 24 hours/day 1–919–684– 4 DAN Trauma/Environmental ALS SaO2 readings that do not improve with supplimental O2 may require RSI EKG monitor Perform 12 lead in patients with Arterial Gas Embolism (AGE) symptoms IV 0. Ped 0.1mg/kg in place of Phenergan or Anzemet 10/7/2009 T-7 .9% NaCl 250 bolus until normotensive. dive computer. then 250cc/hr Aspirin 324-325mg chewable (4 pediatric chewable aspirin) Pneumothorax / Tension Pneumothorax consider the following treatments: MCFR uses Ondansetron (Zofran) 4mg IV/IM over 30 seconds. Mary’s ER Nurses Desk (561) 881–2900 Spinal immobilization if suspected trauma Immobilize prior to removal from water if possible Transport supine Monitor for complications Consider bringing in dive tables.TRAUMA AND ENVIRONMENTAL GUIDELINES Contact the nearest hospital with HBOC ASAP. referrunoff to Pain Management *Contain irrigation if possible Guideline (see page M-10) Phenergan 6. refer to Seizure Treatment Guideline (see page M-14) Physician Consult Nasogastric tube SPECIFIC TOXICOLOGICAL EMERGENCIES BENZODIAZEPINE OVERDOSE Common Benzodiazepines: Alprazolam (Xanax) Clonazepam (Klonopin) Chlorazepate (Tranxene) Diazepam (Valium) Esfazolam (Prosom) Flurazepam (Dalmane) Halazepam (Paxipam) Lorazepam Midazolam Oxazepam Prazepam Quazepam Temazepam Triazolam (Ativan) (Versed) (Serax) (Centrax) (Doral) (Restoril) (Halcion) T-8 10/7/2009 . refer to Altered Level of Consciousness Treatment Guideline (see page M4) Seizures. refer to PERICARDIOCENTESIS PROCEDURAL GUIDELINE (See Page P-29) Consider transport to facility with hyperbaric chamber early Toxicology Toxicology OVERDOSE BLS Vitalize/Prioritize Oxygen/Airway consider notification of poison control Poison Control Center 1–800–282–3171 ALS EKG monitor IV 0.5mg IVP for nausea/vomiting Physician Consult Pericardial emphysema with signs of pericardial tamponade. refer to PLEURAL DECOMPRESSION PROCEDURAL GUIDELINE (See Page P-11) Pain control.5mg IM or Anzemet 12.25 .EMERGENCY MEDICAL GUIDELINES observe for signs of tension pneumothorax decompression of tension pneumothorax.12.9% NACL KVO or Saline Lock (if stable) Altered LOC. Ipecac. refer to Altered Level of Consciousness Treatment Guideline (see page M4) Seizures.TRAUMA AND ENVIRONMENTAL GUIDELINES BLS Vitalize/Prioritize Oxygen/Airway ALS EKG monitor IV 0.4% 50cc/500cc NACL infused @ 50cc/hr 10/7/2009 T-9 .9% NACL KVO or Saline Lock (if stable) Alerted LOC. refer to Seizure Treatment Guideline (see page M-14) TRICYCLIC ANTIDEPRESSANT OVERDOSE (TCA) Contraindications Administration of Procainamide. refer to Altered Level of Consciousness Treatment Guideline (see page M-4) Seizures. Magnesium Sulfate.9% NACL KVO Altered LOC.9% NACL KVO or Saline Lock (if stable) Alerted LOC. Romazicon. refer to Seizure Treatment Guideline (see page M-14) Sodium Bicarbonate 8. Common Narcotics Codeine Darvocet Demerol Dilaudid Fentanyl Heroin Lortab Methadone Morphine MS Contin Oxycontin Percocet Percodan Ultram Vicodin Toxicology BLS Vitalize/Prioritize Oxygen/Airway ALS EKG monitor IV 0. Only administer Narcan to maintain airway. or Calcium Chloride is contraindicated. refer to Altered Level of Consciousness Treatment Guideline (see page M-4) Seizures. Vicatil) Amoxapine Desipramine Imipramine Nortriptyline Trimipramine (Asendin) (Norpramin) (Tofranil) (Pamelor) (Surmontil) BLS Vitalize/Prioritize Oxygen/Airway ALS EKG monitor 12 Lead EKG IV 0. refer to Seizure Treatment Guideline (see page M-14) NARCOTIC OVERDOSE Caution Administer Narcan with caution in patients that are chronic users of narcotics. Common Tricyclics Amitriptyline Clomipramine Doxepin Maprotiline Protryptyline (Elavil) (Anafranil) (Sinequan) (Ludiomil) (Triptil.4% 50cc IVP Sodium Bicarbonate 8. III.5mg/kg no faster than 3mg/min. refer to Seizure Treatment Guideline (see page M-14) 12 Lead EKG V4R should be manually evaluated if any ST elevation in leads II.1mg/kg. Ativan.4% solution and draw up 25 cc of 0.9% NaCl) CARBON MONOXIDE Caution If intubation is necessary. or Versed Notify emergency department if patient ingests cocaine powder. Ativan.9% NACL KVO or Saline Lock (if stable) Seizures. or Versed or chest pain greater than 12 hours after use. air packs) if indicated If multiple patients.9% NACL KVO Physician Consult Request orders for transport to a hyperbaric chamber facility MCFR drug of choice is Ativan 1mg IV push or nasally COCAINE OVERDOSE BLS Vitalize/Prioritize Oxygen/Airway ALS EKG monitor IV 0. or aVF Valium 5mg IVP. Ativan 1mg IVP. Pulse oximetry does not read carbon monoxide BLS Toxicology Remove patient from contamination source while maintaining rescuer safety Use personal protective equipment w/respiratory protection (i. or packed condom Pediatric Valium 0.2% solution (expel 25 cc out of 8. or Versed 1-2mg T .10 10/7/2009 .e.2-0. or Versed 1-2mg IVP for relief of chest pain may be administered rectally if no IV access (also nasally for Ativan or Versed) may repeat once after 10 minutes if chest pain persists Chest pain unrelieved by Valium. page P-74) Vitalize/Prioritize Oxygen/Airway Consider aeromedical transport with long transport distance to a facility with a hyperbaric chamber Transport in semi–fowlers position ALS EKG monitor IV 0.EMERGENCY MEDICAL GUIDELINES Refer to appropriate guideline for arrhythmias Physician Consult Nasogastric tube Pediatric Sodium bicarbonate 1 mEq/kg Under 1 year of age use 4. refer to MCI Procedural Guideline. crack. Ativan 0. DO NOT HYPERVENTILATE (hypervetilation hinders the elimination of carbon monoxide) SaO2 readings may be inaccurate. refer to Chest Pain Treatment Guideline (see page C-4) Physician Consult Repeat Valium. refer to Seizure Treatment Guideline (see page M-14) Toxicology PHYSICIAN CONSULT Nasogastric tube GHB (GAMMA HYDROXYBUTYRATE) OVERDOSE CAUTION The patient.7 degrees Celsius) BLS Vitalize/Prioritize Oxygen/Airway Ice packs in the axilla and groin areas and / or cover patients with wet sheets and fan them. despite a comatose condition. BLS Remove the patient from the contamination source while maintaining rescuer safety Remove contaminated clothing Brush off dry chemicals T .9% NaCl or LR KVO Altered level of consciousness. refer to the ALTERED LEVEL OF CONSCIOUSNESS TREATMENT GUIDELINE (SEE PAGE M-4) Seizures. will occasionally respond to stimuli violently. This includes fighting attempts at ventilation. refer to Medical Shock Syndromes Treatment Guideline (see page M8) Seizures.11 10/7/2009 . Assistance will normally prove necessary to adequately restrain the patient in the ambulance during transport.9% NaCl or LR KVO Altered level of consciousness. BLS Vitalize / Prioritize Oxygen / Airway Restrain patient if necessary ALS EKG Monitor IV 0. refer to Altered Level of Consciousness Treatment Guideline (see page M-4) Hypotension.TRAUMA AND ENVIRONMENTAL GUIDELINES ECSTASY (MDMA) OVERDOSE CAUTION Hyperthermia associated with MDMA overdoses can reach as high as 109 degrees Fahrenheit (42. Do not handle any toxic chemical exposure without the correct level of personal protective equipment (PPE) Consult DOT Handbook. ALS EKG Monitor IV 0. refer to the SEIZURE TREATMENT GUIDELINE (SEE PAGE M-14) PHYSICIAN CONSULT Nasogastric tube TOXIC CHEMICAL EXPOSURE Caution Consider early notification of your Hazardous Materials Team. refer to MCI Procedural Guideline (see page P-74) Vitalize/Prioritize Oxygen/Airway 10/7/2009 S–Salivation L–Lacrimation U–Urination D–Diarrhea G–Gastrointestinal E–Emesis T .1mg maximum single dose 0. 1mg for adolescent methylprednisolone (Solu-Medrol) 2mg/kg or dexamethasone (Decadron) 0.2mg/kg maximum dose 125mg of Solu-Medrol maximum dose 4mg of Decadron furosemide (Lasix) 1.5mg for child. repeat as needed up to 3mg Pediatric Albuterol 1.EMERGENCY MEDICAL GUIDELINES Make sure chemical is not water reactive Flush with copious amounts of water for at least 20 minutes Contain run–off of toxic chemicals If multiple patients.0mg/kg IVP slowly over 1–2 minutes ORGANOPHOSPHATE POISONING BLS SLUDGE Remove the patient from the contamination source while maintaining rescuer safety Remove contaminated clothing Brush off dry chemicals Make sure chemical is not water reactive Flush with copious amounts of water for at least 20 minutes Contain run-off of toxic chemicals If multiple patients.25mg via mini–nebulizer for wheezing Atropine 0. refer to MCI PROCEDURAL GUIDELINE (see page P-74) Vitalize/Prioritize Oxygen/Airway ALS EKG monitor IV 0.02mg/kg minimum dose 0.12 . refer to INHALED TOXINS TREATMENT GUIDELINE (see page T-12) Physician Consult Use of any chemical antidote kit available on scene Toxicology INHALED TOXINS BLS If multiple patients. refer to MCI Procedural Guidelines (see page P-74) Vitalize/Prioritize Oxygen/Airway ALS EKG monitor IV 0.9% NACL KVO or Saline Lock (if stable) Altered LOC. refer to ALTERED LEVEL OF CONSCIOUSNESS TREATMENT GUIDELINE (see page M-4) Seizures. refer to SEIZURE TREATMENT GUIDELINE (see page M-14) Inhaled toxins.9% NACL KVO or Saline Lock (if stable) Albuterol (Proventil) 2.5mg via mini–nebulizer for wheezing may repeat once methylprednisolone (Solu-Medrol) 125mg IVP or dexamethasone (Decadron) 4mg IVP furosemide (Lasix) 40mg IVP with PE signs and/or symptoms Atropine 0.5-1mg IVP. refer to Inhaled Toxins Treatment Guideline (see page T-12) Atropine 2. refer to Altered Level of Consciousness Treatment Guideline (see page M-4) Seizures.TRAUMA AND ENVIRONMENTAL GUIDELINES ALS EKG monitor IV 0. refer to Seizure Treatment Guideline (see page M-14) Inhaled toxins.1mg maximum single dose 0.9% NACL KVO or Saline Lock (if stable) Altered LOC.0mg IVP every 5 minutes until SLUDGE symptoms are controlled No maximum dose of Atropine Pediatric Atropine 0.5mg for child and 1mg for adolescent Toxicology T .13 10/7/2009 .02mg/kg minimum dose 0. DRUG REFERENCE Drug Reference D-1 03/01/05 . rash. and saccharin. alcohol. APAP) CLASS Non-narcotic analgesic/Antipyretic ACTIONS Reduces fever May block pain impulses peripherally INDICATIONS Pediatric fever over 101 degrees F. WARNINGS Verify fever SIDE EFFECTS Anemia. alcohol. CONTRAINDICATIONS History of hypersensitivity Intolerance to tartrazine. rash.EMERGENCY MEDICAL GUIDELINES ACETAMINOPHEN (TYLENOL*. hives DOSAGE Pediatric: 10 mg/kg PO ACETAMINOPHEN SUPPOSITORIES (RECTAL TYLENOL) CLASS Non-narcotic analgesic/Antipyretic ACTIONS Reduces fever May block pain impulses peripherally INDICATIONS Use in febrile seizures post Valium administration Establish time of last dose of Tylenol if possible. when level of consciousness permits. WARNINGS Verify fever SIDE EFFECTS Anemia. hives DOSAGE Adult: 325mg Pediatric: 125mg D-2 03/01/05 . Tylenol is given every 4-6 hours PRN. table sugar. CONTRAINDICATIONS History of hypersensitivity Intolerance to tartrazine. table sugar. and saccharin. CONTRAINDICATIONS Second. It interrupts the reentry circuit – the etiology of most SVT’s (WPW included). consider themselves allergic to acetylsalicylic acid. If rhythm has not converted in 1 to 2 minutes. 12 mg rapid IVP (92% conversion). HOW SUPPLIED 6 mg and 12mg prefilled syringes D-3 03/01/05 . INDICATIONS To convert hemodynamically stable supraventricular tachycardia (rate above 160) after vagal maneuvers were unsuccessful for conversion.DRUG REFERENCE ACETYLSALICYLIC ACID (ASPIRIN. Adenocard is rapidly eliminated by vascular components (halflife <10 seconds so side effects are minimal and short-limiting). It directly slows electrical conduction through the AV node of the heart.Degree A-V blocks Sick sinus syndrome History of hypersensitivity SIDE EFFECTS Hypotension < 1% of time used May produce short lasting 1st. DOSAGE 324mg PO (4 Tablets) ADENOSINE (ADENOCARD) CLASS Nucleoside. antiarrhythmic ACTIONS Adenocard is a naturally occurring nucleoside (a glycoside formed by the union of a purine base with sugar) which is normally present in all cells of the body. may be repeated. or 3rd degree heartblocks 55% of patients develop a few seconds of conversion arrhythmias (asystole. anti-platelet ACTIONS Impedes clotting by anti-prostaglandin properties INDICATIONS Chest pain of suspected cardiac origin CONTRAINDICATIONS Active gastro-intestinal bleeding Patient taking coumadin Allergy Children under 16 due to Reye’s Syndrome SPECIAL CONSIDERATIONS Some asthmatics. PVC’s. headache and shortness of breath.or third. or PAC’s) at the time of conversion Facial flushing. DOSAGES Initial dose 6 mg rapid IV push (60% conversion). 2nd. especially those with environmental allergies. lightheadedness and nausea WARNINGS No studies have been performed on the effects of Adenocard in pediatrics. ASA) CLASS Salicylate. Often this “allergy” is actually a predisposition toward acetylsalicylic acid induced bronchospasm. AMIODARONE (CORDARONE. peaks in 60-90 minutes.blockers and Albuterol will inhibit each other. CONTRAINDICATIONS History of hypersensitivity SIDE EFFECTS AND ADVERSE REACTIONS CNS: Nervousness. Administer cautiously to patients on MAO inhibitors (Nardil. INDICATIONS Albuterol inhaler is indicated for relief of bronchospasm in patients with reversible obstructive airway disease including asthma. either may be used subsequent to a failure of the other.5mg/cc) IV Infusion pump: 40cc/hr with 100cc volume to be infused. syncope. Onset is within 15 minutes. dizziness. vomiting. hypertension. DOSAGE V-Fib / Pulseless V-Tach 300 mg IVP may repeat with 150mg IVP Perfusing patients (V-Tach. dizziness. DOSAGE 2. numbness or tingling in fingers or toes. Rapid atrial dysrhythmias with poor LV function.5gtts/sec) D-4 03/01/05 . headache. unusual taste WARNINGS Use cautiously in patients with coronary artery disease. tremor. Therapeutic effects may be active up to 5 hours. IV drip set (60gtts/cc) 40gtts/min (1. Eutonyl) or tricyclic antidepressants. however. painful breathing. insomnia CV: Tachycardia. nausea. diabetes. angina GI: Drying of oropharynx. CONTRAINDICATIONS Known allergy Pregnancy Liver disease Thyroid problems Patients taking Dilantin.5 mg in 3 ml in a nebulizer at 6 lpm.EMERGENCY MEDICAL GUIDELINES ALBUTEROL (PROVENTIL. PACERONE) CLASS Antiarrythmic ACTIONS Slows nerve impulses on the heart and acts directly on heart tissues. SIDE EFFECTS Cough. Epinephrine should not be used at the same time as Albuterol. Beta. INDICATIONS Used to correct ventricular arrythmias to a regular rhythm. shortness of breath. unusual and uncontrolled movements of the body. hypertension. lightheadedness. VENTOLIN) CLASS Adrenergic bronchodilator ACTIONS Albuterol is primarily a beta-2 sympathomimetic and as such produces bronchodilation.) 150mg IV given over 10 min Maintenance Drip Infuse 1mg/min (40gtts/min) with mini drip Mix 150mg in 100cc of D5W (1. hyperthyroidism. Because of its greater specificity for beta-2 adrenergic receptors. Marplan. it produces fewer cardiovascular side effects and more prolonged bronchodilation than Isuprel. Tachycardia. agitation. then repeat in 3 – 5 minutes.04 mg/kg should not be exceeded.5 to 1 mg IV or ET may repeat every 3 – 5 minutes until improved or total dose of 0. Symptoms: Chest pain. flushing of skin GI: Dry mouth. blurred vision. palpitations. thus freeing the hemoglobin to react with oxygen. HOW SUPPLIED Prefilled syringes containing 1 mg in 10 cc of solution Multi-dose vials containing 4 mg in 10 cc of solution D-5 03/01/05 . INDICATIONS Cyanide poisoning Angina CONTRAINDICATIONS None when used for cyanide poisoning SIDE EFFECTS Hypotension. pulmonary congestion. headache CV: Increase heart rate. confusion. Go at once to pacing. Clinical manifestations include: 1. decreased level of consciousness Do not delay TCP while awaiting IV access or for Atropine to take effect if patient is symptomatic. Acute MI 2. Signs: Low BP. catecholamine infusion. Effective in the treatment of cyanide poisoning by causing the oxidation of hemoglobin to the compound methemoglobin. CONTRAINDICATIONS None in emergency situations for adults Not to be used in infants below 1 month in age SIDE EFFECTS CNS: Restlessness. ventricular fibrillation. Methemoglobin reacts with the cyanide ion to form cyanomethemoglobin. dizziness. Repeat continuously as needed. A maximum dose of 0.04 mg/kg has been reached. nausea / vomiting. ATROPINE SULFATE (AS A CARDIAC AGENT) CLASS Anticholinergic ACTIONS Atropine is a potent parasympatholytic anticholinergic that reduces vagal tone and thus increases automatically the SA node and increases A-V conduction. headache.1 mg in the pediatric patient) or if pushed too slowly may initially cause the heart rate to decrease. shortness of breath. Serious signs and symptoms must be related to the slow rate.DRUG REFERENCE AMYL NITRATE CLASS Vasodilator ACTIONS Amyl nitrate is chemically related to nitroglycerin. ventricular tachycardia. CHF. or both. shock.02 mg/kg IV or ET – minimum dose is 0. Asystole: 1 mg IV or ET. may worsen ischemia or increase area of infarction. Atropine is potentiated by antihistamines and antidepressants. difficulty swallowing GU: Urinary retention Other: Worsened pre-existing glaucoma WARNINGS Too small of a dose (<0. INDICATIONS Asystole Bradycardia.1 mg and maximum dose is 1 mg. blurred vision WARNINGS Use with caution when treating poisoning with a combination of cyanide and carbon monoxide DOSAGE Administer vapors from crushed inhalant for 30 – 60 seconds. psychotic reaction. syncope. which has less affinity for oxygen. DOSAGES Adult: Bradycardia: 0.5 mg in the adult or 0. either absolute (<60 BPM) or relative A. Pediatric: 0. angina. pupil dilation. Denervated transplanted hearts will not respond to atropine. malathion. SIDE EFFECTS Victims of organophosphate poisoning can tolerate large doses (1000 mg) of atropine. POISONING SIGNS ARE “SLUDGE”: Salivation Lacrimation Urination Defecation GI Cramping Emesis Also: pinpoint pupils. Also acts as an activator in the transmission of nerve impulses and contraction of cardiac. WARNINGS It is important that the patient be adequately oxygenated and ventilated prior to using atropine as atropine may precipitate ventricular fibrillation in a poorly oxygenated patient. rid-a-bug) and carbamate (baygon. Signs of atropinization is the end point of treatment: flushing. pupil dilation.05 mg/kg repeat q 25 minutes if necessary CALCIUM CHLORIDE CLASS Elemental Calcium for electrolyte balance ACTIONS Calcium chloride is a calcium salt that maintains cell membrane and capillary permeability. INDICATIONS Organophosphate (e. syncope. tachycardia. nausea and vomiting SPECIAL CONSIDERATIONS Should be given with extreme caution and in reduce dosage to persons taking digitalis. INDICATIONS Magnesium sulfate toxicity As an antidote to calcium channel blocker overdose Hyperkalemia (renal dialysis. bradycardia and excessive sweating. bradycardia. CONTRAINDICATIONS None when used in the management of severe organophosphate poisoning. cardiac arrest. IV line should be flushed between calcium chloride and sodium bicarbonate administration. May repeat with 2-5 mg q 5 minutes until atropinization occurs. skeletal and smooth muscles.g. parathion. sevin and many common roach and ant sprays). phlebitis at IV site. Pediatrics: 0.EMERGENCY MEDICAL GUIDELINES ATROPINE SULFATE (AS AN ANTIDOTE FOR POISONINGS) CLASS Anticholinergic ACTIONS Atropine is a potent parasympatholytic that binds to acetylcholine receptors thus diminishing the actions of acetylcholine. dry mouth. may be repeated every 10 minutes PEDIATRIC: 5 to 7 mg/kg of a 10% solution slow IVP D-6 03/01/05 . DOSAGE Adult: 2 mg IV. DOSAGE ADULT: 10 mg/kg of a 10% solution slow IVP. cardiac arrest) To relieve muscle spasm and pain caused by a black widow spider bite or portuguese man-o-war sting CONTRAINDICATIONS Hypercalcemia Renal calculi SIDE EFFECTS Arrhythmias. Dilantin and Theophylline. cardiac dysrhythmias WARNINGS Patient’s EKG must be monitored Necrotic to exposed tissue if infiltration occurs DOSAGE 500mg – 1000mg IV over 5 – 10 minutes Peds: 20-25mg/kg IV or IO slowly CIMETIDINE (TAGAMET) CLASS H2 blocker ACTIONS Inhibits the action of histamine on the stomach cells. thus reducing acid production. headache. nausea and vomiting WARNINGS May alter blood levels in patients taking Coumadin. dizziness. bradycardia.DRUG REFERENCE CALCIUM GLUCONATE CLASS Calcium electrolyte ACTIONS Supplemental Calcium therapy INDICATIONS Hypocalcemia Hyperkalemia Hypermagnesemia Calcium channel blocker overdose CONTRAINDICATIONS Hypercalcemia V-fib Digitalis toxicity SIDE EFFECTS Venous irritation. hypotension. INDICATIONS Allergic reaction Anaphylaxis CONTRAINDICATIONS None in the emergency setting SIDE EFFECTS Fatigue. DOSAGE 300mg in 50cc infused over 15 minutes D-7 03/01/05 . blurred vision. DOSAGES Adult: 2 – 10 mg IV. WARNINGS Diazepam is incompatible with many medications.25 – 0. nausea and vomiting.. Flumazenil should be readily available to reverse sedation effects. amnesia.5mg/kg in Pediatrics D-8 03/01/05 .5 mg/kg IV or rectal HOW SUPPLIED Ampule containing 10 mg in 2 cc Anaphylaxis (after epinephrine and diphenhydramine) Asthma COPD CONTRAINDICATIONS None in the emergency setting PRECAUTIONS Should be protected from heat Onset of action may be 2-6 hours and thus should not be considered to be of use in the critical first hour following an anaphylatic reaction SIDE EFFECTS Gastrointestinal bleeding Prolonged wound healing DOSAGE 4-24 mg IV or IM 0. violent patient (physician consult) Eclampsia (physician consult) CONTRAINDICATIONS History of hypersensitivity SIDE EFFECTS Hypotension.EMERGENCY MEDICAL GUIDELINES DEXAMETHASONE (DECADRON) CLASS Steroid ACTIONS Anti-inflammatory Suppresses immune response (especially in allergic reactions) INDICATIONS DIAZEPAM (VALIUM) CLASS Anticonvulsant/sedative ACTIONS Diazepam suppresses the spread of seizure activity through the motor cortex of the brain. INDICATIONS Major motor seizures Status epileptieus Premedication before cardioversion Skeletal muscle relaxant Acute anxiety states Airway management (when RSI not indicated or available) External pacing Altered L. headache. May cause respiratory depression or compromise.2-0. respiratory depression. drowsiness.O.C. IM or rectal Pediatric: 0. IV line should be adequately flushed. It should not be mixed with any other drugs. sedation and disturbed coordination. INDICATIONS Allergic reactions Anaphylaxis CONTRAINDICATIONS Newborns Premature infants Nursing mothers Lower respiratory tract symptoms Asthma SIDE EFFECTS AND ADVERSE REACTIONS Hypotension. WARNINGS Use with caution for patients with a heart rate of less than 100 bpm. they may produce excitation. headache. headache. antihistamines in overdosage may cause hallucinations. and blood vessels. dizziness. convulsions. Diphenhydramine prevents. Diphenhydramine has additive effects with alcohol and other CNS depressants (hypnotics. Also dilates coronary arteries and inhibits coronary artery spasm. weakness. but does not reverse histamine medicated response. As in adults.25 mg/kg HOW SUPPLIED 50 mg diphenhydramine HCL in 1 ml ampules/prefilled syringes D-9 03/01/05 . or death. sedatives.DRUG REFERENCE DILTIAZEM (CARDIZEM) CLASS Calcium Channel Blocker ACTIONS Inhibits calcium influx through slow channels into the cells of the myocardium and smooth muscle. palpitations. bradycardia. If no effect in 15 minutes:0. INDICATIONS PSVT Rapid atrial fibrillation Atrial flutter CONTRAINDICATIONS 2 or 3 degree block Hypotension Sick sinus syndrome VT WPW Do not give with oral beta blockers Do not give with Furosemide in the same IV line (flush the line first) SIDE EFFECTS Hypotension.) DOSAGE Adult: 25 – 50 mg IVP Pediatric: 1 mg – 1. In young children. DOSAGE 0. May cause hypotension.35mg/kg slow IVP DIPHENHYDRAMINE (BENADRYL) CLASS Ethanolamine derivative antihistamine ACTIONS Diphenhydramine is an antihistamine with anticholinergic (drying) and sedative side effects. uterus. CHF. antihistamines may diminish mental alertness in children.25mg/kg slow IVP over 2 minutes. tachycardia. etc. WARNINGS In infants and children especially. N/V. gastrointestinal tract. drowsiness. tranquilizers. Antihistamines appear to compete with histamine for cell receptor site on effector cells. particularly histamines effects on the smooth muscle of the bronchial airways. 5 mg Pediatric: 0. cardiac output.EMERGENCY MEDICAL GUIDELINES DOBUTAMINE (DOBUTREX) CLASS Inotrope ACTIONS Stimulates beta-1 receptors in the heart. diarrhea.10 03/01/05 . V-Tach. Acute Coronary Syndrome. nausea / vomiting. V-fib. therefore increasing cardiac function. arrhythmias DOSAGE Adult: 12. dizziness.5mg) 2 yrs – 16 yrs D . headache DOSAGE 2-20ug/kg/min IV infusion. and stroke volume with only minor effects on the heart rate.35mg/kg (not to exceed 12. hypertension. INDICATIONS Congestive Heart Failure CONTRAINDICATIONS Shock Hypovolemia Tachydysrhythmias SIDE EFFECTS Tachydysrhythmias. Mix 250mg in 250cc (1mg/cc) DOLASETRON MESYLATE (ANZEMET) CLASS Antiemetic INDICATIONS Nausea and Vomiting CONTRAINDICATIONS Hypersensitivity to Anzemet SIDE EFFECTS Headache. ventricular ectopy. systolic blood pressure above 160 mm Hg. 1:1000 epinephrine cannot be given intravenously. INDICATIONS To treat shock and correct hemodynamic imbalances Improve perfusion to vital organs and to increase cardiac output. hypotension. DOSAGE Mix 400 mg into 250 cc NaCl or 800 mg into 500 cc NaCl to yield a concentration of 1. Pediatric: 0. Intropin has alpha receptor stimulating actions that result in peripheral vasoconstriction and marked increases in pulmonary occlusive pressure.01 mg/kg up to 0. unless diluted first to 10 cc 0.3 mg subcutaneously.5 cc) subcutaneously. vomiting Local: Necrosis and tissue sloughing with extravasation. CONTRAINDICATIONS Intropin should not be used in patients with tumor of the adrenal gland. At high doses. Intropin dilates renal and mesenteric blood vessels at low doses that may not increase heart rate or blood pressure. It exerts an inotropic effect on the myocardium resulting in an increased cardiac output. hypertensive or cardiac history. Epinephrine should be used with caution to patients >60 years of age. HOW SUPPLIED Intropin is supplied in 5 ml ampules containing 400 mg.3-0. palpitations. pulse above 120 bpm.5 mg (0. May be repeated every 15 minutes x 3 if patient in anaphylaxis is hypotensive. Intropin produces less increase in myocardial oxygen consumption than does isoproterenol and it’s use if usually not associated with tachydysrhythmias. tachycardia. GI: Nausea. INDICATIONS Asthma Anaphylaxis Allergic reaction CONTRAINDICATIONS Hyperthyroidism Hypertension Cerebral arteriosclerosis in asthma In anaphylaxis. Patients who have been treated with monoamine oxidase (MAO) inhibitors will require substantially reduced dosage.000 WARNINGS Same as epinephrine 1:10. Begin infusion at 2 to 5 mcg/kg/min and titrate to effect. anginal pain. Other: Piloerection. Dosages of over 20 mcg/kg/ min have been required occasionally to obtain desired effect. SIDE EFFECTS AND ADVERSE REATIONS CNS: Headache CV: Ectopic beats.000 solution IV push. DOSAGE Adult: 0.3-0. Subcutaneous dose lasts 5-15 minutes.11 03/01/05 . Also causes hyperglycemia. Therapeutic doses have predominant beta adrenergic receptor stimulating actions that result in increases in cardiac output without marked increases in pulmonary occlusive pressure.9 % NaCl. dyspnea WARNINGS Do not administer Intropin in the presence of uncorrected tachyarrythmias or ventricular fibrillation. start an IV and administer 3-5 cc of a 1:10. there are no contraindications SIDE EFFECTS Same as epinephrine 1:10.DRUG REFERENCE DOPAMINE (INTROPIN) CLASS Sympathetic Agonist ACTIONS Intropin stimulates dopaminergic beta-adrenergic and alpha-adrenergic receptors of the sympathetic nervous system.600 mcg/ml. Can also be given sublingually.000. Do not add Intropin to any alkaline diluent solution since the drug is inactivated in alkaline solution. HOW SUPPLIED Ampule containing 1mg/cc Multi-dose vial containing 30 mg in 30 cc D . however. EPINEPHRINE (1:1000) CLASS Sympathetic Agonist ACTIONS Epinephrine is a sympathomimetic which stimulates both alpha and beta adrenergic receptors causing immediate bronchodilation increase in heart rate and an increase in the force of cardiac contraction. For Cardiac Arrest: 1 mg IVP every 3 to 5 minutes Pediatric: 0. As a vaso-pressor infusion 1 mg/ 250 cc NaClstart 1 mcg/min And titrate to desired effect.1 mcg/kg/min up to 1.3mg/kg) IVP over 30-60 seconds Some agencies administer 20mg non-weight based D . myocardical and cerebral blood flow are increased during ventilation and chest compression. Lowers ICP and cerebral metabolic rate of oxygen consumption Duration of action 3-5 minutes INDICATIONS Pre-medication for RSI Cardioversion Convulsions.EMERGENCY MEDICAL GUIDELINES EPINEPHRINE (1:10. angina. Ventricular fibrillation unresponsive to defibrillation PEA and severe anaphylaxis Other pediatric indications: Hypotension in patients with circulatory instability Bradycardia unresponsive to atropine CONTRAINDICATIONS None in the cardiac arrest situation. HOW SUPPLIED Prefilled syringes containing 1 mg/10 cc ETOMIDATE (AMIDATE. Antidepressants potentiate the effect of Epinephrine.12 03/01/05 . HYPNOMIDATE) CLASS Short acting non-barbiturate hypnotic ACTIONS Etomidate is a short acting non-barbiturate hypnotic that acts at the level of the reticular activating system thereby causing sedation and amnesia. cerebral hemorrhage CV: Tachycardia. apnea WARNINGS Be aware of increased myoclonic activity. Epinephrine increases systemic vascular resistance and thus may enhance defibrillation. headache. repeat every 5 minutes as necessary as in infusion – start at 0.0 mcg/kg/min. It also works well as an anti-convulsant since it does not require locked access.01 mg/kg (0. SIDE EFFECTS CNS: Anxiety. ventricular dysrythmias. DOSAGE 0.2mg/kg-0.1 ml/kg) IV or Double-Dose down ET tube. Nausea is common post recovery. As a result of its effect. INDICATIONS Asystole. DOSAGES Adult: 0.000) CLASS Sympathetic Agonist ACTIONS Epinephrine is a sympathomimetic which stimulates both A & B receptors. palpitations GI:Nausea and vomiting WARNINGS Epinephrine is inactivated by alkaline solutions – never mix with Sodium Bicarbonate. Do not mix Isuprel and Epinephrine – will get exaggerated response. hypertension.0 mg (5-10 cc) IV every 5 minutes Can also be given double-dose down the ET tube repeat every 5 minutes. Action of catecholamines is depressed by acidosis – attention to ventilation and circulation is essential. CONTRAINDICATIONS Under 10 years old Hypoventilation Laryngospasm Bradycardia Vomiting SIDE EFFECTS Respiratory depression.5 to 1.6mg/kg (usually 0. muscle cramping WARNINGS Furosemide should be protected from light. blurred vision. tinnitus.2mg IVP over 30 seconds. HOW SUPPLIED Ampules of 10 cc containing 10 mg/cc Prefilled syringes containing 40 mg/4 cc or 100 mg/10cc D .2mg single dose. Peds: 0. after 30 seconds. 0. Max dose of 1mg. Flumazenil competitively inhibits the activity at the benzodiazepine receptor site to reverse the sedative effects of the benzodiazepines INDICATIONS Benzodiazepine overdose CONTRAINDICATIONS Tricyclic antidepressant overdose Status epilepticus Increased ICP SIDE EFFECTS Nausea / vomiting. Dehydration and electrolyte imbalance can result from excessive dosages. Onset of diuresis is 5-15 minutes and effects can last up to 2 hours. SIDE EFFECTS CNS: Dizziness. weakness GI: Anorexia. dizziness. nausea CV: Hypotension Others: Pruritus. withdrawal symptoms. IO up to 0.3mg IVP over 30 seconds. Should be used in pregnancy only when benefits clearly outweigh risks. repeat in 20 minute intervals to a total of 3mg. headache. thus decreasing cardiac work. INDICATIONS Pulmonary edema Hypertension Congestive heart failure Cerebral edema CONTRAINDICATIONS Furosemide is contraindicated in patients who are allergic to sulfa. after 1 minute 0. urticaria. blurred vision WARNINGS Not recommended for use in the elderly Can possibly cause seizures in the overdose patient DOSAGE 0.5mg IVP over 30 seconds. Following administration.5 – 1.13 03/01/05 . DOSAGE Adult: 0.01mg/kg IV.DRUG REFERENCE FLUMAZENIL (ROMAZICON) CLASS Benzodiazepine antagonist ACTIONS Antagonizes the actions of benzodiazepines on the central nervous system. hearing loss. FUROSEMIDE (LASIX) CLASS Diuretic ACTIONS Furosemide is a loop diuretic which inhibits the reabsorption of sodium and chloride in the kidneys. seizures. agitation. Not to be used on renal dialysis patients. vomiting. Rapid diuresis can lead to hypotension and thromboembolic episodes. venous dilation occurs within 5 minutes which causes reduction in pre-load.0 mg/kg IV slowly over 1-2 minutes (40-80 mg) Can be given IM or double patient’s daily dose. Physician consult should be obtained regarding treatment of low blood glucose levels associated with pregnancy and stroke.5 – 1 gm/kg slow IVP Expel 37. INDICATIONS Hypoglycemia when IV access is unobtainable b-blocker overdose CONTRAINDICATIONS Hyperglycemia SIDE EFFECTS Hyperglycemia DOSAGE Reconstitute glucagen powder with 1cc of diluting solution. hyperglycemia. alkalosis.9% NaCl Age: 1 . Hypertonic solution. CONTRAINDICATIONS CVA with suspected intracranial or intraspinal hemorrhage DT’s with dehydration SIDE EFFECTS CV: Thrombosis. spares body proteins and loss of electrolytes. then 1mg IM GLUCOSE 50% (DEXTROSE 50%) CLASS Carbohydrate ACTIONS A monosaccharide which provides calories for metabolic needs.5 – 1. IM or IV. Perform an Accucheck (if possible) and draw a blood sample (red top tube) prior to administering Dextrose. hypokale . DOSAGE Adult: 50 cc of a 50% solution (25 grams) IV Pediatric: Age: birth – 1 year Dextrose 12. Readily excreted by kidney producing diuresis.5% 0. INDICATIONS Hypoglycemia Coma of unknown origin.8 years Dextrose 25% 0.5 cc 0.14 03/01/05 .5 cc of D-50 and draw 37.0 gm/kg slow IVP Expel 25 cc of D-50 and draw 25 cc of 0.EMERGENCY MEDICAL GUIDELINES GLUCAGON (GLUCAGON) CLASS Polypeptide Hormone ACTIONS Assists with the breakdown of glycogen into glucose. sclerosing if given in peripheral vein INTEG: Tissue irritation if infiltration occurs OTHERS: Acidosis.mia WARNINGS May cause Wernicke-Korsakoff syndrome in acute alcohol intoxication – usually this is prevented by administering Thiamine 100 mg.9% NaCl D . lemon flavoring. Use with caution in geriatric patients. alkalosis. Use reasonable doses in amounts small enough not to occlude the airway.15 03/01/05 . HEPARIN CLASS Anticoagulant ACTIONS Inhibits the action of antithrombin III on various coagulation factors including factors IIa. glycerin. SIDE EFFECTS Other: Acidosis. Heparin also increases the rate of formation of antithrombin III-thrombin complex causing inactivation of thrombin and preventing the conversion of fibrinogen to fibrin. Xa. purified water. Use extreme precautions and aggressive management to protect the airway of patients with altered level of consciousness (LOC) providing suction PRN. XIa and XIIa. therefore the action of thrombin in coagulation is inhibited. the kind of sugar the body most readily absorbs. IXa. heparin also prevents the formation of a fibrin clot. CONTRAINDICATIONS Airway obstruction When suction is not available to maintain the airway of a patient with altered level of consciousness. INDICATIONS Acute Coronary Syndrome Pulmonary embolism Stroke CONTRAINDICATIONS Active bleeding Hemophilia Thrombocytopenia Suspected intracranial hemorrhage SIDE EFFECTS Hemorrhagic reaction WARNINGS Use with caution in women who are menstruating and pregnancy. hypokalemia WARNINGS For oral use only. By inhibiting the activation of fibrin-stabilizing factor by thrombin. DOSAGE Adult: utilize 15 gm dosage tube PRN Pediatric: utilize 15 gm dosage tube PRN HOW SUPPLIED Prefilled tube containing 15 grams of Glucose (d-glucose). Use care in application to avoid being bitten by patient. Draw a blue top tube for PT and PTT levels. INDICATIONS Hypoglycemia in the emergent setting when IV access cannot be obtained. and preservatives in an oral gel base. hyperglycemia. DOSAGE 5000 units IVP D .DRUG REFERENCE GLUCOSE ORAL (GLUTOSE) CLASS Carbohydrate ACTIONS Glutose 15 is oral Glucose gel containing 40% Dextrose (dglucose). Inhibition of factor Xa results in interference with thrombin generations. and burns CONTRAINDICATIONS History of hypersensitivity Presence or possibility of intracranial pressure (ICP) Pre-existing respiratory depression (i. emphysema.5mg of albuterol D . rash. Also reduces vagally mediated reflexes bronchospasms. 0. myocardial infarction.0. IM. blurred vision.EMERGENCY MEDICAL GUIDELINES HYDROMORPHONE HCL (DILAUDID) CLASS Narcotic analgesic ACTIONS Binds with opiod receptor sites in the CNS. fractures. nursing mothers. May repeat to a total of 4mg In elderly (65 yrs and older). headache. IM.5mg nebulized with 2. altering perception of and emotional response to pain. dislocations. COPD. by inhibiting acetylcholine at receptor sites. 0. May repeat as tolerated Pediatric: not approved for pediatric use IPRATROPIUM (ATROVENT) CLASS Parasympatholytic Bronchodilator ACTIONS Anticholinergic agent acts directly on the smooth muscles of the bronchial tree. cough.25 . SIDE EFFECTS Dry mouth.5mg slow IV.16 03/01/05 .e. INDICATIONS COPD Bronchospasm Asthma CONTRAINDICATIONS History of hypersensitivity Glaucoma Allergy to soy or peanut products Use caution in pregnancy. INDICATIONS Relief of moderate to severe pain from trauma. status asthmaticus CAUTIONS May produce respiratory depression Not to be used in abdominal pain or head injury patients SIDE EFFECTS Respiratory depression Nausea and vomiting Circulatory depression and cardiac arrest have occurred after rapid intravenous injection DOSAGE 1-2mg slow IV. hives DOSAGE One time use. causing a fall in blood pressure and a slight decrease in heart rate. INDICATIONS Hypertension CONTRAINDICATIONS Bronchial asthma Congestive heart failure Heart blocks greater than first degree Cardiogenic shock Severe bradycardia Chronic bronchitis Emphysema COPD Preexisting vascular disease SIDE EFFECTS Dizziness. Ketorolac has been used with morphine and meperidine without adverse effects. DOSAGE 0. INDICATIONS Mild to moderate pain. heartburn. and antipyretic effect. drowsiness. TRANDATE) CLASS Beta blocker ACTIONS Adrenergic receptor blocker (both alpha and beta). Nitroglycerine and Labetalol have additive effects and should not be used together except with great caution. and dizziness. itching. and 60 mg of the drug LABETALOL (NORMYDYNE. CONTRAINDICATIONS History of hypersensitivity Not administered to patients with allergies to aspirin or the non-steroidal anti-inflammatory drugs. in patients also receiving diuretics. Will decrease heart rate and should be used with extreme caution in patients with heart rates less than 100. It has analgesic. It does not have the sedative properties of the narcotics. diarrhea. Orthostatic hypotension will occur so patients must remain supine. anti-inflammatory. rash.25 mg/kg IV slowly over 2 minutes (20 mg dose for average adult) 5 mg IV over 2 minutes (max 300 mg) NOT FOR USE IN PEDIATRICS D . When administered IV for hypertensive emergencies. nausea. Ketorolac is considered a peripherally acting analgesic. increased airway resistance. SIDE EFFECTS Can cause edema. hypertension. nausea. Labetalol produces a rapid. Dizziness is the most common side effect and tends to occur in earlier stages of the treatment. This drug masks common signs of shock and hypoglycemia. WARNINGS Use with caution in patients with heart disease.17 03/01/05 .DRUG REFERENCE KETOROLAC (TORADOL) CLASS Analgesic/Non-steroidal anti-inflammatory ACTIONS Ketorolac is a non-steroidal anti-inflammatory drug (NSAID). WARNINGS May cause gastrointestinal irritation and bleeding. Unlike narcotics which act on the central nervous system. predictable fall in blood pressure within 5 to 10 minutes. vomiting. 30. DOSAGE 30 – 60 mg IM 30 mg IVP HOW SUPPLIED Prefilled syringes containing 15. EMERGENCY MEDICAL GUIDELINES LIDOCAINE HCL (XYLOCAINE) CLASS Antiarrhythmic ACTIONS Decreases ventricular automaticity and raises the ventricular fibrillation threshold. RESP: At toxic levels – respiratory depression and/or arrest. D . tinnitus. Average anesthesia of at least 60 minutes.5 – 1.000 CLASS Amide derivative ACTIONS Provides profound local anesthesia of intermediate duration. widening of QRS complex. CONTRAINDICATIONS None SPECIAL CONSIDERATIONS None 03/01/05 . cardiac arrest. (i. repeat with 0. euphoria. tremors. INDICATIONS PVC’s: >6 minute. Convulsions. the bradycardia should be treated first SIDE EFFECTS CNS: Drowsiness. NOTE: The larger dosage approach is recommended in cardiac arrest HOW SUPPLIED Prefilled syringes: 1% = 100 mg/10 cc 2% = 100 mg/5 cc Prefilled bag: 2 gm/500 cc D5W NOTE: Lidocaine jelly is a viscous preparation of 2% Lidocaine that facilitates nasotracheal intubation by providing lubrication and acting as a local anesthetic. Pediatrics: 1 mg/kg IV bolus. Can also be administered IM or Double-Dose down ET tube followed by an infusion at 2-4 mg/min. and Stokes-Adams syndrome If PVC’s occur in conjunction with sinus bradycardia. congestive heart failure and/or patient older than 70 years of age. R-on-T phenomenon.e. CONTRAINDICATIONS Lidocaine is contraindicated in second-degree heart block Mobitz II: complete A-V block. blurred vision. but with toxic levels – hypotension.18 LIDOCAINE HCL 2% WITH EPINEPHRINE 1:100. IV infusion should contain 120 mg LIDOCAINE/100 cc D5W.0 – 1. WARNINGS Lidocaine is metabolized in liver. CV: Rare. multifocal. infuse at a rate of 20-50 mcg/ kg/min. bradycardia.5 mg/ kg q 5-10 minutes if necessary to a total of 3 mg/kg. or in bursts of >2 or more in a row. muscle twitching. numbness.) DOSAGE Adults: 1.5 mg/kg* IV bolus. INDICATIONS Utilized prior to sternal interosseous infusions (FAST 1 or BIG). Ventricular tachycardia Ventricular fibrillation Prophylactic treatment in patients highly suspected of having myocardial infarction. shock. Maintenance infusion should be decreased by half in patients with liver disease and low cardiac output states. dizziness. the jelly may dry on the inner surface leaving a residue which tends to clump with flexion.19 03/01/05 . Lidocaine is metabolized rapidly by the liver. It suppresses the spread of seizure activity through the motor cortex of the brain. additional doses may be required. CONTRAINDICATIONS History of hypersensitivity to local anesthetics.DRUG REFERENCE LIDOCAINE HCL TOPICAL (XYLOCAINE 2% JELLY) CLASS Amide derivative ACTIONS Lidocaine stabilizes the neuronal membrane by inhibiting the ionic fluxes required for the initiation and conduction of impulses. the rate of absorption of local anesthetic agents following topical application occurs most rapidly after itratracheal administration. Lidocaine may be absorbed following topical administration to mucus membranes. Do not use the jelly to lubricate the endotrachial stylette.0mg/lb) of body weight. Romazicon can be used as an antidote. When used for endotracheal tube lubrication.1 mg/kg over 2 – 5 minutes. INDICATIONS Major motor seizures Status epilepticus Premedication before cardioversion Acute anxiety states CONTRAINDICATIONS History of hypersensitivity SIDE EFFECTS Hypotension. DOSAGE Adults: No more than 600 mg in a 12 hour period. or short intervals between doses. Monitor respiratory status closely. respiratory depression. May be Repeated after 15 – 20 minutes. headache. acutely ill patients. Pediatrics: Not to exceed 4. In such cases. There have been rare reports in which this residue has caused the lumen to occlude. amnesia. and duration of exposure. May cause respiratory depression. can result in high plasma levels and serious adverse effects. Maximum single dose 4 mg. Benzodiazepine ACTIONS Lorazepam is a benzodiazepine with a shorter half-life than diazepam. SPECIAL CONSIDERATIONS Use caution in patients with severe shock or heart block. LORAZEPAM (ATIVAN) CLASS Anticonvulsant/Sedative. since under such conditions there is the potential for rapid systemic absorption. and 4 mg in 2 ml of solvent. Debilitated elderly patients.05 mg/kg not to exceed 2 mg.5 mg – 1. thereby effecting local anesthetic action. drowsiness. Infants & Children: 0. nausea and vomiting. xylocaine 2% Jelly should be used with extreme caution in the presence of sepses or severely traumatized mucosa in the area of application. the specific site of application. In general. care should be taken to avoid introducing the product into the lumen of the tube. HOW SUPPLIED Lorazepam is supplied in ampules and tubex syringes containing 1. INDICATIONS As an anesthetic lubricant for endotracheal intubation (Oral or Nasal). WARNINGS Because of its short half-life. narrowing the lumen.0 mg. The onset is 3-5 minutes. It is effective when applied to intact skin. its rate and extent of absorption depending upon concentration and total dose administered. seizure activity may recur. HOW SUPPLIED 30 ml Aluminum tube D . Excessive dosage.5 mg/kg (2. 2. and children should be given reduced doses commensurate with their age and physical status. If allowed into the inner lumen.5 – 2 mg IVP Seizures: 0. may repeat after 15 minutes Neonate (<1 month): 0. May be repeated after 10 minutes. DOSAGE Anxiety: 0. blurred vision. Also suppresses the immune response. hypertension. bronchospasm. DOSAGE Usual dose is 125 mg IV but can be up to 30 mg/kg IV over 30 minutes. Decreases inflammation. fat and carbohydrate metabolism. and hiccups.20 03/01/05 . HOW SUPPLIED 50% Magnesium Sulfate injection. INDICATIONS Eclampsia including pre-eclampsia Torsades De Pointes Refractory V-fib/pulseless v-tach Status asthmaticus CONTRAINDICATIONS Renal diseases Heart blocks CHF Bradycardia Cardiogenic shock SIDE EFFECTS Respiratory depression. up to 4 – 6 gms. INDICATIONS Head trauma Severe asthma Allergic reactions COPD CONTRAINDICATIONS Patients with reduced immune system. stimulates bone marrow and influences protein. 5 grams {500 mg/ml (4mEq/ml)} prefilled syringe. DOSAGE Eclampsia: Loading dose 4 gm/100 cc IV 0. WARNINGS Must be reconstituted and used promptly. Onset of action may be 2-6 hours and thus should not be of use in the critical first hour following an anaphylactic reaction. Status Asthmaticus: 2 gm diluted in 10 cc NaCl administered IV over 3 minutes. The time interval to repeat the dose will be based on the patient’s condition. vertigo. HOW SUPPLIED Vial containing 125 mg D . malaise. headache.5 g/cc) MEHTYLPREDNISOLONE (SOLU-MEDROL) CLASS Corticosteroid/Anti-inflammatory ACTIONS Steroid which is used to stabilize cell membranes to decrease edema in head trauma and used as an anti-inflammatory drug. heart block. CHF. CHF. Dose may be repeated if patient is still symptomatic. SIDE EFFECTS May cause fluid retention. up to 4 – 6 gms. mainly by stabilizing leukocyte lysosomal membranes.9% NaCl wide open Maintenance dose 2 gm/100 cc at 100 cc/hr Pre-Eclampsia: Loading dose 4 gm/100 cc IV 0. bradycardia. Vials containing 5 grams in 10 cc solution (0.EMERGENCY MEDICAL GUIDELINES MAGNESIUM SULFATE CLASS Anticonvulsant/Antiarrhythmic ACTIONS Magnesium Sulfate is a central nervous system depressant and vasodilator. postural hypotension.9% NaCl over 15 minutes Maintenance dose 2 gm/100 cc at 100 cc/hr Refractory V-fib: 1 – 2 gm slow IVP over 1-2 minutes Torsades De Pointes: 1 – 2 gm diluted in 10 cc NaCl administered IV over 3 minutes. abdominal distension. It increases venous capacitance.0mg – 10.1 – 0. Can also be given IM or SC.21 03/01/05 . sedatives and beta-blockers. nausea and vomiting GU: Urinary retention RESP: Bronchial constriction. antihistamines. Morphine also decreases myocardial oxygen demand. decreases venous return and produces mild peripheral vasodilation. Premedication for tracheal intubation CONTRAINDICATIONS History of hypersensitivity Glaucoma Shock Alcohol intoxication Overdose Hypotension SIDE EFFECTS Over sedation. INDICATIONS Pain from acute MI Pulmonary edema Pain from burn Pain from Fx or dislocation to facilitate moving patient CONTRAINDICATIONS Pain due to trauma or acute abdomen Volume depletion or hypotension Head trauma Acute alcoholism Acute asthma History of hypersensitivity SIDE EFFECTS CNS: Euphoria.0mg IVP below 60 years old Peds: 0. INDICATIONS Conscious sedation.2mg/kg IM.5mg/kg dose 0. respiratory depression / arrest. It is potentiated by alcohol. respiratory arrest CV: Bradycardia. Avoid high doses! May cause hypotension. hypotension GI: Decreases gastric motility.DRUG REFERENCE MIDAZOLAM (VERSED) CLASS Benzodiazepine ACTIONS Short acting CNS depressant that impairs the memory. max 5mg MORPHINE SULFATE (MS) CLASS Narcotic Analgesic ACTIONS Morphine is a narcotic analgesic which depresses the central nervous system and sensitivity to pain.2 mg/kg IV slowly. Repeat with small increments every 5 minutes until desired response is achieved.0mg IVP over 60 years old 5. Should not be used in patients who have taken CNS depressants. Pediatrics: 0. alcohol.1mg/kg IV. hypotension. HOW SUPPLIED Ampule containing 10 mg/l cc D . drowsiness. DOSAGE Adults: 1 – 5 mg IV slowly. decrease cough reflex WARNINGS Morphine is detoxified by the liver. DOSAGE 2. max of 2.5mg – 5. pupillary constriction. headache. or narcotics. blurred vision. barbiturates. nausea and vomiting WARNINGS Sedative effects may be accentuated by concomitant use of barbiturates. might result in physical dependence DOSAGE 2mg – 4mg IVP or IM NALOZONE (NARCAN) CLASS Narcotic Antagonist ACTIONS Naloxone is chemically similar to narcotics. percodan Suspected acute opiate overdose Unconscious/unresponsive patient of unknown origin. dry mouth. marine injuries. or SC. chest pain. It competes for opiate receptors in the brain.4 mg/ml). then condition is probably not due to narcotic. DOSAGE Adult: An initial dose of 0. ventricular fibrillation. meperidine (Demerol). 0.1 mg/kg second dose if needed. belligerence. headache. pupillary dilation seizures. CONTRAINDICATIONS History of hypersensitivity SIDE EFFECTS AND ADVERSE REACTIONS CNS: Tremor. hypotension. INDICATIONS Complete or partial reversal of narcotic depression Respiratory depression secondary to narcotics or related drugs: heroin. Maximum cummlative dose of 2. methadone. Pediatric: 0. May be titrated to effect and repeated in 2-3 minutes if necessary.22 03/01/05 . pulmonary edema. CV: Hypertension. increased tear production. INDICATIONS Pain Management (burns. hydromorphone (darvon).01 mg/kg initial dose. vomiting WARNINGS Naloxone should be administered cautiously to persons including newborns of mothers who are known or suspected to be physically dependent on opiates – may precipitate an acute abstinence syndrome. hypotension WARNINGS Not indicated for use in children Use may impair the mental or physical abilities Use care with susceptible individuals. Use caution during administration as patients may become violent as level of consciousness increases.EMERGENCY MEDICAL GUIDELINES NALBUPHINE (NUBAIN) CLASS Synthetic narcotic agonist / analgesic ACTIONS Nubain is a potent analgesic. Use caution in patients with pre-existing cardiac disease or who have received potentially cardiotoxic drugs. it has only antagonistic properties. If no response after 10 mg. propoxyphene. and also 1 mg/2 ml prefilled syringes. It can reverse respiratory depression associated with narcotic overdose. For childern: 2 ml (0. sickle cell crisis) CONTRAINDICATIONS History of hypersensitivity Respiratory depression Hypotension SIDE EFFECTS Respiratory depression.4 mg – 2 mg may be administered IV. ventricular tachycardia. However.2 mg/ml) ampule D . agitation. codeine. nausea/vomiting. HOW SUPPLIED NALOXONE is available in 1 ml (0. fractures. 10 ml (. GI: Nausea.04 mg/ ml). sedation. sweating. Analgesic potency is essentially equivalent to that of morphine on a milligram basis. It also displaces narcotic molecules from opiate receptors. morphine (dilaudid). Naloxone is not effective against a respiratory depression due to non-opiate drugs. lomotil. pentazocine (talwin) .0 mg. May need to repeat Naloxone since duration of action of some narcotics may exceed that of Naloxone. IM. reflex tachycardia PRECAUTIONS Tolerance to nitrates easily develops which necessitates increasing the dosage. monitor vital signs often. Pain relief occurs within one minute and therapeutic effects can last up to 30 minutes. Pediatrics: Not indicated D . antianginal agent (coronary vasodilator) ACTIONS Increases coronary blood flow by dilating coronary arteries and improving collateral flow to ischemic regions. flushing. NITROGLYCERINE SL (NITROLINGUAL) (NITROBID) (NITROSTAT) CLASS Nitrate. antianginal agent (coronary vasodilator) ACTIONS Nitroglycerin is a direct vasodilator which acts principally on the venous system although it also produces direct coronary artery vasodilation as a result. DOSAGE 1 spray or 1 SL tab contains 0. Sublingual Nitroglycerin is readily absorbed. nausea and vomiting CV: Hypotension.23 03/01/05 . flushing Tachycardia SPECIAL CONSIDERATIONS Avoid Nitroglycerin in the setting of right ventricular infarction. DOSAGE 5 – 10 mcg/min IV drip. may increase by 5 to 10 mcg/min until desired effect is achieved or systolic blood pressure <100 mmHg. May repeat in q3-5 minutes for total of 3 doses. Produces vasodilation (venous greater than arterial). INDICATIONS Chest pain of suspected cardiac origin Acute pulmonary edema Hypertension CONTRAINDICATIONS Hypotension Patients <12 years old SIDE EFFECTS Headache Nausea and vomiting Hypotension Dizziness. There is a decrease in venous return which decreases the workload on the heart and thus decreases myocardial oxygen demand.4 mg Nitroglycerin Adult: 1 spray or 1 tab SL. Pediatric dosage is contraindicated. reduces myocardial oxygen demand. Use IV pump or Dial-A-Flow to deliver specific ml/hr. dizziness. INDICATIONS Angina Pectoris Hypertensive crisis Pulmonary edema with hypertension CONTRAINDICATIONS Patients with increased intracranial pressure Systolic blood pressure <100 mmHg Children under age 12 SIDE EFFECTS CNS: Headache. decreases preload and afterload.DRUG REFERENCE NITROGLYCERINE IV (TRIDIL) CLASS Nitrate. therefore results in peripheral vasodilation of arteries and veins. preload and afterload and increases cardiac output. hypoxemia. Mix 50mg in 250cc of D5W (200ug/cc) D .1ug/kg/min and titrated to effect. Decreases systemic resistance. Dosage has not been established in children. nausea / vomiting WARNINGS Wrap IV set in an opaque cover because the drug is light sensitive. INDICATIONS Hypertensive Crisis Congestive heart failure CONTRAINDICATIONS Recent use of Viagra within 24 hours Hypotension Aortic stenosis SIDE EFFECTS Tachycardia. DOSAGE 0. antianginal agent (coronary vasodilator) ACTIONS Transdermal absorption. headache. Increase dose every 3-5 minutes until desired effects are achieved. Caution must be used. dizziness WARNINGS Use with caution for right side injury / infarct. blurred vision. nausea and vomiting.EMERGENCY MEDICAL GUIDELINES NITROGLYCERINE TOPICAL (NITRO-BID) CLASS Nitrate. headache.24 03/01/05 . Start at 0. 1 inch = 15mg nitroglycerin NITROPRUSSIDE (NIPRIDE) CLASS Vasodilator ACTIONS Directly acts on vascular smooth muscle. hypotension.1– 10ug/kg/min. can result in toxic levels of cyanide. causes coronary vasodilation INDICATIONS Prophylaxis Treatment of angina pectoris CONTRAINDICATIONS History of hypersensitivity Hypotension (systolic < 100mmhg) SIDE EFFECTS Hypotension. dizziness. DOSAGE 1 inch applied topically to the chest wall. CO2 retention. seizures. INDICATIONS Post partum hemorrhage CONTRAINDICATIONS Oxytocin should be administered only to patients suffering from severe post-partum bleeding. tachycardia.25 03/01/05 . nausea and vomiting. WARNINGS Can cause overstimulation of the uterus and uterine rupture. and that there is not an additional fetus in the uterus. DOSAGE 50% N2O/50% O2 self administered by patient through the mask or mouth piece.DRUG REFERENCE NITROUS OXIDE (NITRONOX) CLASS Analgesic/Anestetic Gas ACTIONS Nitrous Oxide is a central nervous system depressant that causes rapid but easily reversible pain relief. administer supplemental O2 4 lpm/nasal cannula approx. It is essential to verify that the baby and the placenta have been delivered. SIDE EFFECTS Can cause hypotension. When administering Nitrous Oxide to a minor. HOW SUPPLIED Vials containing 10 units in 1 cc D . nausea and vomiting DOSAGE 20 units/1000 cc 0. arrhythmias. Upon discontinuation of Nitronox. 15 minutes. Musculoskeletal pain Burns. INDICATIONS Substernal chest pain of suspected cardiac origin that does not respond to nitroglycerin or morphine sulfate. SPECIAL CONSIDERATIONS Vehicle should be well ventilated during Nitrous Oxide administration (turn on the exhaust fan and open windows).9% NaCl infused at 120 – 150 cc/hr. coma. It is used in the emergency setting to control post partum hemorrhage by contracting uterine smooth muscle and lactation. (excluding respiratory tract burns) Normal and breech childbirth ?? CONTRAINDICATIONS Altered level of consciousness Patients intoxicated with drugs or alcohol COPD Acute pulmonary edema Pneumothorax Barotrauma Acute abdomen Head injury Respiratory tract burns SIDE EFFECTS Headache. dizziness. OXYTOCIN (PITOCIN) CLASS Hormone/Uterine stimulant ACTIONS Oxytocin is a naturally occurring hormone. obtain parental consent or contact the EDP for orders. giddiness. EMERGENCY MEDICAL GUIDELINES PROCAINAMIDE (PRONESTYL) CLASS Antiarrhythmic ACTIONS Slows conduction through myocardium Elevates V-fib threshold Suppresses ventricular ectopic activity Decreases automaticity of ectopic pacemakers INDICATIONS Persistent cardiac arrest due to ventricular fibrillation and retractory to lidocaine. PVC’s refractory to lidocaine V-tach refractory to lidocaine Patients allergic to lidocaine CONTRAINDICATIONS High degree heart blocks PVC’s in conjunction with bradycardia (treat rate first) Torsades de Pointes WARNINGS Procainamide should be discontinued when any of the following four occurs: • Rhythm resolved • Hypotension • QRS widens by 50% • Maximum dose of 17mg/kg administered SIDE EFFECTS May cause drowsiness, seizures, hypotension, bradycardia, heart blocks, nausea, vomiting, respiratory and cardiac arrest. DOSAGE Bolus drip mix 2 grams in 50 cc 0.9% NaCl run at 20mg/min. Maintenance drip 2 grams in 500 cc run 1-4 mg/min. May give up to 50 mg/min. for shock resistant or recurrent pulseless VT/VF. HOW SUPPLIED Vials containing 1 grams in 10 ml PROMETHAZINE (PHENERGAN) ACTIONS A derivative of phenothiazine (thorazine) with antiemetic; anticholinergic and antihistamine effects. INDICATIONS Severe nausea and vomiting Antiemetic Sedation CONTRAINDICATIONS Abdominal pain SIDE EFFECTS Dry mouth, blurred vision, dizziness, confusion, extra pyramidal symptoms (muscle rigidity, tremor) may occur. It may also worsen glaucoma, bladder obstruction or stenosis peptic ulcer. Hemothiazines tend to lower blood pressure and also lower the seizure threshold (i.e. make seizures more likely in seizure prone patients such as alcoholic or epileptics). DOSAGE Adult: 6.25 – 25 mg IM, IV, oral or rectal Pediatric: 0.2 – 0.5 mg/kg not to exceed 12.5 mg NOTE: Should be used following Morphine Sulfate administration. D - 26 03/01/05 DRUG REFERENCE PROPOFOL (DIPRIVAN) ACTIONS Diprivan injectable emulsion is an intravenous sedativehypnotic agent producing rapid sedation with minimal excitatory activity, however it has no analgesic properties. The actual mechanism of action is unknown. Onset of sedation usually occurs within 1-3 minutes. After bolus, titrating a maintenance infusion can control the level of sedation. After discontinuing the infusion the effects of the sedation clear within 5-7 minutes. INDICATIONS Induction and maintenance of general anesthesia in the intubated and mechanically ventilated patients. CONTRAINDICATIONS History of hypersensitivity to Propofol or its components (soybean oil, egg lecithin, glycerol) Patients in which sedation is not needed. SIDE EFFECTS Hypotension Bradycardia and decreased cardiac output Respiratory acidosis during weaning May produce copious secretions, larnygospasm and hypotension. Pain or burning at the injection site is common especially when the IV is in a small peripheral vein. SPECIAL CONSIDERATIONS Diprivan is extensively distributed throughout the body. It is eliminated from the body by the liver and the pulmonary system. No dosage adjustments are needed for patients with renal or hepatic failure. SODIUM BICARBONATE CLASS Alkalizing agent ACTIONS An alkalizing agent used to buffer acids present in the body during and after severe hypoxia. Bicarbonate combines with excess acids (usually lactic acid) present in the body to form a weak, volatile acid. This acid is broken down into CO2 and H2O. Sodium Bicarbonate is effective only when administered with adequate ventilation and oxygenation. INDICATIONS Metabolic acidosis due to: Cardiac arrest Shock Salicylate overdose Barbiturate overdose Keto acidosis Hyperkalemia Tricyclic antidepressant overdose CONTRAINDICATIONS Congestive heart failure Alkalotic states SIDE EFFECTS Metabolic alkalosis Hypernatremia Cerebral acidosis Sodium and H2O retention which can cause CHF WARNINGS Excessive Bicarbonate therapy inhibits the release of oxygen. Bicarbonate does note improve the ability to defibrillate. May inactivate simultaneously administered catecholamines. Will precipitate if mixed with Calcium Chloride. Administration should be guided by arterial blood gasses and ph. DOSAGE Adult: 1 meq/kg IV. Repeat with 0.5 meq/kg q 10 minutes Pediatric: 1 meq/kg IV. Repeat with 0.5 meq/kg q 10 minutes Infants: 0.5 meq/kg IV (diluted) slowly. May repeat in 10 minutes HOW SUPPLIED Prefilled syringes containing 50 meq/50 cc D - 27 03/01/05 EMERGENCY MEDICAL GUIDELINES SUCCINYLCHOLINE CHLORIDE (ANECTINE, QUELICIN) CLASS Depolarizing neuromuscular blocker ACTIONS Succinylcholine Chloride is a depolarizing muscle relaxant that prevents acetylcholine from binding to receptors on the post-synaptic neuron, thereby inhibiting the generation of an action potential and effectively paralyzing skeletal muscle. Complete paralysis is obtained within 1 minute and persists for approximately 2 minutes. It has no effects on consciousness whatsoever. INDICATIONS To facilitate intubation in patients where other efforts to obtain definitive airway control have failed. CONTRAINDICATIONS Any patients who can not be effectively ventilated with a BVM and oral airway. SIDE EFFECTS Prolonged apnea, bronchospasm, sinus arrest, tachycardia, bradycardia, PVC’s, increased ICP, muscle fasciculations. SPECIAL CONSIDERATIONS Since Succinylcholine Chloride effects only skeletal movement and not sensation, the patient should be sedated prior to administration. The use of Succinylcholine will not reduce the patients level of consciousness. The paramedic should verbally reassure the patient before intubation. If unable to intubate the patient, ventilate with BVM and oral airway until spontaneous respirations return (this should occur in approximately 5 to 7 minutes). Less than one percent of the population, and a higher percentage of the pregnant population, lack sufficient pseudocholinesterase to rapidly metabolize Succinylocholine. Paralysis may be dramatically prolonged in these patients. DOSAGE Adult: 1 mg/kg IVP repeated in 1 to 2 minutes if desired effect is not achieved. Pediatric: Same as the adult dose. Can be given IM if needed 3 mg/kg HOW SUPPLIED Vials containing 10 ml of a 20 mg/ml Concentration (200 total milligrams) TETRACAINE HCL (PRONTOCAINE) ACTIONS Tetracaine is an ophthalmic solution that produces anesthesia by preventing initiation and transmission of impulses at the nerve-cell membrane. INDICATIONS As an adjunct to facilitate irrigation of foreign bodies in the eye. Toxic/chemical burns to the eye. CONTRAINDICATIONS None in the emergency setting SIDE EFFECTS Rash, irritation, sensitivity SPECIAL CONSIDERATIONS Do not use if the Tetracaine HCL solution contains crystals, or if it is cloudy or discolored. Do not let patient touch or rub the eye after it is anesthetized as this can cause corneal abrasions. May be administered with contact lenses left in eye(s). Patch eye after administering. DOSAGE 1 to 2 drops of a 0.5% solution instilled into the affected eye. Pediatric dose will be the same. D - 28 03/01/05 DRUG REFERENCE THIAMINE (VITAMIN B-1) ACTIONS Thiamine is a sterile solution of Vitamin B1 (can not be produced by the human body). With total absence of Thiamine in the diet, body depletion occurs in approximately three weeks. INDICATIONS For the treatment of Thiamine deficiency Rapid restoration of Thiamine to prevent WernickeKorsakoff in the alcoholic and malnourished patient. Administered to individuals (prior to dextrose) with marginal thiamine status to avoid precipitation of heart failure. CONTRAINDICATIONS History of hypersensitivity WARNINGS Serious hypersensitivity/anaphylactic reactions can occur, especially with repeated dosages. SIDE EFFECTS A feeling of warmth pruritus, urticaria, weakness, sweating, nausea, restlessness, throat tightness, cyanosis, pulmonary edema, and GI bleeding. DOSAGE 100 mg IVP prior to administration of highly concentrated Dextrose solutions. HOW SUPPLIED 100 mg in 1 ml VASOPRESSIN (PITRESSIN) CLASS Antidiuretic Hormone ACTIONS Systemic vasoconstriction, increased contractility, increased cerebral and coronary perfusion without undesired effects of myocardial ischemia and irritability. INDICATIONS Ventricular fibrillation Pulseless ventricular tachycardia CONTRAINDICATIONS All other pulseless dysrhythmias SIDE EFFECTS None in the pulseless patients WARNINGS Currently only to be used for pulseless V-fib and V-tach patients DOSAGE 40 units IVP, one time administration. No Epinephrine for 10 min post administration. D - 29 03/01/05 EMERGENCY MEDICAL GUIDELINES VECURONIUM BROMIDE (NORCURON) CLASS Nondepolarizng neuromuscular blocker ACTIONS Norcuron is a nondepolarizing neuromuscular blocking agent of intermediate duration. It acts by competing for cholinergic receptors at the motor end-plate. Clinically required neuromuscular blockade will occur in 2.5 to 3 minutes and last approximately 25 to 30 minutes. INDICATIONS Long term paralysis for flight or ground transport to facilitate control of combative patients that have already been intubated. CONTRAINDICATIONS Any patient that an RSI has NOT been successful. SIDE EFFECTS Prolonged apnea, tachycardia, bradycardia, bronchospasm, muscle fasciculations. SPECIAL CONSIDERATIONS If Succinylcholine is used prior to Norcuron, the administration of Norcuron should be delayed until the patient starts recovering from the Succinylcholine-induced neuromuscular blockade. Prior administration of Succinylcholine may enhance the neuromuscular blocking effect of Norcuron and its duration of action. The effect of prior use of other nondepolarizing neuromuscular blocking agents on the activity ofNorcuron has not been studied. Norcuron should only be given to a pregnant woman if clearly needed. DOSAGE Adult: Initial dose: 0.1 mg/kg IVP Maintenance dose: 0.015 mg/kg IVP (25 – 40 min. after initial dose) Subsequent maintenance doses, if required, may be administered at 12 – 15 minute intervals. Pediatric: Same as the adult dose. HOW SUPPLIED Vial with 10 mg of a sterile nonpyrogenic freeze-dried buffered cake. VERAPAMIL (ISOPTIN OR CALAN) CLASS Calcium channel blocker ACTIONS Inhibits slow channel calcium activity in cardiac and smooth muscles. It blocks the slow inward current due to changes in both calcium and sodium flux. INDICATIONS Paroxysmal Supraventricular Tachycardia refractory to Adenocard in the stable patient Symptomatic Atrial Fibrillation and Atrial Flutter (above 130 BPM with chest pain and SOB) CONTRAINDICATIONS Hypotension (Blood pressure below 120 systolic) Bradycardia History of Wolf-Parkinson-White syndrome SIDE EFFECTS Causes reflex increase in adrenergic tone due to peripheral vasodilation if given for tachycardia due to Wolf-Parkinson-White syndrome. Decreased blood pressure and increased adrenergic response may extend an acute M.I.. May also cause symptomatic bradycardia. Dizziness, headache, fatigue, AV block, peripheral edema, nausea, and asystole. WARNINGS Verapamil may induce severe hypotension and pre-dispose to V-fib if given to V-Tach. If uncertain of origin (V-Tach or wide complex PSVT) treat the rhythm as V-Tach; Verapamil should be avoided. DOSAGE 5 mg slow IVP (0.075 – 0.15 mg/kg) 10 mg slow IVP in 15 minutes, if necessary D - 30 03/01/05 AEROMEDICAL Aeromedical 03/01/05 A-1 . e. They use an on-call staff and perform long-rang missions. maintenance. Aircraft. B-2 Power: 2x738 shp Turbomeca Arriel 1E2 C-1 MTOW: 3. >150-200 miles) interfacility transports and can operate in weather conditions that may restrict rotorwing aircraft.950kg (4. The private service model represents primarily fixedwing aircraft vendors.385lb) Maximum useful weight: 1. This model is funded primarily through automobile and private insurance billing.980kg (4.700lb) Maximum useful weight: 1.350kg (7.595kg (3.250kg (9. Anthony’s Hospital in Denver. Fixed-wing transport had limited use until World War II.562lb) 03/01/05 . A hospital usually a tertiary or academic center sponsors and/or owns the air medical program. This model has proven to be the most economical by far. and pilots. EDUCATIONAL SECTION THE HISTORY OF AEROMEDICAL TRANSPORT Transport of injured patients by air can be traced to World War I. and medical flight personnel. The private industry aviation vendor supplies the aircraft. These models are primarily funded through insurance and direct cash-for-transport exchanges. pilots. helicopter air medical transport significantly reduced battlefield mortality and became an important and highly visible part of the military trauma system.156lb) Maximum cruise speed: 133kt Maximum range: 294nm (B-2). Awareness of the role military air medical transport made the extension of helicopter use to the civilian arena inevitable. The modern era of air medical transport began during World War II. Since then. equipment. During the Korean and Vietnam conflicts. Fixed-wing transports are particularly useful for long distance (i. The government/private partnership has just came into existence over the last several years. (i. when the Allies evacuated large numbers of casualties by air. AIRCRAFT TYPES OPERATING IN FLORIDA Aeromedical providers who utilize the BK117: Orange County Fire-Rescue Aeromed Bayflite Trauma One Air Care Team Life Flight Eurocopter Kawasaki BK117 Power: 2x684 shp Allied Signal LTS B-1. the number of air medical programs has grown steadily. The government agency supplies the crew housing.618kg (3.299lb) N3 Maximum cruise speed: 150kt Maximum range: 464nm ORGANIZATIONAL MODELS The hospital based model represents the most common type of approach for providing air medical service to the community. when helicopters transported wounded patients in Burma. These models are predominantly operated by a law enforcement agency with medical staffing being supplied by the local hospital or fire department. AEROMEDICAL GUIDELINES. fixed-wing. primarily in C-47 transports. when a French fighter plane was used to evacuate a wounded Serb. The successful air medical experience in Vietnam proved the ability of helicopters to transport injured patients directly from trauma scenes to specialized trauma care centers.365lb) N2 Maximum useful weight: 1.307kg (11. These services generally do not respond directly to the scene. supplies.e. Some services that began with a single rotor-wing aircraft have added additional helicopters. No taxing districts are needed and the start up fee’s are minimal for the local government. The first air medical transport program was established in 1972 at St.370lb) Maximum useful weight: 1. Colorado. These models are A-2 Aeromedical providers who utilize the S-76C+: Palm Beach County Health Care District Miami Children’s Hospital Sikorsky S-76C+ Power: 2x856 shp Turbomeca Arriel 2S1 MTOW: 5. 292nm (C-1) Aeromedical providers who utilize the Dauphin: ShandsCair Eurocopter AS365N2 Dauphin Power: 2x739 shp Turbomeca Arriel 1E2 N2 Power: 2x851 shp Turbomeca Arriel 2C N3 MTOW: 4.EMERGENCY MEDICAL GUIDELINES primarily funded through local taxing districts. The LifeStar aeromedical program was the first in the nation to use this model. Air medical transport services now provide much more than trauma scene response. Tampa General Hospital-Aeromed) The governmental agency model has been used successfully for years. Transfers from rural emergency departments into tertiary care centers occur on a routine basis and in some cases account for 100% of the call volume of the program. reaching more than 160 programs today. or ground critical care transport capability. and maintenance services are often provided by an aviation vendor. helicopters are increasingly used for emergency medical services.845lb) Maximum cruise speed: 140kt Maximum range: 353nm Because of their unique capabilities. Aerospatiale Dauphin SA 365N. Bell 222. Twin-engine helicopters offer a increased safety margin. ground personnel and themselves.996lb) Maximum useful weight: 1.651SM Aeromedical providers who utilize the EC-135: Martin County Fire Rescue Holmes Regional First Flight Collier County EMS Baptist Life Flight Florida Flight 1 Eurocopter EC-135 P1/T1 Power: 2x732 shp Turbomeca Arriel 2B1 T1 Power: 2x621 shp Pratt & Whitney PW206B P1 MTOW: 2.360lbs Max Cruise Speed: .280kg (2. The ability of the helicopter to get in an out of accident scenes. teamwork and coordination are essential for safe helicopter EMS operations.767lb) T1 Maximum cruise speed: 139kt Maximum range: 322nm AEROMEDICAL PROGRAM OPERATION HELICOPTER ORIENTATION AND SAFETY Aeromedical providers who utilize the A119 Koala: St. Lucie County FireDistrict Agusta A119 Koala Power: 1x1002 shp Pratt & Whitney MTOW: 2.734lb) P1 Maximum useful weight: 1.AEROMEDICAL Maximum cruise speed: 155kt Maximum range: 385nm Max Useful Wt: 7. use less fuel and cost less to operate.850kg (6. single-engine helicopters require less time to start.Limitations exist under both visual flight rules (VFR) and instrument flight rules (IFR). Training. usually provide increased payload and require more maintenance and more time to start than the single engine aircraft.255kg (2. Bell 412. the MBB BK117. Helicopter Capabilities Each helicopter has different capabilities.436NM. Types of Helicopters There are many types of helicopters in service in the EMS industry. the patient. Bell 206 LIII Long Ranger. Operational Limitations Ceiling/Visibility . It is imperative that ACMs receive mission-specific training to ensure a safe standard of operation and preclude any errors which could effect the safety of flight.822lb) Maximum cruise speed: 156kt Maximum range: 550nm Aeromedical providers who utilize the Gates Learjet 25: Power: GE CJ610 MTEW: 15. Aeromedical crew members (ACMs) can contribute significantly to the safety of the mission.82 Mach. Aerospatiale Twinstar AS 355F. The standard in the EMS industry is the twin-engine aircraft due to the increased safety margin to the aircraft personnel and patient. the bell 206 BIII Jet Ranger. MBB BO105.732lb) Maximum useful weight: 1. 1.996lb) Maximum useful weight: 1. Aerospatiale A Star AS 350 and the Agusta A119 Koala. Twin Engine: Twin-engine aircraft include but are not limited to.170kg (2.000lbs 03/01/05 A-3 . however. Lucie County Sheriff’s Office & St. Ambient Temperature .720kg (5.240kg (2.203lb) Maximum useful weight: 1. 465kts.600kg (5.Most aircraft have both an Aeromedical providers who utilize the BO105: Life Net Life Flight Lee County EMS Eurocopter BO105 Power 2x500 shp Rolls-Royce Allison 250 C28C MTOW: 2.550lb) Maximum cruise speed: 130kt Maximum range: 278nm Aeromedical providers who utilize the A109: Baptist Aeromed Agusta A109 KII Power: 2x640 shp Pratt & Whitney Canada MTOW: 2. Agusta 109A and Sikorsky S76. remote areas and hospital pads quickly is key in delivery of lifesaving care. 535mph Max Range: 1.720kg (5.290kg (2. In general. The helicopter most commonly used in EMS programs are as follows: Single Engine: Single-engine aircraft include but are not limited to. including aeromedical flights. hover OGE (out of ground effect . The degree of the slope that may be negotiated varies. The hot-mike should be used appropriately. The ACM should advise the pilot prior to use of distracting medical equipment. Patient needs. pilot experience. Oxygen requirements . High-altitude landings may not be possible without decreasing the weight of the helicopter. Thunderstorm and severe weather (TRW) . Night protocols should be strictly adhered to. tall buildings. Loose articles must be securely stowed when no in use. ACMs should be highly disciplined in the use of proper terminology to avoid confusion or misinterpretation of instructions during any phase of the mission. safe approach and departure.specifies rules for air taxi and commercial operators. This decreases the “Golden Hour” time that the patient needs to have the best chance of survival. are governed by appropriate FARs.Most programs require a minimum clear area (i. also should be discussed with the pilot. Helicopter Safety Pilot-In-Command Responsibilities According to federal air regulations. Non-essential conversation should be kept to a minimum during critical phases of the flight. The safety of the EMS mission can be enhanced through ACM cooperation.The amount of wind in which a helicopter can operate varies. airspace. The use of red or amber lighting inside the cabin is preferred because bright Federal Aviation Regulations (FARs) FARs are written and enforced by the Federal Aviation Administration.) and other factors. This figure represents the highest altitude at which flight characteristics and handling for the aircraft have been satisfactorily demonstrated. All passengers must function in and around the aircraft under the pilot’s direction.details general operating and flight rules for aircraft flying within U.e. wind direction and velocity. such as needles and IV catheters. 100' x 100' night) for use as a helicopter landing zone. other than local government (local sheriff’s office’s) or military.Extremely dusty landing zones can reduce visibility to zero due to rotorwash disturbance. etc. The pilot should be warned of converging traffic or of obstructions on landing or takeoff. gust spread. Flotation devices may be required for the aircraft for over the water operations. FAR Part 135 .The limitations section of the helicopter flight manual contains service ceiling information. ACMs must know the location and operation of all exits. such as on board suction.The FAA requires the use of supplemental oxygen by the pilot and passengers above 10. depending on factors such as aircraft type. are regulated under Part135 of the FAR. depending on factors such as aircraft type. ACMs also will ensure the tail rotor is secured by either standing watch themselves or by designating a public safety official upon landing.Flight is prohibited in known icing conditions Wind . should be protected. etc. Surface conditions . Confined areas . etc.These situations should be avoided unless circumnavigation can be safely accomplished. All civil aviation operations. Performance . Terrain Slopes . Confined areas present special problems such as obstacles. Altitude Limitations Service ceiling .S. Excessively rocky or otherwise uneven landing surfaces may not provide a solid enough base for the aircraft. such as altitude or heating/air conditioning requirements. Head winds affect the range of the helicopter and may extend the ETAs. ACMs must always remain clear of the flight controls and switches not designated specifically for medical personnel use. The use of “canned” landing zones are being discouraged due extended transport times from the scene to the “canned” area. Communications with the pilot must be maintained at all times. Medical oxygen does not comply with this regulation. Icing . ACMs must be trained to use all medical equipment and systems used for patient care. turbulence (mountains. responsibility for all aspects of the safe operations of the aircraft rests with the pilot-in-command. Sharp objects. ACMs should direct the activities of ground personnel around the helicopter.Aircraft performance is adversely affected by increasing altitude.increased power requirements). lighting. vertical let-downs.EMERGENCY MEDICAL GUIDELINES upper and lower ambient temperature limit.Normal Operations Seat belts and shoulder harnesses must be used by all personnel. ACM Duties .ACMs must be trained to use all the radio equipment located on board the aircraft. The number of assistants approaching the helicopter should be kept to a minimum. It is recommended that the helicopter LZ be located as close to the actual scene as possible.000 feet under certain conditions.Slope landings require greater precision on the part of the pilot. FAR Part 91 . A-4 03/01/05 . pilot experience. 60' x 60' day. surface condition. Most aeromedical programs. transmissions and rotor systems emit loud. Observers When operating in and around the aircraft. blade clearance may be deceptive. high-frequency noise. The observer shall not disturb or manipulate any equipment. The degree of patient injury or illness has absolutely no bearing on whether or not a flight may be safely accomplished. fire. NEVER approach a aircraft without the pilots or the ACMs permission to do so. Lights should be off or dimmed during night landing approaches. such as sheets. Safety is a dynamic concept and must be continually addressed. Unsecured Landing Zone The ACM shall ensure adequate security of the helicopter while the pilot remains in the aircraft. Blades may flex downward. Don’t be complacent. he or she shall always follow the flight teams instructions. Make suggestions to improve current conditions. Lightweight articles. can cause injury. Permanent high-frequency hearing loss can occur with extended exposure if hearing protection is not used. It is low enough to cause severe injury or death. such as IV poles. tail rotor failure. Safety Attitudes Safety is everyone’s responsibility. ACMs and ground personnel must ensure all wires are clear in the approach and departure path of the aircraft. Always conduct yourself as a role model for safety around the aircraft. hit the rotor blades. When the observer is occupying the aft compartment. The observer will adhere to strict aircraft discipline at all times. Emergency training should include the topics listed in Title 14 Code of Federal Regulations Part 135. especially when turning slowly in windy conditions. the ACM should proceed to a pre-designated point referenced from the aircraft. The A-5 03/01/05 . Stay up to date on the latest changes in aircraft safety. skills. hydraulic failure.AEROMEDICAL white lights destroy the pilot’s night vision. The following topics also should be covered: Pilot directives Stow all equipment. Ground agencies who have been trained in helicopter/landing zone safety can be used to secure the area while the aircraft is on the ground. mattress pads and gravel. Hazard Recognition Main Rotor System On slopes or uneven ground. Avoid tall objects which may AIR TRANSPORT GENERAL INFORMATION Training of flight has evolved into a process of acquiring specialized knowledge. electrical failure. Safety is the highest priority. Wires Wires tend to be more hazardous than other obstructions because they are difficult to see. restrain the patient securely and lock and tighten seat belts/shoulder harness. extremely strong winds are produced. After the emergency. ACMs should be aware of these conditions so they can respond appropriately. Tail Rotor System All personnel should be alert to the hazards of the tail rotor system. Noise Helicopter engines. The safety of the aircraft and its personnel are paramount. Never attempt to influence the decision of the pilot or that of another ACM. as appropriate. Rotor Wash During the landing and departure of helicopters. The ACMs assigned to the aircraft and the pilot have the final word when it comes to the safety and operation of the aircraft on the scene. and experience.Emergency Procedures Some of the malfunctions/emergencies that may occur during transport include engine failure. NEVER approach or leave an aircraft uphill. ACMs or ground crews should not carry tall objects. inadvertent meteorological conditions (IMC) and emergency aircraft shutdown. transfer the patient to a safe location. ACM Duties . If immediate egress is warranted. especially to the eyes. remove all survival equipment and check to ensure the proper operation of the ELT. ALWAYS approach or leave an aircraft downhill. High speed makes tail rotor blades difficult to see. or initiate CPR on stretchers under turning rotor blades.331. the observer is under the direction of the pilot and air crew members. Emergency procedures should be discussed and planned as part of the pre-flight briefing. providing the aircraft can be seen from the air. autorotation. Question anything that you do not fully understand regarding aircraft operation and safety. Crewmember Emergency Training. Remain at or near the aircraft. Standing downwind can dramatically increase the severity of rotor wash. Success or failure in dealing with an emergency usually depends on how prepared you are. FATIGUE HYPOXIA Hypoxia is defined as a inadequate supply of oxygen for cell function. CO poisoning. and the physical condition of both the patient and the flight team. shock. and MAST (Military Anti-Shock Trousers) warrants frequent volume checks of the cuff and bladder. resulting in shock. Glass bottles should be vented if they cannot be replaced with plastic bags. alcohol. when applied to flight. Hypoxia and hypoxemia results and can manifest itself in crew members. Hypoxemia is an abnormal deficiency of oxygen content in the blood. • Hypoxic hypoxia is an inadequate Pa02 caused by reduced oxygen in the atmosphere or an inadequate gas exchange at the alveolar . • Critical stage . smoking. it is advisable to leave nasogastric tubes.carrying capacity of hemoglobin.95% to 21% of the earth’s atmosphere. decreased level of consciousness and belligerence are experienced.night vision decreases by approximately 28%. The use of endotracheal tubes. they are: BAROMETRIC PRESSURE The effects of barometric pressure change and hypoxia are best represented through a combination of the gas law of Boyle and that of Dalton. headache. Gforces. consumed alco- 03/01/05 . hypoxia. These stresses are barometric pressure. When any crew member has an upper respiratory tract infection. night vision is reduced 50%. • Histotoxic hypoxia is prevalent when the tissues are unable to utilize the available oxygen. Compensation stage .capillary membrane. fitness. duration of flight. blood loss.” The significance of this law. the volume of a given gas is inversely proportional to the pressure to which it is subjected. air splints. Nausea and vomiting occur. mainly in children. Dalton’s law of partial pressure states that “the pressure of a gaseous mixture is equal to the sum of the partial pressures of the gases in the mixture. This percentage remains constant. Crew members must be aware that flying with upper respiratory complications can lead to damage to the eardrum. There are nine stresses of flight that we will go over. alcohol use. in which altitude and pressure changes are more extensive than in a pressurized cabin. If signs and symptoms of hypoxia in patients or air crew members are ignored. weather. noise.inability to remain upright is rapidly followed by unconsciousness.EMERGENCY MEDICAL GUIDELINES stresses of flight. • Stagnant hypoxia occurs when the cardiac output does not meet the demands of the tissues. pressurized versus unpressurized environment. smokes.initial awareness of symptoms. seizures.” Oxygen accounts for 20. temperature. acute asthma. hypoxia. temperature. thermal stress. When transporting patients with such conditions as pneumothorax. smoking. venous pooling and possibly cardiac arrest. chest tubes. affecting not only the patient’s condition but the flight crew as well. Conditions that influence these stresses include altitude. and gravitational forces. amnesia.in addition to all indifferent stage signs. etc. as well as in patients. pneumothorax. Boyle’s law states that “at a constant temperature. rotational shifts. as with cyanide poisoning. dehydration. heart attack. foley catheters. and barometric changes. Supplemental oxygen therapy is a prime intervention for both air crew members and patients alike. Several general factors contribute to the stress of the flight: general health status. These include pneumonia. they may result in death. diet. nausea. noise. vibration. or gastrointestinal or genitourinary complications. vibration. • • Disturbance stage . allowing for increased expansion of a gas within a closed or semi closed space. Air hunger. The type and amount of oxygen delivery depends upon the condition of the patient and/or air crew member. and other factors. bowel obstruction. The four categories of hypoxia are: A-6 A multitude of factors contribute to fatigue in the transport team. There are four stages of hypoxia. COPD. • Indifferent stage . coma and death. fatigue. is that as altitude increases. Hypoxia resulting from any abnormal condition experienced by the air crew member or patient is intensified by altitude change. third spacing. • Anemic hypoxia is caused by a reduction in the oxygen . This is especially critical in the transport of patients in an unpressurized aircraft. as demonstrated in sickle cell anemia. particularly in an unpressurized cabin at higher altitudes. barometric pressure decreases. but the gas expands at altitudes directly related to the change in barometric pressure and there is less oxygen available at higher altitudes. and the person is unaware of the symptoms. Other contributing factors also can increase the incidence of hypoxia. especially during ascent and decent. are a subject of great concern but one that has been given little consideration. and similar equipment open to gravity or low suction. Internal gas expansion and possible deterioration of the patient’s status are thus minimized. heart and respiratory rate increases. increased decibel levels in the aircraft interfere with the ability to properly auscultate lung. the incidence of significant fatigue increases. throughout the flight. The mechanical function of the aircraft contributes to fatigue. did not eat properly before or during the shift. can have either an antagonistic or a synergistic effect. this may enhance the -G forces by pooling the blood in the A-7 03/01/05 . high-altitude. increased heart rate and decreased blood pressure. gravitational pull. Second. Subjective Signs: At 5. the vasoconstriction caused by vibration can override or impair the function of the body’s cooling mechanism by decreasing the ability to sweat. VIBRATION.000 feet At 20. both mentally and physically. Patient positioning in some aircraft may minimize or enhance the effects of G-forces. late vasoconstriction and decrease sweating. heart. particularly during hot-weather operations. nausea. dehydration. hol 8 to 12 hours before the flight. depending on whether the change is to greater heat or more cold. jerking of upper limbs. headache. tingling. seizures and rapid unconsciousness. fatigue. cyanosis.000 feet At 18. Compounding these stresses are the crew’s emotional and physical stresses of treating a critically ill patient who is enduring the same physiologic effects. dizziness and hot and cold flashes.000 feet blurred vision and/or tunnel vision air hunger. poor judgment and muscular incoordination. in rotorcraft. The latter two factors relate to blood pooling. Centrifugal force tends to alter the blood flow in the body in proportion to the amount of force imposed. the opposite occurs during negative (-G) application. Whether the duration of the flight is a short 15 to 30 minutes or is extended for 4 to 6 hours. In addition. Adaptive monitoring procedures include palpation of blood pressures and observation and palpation of the chest (for abnormal excursion or increased dyspnea) and abdomen (for increased distension or guarding). NOISE.000 feet At 15. AND THERMAL STRESS Noise creates a twofold problem for the flight crew. the effects of fatigue will be noticed by the crew and patient. winds. apprehension. When positive (+G) forces are applied to the body. euphoria and belligerence. constant exposure to aircraft noise not only temporarily affects hearing ability but may promote hearing loss over a long period. confusion. numbness. and thermal changes (turbulence caused by the meeting of two air masses of different temperatures) contribute to fatigue. On ascent.AEROMEDICAL SIGNS AND SYMPTOMS OF HYPOXIA Objective Signs: At 10.consider positioning the patient with head toward the back (aft) position of the aircraft. and centrifugal force. storms. Factors influencing (G) forces are weight and its distribution. or has not had a restful sleep.000 feet At 10. First. Vibration and thermal changes. blood tends to pool in the lower portions of the body. Signs and symptoms may include edema.000 feet hyperventilation and impaired task performance. The body’s primary response to heart exposure is vasodilatation and activation of the cooling mechanisms. Since the majority of flights are at lower altitudes and of short duration. as follows: Ö Cardiac . particularly in a fixedwing aircraft. flight crews must be cognizant of these physiologic stressors in long-distance. THIRD SPACING AND DEHYDRATION The aforementioned vasoconstrictive and vasodilatory effects can contribute to the stressors that cause “third spacing” and dehydration. weather conditions such as high or low temperatures. Consequently. Cold exposure and vibration stimu- GRAVITATIONAL FORCES Gravitational (G) forces are most relevant in relation to the patient’s position in the aircraft. or multiple short-scene flights. the effects are not often evident. and bowel sounds along with blood pressures. However. The noise level and vibration created by the propellers of the fixed-wing aircraft or the rotor blades of the helicopter are continual stressors to the crew and the patient. and ensure appropriate loading of the most critical patients take place. “www. Once the extrication (if needed) is completed.Consider positioning the patient with head toward the front of the aircraft. No. number of patients. “The Effects of Long Duration Acceleration” Aviation Medicine. References: Airborne Patient Care Management Mosby’s Medical and Nursing Dictionary. presence of hazardous materials. no information shall be given unless its related to the landing zone and safety of the aircraft until the aircraft is on the ground. This may help reduce the risk of a transient increase in ICP on lift-off. National EMS Pilots Association. upon the aircraft’s arrival you not only receive the benefit from its equipment but you also obtain more manpower to treat the patient. the main purpose of rotor-wing aircraft in the EMS environment is for rapid transport to specialized tertiary care centers (i. Ö Fluid Overload . Secondly.fama. trees or bushes in LZ. 1980: 3 Air-Medical Crew National Standard Curriculum. cell-phone towers. If no GPS available. If multiple patients are involved. Placement of a tail rotor guard is a priority once the aircraft has arrived and is secured on the ground. determine if the area is large enough to land a helicopter safely. uneven terrain • Communications: Should be kept to a minimum. Notify aircraft’s dispatch as soon as possible if more than one aeromedical provider is responding to the scene. This cannot be obtained if the aircraft is sitting at the base site 20 minutes from the scene with extrication in progress.org” Physiological Training. Space and Environmental Medicine 57. we have only one (1) hour/60 minutes from the “TIME OF INJURY” to get the patient to the “OPERATING ROOM”.). herbicides. Ö • AIR TRANSPORT PRE-HOSPITAL Radio communication with scene contacts shall be limited to information that affects the flight crews preparation (i. trauma centers). cervical spine immobilize the patient and prepare to move toward the aircraft. When the aircraft is on location.e. FAA. or weapons of mass destruction (WMD) are involved. 4 NEMSPA. • Weather: Advise dispatch to relay on-site information to inbound helicopter. Starting IV’s or splinting is not justification for a delay. No unauthorized vehicle traffic around the aircraft. • Security: Aircraft safety is a priority.” Journal of Emergency Nursing 13. Head Injury . firstly. • Hazardous Material: No patient will be transported via helicopter unless they are first decontaminated if pesticides. Florida Air Medical Association. PRE-HOSPITAL CONSIDERATIONS • • A-8 Day Landing Zone Size: 60 feet x 60 feet Night Landing Zone Size: 100 feet x 100 feet 03/01/05 . The general rule for flight programs is to be “on scene” no more than 10 minutes from the time of initial landing unless extrication or airway problems arise. etc. “Guidebook to Landing Zones” FAMA. If multiple patients are involved. 1st Ed SELECTING AN ON-SCENE LZ First. Do not delay the response of the aircraft because of extended extrication. DOT Manual. free of debris that would blow up into the rotor system. • Obstacles: High-tension wires. No. GPS: Advise ASAP landing zone coordinates. Only transmit needed safety information when on approach. give nearest cross street reference. 2003 “Thermoregulatory Responses to heat and vibration in men.” Aviation.Consider positioning the patient head first. with feet toward the back (aft) portion of the aircraft. “The nine stresses of Flight. A paved roadway. the flight team must communicate carefully with the incident commander. All activity at the scene should be directed toward moving the patient to the helicopter. The landing surface should be flat and firm. it is highly recommended that shutting down of the aircraft be accomplished if reconfiguration of the aircraft is needed.e. which may assist in myocardial perfusion. 11 Basic Human Physiology.EMERGENCY MEDICAL GUIDELINES upper part of the body. • Patients: Advise ASAP if multiple patients. parking lot or other concrete surface is preferred. The reason being is two-fold. This will allow the pilots to communicate and coordinate their approach. • Scene Personnel: Never approach the aircraft unless directed to do so by the pilot or air crew members on scene. This may enhance the +G forces by pooling the blood in the lower extremities. the pilot. This may enhance the +G forces by pooling the blood in the lower extremities. Remember. PERSONAL SAFETY & NIGHT LANDING When an LZ is established other than on a roadway that has been shut down by public safety. are very helpful in finding accident locations and do not affect the pilot’s night vision. chinstraps must be securely fastened (no loose ball caps or helmets blowing up through rotors). If you have a radio and are monitoring the LZ frequency announce “WAVE OFF. The “Golden Hour” can be further broken down. Turn-off non-essential lights. and obstructions such as trees. Assure that everyone wears eye protection. Scene security MUST be maintained and not abandoned at any time during flight operations. GROUND GUIDE CONTINUED The Ground Guide’s sole purpose is to ensure scene security thru protection from the dangers of an idling helicopter. This action is performed to further identify potential problems and execute the proper approach should the pilot need to abort the landing. ensure that the pilot or flight crew member aboard the helicopter see your hand gestures in order to acknowledge your request. Once verbal and visual communication is established with the flight crew and a LZ brief is given. Deploy as many public safety officials as necessary to meet the security requirements of each LZ.AEROMEDICAL Touchdown Area: the touchdown area should be a square with 60-foot sides. Scene security does not end when the helicopter lands. (i. Anyone at anytime can wave-off the helicopter should you see anything of concern to you. increased to100 x 100 feet at night. That person must wear eye protection. posts and large rocks. The only hand signal that you need to be aware of is the “WAVE-OFF”. it is just beginning. Once the helicopter has landed. (i. WAVE OFF. Keep spectators at least 200 feet from the touchdown area. vehicles. The EMT-Paramedic has a “Golden 10 Minutes” to assess the critical trauma patient and provide ESSENTIAL needed on-scene management. the ground guide should clear the LZ. The landing site should be clear of people. the only delay should result A-9 GROUND GUIDE When you hear or see the helicopter. assure the spotlights. please tell the helicopter crew on the initial radio call.e. If helmets are worn. Furthermore. Every minute that you delay the transfer of the patient to the flight crew takes away from their golden hour. Keep in mind that wires are extremely difficult at best to see from the air during the day and nearly impossible at night.e. trees. Do not land the helicopter in an extremely dusty area or areas with excessive loose debris. The ground guide should be far enough from the touchdown area that he can maintain eye to eye contact with the pilot and remain outside the rotor arch. DO NOT under any circumstances abandon your responsibility. the landing site must be free of stumps. etc?)? If there are obstructions. Utilization of a fire engine’s mounted spotlights are preferred while the engine is parked under the wires. Guide the helicopter to the 03/01/05 . brush. poles. Helicopters land and take off into the wind. fresh cut grass) Choose a more appropriate location. . This responsibility includes (1) helicopter stand-by as medical flight crews package one patient. Nighttime operations may facilitate the need to illuminate the corners of the LZ to make it identifiable to the helicopter. AVOIDING PATIENT TRANSFER DELAYS Remember. (3) clearing scene personnel from the LZ during power up and the subsequent lift-off of the helicopter. antennas. Red lights. LZ by utilizing the nose of the aircraft as your 12 o’clock marker. the reason you called for a helicopter is to expedite transport. (2) shut down to reconfigure the aircraft for two patients. At night .e. There is no excuse for holding critical trauma patients at the scene for unmeaningful or unnecessary intervention (i. hay. such as spotlights flash bulbs and hi-beam headlights ruin the pilot’s night vision and temporarily blind him. The helicopter will orbit the LZ conducting recon prior to landing. WAVE OFF. mark the touchdown area with a light source other than road flares. Road flares are an intense source of ignition and are not appropriate. This is the one time utilization of a spotlight pointed up at the pole where wires make their connection is suggested. WIND DIRECTION & TOUCHDOWN AREA Consider the wind direction. or equipment hanging outside the aircraft). Is the approach and departure path free of obstructions (wires. a previously unseen safety hazard. however. The tail rotor guards are especially important to the operation. loading of the patient (s). one person should help guide the helicopter into a safe landing. . White lights. There is no need to deploy a charged hose line. people in the LZ. Handheld lights may also be used. Keep emergency service personnel at least 100 feet away. and if time and personnel permit. Your job is to STOP anyone (other than those escorted by flight crew members) from approaching the aircraft at anytime. Ensure that personnel understand their assignment. poles and wires. He should stand with his back to the wind and with his arms raised over his head to indicate he is the ground guide. This action may cause the helicopter to ingest debris thereby making it mechanically compromised and unsafe to fly. floodlights and hand lights used to define the touchdown area are not pointed toward the helicopter. IV attempts) that can be accomplished in flight. Have fire equipment (if available) standing by.” If you do not have a radio. never approach from the rear. For hazardous material accidents involving radioactive materials. keep the departure path free of vehicles and spectators. Poisonous or irritating gases may cling to a victim’s clothing and go unnoticed until the patient is loaded And the doors of the helicopter are closed. the professionals on the scene. the landing zone must be at least one mile upwind of the accident site. ASSISTING THE FLIGHT CREW Once the helicopter has landed. the crew is then compromised.EMERGENCY MEDICAL GUIDELINES from an inability to secure a difficult airway and requiring the assistance of the flight crew to do so. eye protection and hearing protection is recommended. HAZARDOUS CHEMICALS/GASES Hazardous chemical and gases are extremely dangerous to the unprotected person and may be fatal if inhaled or absorbed through the skin. A Final Note Your helicopter ambulance can serve you only if we arrive safely. Never assume that the crew has already been informed. Always approach and depart the aircraft towards the front so you can see the pilot. and he can see you. Once the patient is cocooned. helicopter landing zones must be prepared UPWIND at least ONE MILE from the hazardous material accident site and never in lowlying areas. When approaching or departing the helicopter. the crew could be poisoned and/or the engines could develop mechanical problems. DO NOT approach the helicopter. the helicopter crew must be made aware of any hazardous gases in the area of a scene or LZ. If the helicopter is landed on a slope. When explosives. remember to keep low to avoid the main rotor. at least ONE QUARTER MILE from the accident. the helicopter landing zone must be prepared UPWIND. and in this case. PLEASE BE PREPARED WITH PROPER PERSONAL SAFETY EQUIPMENT to assist.**Martin County Fire-Rescue LifeStar1 will not be transporting any patients exposed to a hazardous or radioactive material. SIDE BAR NOTE . If A . Please have any pertinent information written down. It is the goal of the flight crew to be off the scene within minutes of their arrival. If an emergency were to occur. Helmet with chinstrap fastened. secured to the stretcher and ready to load. poisonous gases/vapors. unless there are radioactive gases (steam or smoke). These additional items can be found in the LZ kits located on each fire engine. always be aware of the tail rotor and always follow the flight crew’s directions for your safety. Our safety and the safety of the people on the ground depends on you. because winds can cause the rotor to flex downward. approach and depart from the down-slope side only. or chemicals in danger of exploding and burning are on site. Failure to be prepared will cause delay in transport.10 03/01/05 . GENERAL HELICOPTER SAFETY RULES When working around helicopters. we would need this area to execute our landing. additional personnel are generally not required on paved roadways. The flight crew will approach you when it is safe to do so. A patient not requiring additional interventions by the flight crew may be transferred to the helicopter stretcher as report is being taken from the onscene paramedic. HAZARDOUS MATERIAL LIZ’S Helicopter landing zones must be selected to avoid ALL possibility of compromising the safety of the helicopter and its crew. Please bring the patient to the flight crew the aircraft were to fly through the hazardous gases. When approaching the helicopter. the flight crew may select two or three personnel to assist with movement to the helicopter. In order to facilitate lift-off. Upon initial radio contact. When the helicopter is loaded and ready for take off. Haz-Mat Guidelines Haz-Mat Guidelines 03/01/05 H-1 . Ambulance personnel “provide emergency treatment procedures appropriate to the hazards on site”. In any case. Fire service personnel. they should be trained to recognize a hazardous materials incident and be able to initiate a response. they can provide medical care to a fully decontaminated victim. is appropriate for emergency departments and pre–hospital medical care providers because most authorities agree that it is unacceptable to provide sophisticated protective gear to persons who have not been previously properly fitted and trained in its use. They would take no further action beyond notifying the authorities of the release”. conduct rescues. SCBA or respirators unless they have been trained to use them and their responsibilities at the scene require it. They are trained to H-2 INTRODUCTION TO PROTOCOLS Health care providers who care for injured persons exposed to hazardous materials must know how to evaluate and manage a contaminated victim’s medical problems while protecting themselves and others from potential hazardous exposure (secondary contamination). The 40hour Haz-Mat Medic or Tox-Medic class is recommended. health care providers should immediately contact the receiving hospital. In the vast majority of cases. paramedics or other rescue health workers in the field. or for decontamination of protective equipment. and hospital emergency department physicians and nurses.Emergency Medical Guidelines respond in a defensive fashion without actually trying to stop the release from a safe distance. However. decontaminate victims or response personnel. The protocols are intended as guidelines.” ~. “First responders at the operations level are individuals who respond to releases or potential releases of hazardous substances. and that their personnel are trained to follow it. We have evaluated the rule and recommend no less than four hours of training as being sufficient to meet the OSHA requirements for this category of responder. for controlling and containing the release. as part of the initial response to the site for the purpose of protecting nearby persons. Controversies abound in the evolving field of environmental toxicology. Given their typical daily responsibilities and training. and responsibilities at a haz-mat spill site (particularly if they are not part of the fire service) they should be trained at least at the “First Responder Awareness Level”. They may require modification depending on the resources of a particular department or the needs of a particular patient.120 regulations state that EMT’s and Paramedics cannot wear special protective gear. additional medical training to decontaminate and manage victims would probably be necessary. The federal rule does not specify how many hours of training are necessary for this level. These protocols are designed for use by Haz-Mat entry team members. Given EMS personnel’s medical duties. It is essential for the safety of health care personnel and patients that hospitals and emergency medical services agencies have a written plan for management of the contaminated victim. Again. “First responders at the awareness level are individuals who are likely to witness or discover a hazardous substance release and who have been trained to initiate an emergency response by notifying the proper authorities of the release. For example. It categorizes “medical support” as involving “off–site personnel”. For this reason. the protocols are sometimes vague or ambiguous. will be trained at a higher level because of their fire service duties and functions. stopping its spread. EMT’s and paramedics should be trained at the “First Responder Operations Level” if they are expected to select and don protective equipment. and preventing exposures. 03/01/05 . these two EMS classifications should take a course on the medical management of haz-mat victims that is based on these protocols or their equivalent. Decontaminated victims should be brought to them for medical care so that untrained and unprotected EMT’s and Paramedics are not put at risk. if any. or Regional Poison Control Center for advice on managing victims of hazardous materials exposure. keep it from spreading. it is the employer’s responsibility to see that their personnel are properly trained to meet these requirements. EMT’s and Paramedics clearly are not responsible for making a rescue wearing protective gear. In all incidents. Additional medical training to manage hazardous materials victims would probably be necessary. 9329). 29 CFR 1910. HAZARDOUS MATERIALS MEDICAL MANAGEMENT PROTOCOLS INTRODUCTION The NIOSH EPA hazardous waste site operations document is helpful in defining the EMT / Paramedic’s role. The following treatment protocols provide step–by–step information on how to manage medical problems arising from the most common kinds of hazardous materials (“haz-mat”) scenes. no consensus exists on what specific protective gear. Again. Sixteen hours of training is required for this level by Federal OSHA mandates. All of this must be consistent with the haz-mat role that the local EMS agency has defined for EMS personnel. property or the environment from the effect of the release. it is prudent for providers to don the protective gear when appropriate. and telephone numbers of all personnel and victims who have been or may have been exposed at a haz-mat scene should be recorded for future notification if it is subsequently determined that medical evaluation or treatment is required. Refer to your local EMS agency medical director for guidance. If there is any doubt about the potential for secondary contamination. If victims are already properly decontaminated before they are brought to health care providers at the perimeter of the hot zone/decon area. pre–hospital health care personnel may need to repeat or continue decontamination procedures (e. patients with serious trauma or medical illness can be quickly stripped and flushed with water prior to delivery to pre–hospital health providers outside the hot zone. advance arrangements for additional training and protective equipment should be made. Consult the lists above or knowledgeable sources to determine the risk of secondary contamination. In those rare circumstances where they have been in the hot zone or have attended to a victim who was not properly decontaminated. Many toxic substances have delayed onset effects. However. obtain consultation from the Regional Poison Control Center to determine if delayed effects might be seen and for guidance on triage of asymptomatic or mildly symptomatic exposure victims. Note that some of the management protocols may exceed the paramedic scope of practice in a local area. which may appear several hours later. advice from the local environmental health department. Decontamination of Pre–hospital Personnel Pre–hospital workers will not normally need personal decontamination. risk to the pre–hospital health provider or their vehicle. If the transport vehicle is inadvertently contaminated. This is true even in cold or inclement weather. Victim and Response Personnel Follow–up The names. If this cannot be performed because of acute life–threatening conditions or other circumstances. corrosive materials in the eye. they will pose very little. In those jurisdictions where a pre–hospital provider might be placed in such a situation without assistance from a properly trained hazmat specialist. They should practice with the local haz-mat team to become familiar with the steps involved. If the toxic substance is known. In many cases (e. are the only ones who should assist with decontamination or enter the hot zone. or the Regional Poison Control Center. wool or other highly absorbent materials that cannot be decontaminated should be removed prior to providing care. since in many. they should consider themselves to be potentially contaminated. Although specialized protective gear should not be necessary. Pre–hospital Decontamination Unprotected EMS responders must advise on and observe the decontamination procedures from a distance to ensure that they are properly carried out. oily pesticide skin exposure). hazardous materials team. A contaminated appendage can be washed without wetting the whole body if that is the only part contaminated. if not most cases. health care providers will not generally need to use any specialized protective gear. after the victim has returned home. every effort should be made to decontaminate the victim at the scene if the means to do so are available. and dispose of or clean contaminated clothing and personal items. Any persons suspected of being exposed should be seen and evaluated by emergency department staff. then the vehicle must be protected and those providing care during transport and driving the vehicle must be properly fitted and trained with the appropriate level of specialized protective gear. decontaminate the victim.Haz-Mat Guidelines It is imperative that proper decontamination has been initiated by the haz-mat team or other trained responders in the hot zone/decontamination area.g. Thus. All leather items. Pre–hospital Triage Victims with obvious significant illness or injury will need rapid transport and treatment after initial stabilization and basic decontamination is carried out. addresses. to select the appropriate chemical protective suits. and know how to function in them. In virtually all cases.g. the receiving hospital. Victims with few or minimal symptoms are not necessarily safe from progression of illness. If in doubt. if any. Information can be obtained from the Incident Command Safety Officer at the scene. decontaminate... no personal decontamination will be necessary. Rescuers who are trained to use self contained breathing apparatus. No provider should put on a respirator or other specialized gear unless that worker has been previously fitted and trained in its use. Advice should also be sought on how to preserve evidence for law enforcement. Clothing 03/01/05 H-3 . even for substances considered as potential secondary contaminants. Pre–Hospital Care Consult the specific protocols for recommended pre– hospital care of exposed victims. eye irrigation. or local hazardous materials spill clean– up companies should be sought on how to determine the level and location of the contamination and on how to clean it up. soap/water skin wash) after receiving the victim at the perimeter. covering the rest of the body and exposed skin should be carefully checked for contamination. Stabilize the spine (if trauma suspected). Even fairly low airborne concentrations of acid mists or vapors produce rapid onset of eye. Rescuers should don agent–specific protective clothing and gloves. and aerosolized dusts. Ingestion: DO NOT induce vomiting. PRE–HOSPITAL MANAGEMENT Decontaminate – May need to continue to flush skin and/or eyes even after patient has gone through a formal decon process. PRE–HOSPITAL MANAGEMENT ACIDS & ACID MISTS (NOT Including Hydrofluoric Acid) FORMS: Gas. there is no significant risk of secondary contamination. especially with low–solubility gases such as nitrogen oxides (given off by nitric acid). If clothing has been soaked by acid or acid spray. Generally. Remove contact lenses and irrigate eyes with saline via plain IV tubing. Use of the “Morgan Lens” for flushing the eyes is recommended.Emergency Medical Guidelines NOTE: This document is designed to address the most common types of chemicals found. Occasionally. If these requirements cannot be met. Tomes. 5. don appropriate protective equipment consistent with risk of secondary contamination.g. Evaluate and support ABCs (airway. 1. Attach cardiac monitor. nose and throat irritation. CALL YOUR REGIONAL POISON CONTROL CENTER AT: (800) 222–1222 2. breathing and circulation). 4. All areas need to be flushed minimum of 20 minutes. Provide high–flow oxygen by mask. Inhalation of higher concentrations can produce cough. chemical pneumonia or non–cardiogenic pulmonary edema. Please refer to your individual department’s resources (Cameo. and self–contained breathing apparatus particularly if mists or vapors are present. CALL YOUR REGIONAL POISON CONTROL CENTER AT: (800) 222–1222 BACKGROUND: Acids act as direct irritants and corrosive agents to skin and moist mucosal membranes. If victim is NOT decontaminated and responder is properly trained. Victims with minimal or quickly resolving symptoms probably do not require immediate evaluation in the emergency department. Severe injury or permanent damage may be caused from improper use. Remove contact lenses and irrigate exposed eyes if symptomatic. However. clothing which has become soaked with concentrated acid may be corrosive to rescuers.. POTENTIAL FOR SECONDARY CONTAMINATION: Small amounts of acid mists can be trapped in clothing after an overwhelming exposure but are not usually sufficient to create a hazard for health care personnel away from the scene. remember that with certain acids and low–solubility gases (e. If victim is decontaminated. 3. Severe burns may result. FOR ADVICE ON CLINICAL MANAGEMENT. Aerosolized bronchodilators (Albuterol) may be helpful for victims with wheezing. establish airway and breathing. strider or coughing. and consider high flow supplemental oxygen by bag valve mask with reservoir. Also consider contacting the Poison Control Center for South Florida at: FOR ADVICE ON CLINICAL MANAGEMENT. Re–evaluate airway. these substances have very good warning properties. fuming nitric acid forming nitrogen oxides) pulmonary edema may occur after a delay of 12–24 hours. However. Prioritize and Vitalize H-4 03/01/05 . 3. Immediately dilute with 1 glass of water or milk. don appropriate agent–specific protective equipment and self–contained breathing apparatus. intubating the trachea if victim has developed severe respiratory distress. Flush exposed skin with water spray. Toxicology manuals) for clinical management of these and other medical emergencies. pulmonary edema may be delayed for several hours. strider. PATIENT MANAGEMENT IN THE HOT ZONE/ DECON AREA: 1. liquid (variable concentrations). 6. wheezing. Individuals must be trained in the use of this device. 2. Ambulatory patients should be instructed to remove themselves from the hot zone and to decontaminate themselves under the direction of the decontamination supervisor. esophagus and stomach. request assistance from the local haz-mat team or your Regional Poison Control Center. Continue to flush affected skin and eyes with copious water or saline. if possible and practical. Once the victim has been stripped and flushed with water. remove and double–bag clothing and flush skin for 1– 2 minutes. mixtures with water. Decontamination is not necessary for victims with inhalation exposure only. Quickly evaluate and support ABCs. Activate basic decontamination protocol. for at least 10–15 minutes or until symptoms of pain or irritation have resolved. Ingestion of acids can result in severe injury to the airway. maintain 5cm of H2O PEEP. EKG Monitoring Establish IV . Continue to flush affected skin and eyes with copious water or saline. If victim is NOT decontaminated and responder is properly trained. Administer oxygen by mask. POTENTIAL FOR SECONDARY CONTAMINATION: Small amounts of ammonia vapor can be trapped in clothing after an overwhelming exposure but are usually not sufficient to create a hazard for health care personnel away from the scene. Watch for signs of airway closure and laryngeal edema. PRE–HOSPITAL MANAGEMENT AFTER INITIAL DECONTAMINATION: 1. Aerosolized bronchodilators (e. Stabilize the spine (if trauma suspected). to intact skin. If respiratory distress is present or if exposed to low solubility gases such as nitrogen oxides. CALL YOUR REGIONAL POISON CONTROL CENTER AT: (800) 222–1222 AMMONIA (LIQUID AND GAS) FORMS: Gas (anhydrous) and liquid (aqueous solutions.with Normal Saline CPAP for Pulmonary Edema (Non Cardiogenic Shock . Intubate if patient manifests severe respiratory distress from pulmonary edema or upper airway swelling. When intubated. chemical pneumonia or non– cardiogenic pulmonary edema. request assistance from the local haz-mat team or your Regional Poison Control Center. such as hoarseness. there is no significant risk of secondary contamination. and self–contained breathing apparatus. breathing. Remove contact lenses and irrigate eyes with saline via plain IV tubing. > 5%) may cause serious corrosive injury to the esophagus and stomach. The onset of pulmonary edema is usually rapid but may occasionally be delayed for 12–24 hours. or Morgan Lens.. strider. If clothing has been soaked by liquid ammonia. admit and observe 24 to 48 hours for possible delayed onset of pulmonary edema. Evaluate ABCs (airway. Obtain arterial blood gases and chest x–ray if respiratory distress is present. and consider high flow supplemental oxygen by bag valve mask with reservoir device or manually triggered oxygen powered breathing device. Ammonia has very good warning properties. if possible and practical. Individuals must be trained in the use of this device. 3. Remove contacts and irrigate exposed eyes if symptomatic. don appropriate protective equipment consistent with risk of secondary 2. Use of the “Morgan Lens” for flushing the eyes is recommended. Higher concentrations can produce cough. All areas need to be flushed minimum of 20 minutes. intubate early. variable concentrations). Ingestion of concentrated ammonia solutions (e. establish airway and breathing. Even fairly low airborne concentrations produce rapid onset of eye. strider. If these requirements cannot be met. FOR ADVICE ON CLINICAL MANAGEMENT. wheezing. If victim is decontaminated. Bronchodilators maybe helpful for wheezing. Albuterol) may be helpful for victims with wheezing. PRE–HOSPITAL MANAGEMENT Decontaminate – May need to continue to flush skin and/or eyes even after patient has gone through a formal decon process. and circulation).g. nose and throat irritation. to a lesser extent. Repeat as needed. Severe upper airway edema may necessitate endotracheal intubation or cricothyrotomy. NOTE: Liquefied compressed gas may produce cryogenic (freezing) hazard as it is released into the atmosphere. Immediately dilute with 1 glass of water or milk. Administer 100 % O2.g. for at least 10–15 minutes or until symptoms of pain or irritation have resolved.Haz-Mat Guidelines Airway Management – If airway is compromised by secretions or is rapidly closing. Flush skin with water spray for 1 – 2 minutes. 2. However. Ingestion: DO NOT induce vomiting. Once the victim has been stripped and flushed with water. remove and double–bag. Quickly evaluate and support ABCs. Rescuers should don agent–specific protective clothing and gloves. Ambulatory patients should be instructed to remove themselves from the hot zone and to decontaminate themselves under the direction of the decontamination supervisor. or retractions. BACKGROUND: Ammonia (NH3) is a direct irritant and alkaline corrosive agent to moist mucous membranes and. Activate basic decontamination protocol.. don appropriate agent–specific protective a equipment and self–contained breathing apparatus.do not use Furosemide) Valium 5-10mg or Ativan 1-2mg for seizures. PATIENT MANAGEMENT IN THE HOT ZONE/ DECON AREA: 1. Victims with minimal or quickly resolving symptoms after brief inhalation exposure probably do not require immediate evaluation in the emergency department. clothing which has become soaked with concentrated liquid ammonia may be corrosive to rescuers. Severe injury or permanent damage may be H-5 03/01/05 . Evaluate and support ABCs (airway. don appropriate agent–specific protective equipment and self–contained breathing apparatus. there is no significant risk of secondary contamination. Aerosolized bronchodilators (Albuterol) may be helpful for victims with wheezing. Repeat as needed FOR ADVICE ON CLINICAL MANAGEMENT. Approved butyl rubber masks are prefered. The effects of blister agents may not be immediate. Provide high–flow oxygen by mask. coughing and sneezing. colorless liquid while pure. 2. intubate early. irritation of mucious membrane. PRE–HOSPITAL MANAGEMENT AFTER INITIAL DECONTAMINATION: 1. POTENTIAL FOR SECONDARY CONTAMINATION: Small amounts of liquid can be trapped in clothing after an overwhelming exposure but are not usually sufficient to create a hazard for health care personnel away from the scene. Mild exposure may result in tearing. Assistance from the local haz-mat team or your Regional Poison Control Center should be requested to verify that decontaminaiton efforts are sufficent. or butter almond odor. for at least 10–15 minutes or until symptoms of pain or irritation have resolved. 2.with Normal Saline CPAP for Pulmonary Edema (Non Cardiogenic Shock . remove and double–bag clothing and flush skin for 1– 2 minutes. maintain 5cm of H2O PEEP. with severe respiratory distress. don appropriate protective equipment consistent with risk of secondary contamination. BLISTER AGENTS FORMS: There are two agents referred to as blister agents. or liquid form. Sulfur mustard agents are colorless when pure. Though Lewsite effects are immediate.Emergency Medical Guidelines caused from improper use. Remove contact lenses and irrigate eyes with saline via plain IV tubing. EKG Monitoring Establish IV . burns may cause swelling of the airway and bronchiole passagesand patients may present with non-cardiogenic pulmonary edema. formation of blisters on the skin. musty. clothing which has become soaked with blister agents may be corrosive to rescuers. Re–evaluate airway. If victim is decontaminated. Quickly evaluate and support ABCs. Silicone breathing apparatus masks may not protect rescuers for some blister agents due to chemical incompatibility. If clothing has been soaked by acid or acid spray. Continue to flush affected skin and eyes with copious water or saline. eyes. but typically are a yellow to brown oily liquid with a slight mustard to garlic odor. However. Remove contact lenses and irrigate exposed eyes if symptomatic. if possible and practical. These agents produce vapors. Internal organs may also be affected as vapors are taken up in the circulatory system and transported throughout the body. Administer 100 % O2. The lewsites may have the odor of geraniums or garlic-like. In the form of gas or liquid. When intubated. establish airway and breathing. and consider high flow supplemental oxygen by bag valve mask with reservoir. CALL YOUR REGIONAL POISON CONTROL CENTER AT: (800) 222–1222 BACKGROUND: Blister agents are considered to be a chemical warfare agent. intubating the trachea if victim has developed severe respiratory distress. inflammation of the skin. pateints exposed to mustard agents do not show signs or symptoms for 2 to 24 hours after exposure. 4. Lewsites are an oily. CALL YOUR REGIONAL POISON CONTROL CENTER AT: (800) 222–1222 been stripped and flushed with water. If inhaled. fruity. Once the victim has H-6 03/01/05 . Prioritize and Vitalize Airway Management – If airway is compromised by secretions or is rapidly closing. If victim is NOT decontaminated and responder is properly trained. nausea. aerosol. Rescuers should don agent–specific protective clothing and gloves. 3. blister agents affect the skin. but is amber to black when impure. Activate basic decontamination protocol. breathing and circulation). Stabilize the spine (if trauma suspected). FOR ADVICE ON CLINICAL MANAGEMENT. Signs of blister agents include reddening and blistering of effected tissue. Attach cardiac monitor. mustard agents and lewsite. but may be dispersed in a gas. hoarseness. PATIENT MANAGEMENT IN THE HOT ZONE/ DECON AREA: 1. and self–contained breathing apparatus particularly if mists or vapors are present. vomiting and diarrhea. 3. lungs. Severe exposures which are incapacitating may include loss of sight. Ambulatory patients should be instructed to remove themselves from the hot zone and to decontaminate themselves under the direction of the decontamination supervisor. Nitrogen mustards can be colorless to pale yellow with a fishy. Flush exposed skin with water spray. strider or coughing.do not use Furosemide) Valium 5-10mg or Ativan 1-2mg for seizures. and gastro-intestinal tract. Severe injury or permanent damage may be caused from improper use. All areas need to be flushed minimum of 20 minutes. 6. 5. Ambulatory patients should be instructed to remove themselves from the hot zone and to decontaminate themselves under the direction of the decontamination supervisor. establish airway and breathing. BACKGROUND: Chlorine is a highly irritating gas. NOTE: Liquefied compressed gas may produce cryogenic (freezing) hazard as it is released into the atmosphere. choking. and self–contained breathing apparatus. remove and double–bag. Aerosolized bronchodilators (e. don appropriate protective equipment consistent with risk of secondary contamination. Repeat as needed. CHLORINE GAS FORMS: Gas (anhydrous) or liquid (aqueous chlorine) are usually in the form of hypochlorite. Remove contact lenses and irrigate eyes with saline via plain IV tubing. 4. 3. Evaluate and support ABCs (airway. variable concentrations. and circulation). Quickly evaluate and support ABCs. Those with persistent cough. which rapidly forms hydrochloric acid after contact with moist mucous membranes in the upper airway and in the lungs. The liquid hypochlorite solutions are very unstable and react with acids to release chlorine gas. If victim is decontaminated. If clothing has been soaked by hypochlorite solution. clothing which has become soaked with concentrated hypochlorite solution may be corrosive to rescuers and may off–gas chlorine. don appropriate agent–specific protective equipment and self–contained breathing apparatus. nose and throat irritation. chemical pneumonitis.Haz-Mat Guidelines PRE–HOSPITAL MANAGEMENT Decontaminate – May need to continue to flush skin and/or eyes even after patient has gone through a formal decon process. Low concentrations produce eye. 2. Attach cardiac monitor. Valium 5-10mg or Ativan 1-2mg for seizures. intubate early. for at least 10–30 minutes or until symptoms of pain or irrigation have resolved. wheezing. or pulmonary edema. Flush skin with water spray for 1 – 2 minutes. Continue to flush affected skin and eyes with copious water or saline. POTENTIAL FOR SECONDARY CONTAMINATION: Small amounts of chlorine gas can be trapped in clothing after an overwhelming exposure but are not usually sufficient to create a hazard for health care personnel away from the scene. breathing. maintain 5cm of H2O PEEP. Administer 100 % O2. However.with Normal Saline CPAP for Pulmonary Edema (Non Cardiogenic Shock .do not use Furosemide) Treat burns per “Burn” protocol. Consider pain management as appropriate. PRE–HOSPITAL MANAGEMENT AFTER INITIAL DECONTAMINATION: 1. Albuterol) may be helpful for victims with wheezing. Individuals must be trained in the use of this device.g. Use of the “Morgan Lens” for flushing the eyes is recommended. Prioritize and Vitalize Airway Management – If airway is compromised by secretions or is rapidly closing. Once the victim has been stripped and flushed with water. or Morgan Lens. Continue to provide high flow oxygen by mask. Remove contact lenses and irrigate exposed eyes if symptomatic. Ingestion: DO NOT induce vomiting. Immediately dilute with 1 glass of water or milk. EKG Monitoring Establish IV . request assistance from the local haz-mat team or your Regional Poison Control Center. Victims with minimal or quickly resolving symptoms probably do not require immediate evaluation in the emergency department. Decontamination is not necessary after simple inhalation exposure. When intubated.. 2. If these requirements cannot be met. or altered mental status should receive urgent medical evaluation. if possible and practical 3. intubating the trachea if victim has developed severe respiratory distress due to upper airway swelling or pulmonary edema. Re–evaluate airway. Stabilize the spine (if trauma suspected). PRE–HOSPITAL MANAGEMENT Decontaminate – May need to continue to flush skin and/or eyes even after patient has gone through a formal decon process. All areas need to be flushed minimum of 20 minH-7 03/01/05 . Rescuers should don agent–specific protective clothing and gloves. and consider high flow supplemental oxygen by bag valve mask with reservoir. Activate basic decontamination protocol. Higher concentrations produce cough. If victim is NOT decontaminated and responder is properly trained. wheezing. PATIENT MANAGEMENT IN THE HOT ZONE! DECON AREA: 1. Ingestion of concentrated hypochlorite solutions can cause serious corrosive esophageal or stomach injury. there is no significant risk of secondary contamination. Symptoms occur rapidly and provide good warning properties for exposure. If clothing has been soaked by solid or liquid CN– containing material. if regurgetaiton occurs. Quickly evaluate and support ABCs. If patient is not breathing. Repeat as needed FOR ADVICE ON CLINICAL MANAGEMENT. PRE–HOSPITAL MANAGEMENT AFTER INITIAL DECONTAMINATION: 1. liquid (solutions of cyanide salts). Prioritize and Vitalize Airway Management – If airway is compromised by secretions or is rapidly closing. Consider use of sodium thiosulfate IV. 2. Remove contact lenses and irrigate eyes with saline via plain IV tubing. solid). CALL YOUR REGIONAL POISON CONTROL CENTER AT: (800) 222–1222 to remove themselves from the tot zone and to decontaminate themselves under the direction of the decontamination supervisor. This can be done be early recognition and having properly trained personnel and specialized medication available. effects may be delayed until the CN is absorbed from the stomach. establish airway and breathing. vomiting. maintain 5cm of H2O PEEP. Decontaminate – May need to continue to flush skin and/or eyes even after patient has gone through a formal decon process. Victims whose clothing is contaminated with HCN solution can secondarily contaminate rescuers by direct contact or through off-gassing. but after ingestion of a CN salt. Stabilize the spine (if trauma suspected). If exposure is by inhalation of CN gas. and solid (cyanide salts). PRE–HOSPITAL MANAGEMENT Note: Rapid intervention is imperative to a positive outcome. breathing. CN can interfere with the transmission of oxygen. Remove contact lenses and irrigate exposed eyes if symptomatic. tachycardia. Ambulatory patients should be instructed H-8 03/01/05 . Administer 100 % O2. tachypnea. Individuals must be trained in the use of this device. intubate early. remove and double–bag clothing. Severe injury or permanent damage may be caused from improper use. if possible and practical. CYANIDE FORMS: Gas (hydrogen cyanide). CN produces toxicity by interfering with cellular metabolism. 3. Death can occur within minutes of exposure. Individuals must be trained in the use of this device. there is not little risk of secondary exposure to rescuers.with Normal Saline POTENTIAL FOR SECONDARY CONTAMINATION: If the exposure was by inhalation of HCN gas. intubating the trachea if victim is unconscious or has developed severe respiratory distress. Continue to flush affected skin and eyes with copious water or saline. and circulation). Activate basic decontamination protocol. There may be a distinctive odor (“bitter almonds”) on the victim’s clothing or breath. administer Amyl Nitrite inhalant. and coma. dizziness. don appropriate protective equipment consistent with risk of secondary contamination. intubate early. Symptoms and signs include headache. CN gas (HCN) is a major toxic component in cases of smoke inhalation. If patient is unconscious but still breathing. liquid. Attach cardiac monitor. If these requirements cannot be met. Rescuers should don agent–specific protective clothing and gloves. Continue to provide high flow oxygen by mask.Emergency Medical Guidelines utes. Use of the “Morgan Lens” for flushing the eyes is recommended. peak toxic effects are seen within minutes. Prioritize and Vitalize Airway Management – If airway is compromised by secretions or is rapidly closing.with Normal Saline CPAP for Pulmonary Edema (Non Cardiogenic Shock . Use of the “Morgan Lens” for flushing the eyes is recommended. 3. Establish IV .do not use Furosemide) Valium 5-10mg or Ativan 1-2mg for seizures. Secondarily. Victims who have ingested CN solutions pose the greatest risk to responders. which is widely used in industry in a variety of forms (gas. Administer 100% supplemental O2. Re–evaluate airway. Severe injury or permanent damage may be caused from improper use. If victim is decontaminated. Flush skin with water spray for 1–2 minutes. If victim is NOT decontaminated and responder is properly trained. intubate and place perles in the BVM reservoir and ventilate. Hydrogen cyanide gas may be formed when acid is added to a cyanide salt or a nitrile. BACKGROUND: Cyanide (CN) is an extremely toxic compound. All areas need to be flushed minimum of 20 minutes. PATIENT MANAGEMENT IN THE HOT ZONE/ DECON AREA: 1. EKG Monitoring Establish IV . allowing patient to inhale Amyl Nitrite for 20-30 seconds per minute. When intubated. and consider high flow supplemental oxygen by bag valve mask with reservoir. 2. for at least 20 minutes or until symptoms of pain or irrigation have resolved. and self–contained breathing apparatus. don appropriate agent–specific protective equipment and self–contained breathing apparatus. Evaluate and support ABCs (airway. request assistance from the local haz-mat team. vomiting. Prolonged breathing of these high concentrations can cause dizziness.65ml up to 50 ml over 10 minutes). and self–contained breathing apparatus. in health care facilities. PRE–HOSPITAL MANAGEMENT AFTER INITIAL DECONTAMINATION: 1. shoes and boots and throw out. 3. 5. including spontaneous abortions among female hospital workers. CALL YOUR REGIONAL POISON CONTROL CENTER AT: (800) 222–1222 potential for secondary contamination is low and decontamination is not required. (Pediatric dose is 1. Remove and throw out grossly contaminated clothing. Peripheral neuropathy has been infrequently observed. continued exposure results in olfactory fatigue. olfactory fatigue. However. dental. Flush the skin with water spray vigorously for at least 15 minutes. ETHYLENE OXIDE (ETO. Activate basic decontamination protocol. 3. POTENTIAL FOR SECONDARY CONTAMINATION: Following inhalation exposure to ETO gas ONLY. don appropriate agent–specific protective equipment and self–contained breathing apparatus. Symptoms after mild exposure usually clear within a few hours. if possible and practical. breathing. Give bronchodilators if significant wheezing is present. Evaluate and support ABCs (airway. and circulation). Inhalation or direct contact by dermal exposure should be avoided. shoes and boots. Victims with minimal or quickly resolving symptoms may not require hospital emergency department evaluation. Quickly evaluate and support ABCs. onset of pulmonary edema may be delayed up to 24 hours. Liquid formulation of ETO may be absorbed by clothing. Rescuers should don agent–specific protective clothing and gloves. nose. and stabilize C– spine if trauma if suspected. (Pediatric dose is . shoes. Cancer and adverse reproductive effects. Acute exposure to several hundred ppm can lead to nausea. Remove grossly contaminated clothing. medical and scientific equipment and supplies. Valium 5-10mg or Ativan 1-2mg for seizures. explosive and toxic. and consider high flow supplemental oxygen by bag valve mask with reservoir. PATIENT MANAGEMENT IN THE HOT ZONE/ DECON AREA: 1. If these requirements cannot be met. ETO in its pure form is extremely flammable. 4. Remove exposed individual from source of contamination. and. Sodium Thiosulfate – 50 ml of a 25% solution over 10 minutes. Used to produce ethylene glycol for anti–freeze products. weakness. Repeat as needed FOR ADVICE ON CLINICAL MANAGEMENT. have been reported in various studies but long–term effects are not completely known. skin or eyes. don appropriate protective equipment consistent with risk of secondary contamination. The material is a known sensitizer and has produced allergic and anaphylactic reactions. pharmaceutical. however. Do not administer Sodium Thiosulfate in Hydrogen Sulfide poisoning). chest pain and pulmonary edema. Short–term exposure can cause irritation to eyes. Even brief skin contact with liquid ETO can cause edema and erythema with progression to blister formation in 6–12 hours.Haz-Mat Guidelines Sodium Nitrite – 10ml of a 3% solution IV over 2 minutes. BACKGROUND: ETO in a gaseous form can enter the body through the lungs. for at least 10–15 minutes or until symptoms of pain or irrigation have resolved. Symptoms usually clear without residual within hours after termination of exposure. 2.33 ml/kg of a 3% solution over 10 minutes). throat and lungs. fumigate books. Quickly establish airway. If victim is NOT decontaminated and responder is properly trained. sterilize food. Administer supplemental oxygen as soon as it is practical. EO) FORMS: Liquid and gas. If victim is decontaminated. Remove contact lenses and irrigate eyes with saline via plain IV tubing. the PRE–HOSPITAL MANAGEMENT Decontaminate – May need to continue to flush skin and/or eyes even after patient has gone through a formal decon 03/01/05 H-9 . Stabilize the spine (if trauma suspected). 2. to gas sterilize equipment. establish air–way and breathing. nervous system injury and respiratory distress. Ambulatory patients should be instructed to remove themselves from the hot zone and to decontaminate themselves under the direction of the decontamination supervisor. Remove contact lenses and irrigate exposed eyes if symptomatic. ETO is a colorless gas with an ether–like (sweetish) odor that is readily detected at first. Continue to flush affected skin and eyes with copious water or saline. and boots from which it can off– gas. request assistance from the local haz-mat team or your Regional Poison Control Center. Severe injury or permanent damage may be caused from improper use. 6. Formaldehyde is a known animal and suspected human carcinogen. don appropriate protective equipment consistent with risk of secondary contamination. Attach cardiac monitor. intubating the trachea if victim has developed severe respiratory distress due to upper airway swelling or pulmonary edema. and consider high flow supplemental oxygen by bag valve mask with reservoir. for at least 20 minutes or until symptoms of pain or irrigation have resolved. Immediately dilute with 1 glass of water or milk.do not use Furosemide) Valium 5-10mg or Ativan 1-2mg for seizures. carpeting. Individuals must be trained in the use of this device. pre–form insulation. even if the characteristic residual odor of formaldehyde is still detectable. 3. When intubated. Administer 100 % O2. Aerosolized bronchodilators (Albuterol) may be helpful for victims with wheezing. Repeat as needed FOR ADVICE ON CLINICAL MANAGEMENT. or Morgan Lens. It is a highly water soluble gas with toxicity beginning at very low levels of exposure. 4. maintain 5cm of H2O PEEP. Activate basic decontamination protocol. Prioritize and Vitalize Airway Management – If airway is compromised by secretions or is rapidly closing.Emergency Medical Guidelines process. wheezing. If victim is decontaminated. Those with persistent cough. and direct contact with concentrated aqueous solutions can cause burns. usually about 35% formaldehyde that may also contain 5-15% methanol. POTENTIAL FOR SECONDARY CONTAMINATION: Victims who have inhaled formaldehyde gas are not contaminating to others and do not require decontamination. Rescuers should don agent–specific protective clothing and gloves. All areas need to be flushed minimum of 20 minutes. and absorption of the formaldehyde and methanol can cause metabolic acidosis and blindness due to metabolism to formic acid. intubate early. wheezing. Continue to provide supplemental oxygen. Victims whose clothing or skin is soaked with formalin solution may off–gas formalin and methanol. Severe injury or permanent damage may be PATIENT MANAGEMENT IN THE HOT ZONE/ DECON AREA: H . All areas need to be flushed minimum of 20 minutes. and circulation). and self–contained breathing apparatus. Victims with minimal or quickly resolving symptoms of eye and throat irritation do not require immediate evaluation in the emergency department. furniture. Stabilize the spine (if trauma suspected). PRE–HOSPITAL MANAGEMENT AFTER INITIAL DECONTAMINATION: 1. If these requirements cannot be met. there is no significant risk of secondary contamination of rescuers outside of the hot zone. CALL YOUR REGIONAL POISON CONTROL CENTER AT: (800) 222–1222 1. if possible and practical. Ingestion of Formalin may cause corrosive injury of the esophagus and stomach. Formalin is an aqueous solution. Quickly evaluate and support ABCs. If victim is NOT decontaminated and responder is properly trained. 5.with Normal Saline CPAP for Pulmonary Edema (Non Cardiogenic Shock . or altered mental status should receive urgent medical evaluation. PRE–HOSPITAL MANAGEMENT Decontaminate – May need to continue to flush skin and/or eyes even after patient has gone through a formal decon process. wood products. Individuals must be trained in the use of this device. BACKGROUND: Formaldehyde is a gas with a pungent odor used widely in paper processing. establish airway and breathing. and fabrics. remove and double bag clothing and flush skin for 1– 2 minutes. Continue to flush affected skin and eyes with copious water or saline. Use of the “Morgan Lens” for flushing the eyes is recommended. Evaluate and support ABCs (airway. and non–cardiogenic pulmonary edema. 2. If the victim has been soaked by formalin solution.10 03/01/05 . Skin and eye irritation may occur. 3. Reevaluate the airway. don appropriate agent–specific protective equipment and self–contained breathing apparatus. FORMALDEHYDE FORMS: Formaldehyde is a gas. EKG Monitoring Establish IV . Ingestion: DO NOT induce vomiting. Inhalation of high concentrations can cause severe coughing. 2. Ambulatory patients should be instructed to remove themselves from the hot zone and to decontaminate themselves under the direction of the decontamination supervisor. breathing. Remove contact lenses and irrigate eyes with saline via plain IV tubing. but once the clothing has been removed and the skin flushed with water. Use of the “Morgan Lens” for flushing the eyes is recommended. Remove contact lenses and irrigate exposed eyes if symptomatic. request assistance from the local haz-mat team or your Regional Poison Control Center. for at least 10–15 minutes or until symptoms of pain or irrigation have resolved. 3. Treat tetany or cardiac arrest with IV 5 cc calcium chloride 10% (or 10 cc calcium gluconate 10%). maintain 5cm of H2O PEEP. In contrast.with Normal Saline CPAP for Pulmonary Edema (Non Cardiogenic Shock .11 . PATIENT MANAGEMENT IN THE HOT ZONE DECON AREA: 1. 2. request assistance from the local haz-mat team or your Regional Poison Control Center. and hyperkalemia. liquid (variable concentrations). Ambulatory patients should be instructed PRE–HOSPITAL MANAGEMENT Decontaminate – May need to continue to flush skin and/or eyes even after patient has gone through a formal decon 03/01/05 H . a. Continue to provide high–flow oxygen by mask. Administer 100 % O2. 3. HYDROFLUORIC ACID FORMS: Gas. from a burn or after ingestion) may result in severe hypocalemia. Attach cardiac monitor.do not use Furosemide) Valium 5-10mg or Ativan 1-2mg for seizures. Quickly evaluate and support ABCs. If available. there is some hazard to treating health care personnel. Ingestion may produce severe corrosive burns of the esophagus and stomach. Following basic decontamination. Provide continuous cardiac monitoring to look for QT interval prolongation. Evaluate and support ABCs (airway. establish airway and breathing. Re–evaluate airway.e. give magnesium or calcium–containing antacid (both will bind fluoride). the highly toxic fluoride ion has the ability to penetrate tissue and produce indolent ulceration or bony destruction. When intubated. and delayed onset pulmonary edema. 5.Haz-Mat Guidelines caused from improper use. and self–contained breathing apparatus. Consider prophylactic calcium for victims with high concentration (10–20%) exposure to greater than 3–5% body surface area. The “acid” moiety (hydrogen ion) is relatively unimportant. hypomagnesia. magnesium– containing antacids such a Maalox® or Mylanta® can be applied topically. depending on the concentration. intubating the trachea if victim is unconscious or has developed severe respiratory distress due to upper airway swelling or pulmonary edema. Remove and double–bag clothing. Flush skin with water spray for 1 – 2 minutes with water spray. If available. PRE–HOSPITAL MANAGEMENT AFTER INITIAL DECONTAMINATION: 1. nose and throat irritation. Solutions of greater than 60% concentration can cause significant respiratory exposures. Stabilize the spine (if trauma suspected). if possible and practical. there is usually no significant risk of secondary contamination. cough. Systemic absorption of fluoride (i. and circulation). b. intubate early. Remove contact lenses and irrigate exposed eyes if symptomatic. CALL YOUR REGIONAL POISON CONTROL CENTER AT: (800) 222–1222 to remove themselves from the hot zone and to decontaminate themselves under the direction of the decontamination supervisor. Prioritize and Vitalize Airway Management – If airway is compromised by secretions or is rapidly closing. and consider high flow supplemental oxygen by bag valve mask with reservoir. Repeat as needed FOR ADVICE ON CLINICAL MANAGEMENT. 4. Ingestion: DO NOT induce vomiting immediately dilute with 1 glass of water or milk. BACKGROUND: Hydrofluoric acid (HF) produces toxicity quite distinct from other mineral acids. As well inhalation may cause eye. Solutions of greater than 10–20% are particularly destructive. If victim is NOT decontaminated and responder is properly trained. POTENTIAL FOR SECONDARY CONTAMINATION: Until the soaked clothing has been removed and the affected body part has been flushed. producing little burning sensation on initial contact. If these requirements cannot be met. which is an early sign of hypocalemia. If victim is decontaminated. tracheal bronchitis. don appropriate agent–specific protective equipment and self–contained breathing apparatus. Also. Remove contact lenses and irrigate eyes with saline via plain IV tubing. Rescuers should don agent–specific protective clothing and gloves. breathing. Activate basic decontamination protocol. resulting in tetany and cardiac arrest. EKG Monitoring Establish IV . magnesium sulfate solution (Epsom salt) or lime water (calcium hydroxide) is effective irrigating solutions. don appropriate protective equipment consistent with risk of secondary contamination. and fluoride salts in the presence of acids may generate toxic quantities of hydrogen fluoride. Continue to flush affected skin and eyes with copious water or saline. 2. Burns to skin – After flushing with copious amounts of water. they may develop delayed onset peripheral neuropathy. or who has a combination of two or more organ systems affected (respiratory effects. disturbances in level of consciousness). The vapor pressure of these agents varies widley. For certain organophosphates. These agents may be dispersed through the use of solvents to increase vapor pressure. Organophosphate H . twitching and seizures. or explosive devices to atomize the material. CALL YOUR REGIONAL POISON CONTROL CENTER AT: (800) 222–1222 pesticides inhibit the enzyme cholinesterase. establish airway and breathing and consider high flow supplemental oxygen by bag valve mask with reservoir. Inhalation Injury – Mix 6 cc of Normal Saline with 3 cc of 10% Calcium Gluconate and nebulize. Rescuers should don agent–specific protective clothing and gloves.Emergency Medical Guidelines process. Death is due to respiratory muscle paralysis. Remove contact lenses and irrigate exposed eyes if symptomatic. All areas need to be flushed minimum of 20 minutes. GB. but must be closely monitored for heat stress. Stabilize the spine (if trauma suspected). Nerve agents can pose an exposure risk through all routes.Quickly evaluate and support ABCs. Included in this category are casualties with no respiratory or cardiac activity.with Normal Saline Eye Injury from Hydrofluoric Acid– Apply 1-2 drops of Tetracaine to eye. who is not breathing or is having breathing difficulties. gastrointestinal effects. sweating. Flush skin with water spray for 1 – 2 minutes.An individual who suspects he has had or has had liquid agent on his skin.do not use Furosemide) Valium 5-10mg or Ativan 1-2mg for seizures. Severe injury or permanent damage may be caused from improper use. POTENTIAL FOR SECONDARY CONTAMINATION: Many organophosphates are well–absorbed through intact skin. NERVE AGENTS (GA. BACKGROUND: Organophosphate pesticides are widely used in home gardening and commercial agriculture. but who has no PESTICIDES – ORGANOPHOSPHATES FORMS: The typical way organophosphates are found is either in a liquid (usually solution with xylene or other organic solvent) or solid (wettable powder) state which may be inhaled in an aerosol form or as a component of smoke. if possible and practical. Repeat as needed FOR ADVICE ON CLINICAL MANAGEMENT. prepare a skin gel by mixing Calcium Gluconate (10%) 10ml into a 2-ounce tube of KY jelly (making a 2. dizziness. 3. Remove and double–bag clothing. 2. A variety of products are available. Potential toxicity of the solvent vehicle should always be considered. muscle weakness. VX) FORMS: All nerve agents in the pure form are a colorless liquid. with widely varying potencies. xylene) and not due to cholinesterase inhibition. skeletal muscular twitching or weakness. These persons require antidotes immediately to save their lives. EKG Monitoring Establish IV . Individuals must be trained in the use of this device. Prioritize and Vitalize Airway Management – If airway is compromised by secretions or is rapidly closing. GF. Nonspecific symptoms such as upper respiratory irritation. resulting in buildup of excessive acetylcholine. PRE–HOSPITAL MANAGEMENT (See Organophospate Poisoning) FOR ADVICE ON CLINICAL MANAGEMENT. Yellow (Medium Priority). Prepare an eye wash solution by mixing Calcium Gluconate (10%) 50ml in NS 500ml. Ambulatory patients should be instructed to remove themselves from the hot zone and to decontaminate themselves under the direction of the decontamination supervisor. they should immediately administer a “Mark I” auto-injector to prevent becoming incapacitated. bronchospasm. and self–contained breathing apparatus.12 03/01/05 . Signs and symptoms include hypersalivation. If rescuers begin to exibit signs and symptoms of OP poisoning. CALL YOUR REGIONAL POISON CONTROL CENTER AT: (800) 222–1222 TRIAGE Red (Highest Priority). small pupils. Apply eyewash solution by using a Morgan Theraputic Lens.5% gel). Rescuers who have been treated with Atropine may be able to continue working. PATIENT MANAGEMENT IN THE HOT ZONE/ DECON AREA: 1.g.An individual who is convulsing or who is postictal. Administer 100 % O2. and thus may pose a serious hazard to rescuers or health care personnel. nausea and headache after inhalation exposure may be due to the solvent vehicle (e. intubate early. GD. diarrhea. Use of the “Morgan Lens” for flushing the eyes is recommended. if resources are available to provide appropriate immediate care. Water decontamination may be insufficient to remove oily compounds. abdominal cramps. if victim survives the acute poisoning. CPAP for Pulmonary Edema (Non Cardiogenic Shock . responders should make worst-case assumptions about the material.(2-Pam) 1 gram diluted in 20 mL of Sterile Water mixed in 100 ml normal saline and given IVP over 20-30 minutes. b. This patient must be kept under observation for at least 18 hours. rescuers should assume that the victim poses a risk of secondary contamination until decontaminated. Atropine administration in a hypoxic patient may precipitate Ventricular Fibrillation If the patient is hypoxic. was to small amounts of gas or vapor. e.). liquid. the patient’s respiratory effort is a better indicator to determine if sufficent atropine has been administered. 1mg (2-9 y. Reactive and likely to give rise to irritant or poisonous gases on contact with water or heat. For exposures involving direct contact with an unknown liquid or solid material or dust. or more of atropine. or other means.o. If the victim’s only exposure.An individual who is able to walk and talk after a vapor exposure. In general. CPAP for Pulmonary Edema (do not use Furosemide) “Mark-1”. Corrosive (either acidic or alkaline). Dosages may be repeated every 15 minutes until signs/ symptoms are eliminated. Oily and persistent on skin and clothing.o. or solid/dust. PATIENT MANAGEMENT IN THE HOT ZONE/ DECON AREA: 1. and. the risk of secondary contamination to health care personnel away from. if the exposure involved an aerosol which might condense on a victim’s skin or clothing.). An individual who was given 4 mg. which cannot be identified in the form of a gas or vapor. Individuals may only need monitoring for at least one hour. Green (Low Priority). EKG Monitoring Establish IV . “CANA” or “Atrox” Auto-Injector kit is the preferred method of administration. “Atrox” autoinjectors area available in multiple dose ranges based on patients age. or 10 to 15 if IM until SLUDGE symptoms are relieved. rescuers will not enter the Hot Zone.) Pralidoxime . Atropine may be given via ET tube. and therefore difficult to decontaminate. UNKNOWN MATERIAL FORMS: This section assumes that a victim has been exposed to a hazardous material. Labetolol may be indicated if hypertension persists for more than 20 minutes. explosion. (pt’s heart rate may be >60/min. However. Though the patients heart rate is one indicator to determine if the patient needs more atropine.Haz-Mat Guidelines FOR ADVICE ON CLINICAL MANAGEMENT. In such a situation once the clothing had been removed and double bagged. However. decontaminate the victim. CALL YOUR REGIONAL POISON CONTROL CENTER AT: (800) 222–1222 effects.13 .) every 5 minutes if IV. and able to be absorbed through intact skin. Some miosis without other effects. Once entry appears to be 03/01/05 H . Poisonous by inhalation. Administer 100 % O2. or serious reactivity has been ruled out. Brochoconstriction may prevent intubation efforts and should be treated with an initial dosage of Atropine.0 mg. the initial dosage of atropine must be given IM to prevent ventricular fibrillation. or 2. the scene is probably very small. the risk to rescuers would be minimal. if such identification is impossible. atropine administration should be given immediately. When intubated. PRE–HOSPITAL MANAGEMENT Decontaminate Prioritize and Vitalize Airway Management – If airway is compromised by secretions or is rapidly closing. and who is recovering from the effects of both the agent and the antidote. shipping papers. 600 mg IM may be used if no IV access is available. “CANA” auto-injectors contain 10 mg of Valium for the treatment of seizures in a severely exposed victim. and therefore able to penetrate certain types of protective clothing and protective gear. Lipid soluble. Theoretically.The “Mark I” kit contains two auto-injectors.0 mg dosages. BACKGROUND: Every attempt should be made to identify the substance involved using placards. maintain 5cm of H2O PEEP. small amounts of gas might be trapped in a victim’s clothing. The administration of atropine will aid the intubation efforts. When in doubt. IV administration may cause prolonged marked hypertension if given too rapidly. until the possibility of fire. They can be self administered through an IM route and are designed to be re-administered PRN.with Normal Saline Atropine . one Atropine (2 mg) and one Pralidoxime (600 mg). d. May substitute Lorazapam (Ativan) 1-2 mg for Diazepam. c. POTENTIAL FOR SECONDARY CONTAMINATION: Victims contaminated with an unknown liquid or solid/dust material should be assumed to be carrying a risk of secondary contamination. there would be a potential for secondary contamination until decontamination had been carried out. Diazepam – 5-10 mg for seizures.5mg.5mg (0-2 y. ingestion. .o. The pediatric dosage for Pralidoxime is 15mg/kg. These units are available in 0. 1. Rescuers should assume that the material might be: a. and cutaneous absorption.2mg (>9 y. with IV crystalloid solutions. Flush skin with water spray for 1 – 2 minutes. Quickly evaluate and support ABCs. Remove and double bag clothing. immediately dilute with 1 glass of water and give activated charcoal 60 – 100 grams if available. and 0. with soap and/or shampoo. 6. Stabilize the spine (if trauma suspected). 3. 3. FOR ADVICE ON CLINICAL MANAGEMENT. establish airway and breathing. CALL YOUR H . Instead. request assistance from the local hazmat team or your Regional Poison Control Center. Re–evaluate airway.1 mg/kg over 2-5 minutes. Even if significant ingestion is suspected. 7. including skin or hair. 2. do not induce vomiting. 4. have the victim remove contact lenses if able to do so. for at least 10–15 minutes or until symptoms of pain or irritation have resolved. Irrigate exposed eyes if symptomatic. and consider high flow supplemental oxygen by bag naive mask with reservoir. if possible and practical. if the victim is conscious and able to protect the airway. 8. Continue to irrigate injured eyes or exposed areas of skin for at least 15 to 20 minutes if the victim continues to complain of discomfort.10 mg IV for an adult. Continue to flush affected skin and eyes with copious water or saline. Remove contact lenses and irrigate eyes with saline via plain IV tubing. If the victim complains of eye irritation. and 1 – 2 mg IV for children or Ativan (Lorazepam): 5 . Treat bradycardia with Atropine or other modality appropriate to the patient’s clinical status. Do NOT give activated charcoal if a corrosive is suspected. Consider aerosolized bronchodilators if significant wheezing is present. 2. In addition.Emergency Medical Guidelines feasible. Continue to provide high–flow oxygen by mask.14 03/01/05 . REGIONAL POISON CONTROL CENTER AT: (800) 222–1222 PRE-HOSPITAL MANAGEMENT AFTER INITIAL DECONTAMINATION: 1. don protective equipment (self– contained breathing apparatus) capable of withstanding brief exposure to both corrosives and hydrocarbon solvents. If these requirements cannot be met. Support BP if needed. Attach cardiac monitor. Activate basic decontamination protocol. If victim is NOT decontaminated and responder is properly trained. and self–contained breathing apparatus. rescuers should don fully encapsulated protective clothing and gloves capable of withstanding both corrosives and hydrocarbon solvents. 5. wash oily contaminated areas. Treat seizures with Diazepam (Valium): 5 – 10 mg IV for an adult. intubating the trachea if victim is unconscious or has developed severe respiratory distress. Haz-Mat Guidelines 03/01/05 H .15 . 5mg IV/IO q 3-5 minutes to max of 3.04mg/kg) Transcutaneous Pacing Dopamine 5-20 ug/kg/min Epinephrine 2-10ug/min Pulseless Electrical Activity Think 6 “H’s” & 6 “T’s” (See table A) Vasopressin 40u IV/IO to replace 1st or 2nd dose of Epinephrine OR Epinephrine 1.0mg (0.03-0. aVF Asystole Think 6 “H’s” & 6 “T’s” (See table A) Vasopressin 40u IV/IO to replace 1st or 2nd dose of Epinephrine OR Epinephrine 1.000 IVP/IO q 3-5 minutes Atropine 1.Immediate defibrillation (See table B) Unwitnessed Arrest – CPR for 5 cycles / 2 minutes.04mg/kg) **CPR——Intervention—CPR pattern (Minimize interruptions in CPR)** Ventricular Fibrillation (VF) / Pulseless Ventricular Tachycardia (PVT) Think 6 “H’s” & 6 “T’s” (See Table A) Witnessed Arrest .0mg 1:10.000 IVP/IO q 3-5 minutes Atropine 1.0mg IV/IO q 3-5 minutes to max of 3.03-0. 1meq/kg IV/IO **CPR——Intervention—CPR pattern (Minimize interruptions in CPR)** 03/06/06 AA.0mg (0.0mg (0.04mg/kg) **CPR——Intervention—CPR pattern (Minimize interruptions in CPR)** Bradycardia Atropine 0. repeat 150mg IV/IO in 5 minutes OR Lidocaine 1. then defibrillation (See table B) Vasopressin 40u IV/IO to replace 1st or 2nd dose of Epinephrine OR Epinephrine 1.1 .0mg 1:10.0mg IV/IO q 3-5 minutes to max of 3.5mg/kg IV/IO to max 3mg/kg Magnesium Sulfate 1-2g diluted in 10cc over 2 minutes for torsades de pointes Sodium Bicarb. III.03-0.0mg 1:10.0-1.Appendix A APPENDIX A ACLS Quickie All patients: Vitalize/Prioritize Oxygen/Airway EKG Monitored 12 Lead EKG V4R if any ST elevation in leads II.000 IVP/IO q 3-5 minutes Amiodarone 300mg IV/IO. 5 . A-Flutter or M. repeat as needed to max 2.75mg/kg to max of 3mg/kg Prepare for synchronized Cardioversion (See page C-3 & Table B) If SVT with aberrancy: Adenosine 6mg IVP/IO.25mg/kg IV/IO over 2 minutes.5 .Emergency Medical Guidelines Tachycardia (Wide Complex = QRS > 0.75mg/kg IV/IO.2g in 24 hours OR Lidocaine 0. repeat 0.35mg/kg IV/IO over 2 minutes Irregular Rhythm: (Probable A-Fib.0.0.Defibrillate (See Table B) Amiodarone 150mg IV/IO over 10 minutes.5 .5 . 12mg IVP/IO.0. repeat as needed to max 2.35mg/kg IV/IO over 2 minutes Table A 6 H’s 6 T’s Hypovolemia (volume infusion) Hypoxia (ventilation) Hypothermia Hydrogen Ion (acidosis) Hyper/Hypokalemia Hypoglycemia Tamponade Tension pneumothorax Thrombosis-Coronary Thrombosis-Pulmonary Toxins Trauma (Hypovolemia) 03/06/06 AA-2 .2g in 24 hours Lidocaine 0.75mg/kg to max of 3mg/kg Magnesium Sulfate 1-2g IV diluted in 10cc over 2 minutes for Torsades de Pointes Tachycardia (Narrow Complex = QRS < 0.25mg/kg IV/IO over 2 minutes. 12mg IVP/IO Cardizem 0.0.A. 12mg IVP/IO.T.75mg/kg IV/IO.12 seconds) Unstable (Serious Signs and Symptoms) Immediate synchronized cardioversion (See page C-3 & Table B) Regular Rhythm: Attempt vagal maneuvers Adenosine 6mg IVP/IO. may repeat in 15 minutes at 0. 12mg IVP/IO Irregular Rhythm: (Polymorphic VT) Unstable .12 seconds) Unstable (Serious Signs and Symptoms) Ventricular rate > 150 BPM Immediate synchronized cardioversion (See page C-3 & Table B) Regular Rhythm: (V-Tach or Uncertain Rhythm) Amiodarone 150mg IV/IO over 10 minutes. repeat 0. may repeat in 15 minutes at 0.) Cardizem 0. Phillips) Subsequent = 120j or higher Biphasic truncated exponential waveform – Initial = 150j (i. 300j. 360j Biphasic – Initial = 100j Subsequent = 120j. Zoll.0j/kg Subsequent = 2j/kg 03/06/06 AA. 200j Cardioversion: (Wide Complex Tachycardia) Monophasic – Initial = 100j Subsequent = 200j. Medtronics) Subsequent = 150j or higher Monophasic waveform – Initial = 360j Subsequent = 360j Cardioversion: (Narrow Complex Tachycardia) Monophasic – (A-Flutter or Re-entry SVT) – Initial = 50j Subsequent =100j. 150j. 200j Pediatric Electrical Therapy Defibrillation: Monophasic / Biphasic – Initial = 2j/kg Subsequent = 4j/kg. 360j Monophasic – (A-Fib) – Initial = 100j Subsequent = 200j. 200j. Appendix A Table B Adult Electrical Therapy Defibrillation: Biphasic rectilinear waveform – Initial = 120j (i.e.e. 360j Biphasic – Initial = 100j Subsequent 120j. 4j/kg Cardioversion Monophasic / Biphasic – Initial = 0.3 . 300j. 150j.5j/kg – 1. 300j. FL 33435 Boca Raton. FL 34997 1796 Highway 441 North 1414 Kuhl Avenue 2815 South Seacrest Boulevard 800 Meadows Road 2201 45th Street 5301 South Congress Avenue 5352 Linton Boulevard 1201 South Main Street 1300 North Flagler Drive 1210 South Old Dixie Highway 3360 Burns Road 2829 10th Avenue 13001 Southern Boulevard 901 45th Street 7305 N. FL 34994 2100 Southeast Salerno Road Stuart. Fl 33410 West Palm Beach. FL 33461 Loxahatchee. FL 33428 OKEECHOBEE COUNTY Columbia Raulerson Hospital ORANGE COUNTY Orlando Region Medical Center *** PALM BEACH COUNTY Bethesda Memorial Hospital Boca Raton Community Hospital Columbia Hospital Columbia JFK Medical Center Delray Medical Center Glades General Hospital Good Samaritan Hospital Jupiter Medical Center Palm Beach Gardens Medical Center Palm Beach Regional Hospital Palms West Hospital St. Lucie. FL 32901 Vero Beach. Military Trail 10101 Forest Hill Boulevard 21644 State Road Seven Okeechobee. FL 34972 Orlando. Lucie Lawnwood Regional Medical Center 1800 Southeast Tiffany Avenue Port St. FL 33484 Belle Glade. FL 33407 West Palm Beach. FL 33486 West Palm Beach. LUCIE COUNTY Columbia Medical Center – Port St. FL 33410 Lake Worth. FL 32806 Boyton Beach. FL 33430 West Palm Beach. FL 33470 West Palm Beach. FL 32960 Sebastian.S. FL 32958 800-541-1928 772 567–4311 772 589–3186 772 223–5995 772 223–5721 941 763–2151 407-841-5111 561 737–7733 561 395–7100 561 842–6141 561 965–7300 561 498–4440 561 996–6571 561 655–5511 561 744–4460 561 622–1411 561 967–7800 561 798–3300 561 844–6300 561 882-8262 561 798–8500 561 488–8000 772 335–4000 772 461–4000 *** INDIAN RIVER COUNTY Indian River Memorial Hospital Sebastian River Medical Center MARTIN COUNTY Martin Memorial Medical Center Martin Memorial Hospital – South 300 Southeast Hospital Avenue Stuart. Highway One Melbourne.Appendix B APPENDIX B Guide to the Hospitals in the Operating Region BREVARD COUNTY Holmes Regional Medical Center 1350 South Hickory St 1000 36th Street 13695 U. FL 33458 Palm Beach Gardens. FL 33407 Atlantis. Mary’s Medical Center VA Medical Center Wellington Regional Medical Center West Boca Medical Center *** *** ST. FL 34950 *** Area Trauma Centers Poison Control Center 1-800-282-3171 03/01/05 AB-1 . FL 33401 Jupiter. FL 33414 Boca Raton. FL 33462 Delray Beach. FL 34952 1700 South 23rd Street Port St. Lucie. Appendix C APPENDIX C TRAUMA TRANSPORT PROTOCOLS AC-1 . Emergency Medical Guidelines Wong-Baker FACES Pain Scale Instructions Explain to the patient that each face is for a person who feels happy because they have no pain (hurt) or sad because they have some or a lot of pain. Face 0 is very happy because they do not hurt at all Face 1 hurts just a little bit Face 2 hurts a little more Face 3 hurts even more Face 4 hurts a whole lot more Face 5 hurts as much as you can imagine. although you do not have to be crying to feel this bad Ask the patient to choose the face that best describes how he/she is feeling 03/01/05 AD-2 . black tarry stools or vomiting blood). History of stroke or TIA at any time. Patient in cardiogenic shock (systolic BP<90 mm Hg) or the patient is intubated. Radiating pain through to the upper back characterized as a ripping or tearing pain YES NO accompanied by unequal blood pressures or distal pulses when comparing the right and left arms (suggestive of a Dissecting Aortic Aneurysm). 9. AVM (arterial–venous malformation).Appendix E PREHOSPITAL FIBRINOLYTIC CHECKLIST Inclusion Criteria 1. 8. Is the patient 18 years of age or older? 2. 2.g. Hemophilia or any known bleeding disorder. 4. ST segment elevation >1mm in 2 or more anatomically contiguous limb leads or ST YES NO segment elevation >2 mm in 2 or more anatomically contiguous precordial leads (V1–V6) or new or presumably new LBBB? INCLUSION / EXCLUSION CHECKLIST Note: Any YES answer to the questions listed below will EXCLUDE the patient from the administration of a fibrinolytic medication. Hypertension at the time of presentation that exceeds 180 systolic or 110 diastolic. Ischemic discomfort present for greater than 20 minutes but less than 12 hours? YES NO YES NO APPENDIX E 3. Use of cocaine or other amphetamines within the past 3 days. Any major surgery. YES NO YES NO 01/09/06 AE-1 . Pregnancy. trauma (including CPR for greater than 2 minutes). or cerebral aneurysm. 3. 5. 1. 6. YES NO YES NO YES NO YES NO YES NO YES NO 7. or any type of internal bleeding or hemorrhage within the past 4 weeks (e. Brain tumor. uses inappropriate words. 01/09/06 AE-2 . Arm Drift Action: Have the patient close their eyes and hold both arms out Normal: Both arms move the same or both arms do not move at all Abnormal: One arm does not move or one arm drifts down compared to the other Speech Action: Have the patient say: “ You can’t teach an old dog new tricks” Normal: Patient uses correct words with no slurring Abnormal: Patient slurs words. or is unable to speak Interpretation: If any one of these 3 signs fall into the “Abnormal” category. the probability of a stroke is 72%.Emergency Medical Guidelines Cincinatti Stroke Scale Facial Droop Action: Have the patient show their teeth or smile Normal: Both sides of the face move equally well Abnormal: One side of the face does not move as well as the other side. Trauma Alert with scene extrication time greater than 15 minutes. transport patient upon request by a provider. Stroke and Cardiac Alert patients located in areas that would otherwise be outside the three hour window of opportunity for thrombolitic therapy.Appendix F APPENDIX F HELICOPTER ACTIVATION CRITERIA The guidelines for helicopter response include but are not limited to the following: Trauma patients that meet the trauma scorecard methodology and criteria as set forth by your agency. burn unit. Inter-Facility Transfers (IFT) when rapid transport is deemed medically necessary. Ground response to specific scenes greater than 15 minutes Mass Casualty Incidents evacuations (MCI) To augment or expedite pre-hospital transport. Scene to trauma center by ground transport is greater than 20 minutes. For the critically ill patients requiring specialized services and facilities located in other areas. 03/01/05 AF-1 . Example: Pediatrics. Obstetrics. cardiac cath labs etc. Due to the nature of these incidents. III or aVF IV 0. etc. EMS providers should always err on the side of caution and recommend transport of these patients.9 % NaCl Treat underlying conditions.Appendix G APPENDIX G TASER INJURIES Caution Most injuries from a taser devise are the result of secondary injuries such as from a fall.76 Joules per pulse. altered mental status. as needed (cardiac arrhythmias. EMS personnel do not medically clear persons in police custody who were subdued with a tazer. Do not remove the prongs unless they interfere with critical life care measures Advanced Life Support 12 lead EKG monitor V4R should be evaluated if any ST elevation in leads II.) 02/15/06 AG-1 . The electrical current is considered safe with an output of 1. Basic Life Support Confirm that law enforcement has disconnected the wires from the hand held unit Oxygen / Airway Spinal Immobilize. if indicated Secure the taser prongs in place as an impaled object if not already removed by law enforcement. Emergency Medical Guidelines 02/15/06 AG-2 . infusion rates should be slowed to have all infusion administered over 5 minutes. Florida 34994 Chief Wouters. D. To reduce side effects of Cardizem.Lillian Avner. The administration of Cardizem (Diltiazem) is referenced in the current protocols on pages D-9 and C-6 as being administered by infusion over 2 minutes. I would like to have the following changes made to the Emergency Guidelines as they pertain to Martin County.O. Medical Director July 1. As the Medical Director for Martin County Fire Rescue. please contact me at your convenience. 2009 Martin County Fire Rescue 800 SE Monterey Road Stuart. D.O. Lillian Avner. If you have any questions or concerns. Sincerely. Medical Director Martin County Fire Rescue .
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