EKG Rhythm Recognition

600905.8 Contact Hours Rhythm Recognition: Getting to the Heart of the Matter By Susan Manifold, RN, MS, NP-BC ©2014 Gannett Education All Rights Reserved. HOW TO TAKE THIS COURSE 1. Examine the objectives: The course and chapter objectives provide an overview of the course. Focus your attention on the learning goals. 2. Study the chapters in order: Each chapter contains information essential to understanding materials in succeeding sections. Keep your learning “programmed” by reviewing the materials in order. 3. Take the test. 4. Send the answer form to the address below. Gannett Healthcare Group 7950 Jones Branch Drive 7th Floor McLean, VA 22107 Or fax your answer form to 866-704-3752. 5. Certificates indicating successful completion of this offering will bear the date your answer form is received at Gannett Education in Virginia. 6. Answer forms must be postmarked by February 28, 2016. 7. To earn continuing education, you must achieve a score of 75%. If you do not pass the test, you may take it again once at no additional charge. 8. Certificates will be sent to your home e-mail address within two weeks of our receipt of your answer form in our Virginia office. If you do not provide an e-mail address, we will mail your certificate to the address you provide. If you have any questions about continuing education, call (800) 866-0919. 9. Gannett Education is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center’s Commission on Accreditation. Accredited status does not imply endorsement by the provider or ANCC of any commercial products displayed in conjunction with this activity. Gannett Education is also accredited by the Florida Board of Nursing (provider no. FBN 50-1489) and the California Board of Registered Nursing (provider no. CEP13213). Copyright All rights reserved. No part of this book may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from Gannett Education. Gannett Education (800) 866-0919 Nurse.com/CE ContinuingEducation.com 2 GOAL AND OBJECTIVES The purpose of this course is to provide nurses with a step-by-step approach to rhythm analysis and interpretation to enhance their ability to recognize and interpret cardiac dysrhythmias. After studying the information presented here, you will be able to: • Describe the components of the cardiac conduction system, incorporating cardiac anatomy and physiology • Interpret and analyze ECG strips and determine rate, regularity and rhythm • Identify rhythms originating in the sinus node and atria, atrioventricular (AV) node and ventricles and discuss their significance and treatment • Recognize Type I, II and III AV blocks and discuss their significance and treatment • Identify potentially life-threatening rhythms and discuss initial interventions/approach to treatment • Understand the relationship between coronary blood flow, myocardial infarction and associated ECG findings Gannett Education guarantees this educational activity is free from bias. The planners and authors have declared no real or perceived conflicts of interest that relate to this educational activity. ABOUT THE AUTHOR Susan Manifold, RN, MS, NP-BC, a nurse practitioner working at the Heart Center for Excellence in Kalamazoo, Mich., updated this course in 2013. Manifold has more than 25 years of experience in critical care and emergency nursing, having served in an educator role in those areas. She has taught at the associate, diploma, undergraduate and graduate nursing levels. Manifold is also a lecturer for national nurse practitioner meetings, ACLS AHA-certified, a member of the Michigan Coalition for Nurse Practitioners and an associate member of the American College of Cardiology. 3 ............ 41 Chapter 6: Ventricular Rhythms ...................... 31 Chapter 5: Junctional (Nodal) Rhythms ............ 47 Chapter 7: Atrioventricular (AV) Blocks ............................................................................................................................................................................. 15 Chapter 3: Sinus Rhythms ............. 7 Chapter 2: The Electrocardiogram ................................................................................................................................................................................................. 67 Test ..........................................................................................................................................................................................................CONTENTS How to Take This Course .......... 3 Introduction ....................................................................... 2 Goal and Objectives ............................................................ 25 Chapter 4: Atrial Rhythms..... 55 Chapter 8: Myocardial Infarction and Coronary Vessels .... 61 References .............................................................................. 5 Chapter 1: Basic Physiology: The Cardiac Conduction Systems ................................................ 3 About the Author ..................................................................................................................................... 69 4 ........................................................................................................................ hypertension and tobacco abuse. improve patient outcomes. the ability to understand and interpret a bedside monitor is no longer an expectation of only critical care and emergency nurses. Her risk factors include a premature family history of coronary artery disease. ECG tracings can look unintelligible to the untrained eye. with an understanding of basic cardiac physiology and practice. Gaining competence in ECG interpretation and rhythm recognition can assist the bedside nurse to intervene efficiently and effectively in a potentially difficult clinical situation and. However. ECG rhythm recognition and analysis continues to be a major nursing responsibility in the acute care setting. successful ECG interpretation is possible. diabetes. What are they? Are they dangerous or not? Should you notify the physician. Smith has been admitted to the observation unit for evaluation of chest pain unrelieved by nitroglycerin. After connecting her to an ECG monitor and running a “strip” recording you notice unusual-looking beats. 5 . Since the advent of bedside monitoring and coronary care units in the 1960s. Medical/surgical nurses need to be competent in ECG rhythm analysis supported by the notable increased acuity of hospitalized patients requiring ECG monitoring.INTRODUCTION Mrs. initiate emergency protocols or simply continue to monitor closely? The answer lies within the information ahead. ultimately. 6 . Cardiac cells are of two types: conduction and contractile. Collectively this process of electrical activation and myocardial contraction is called a cardiac cycle. The conduction cells create and conduct electrical signals that stimulate the cardiac muscle to contract.Chapter 1: Basic Physiology: The Cardiac Conduction System Electrocardiographic (ECG) monitoring measures the heart’s electrical activity and records it as waveforms on paper. Stimulation of the vagus nerve slows the heart rate via its influence on the SA node. and the atrioventricular (AV) node.1 The Electrical Event The SA node is a collection of cells within the right atrium of the heart that serves as the primary pacemaker of the heart. This spontaneous generation of an impulse is termed “automaticity. This process incorporates an electrical and mechanical event involving cardiac cells with unique properties. These cells comprise the sinoatrial (SA) node. inhibition of the vagus nerve results in an increase or acceleration of heart rate.1 The conduction cells result in an electrical event. These cells result in electrical activation of the myocardium (heart muscle). Electrical activation is necessary before any heart tissue can contract. 7 . The heart’s conduction system causes it to contract. The contractile cells cause the heart muscle to contract and eject blood to the pulmonary and systematic circulation. resulting in an increase in heart rate. The electrical event precedes the mechanical event. (See Diagram 1. Conversely.3 The SA node cells control the rhythm of the heart by retaining an automatic or inherent rate of 60 beats to 100 beats per minute (bpm). It is a visual representation of the electrical events in the heart that occur with each contraction or heartbeat. which prompts myocardial contraction. resulting in blood flow throughout the body. also known as the sinus node.”2. specifically the vagus nerve.2 The conduction cells within the SA node are capable of spontaneously generating an electrical impulse and thereby start the cardiac cycle by initiating contraction of the heart. the contractile cells result in a mechanical event.) The SA node remains predominantly under the influence of the parasympathetic division of the autonomic nervous system. The sympathetic division of the autonomic nervous system may also influence heart rate via the SA node due to a release of stimulatory chemicals known as adrenergic agents or catecholamines. the electrical impulse travels down both ventricles via the bundle of His. The AV node.1-3 The AV node’s rate of automaticity. This delay allows the atria to fill the ventricles prior to ventricular systole. or “junction. The His bundle divides into a right and left bundle branch extending to the Purkinje fibers. The AV node serves as a “gatekeeper” of impulses it receives. thereby providing a conduction delay of the impulses it receives. By this process. it is propagated through the right and left atrium to the AV node. also known as the atrioventricular (AV) bundle. (See Diagram 2.Once the electrical impulse in initiated at the SA node. the ventricles are activated and ventricular contraction (systole) follows.3 This completes the electrical portion of the cardiac cycle. another collection of conduction cells. is located near the interatrial septum. located in the interventricular septum.) The left bundle further divides into the left anterior and posterior fascicles.4 Diagram 1: Cardiac Conduction System/Pathway From the AV node. is 40 bpm to 60 bpm and can function as a backup pacemaker if the SA node should fail. is called “atrial kick” and augments total cardiac output up to 30%. provided by the atria. 8 . or inherent rate.” as it is located between the right atrium and ventricle. This contribution of blood to the ventricles. Ventricular tissue’s rate of automaticity or inherent rate is 20 bpm to 40 bpm. Diastole is the filling of the ventricles with blood returning to the atria via the inferior and superior vena cava and coronary sinus and pulmonary veins. potassium. The resting cardiac conduction cells are polarized. it is important to monitor and maintain normal values of these ions. There are two phases of the cardiac cycle: systole and diastole. ions shift back to their original places and return the cell to its resting state.) Depolarization of the myocardium results in myocardial contraction. This exchange of ions represents a process of depolarization and repolarization. causing the cells to become positively charged. This is referred to as repolarization and represents myocardial relaxation. Systole is the contraction of the ventricles resulting in expulsion of blood into the pulmonary artery and aorta.Diagram 2: Complete Pathway of Cardiac Conduction The Mechanical Event The electrical events previously described precede and ultimately trigger mechanical events that occur during each cardiac cycle.4 The electrocardiogram is a visual representation of the electrical activity of the heart.3.1-4 9 . (See Diagram 3. or depolarized. (See Diagram 4.) When the cells are stimulated by an electrical impulse. calcium and magnesium) influence the process of depolarization and repolarization. that is. Electrolytes (sodium. they are electrically negative on the inside as compared with the outside. which occurs due to an exchange of electrically charged ions across the cardiac cell membrane. Therefore. sodium ions rush into the cells and potassium ions leak out. Once myocardial contraction or systole is complete. QRS complex: A tall. it may be indicative of myocardial ischemia or injury. which should be less than half the time of the preceding R-R interval (distance between two consecutive R waves of the QRS complex).Diagrams 3 and 4: Polarization and Depolarization ECG Waveforms and Complexes The placement of electrodes on the skin transforms the electrical activity of the heart (depolarization and repolarization) into waveforms and complexes representing the cardiac cycle. The normal QRS complex. is less than 0.) T wave: An upright wave occurring after the QRS complex. Electrolytes and certain clinical conditions can alter its shape. QT interval: Measured from the beginning of the Q wave to the end of the T wave. It represents early ventricular repolarization. There are no parameters for timing but there should be no elevation or depression from baseline. 10 . Represents total ventricular depolarization and repolarization time. These waveforms and complexes have normal characteristics and timings as follows:1-5 P wave: A small. upright. A widened QRS complex may be due to a ventricular dysrhythmia (Discussed in Chapter 6). spiked waveform arising from the baseline that may be either upright or inverted representing ventricular depolarization. or ventricular depolarization.12 and 0. (If noted. PR interval: Measured from the beginning of the P wave to the beginning of the R wave of the QRS complex. ST segment: The horizontal line between the end of the QRS complex and the beginning of the T wave. Normal PR interval time is between 0. This interval represents the time it takes for the electrical impulse to pass from the SA node through the complete cardiac conduction system.12 seconds. rounded wave representing atrial depolarization. Atrial contraction follows.20 seconds. representing ventricular repolarization. Atrial muscle mass is small so the electrical charge is small. Diagram 5: The Cardiac Cycle and ECG Complexes. This is manifested by the QRS complex. Collectively. it follows the T wave and represents late repolarization of the ventricle or may indicate electrolyte imbalances. The QRS is altered in ventricular dysrhythmias. or cardiac cycle. each P-QRS-T complex represents one heartbeat. All atrial dysrhythmias relate to the P wave. The atrial contraction on the ECG is manifested by the P-wave. It may become wide or narrow. The ventricular mass is larger and creates a bigger deflection on ECG.U wave: Not normally visualized. If present. (Diagram 5) The horizontal line between the T wave of one beat and the P wave of the next is a time of electrical inactivity and is called the baseline or isoelectric line. 11 . • The T wave represents ventricular repolarization.20 second • QRS complex: 0. or heartbeat. The two phases of the cardiac cycle are systole and diastole. T wave and U wave. QRS complex. Normal segments and intervals for P-QRS-T are: • P-R interval: 0. Electrical stimulation of the heart results in an exchange of ions across the cardiac cell membrane and the initiation of cardiac depolarization and repolarization.12 to 0. • The QRS complex represents ventricular depolarization. • The P wave represents atrial depolarization. The waveforms and complexes reflective of depolarization and repolarization are the P wave.12 second • QT interval: less than or equal to one-half the distance between successive R-R intervals 12 . initiated by contractile cells. bundle of His and Purkinje fibers to the ventricles. The electrical event is initiated in the SA node. • Each P-QRS-T represents one cardiac cycle.Diagram 6 ECG Waveforms/Complexes Chapter Review The electrical event initiated by the cardiac conduction cells precedes the mechanical event of myocardial contraction.06 to 0. propagated through the atria to the AV node. In the diagram below. QRS complex and QT interval.gif 13 . http://www.edu/pic/224/ekg.msjc. note the PR interval. 14 . the left leg is positive. aVL and aVF. The 12 leads include six standard leads (the “limb leads”) that depict cardiac electrical events from six angles in the frontal or vertical plane. II and III Lead I: Measures the current traveling between the right and left arms. 15 . III. The limb leads are leads I. The electrodes are placed at specific locations across the chest. Leads I. II and III are also called bipolar because they measure current traveling between a positive and negative pole. These leads are positive and unipolar. Lead III: Measures the current traveling between the left arm and the left leg. the left leg is positive. The right arm is negative. The greater the number of leads.Chapter 2: The Electrocardiogram The wave of electrical impulses traveling via the SA node to the AV node to the bundle of His to the bundle branches moves in a right-shoulder-to-left-foot direction (downward and to the left). the size of the waveforms so they will be evident on the ECG paper. aVL and aVF are augmented leads. The right arm is negative. II. Electrodes. aVR. Diagram 7: Limb Leads I. are sensors that pick up the heart’s electrical impulses and transform them into a recording on paper. the left arm is positive. Lead II: Measures the current traveling between the right arm and left leg. known as leads. so named because they generate such small waveforms on the ECG paper that the ECG machine must increase. The left arm is negative. Six additional leads (the “chest leads”) depict electrical events in the horizontal plane. requiring only one electrode to make the waveform. These leads provide 12 different views of the heart’s electrical activity. called the electrocardiogram (ECG/EKG). the better the interpretation of the heart’s electrical activity. aVR. placed at various locations on the body. or augment. aVL: Measures the current traveling toward the left arm. V2. (See Diagram 8) They are located across the chest from the fourth intercostal space. midaxillary line.1 Diagram 8 Precordial Chest Lead Placement Twelve-lead ECGs are used for the diagnosis and recognition of acute coronary syndrome in the patient who presents to the hospital or clinic with the complaint of chest pain. or positive (rising above the baseline). or telemetry. V4. Twelve-lead ECGs are often done as well during physical exams and prior to surgery as part of routine health screening and preoperative evaluation. are unipolar. The electrode is on the left arm. The electrode is on the right arm. 16 . if they have a known history of coronary artery disease or dysrhythmia (abnormal rhythm). The two most common three-lead systems place electrodes on the chest to monitor the cardiac cycle in Lead II and via a modified chest lead system (MCL-1). V5 and V6. The chest leads (also called precordial) see the heart from the horizontal plane and are named V1. (See Diagram 8.aVR: Measures the current traveling toward the right arm. These. each one being a positive electrode. The electrode is on the left leg. right sternal border to the fifth intercostal space. like the augmented leads. These patients are attached to either a three-lead or five-lead cable. aVF: Measures the current traveling toward the left leg. which is then attached to a transmitter to allow continuous observation of the heart’s electrical activity. V3.3 Hospitalized patients may require continuous ECG monitoring.) These systems are used because they typically produce ECG waveforms and complexes that are upright. thereby allowing for easier interpretation. or ECG rhythm.2. which then are attached to the monitoring system. (See Diagram 10. 17 . the chest leads (V1 through V6) may be monitored by moving the chest lead into any of the V1 to V6 lead placement positions. A five-lead system places electrodes on the chest in such a way to allow monitoring in both lead II and MCL 1.inch paper. The electrodes are connected to color-coded wires. Diagram 10: 5-lead Monitoring System ECG Paper Recordings of ECG rhythms are recorded on small rolls of special paper measuring about 3 inches wide and several hundred feet in length.Diagram 9: MCL-1 Depicted in Diagram 9 is lead placement for MCL-1 (modified chest lead) with the positive electrode in the V1 position and the negative electrode just below the left clavicle and adjacent to the shoulder.) Additionally. using a recorder that prints a simultaneous view of all 12 leads. A 12-lead ECG is done on 8-by-11. Horizontal counting measures time in seconds. • Each small box on the ECG paper measures 0.04 seconds x 5 = 0.2. Amplitude is measured in millimeters. (5 boxes X 0. • One large box contains five small boxes. • One large box equals 0.20 seconds.Diagram 11 The ECG paper is ruled into small boxes that are 1 millimeter (mm) in height and width. There are five small boxes horizontally and vertically contained within the darker lines. horizontally and vertically. Time intervals are determined by counting these boxes along the horizontal axis. or height. or large box. Each small (1 mm) box represents 0. (See Tracing 1. composed on the horizontal axis of five smaller boxes.20 seconds (0. Each large box. represents 0. ECG waves and complexes are measured by counting these blocks horizontally and vertically. 18 .04 seconds) With ECG paper it is possible to determine heart rate and time intervals for electrical impulses to travel from the atria to the ventricles (depolarization and repolarization) by counting and measuring the boxes. These occur every 5 mm.04 seconds. of the complexes and waves.) Vertical counting measures amplitude.20 seconds.3 Restated: • Each small box measures 1 mm.04 seconds.) Darker lines are present at every fifth block. Approach to the ECG There are many ways to read an ECG but each person has his or her own method. Sometimes. This interval may be prolonged due to certain medications or metabolic disorders. In some asymptomatic adults. isolated T wave inversions may be normal. The following outlines one such approach. The QT interval is usually less than or equal to 0. Q waves that are more than 1 mm duration and greater than one-third of the R wave amplitude are considered pathological. pericarditis.44 seconds for females. 1. This can be assessed by using calipers or markings on a piece of paper and comparing successive waves. It must be corrected for heart rate because it is rate dependent. QT interval: Count the number of small boxes between the beginning of the QRS and the end of the T wave.04 second. myocardial ischemia or ventricular aneurysm. 4. the RR interval or QRS complex is constant. Multiply by 0. Look for Q waves. not notched or peaked. QRS interval: Count the number of small boxes between the beginning and end of the QRS complex. P waves are usually upright. Assessing for Q waves should be done to look for an acute myocardial infarction and a patient history may help. Assess the rhythm of the heart: is it regular or irregular? When the rhythm is regular. ST segment elevation may be an indication of acute myocardial infarction. l. 2.5 mm in any lead. T wave is generally upright and in the same direction as the QRS complex. The ST segment is almost never normally depressed greater than 0. The P wave shape is generally smooth. It is important to know that small Q waves are normal in leads III and aVF and in anterolateral leads aVL. Determine if the ST segment is elevated or depressed. 3.04 second. Multiply by 0. angina. They may be slightly elevated in some leads over the heart (precordial leads). The aim is to develop a systematic approach so that nothing is missed. Developing a systematic approach to the interpretation of the ECG is a critical skill for all clinicians. Look at the ST segment. 6.PR interval: Count the number of small boxes between the beginning of the P and the beginning of the QRS. 5. Always check to see if there is a P wave before the QRS. This reveals if the rhythm is sinus. Learn to measure the QT interval. the rate may be very fast and the P waves may not be visualized.40 seconds for males and 0. 19 .04 second. Multiply by 0. V5 and V6. Determining Heart Rate ECG is printed on a paper at a speed of 25 mm/second. the heart rate is 150 bpm (300/2). If the QRS is separated by three large boxes. In method 2. If the QRS complex is separated by two large boxes. shown below. In the above ECG. Hence. the heart rate is 300 bpm (300/1).2 seconds or one large square. The squares highlighted in red show the distance from R-R wave.7. Therefore. If there’s another QRS complex separated by one large box. the ECG shows regular R waves. the heart rate is 75 bpm (300/4) and so on. locate a QRS complex at the beginning of a large square. First. If there are dysrhythmias. one can use the ECG grid to calculate heart rate. There are a number of ways to determine the heart rate. the heart rate is 100 bpm (300/3). The successive R waves occur after five large squares (which represents one second). the next QRS complex occurs at the 5th box and hence the rate is 300/5=60 bpm. five large squares represent one second. In method one. If the QRS is separated by four boxes. This is standardized and 5 mm = 0. Then locate the next QRS complex (see below). 20 . are they ventricular or supraventricular (another term to describe atrial dysrhythmias that arise above the AV node). there is one beat (R wave per second) and this equals 60 beats per minute (BPM). the PR interval is normal in that it is between 0.12 seconds. as it is less than 0.12 seconds represents a delay in conduction time through the ventricle.3 21 .12 and 0. PR: 0. Most digitally derived ECGs obtain a reliable heart rate within 1% to 5% of the true heart rate (obtained by pulse measurement). Yet another method to calculate heart rate is to count the number of QRS complexes in a sixsecond interval and multiply by 10. A prolongation of the interval may be noted during certain types of drug therapy and increases the susceptibility for a more dangerous ventricular rhythm. the QT interval is evaluated. PR intervals are always calculated every time a rhythm strip is run. The QRS duration is normal.06 sec (1.20 seconds.12 seconds. A QRS interval longer than 0. Tracing 1 Practice: Intervals. Beats that originate in the ventricles or at some point below the AV node always have a conduction time greater than 0.20 sec (5 boxes) QRS: 0. QRS and QT intervals. This interval reflects the depolarization-repolarization process. This interval is less than or equal to one-half the distance between successive QRS complexes for a heart rate between 60 and 100. Finally.32 sec (8 boxes) In the tracing.Remember this is a rough estimate and depends on regular waves.5 boxes) QT: 0. Rhythm Patterns Look at tracing 1 and determine the PR. Tracing 2 Six Second Interval Calculate the heart rate by counting the number of QRS complexes in the six-second interval indicated above. QRS. This is an approximation only. QRS complex. Counting from this line to the next darkened vertical line and then to the next nearest QRS complex. then 150 when you run into the next consecutive R wave. you would count: 300. 75. ST segment.or five-lead cable. Find an R wave that lies on a darker vertical line and counting to the next consecutive R wave. 60. turns out to be quite accurate. multiply by 10 = 80 Summary A systematic approach to ECG analysis is important. QT interval. 50. The number sequence changes each time a darker vertical line is encountered.Another important factor in analyzing ECG tracings is to determine the regularity of the rate. T and U (if present) • Intervals and segments: PR interval. The heart rate is 150 bpm. which allows for ECG waveforms and complexes that are easier to interpret. you should be evaluating: • The waveforms and complexes: P. use the following sequence of numbers to determine heart rate: 300. Answer: 80 bpm. 40. and in most instances. This refers to the pattern of the recording. 22 . 30. 100. Using Tracing 2. This complex lies on a darkened vertical line. look at the sixth QRS complex. The 12-lead ECG provides 12 different views of the heart’s electrical activity and consists of “limb” and “chest leads. as there are eight complexes in the six-second interval.” Hospitalized patients requiring ECG monitoring are usually attached to a three. • Heart rate • Rhythm/regularity Chapter Review The electrocardiogram is a recording of the heart’s electrical activity and impulses. In summary. 150. Leads II and MCL-1 are the two monitoring systems primarily used among hospitalized patients connected to telemetry. ECG paper is standardized so that one small box on the horizontal plane is 0.04 second and a large box of five small boxes is 0.20 second. There are various ways to calculate the heart rate from an ECG tracing: • Dividing 1,500 by the number of small boxes (from R wave to R wave). • Finding an R wave that lies on a darkened vertical line and counting a succession of numbers: 300, 150, 100, 75, 60, 50, 40 each time a darkened vertical line is encountered; with the rate being the number associated with the next R wave reached. • Counting the number of QRS complexes in a six-second interval and multiplying by 10. Using the ECG strip recording below, calculate the heart rate using any of the methods above. 6-second interval Heart rate: 40: The sinus beat circled lies beyond the six-second interval hash mark at the top of the ECG strip recording. 6-second interval Heart rate: 130 23 24 CHAPTER 3: Sinus Rhythms Normal Sinus Rhythm Normal sinus rhythm is a rhythm that originates from the SA (sinoatrial) node, follows the normal conduction pathway, is regular and has a rate between 60 to 100 beats per minute. (See Tracing 3.) Under normal circumstances, the electrical stimulus that initiates the cardiac cycle begins in the SA node and proceeds to the AV node and then down both ventricles via the bundle of His and Purkinje fibers system. Because the stimulus originates above the ventricles in the SA node, it is called supraventricular, or above the ventricles. This is the normal response depicted on the ECG as the P wave and reflects atrial depolarization followed by atrial contraction. The first step in analyzing an ECG strip should include an analysis of waveforms and complexes. A P wave should precede each QRS complex and be followed by a T wave. This represents normal conduction through the heart. Ultimately, with a normal-appearing QRS (with a duration of less than 0.12 second) and a normal-appearing P wave and PR interval (0.12-0.20 second), it can be assumed that the conduction from the SA to the AV node and bundle of His is normal; that is, without any delays or abnormal electrical impulses arising from another electrical “focus,” or location within the heart. Tracing 3: Normal Sinus Rhythm After looking at the waveforms and intervals, determine the regularity of the rhythm and rate. In normal sinus rhythm, the rhythm is regular and the atrial and ventricular rates are the same. The rhythm is described as normal sinus rhythm (NSR) under the following circumstances: (a) The impulse arises from the SA node and passes through the normal conduction pathway, indicated by normal appearing waves; (b) There is a normal PR interval; (c) There are normal QRS configurations; and (d) The heart rate is between 60 bpm to 100 bpm.1 Each rhythm should be evaluated incorporating the following points: • Is the rhythm regular? • What is the atrial and ventricular rate? 25 ) Sometimes the dysrhythmia is cyclical in nature. Each beat follows the normal conduction system.1. however. (See Tracing 4.1-3 • Sinus dysrhythmia • Sinus bradycardia • Sinus tachycardia • Sinus arrest A description of each with additional details follows. it is also sometimes called an arrhythmia. or rate. fast). Sinus dysrhythmia: A rhythm initiated by the SA node at an irregular rate. The rhythms listed below refer to those originating from an impulse arising from the SA node. The rate may vary (slow.3 Tracing 4: Sinus Arrhythmia Sinus bradycardia: A rhythm that originates in the SA node (P wave preceding each QRS with normal P-R interval) with a rate less than 60 bpm.) Well-conditioned athletes 26 . normal. This may be a normal finding in some people. because the rhythm.• • • • • • Are P waves present? Are the P waves of normal shape (rounded and upright)? Is there a P wave preceding each QRS? What is the duration of the PR interval? What is the duration of the QRS interval? Are T waves present of normal shape (rounded and upright)? Sinus Dysrhythmia An ECG rhythm not fitting the criteria for NSR is referred to as a dysrhythmia. is not within defined normal limits as described above. corresponding with inspiration and expiration. There are usually no symptoms noted unless the rhythm is associated with a sinus bradycardia or tachycardia (discussed below) with the treatments corresponding with each. although technically this term is inaccurate. the normal pacemaker of the heart. (See Tracing 5. as “arrhythmia” literally translates to “without rhythm” (at all). They do not qualify as NSR. frequently have sinus bradycardia. Elevated heart rates can result in hemodynamic compromise (decreased blood pressure). when a patient demonstrates signs and symptoms of poor perfusion caused by sinus bradycardia.5 mg IV push.. When the heart rate drops with these conditions. Some medications (e.12 to 2 sec Normal <0. beta-blockers.6 The expected result is an increase in heart rate back to normal (60 bpm to 100 bpm) and normalization of blood pressure and level of consciousness. it is important to determine how the patient “tolerates” this rhythm.6 If atropine is ineffective. If the rate is too slow to maintain an effective cardiac output. Examples of conditions that stimulate the vagus nerve include vomiting and pain.” When this response or state of bradycardia is sustained and results in a change in hemodynamics and level of consciousness. light headedness. it is called a “vagal response. digoxin. which may include preparation for temporary or permanent transvenous pacemaker insertion. Physician consultation should occur for further direction. Inadequate filling results in decreased cardiac output and subsequent decreased tissue and organ 27 . This is an example of the patient not “tolerating” the rhythm. such as altered mental status. lightheadedness or chest pain. which causes slowing of the heart rate. Sinus tachycardia: A rhythm that originates within the SA node (P wave preceding each QRS with normal P-R interval). calcium channel blockers.) As with sinus bradycardia. rarely exceeding 180 bpm. anything that stimulates this nerve may result in sinus bradycardia. the blood pressure will fall below normal and the patient may feel faint or light-headed.12 sec Rhythm Regular Regular Regular Regular Based on ACLS guidelines. This is determined by noting the patient’s state of hemodynamics (blood pressure) and level of consciousness. it should be treated with the administration of atropine 0. epinephrine) or TCP can be effective. chest pain or hypotension. Because the heart rate is influenced by the vagus nerve. because of inadequate time for cardiac filling during diastole.1 (See Tracing 6. with a rate greater than 100 bpm. then IV infusion of betaadrenergic agonists with rate-accelerating effects (dopamine. It is important to evaluate whether the patient with sinus bradycardia “tolerates” the rhythm. atropine should be given.g. antiarrhythmics) will decrease the heart rate. Tracing 5: Sinus Bradycardia Quick Check: Sinus Bradycardia Ventricular Rate Atrial Rate P wave PR interval QRS complex <60 Same as ventricular Normal Normal 0. 1-3 Tracing 7: Sinus Arrest/Block 28 . beta-blockers. digitalis are common culprits). (See Tracing 7. pain. Many conditions of noncardiac origin can cause sinus tachycardia: exercise (normal physiological response). as sinus dysrhythmia.12 sec Rhythm Regular Regular Regular Sinus arrest/block: This dysrhythmia occurs when the SA node fires its impulse on time. hyperthyroidism and hypovolemia. hypoxemia. bradycardia.perfusion. hypoxia) coronary artery disease (CAD). but the impulse exiting from the SA node to the atrial tissue is blocked. fever. correction of the possible cause should be considered and may be all that is indicated for treatment and stabilization. Therefore. The underlying rhythm is usually very regular. nausea. or tachycardia can be. This rhythm may occur in response to vagal stimulation (e. pain. The result is that one or more cardiac cycles (P-QRS-T) are missing as if dropped. anxiety. Patients with a history of heart disease may become symptomatic at lower rates than those with no pre-existing cardiac history. fear. It is not a dominant or sustained rhythm. cardiomyopathy or as a side effect of medication (calcium channel blockers.20sec Normal <0. Tracing 6: Sinus Tachycardia Quick Check: Sinus Tachycardia Ventricular Atrial rate P wave PR interval QRS complex >100 to 180 Same as ventricular Normal Normal 0.) The beat that the sinus node initiated is not conducted..12 to 0.g. Sinus dysrhythmias are rhythms that originate from the sinus node and include sinus dysrhythmia. In this dysrhythmia. Sinus dysrhythmia is an irregular rhythm arising from the SA node that often corresponds with inspiration and expiration and is a normal finding in some people. you will note that exactly one QRS is missing during this time of sinus arrest/block. but a pause is evident. In fact. exactly two RR cycles will fit into the pause. bradycardia. is regular and has a rate between 60 and 100 bpm.Quick Check: Sinus Arrest/Block Ventricular Rate Atrial Rate P wave PR interval QRS Varies Same as ventricular Normal except for period of sinus arrest Normal (when P wave is present Normal Rhythm Regular except for pause Regular except for pause Regular except for pause Note on Tracing 7 that the dominant rhythm is NSR. resulting in a missed cardiac cycle (P-QRS-T).6 As with sinus bradycardia. As with sinus bradycardia and tachycardia. tachycardia and sinus arrest/block. If you mark out the RR intervals. Sinus bradycardia is a regular rhythm arising from the SA node with a rate less than 60 that may be induced by vagal stimulation. a temporary or permanent pacemaker may be considered should the patient remain symptomatic or with unstable vital signs. Sinus tachycardia is a regular rhythm arising from the SA node with a rate above 100. the pause always results in a multiple of the previous RR intervals. Sinus arrest/block is a pause that occurs when the initiation of a SA node impulse is blocked. the patient should be evaluated for symptoms of decreased perfusion such as blood pressure drop. Either alleviate or remove the possible cause or administer atropine to increase the heart rate. 29 . lightheadedness or chest pain. follows the normal conduction pathway. Chapter Review Normal sinus rhythm is a rhythm that originates from the SA node. Recurrent and prolonged pauses will require action. Label the following rhythm strips as: • Normal sinus rhythm • Sinus dysrhythmia • Sinus bradycardia • Sinus tachycardia • Sinus arrest Answer: Sinus dysrhythmia Answer: normal sinus rhythm Answer: Sinus bradycardia 30 . 1-3 Loss of atrial kick may result in dizziness. firing hundreds of impulses from different locations at the same time. Because there are no P waves. multifocal atrial contractions • Atrial tachycardia • Wandering atrial pacemaker Atrial fibrillation (AF): As the name implies.CHAPTER 4: Atrial Rhythms Atrial Dysrhythmias Atrial dysrhythmias are initiated in the atrial tissue of the heart at a site outside of the normal pacemaker. The ectopic atrial focus may fire rapidly. This rhythm may be sustained or intermittent. The AV node. Two criteria aid in the diagnosis of AF: the ventricular rate is irregularly irregular.2 This rhythm may be either sustained or intermittent. the SA node. is bombarded with impulses and cannot depolarize fast enough to let all of the impulses through. usurping or overriding the sinus node. First. and a P wave is not discernable. Nomenclature often reflects rate-related severity. An abnormal or “ectopic” focus generates the impulse that is propagated down the conduction system. usually a “gatekeeper” or “filter” of electrical impulses it receives from the SA node. lightheadedness. the atria are fibrillating. For example. resulting in a reduced filling of blood into the ventricle. When one of the impulses does get conducted through. In this rhythm. As a result. or quivering. generally producing normal-appearing QRS complexes. AF with a “controlled” ventricular response implies that the ventricular rate is normal: between 60 bpm and 100 bpm. fatigue. Two serious hemodynamic problems may arise with AF.1-4 Atrial dysrhythmias to be discussed include: • Atrial fibrillation • Atrial flutter • Premature atrial contractions.” AF with a ventricular rate greater than 150 bpm is said to be “uncontrolled. One of the distinguishing features of atrial fibrillation is the marked irregularity of the ventricular response.” The QRS could potentially be wider than normal if there is delayed conduction of the impulse though the ventricle as is seen with a bundle branch block (BBB) or intraventricular conduction defect.” AF with ventricular rates less than 60 bpm is called “slow atrial fibrillation. it causes a drop in cardiac output because of the loss of effective and synchronous atrial contraction (atrial kick). Atrial contraction contributes up to 30% to overall cardiac output. 31 . there is no PR interval. atrial rhythms often result in elevated heart rates and patients are usually symptomatic. it is propagated normally. The quivering atria contract inefficiently. A ventricular rate greater than 100 bpm is called “rapid atrial fibrillation.3 The ventricular rate will depend on the degree of blockade (of impulses) at the AV node. shortness of breath or syncope because of a subsequent drop in cardiac output and blood pressure. atrial rates can be as high as 350 bpm to 700 bpm. S. Pooled blood may form clots and precipitate MI. which maintains a drug information portal with additional information from the U. is a therapeutic option to anticoagulate an individual in nonvalvular atrial fibrillation to prevent strokes that could result from systemic emboli formation (in lieu of warfarin).7 (Level ML) The decision for anticoagulation is individually determined for each person with AF. a direct thrombin inhibitor.9 Tracing 8: Atrial Fibrillation Tracing 9a Atrial Fibrillation With Controlled Ventricular Response 32 .8 (Level ML) For all anticoagulants. Food and Drug Administration.8 (Level ML) Rivaroxaban (Xarelto) is a Factor XA inhibitor found to be noninferior to warfarin for the prevention of stroke in patients with nonvalvular atrial fibrillation and is yet another therapeutic option to be used in place of warfarin among patients with atrial fibrillation.A second problem is an increased threat of blood clots. Detailed prescribing information is available at the National Library of Medicine. The 2011 guideline update for AF advises the clinician on use of the addition of clopidogrel to aspirin therapy for those patients unable to tolerate warfarin or comply with the required testing associated with this medication. stroke or pulmonary embolism. the most worrisome complication is bleeding. Most certainly the estimated benefit of anticoagulation must outweigh any and all risks associated with their use. As a result. Close monitoring and patient education are therefore crucial in addition to appropriate patient selection for these drugs. many patients with AF are anticoagulated with warfarin unless the potential risks of anticoagulation would outweigh the risks of untoward bleeding. as the blood in the atria is allowed to pool when the atria are fibrillating rather than contracting completely.7 Dabigatran (Pradaxa). calcium channel blockers and antiarrhythmics may be used.Tracing 9b Rapid Atrial Fibrillation Quick Check: Atrial Fibrillation Ventricular Rate Atrial rate P wave PR interval QRS complex 60 to 100 if controlled Rapid Indiscernible Absent Normal or widened if BBB Rhythm Irregularly irregular Irregular. hypoxia. flecainide (Tambocor). which is used in treatment of paroxysmal atrial fibrillation or after conversion of persistent atrial fibrillation to normal sinus rhythm. Atrial flutter results from a re-entrant circuit with circular activation most often in the right atrium near the tricuspid valve. dofetilide (Tikosyn). Electrical cardioversion. dizzy or short of breath).4 Droneradone (Multaq) is the newest antiarrhythmic agent. beta-blockers. ibutilide (Corvert). pericarditis. hyperthyroidism.7 Atrial flutter: This dysrhythmia results when one single ectopic focus in the atrium fires regularly at a rapid rate.. Atrial fibrillation occurs more frequently in older patients (> age 65) and in association with increased sympathetic nervous system activity. The ectopic focus supersedes the SA node and predominates. AV node ablation or pacing can be done if the medications do not control the rhythm and the patient is hemodynamically unstable or symptomatic (e. The 2011 guidelines on atrial fibrillation caution against using droneradone for patients with Class IV (severe) heart failure or a recent episode of decompensated heart failure in the past month. sotalol (Betapace). amiodarone (Pacerone) and dronederone (Multaq) may be used to convert the rhythm back to NSR (or used selectively to maintain NSR).2 Medications such as digitalis. The treatment objectives for atrial fibrillation consist of ventricular rate and rhythm control. digitalis toxicity. coronary artery disease and pulmonary embolism. Antiarrhythmic agents. such as propafenone (Rhythmol).g. fibrillatory Some of the clinical conditions associated with atrial fibrillation include COPD. producing fluttery or sawtooth P waves. valvular heart disease.3. acute illness. pneumonia.2 33 . The ventricular rhythm may be regular or irregular. depending on the degree of AV node blockage. As with atrial fibrillation. The ventricular rate may range from 60 bpm to 180 bpm. (See Tracing 10. e. three. (See Tracing 11. The number of flutter waves before each QRS will vary. The P waves march out regularly. so many of the impulses never get through to the ventricle.g. the QRS could potentially be wider than normal if there is delayed conduction of the impulse through the ventricle. flutter-like PRI (PR interval) Unmeasurable *A variable atrial flutter will cause the rhythm to become irregular 34 . the rhythm may be denoted as a ratio. four or more flutter waves before the QRS. there may be an irregular response from the ventricle.Tracing 10: Atrial Flutter The flutter or sawtooth-shaped waves signaling atrial depolarization may occur at a rate in excess of 250 bpm.. This would be called atrial flutter with variable ventricular response.2 Less commonly. as is seen with a bundle branch block or intraventricular conduction defect. with one often being buried in (hidden within) the QRS. There may be two. depending on the degree of AV blockage. This rate is too fast for the AV node to depolarize. up to >300 Regular P wave Sawtooth. 3:1 response if there are three P waves for each QRS complex. the rhythm will be regular.) Tracing 11: Atrial Flutter with Variable Ventricular Response Quick Check: Atrial Flutter Rhythm Regular/irregular* Ventricular Rate Depends on AV block QRS complex Normal or widened Atrial Rate Very rapid.) Depending on the number of P waves preceding the QRS. If ventricular depolarization follows regularly at set intervals. synchronized cardioversion should be administered immediately. It is followed by a normal-appearing QRS as the impulse follows down the same conduction pathway once it reaches the AV node. resulting in symptoms associated with decreased cardiac output. There’s often a pause that follows the QRS of a premature atrial contraction that occurs as the sinus nodes resets itself.. amphetamines. valvular heart disease.2 Clinical conditions associated with AF may also result in the development of atrial flutter. ischemia. PACs are benign.g.1-3 35 . If the AV node does not block out a controlled number of impulses. therefore. hypoxia. If the patient is hemodynamically unstable. hyperthyroidism. The treatment is to avoid stimulants and treat or avoid the underlying cause. pericarditis. fear. They may signal impending heart failure. e. representing no pathology and presenting no hemodynamic compromise. Increased sympathetic nervous system activity stimulation (e. ephedrine or tobacco. excitement.or rhythm-controlling drugs. As with atrial fibrillation. (See Tracing 12. Tracing 12 PACs often occur in response to stimulation or irritability of the atrial tissue caused by caffeine. or repolarizes.2-4 Premature atrial contraction (PAC): A premature atrial contraction is a single beat that is prematurely conducted by an irritable focus within the atrium. Medications such as beta-blockers or calcium channel blockers may be used if a person is symptomatic with the PACs. ventricular rates in excess of 250/min are possible. This dysrhythmia is more rare and potentially more unstable and serious than atrial fibrillation. Often.g. digitalis toxicity and cardiac surgery.. in preparation for the next electrical impulse. This premature beat produces a P wave that varies in shape from that obtained with “normal” atrial depolarization arising from the SA node. CAD. COPD. requiring no treatment. pneumonia. the treatment of this dysrhythmia consists of administering rate.) It arises before the regular beat arising from the SA node is due. hyperthyroidism or hypoxia. anxiety) or an electrolyte abnormality may also result in a PAC.Clinical conditions that may cause atrial flutter include any condition that results in an enlargement of the atrial chamber and an increase in atrial pressure. excitement. the greater the possibility for hemodynamic compromise and symptoms. Once the impulse is conducted through the AV node. CAD. Heart rates may range from 150 to 250 bpm. Increased irritability or stimulation of the atria caused by caffeine or increased CNS stimulation (fear. The ratio of P waves to QRS complexes is 1:1.2 Young. therefore. heart failure. healthy people can tolerate this rhythm without symptoms. anxiety) may precipitate this dysrhythmia. or supraventricular tachycardia or SVT). because the ventricles are not allowed to fill and empty adequately due to the rapid rate. drops. The QRS is of normal appearance and duration unless there is abnormal conduction through the ventricle. The P wave associated with the PAC varies from that associated with the normal sinus rhythm. Other causes may signal more serious disorders such as digitalis toxicity (most common). it follows a normal conduction through the ventricle.) This rhythm is distinctive in that it occurs suddenly and is self-limiting. (See Tracing 13. hypoxia or COPD. The longer the rhythm is sustained. electrolyte imbalances. The PRI may be indiscernible as a result. Cardiac output. 36 . Tracing 13: Atrial Tachycardia This dysrhythmia may result in hemodynamic instability. but those with heart disease may develop symptoms rapidly. The P wave may be difficult to detect due to the rapid rate and as it may be hidden within the previous ST segment or T wave. It occurs from a burst of three or more PACs in a row that resets the pacemaker of the heart to a rhythm that is much faster than normal. resulting in a corresponding fall in blood pressure and symptoms of syncope/lightheadedness. hyperthyroidism.Quick Check: Premature Atrial Contraction Ventricular Rate QRS complex Atrial Rate P wave PRI (PR interval) Normal Normal Same as ventricular Varies from sinus P wave Varies from sinus PRI Rhythm Irregular Irregular Atrial tachycardia (AT): This dysrhythmia often starts and stops suddenly and is designated as paroxysmal (paroxysmal atrial tachycardia or PAT. This rhythm is often intermittent. Once the stimulus passes through the AV node. resulting in cardiac conduction. vagal maneuvers intended to stimulate the parasympathetic system may be initially tried. less than 10 seconds. but these are usually very transient and self-limiting due to the short half-life of adenosine. Other medications that may be used include digoxin. the ECG Learning Center and Intermountain Healthcare. a naturally occurring nucleoside. It is given as a 6 mg IV bolus rapidly (over one to three seconds) followed by a saline bolus of 10 mL to 20 mL. If medication-induced conversion of this rhythm does not work. the shape of the P wave and PR interval may vary from beat to beat. Wandering atrial pacemaker (WAP): This dysrhythmia occurs when multiple foci within the atria depolarize. Tracing 14: Wandering Atrial Pacemaker Used with permission of Frank G. Yanowitz. MD. it is conducted normally through the ventricle. and PR intervals. (See Tracing 14) The foci “wander” from different sites in the atria. such as having the patient cough or bear down (Valsalva maneuver). producing normal and uniform-appearing QRS waves.6 Adverse reactions include asystole (complete lack of electrical activity) and hypotension. Adenosine (Adenocard) is the primary drug of choice for treatment of this dysrhythmia.Quick Check: Atrial Tachycardia Ventricular Rate QRS complex Atrial Rate P wave PRI (PR interval) Rhythm Irregular 150 to 250 Normal or widened Same as ventricular Variable if seen Variable if seen Irregular To treat this rhythm. electrical cardioversion may be done if the rhythm persists with hemodynamic compromise and symptoms. medications may be used to interrupt the rhythm. acts on the AV node to slow conduction and inhibit re-entry pathways. Another 12 mg may be administered if the dysrhythmia is not eliminated in one to two minutes. usually three or more different P wave morphologies. intravenous calcium channel blockers or beta-blockers. creating variable P wave configurations. alternating with normal sinus rhythm. Wandering atrial pacemaker may be 37 . Adenosine.10 Due to variations in the location of initiation of the beat. If these do not work. Tracing 15: Multifocal Atrial Tachycardia 38 .1 Wandering atrial pacemaker may be caused by side effects from medications that may affect serum electrolytes.mistakenly diagnosed as AF due to the irregular nature of the rhythm. may be slower* Normal Same as ventricular Variable Variable Irregular This rhythm may be seen in healthy people during sleep or in athletes.2 Treatment is based on determining and treating the underlying cause. In people with no preexisting cardiac disease and without symptoms.2. a person could experience symptoms of decreased cardiac output such as weakness or fatigue. it can also be caused by hypoxia. If the heart rate slows too much.3 When the ventricular rate is above 100 bpm. nothing other than surveillance for symptoms may be necessary. It is often associated with no symptoms. such as diuretics. Heart rates may range from 60 bpm to 100 bpm and in some cases may be bradycardic. this dysrhythmia is referred to as multifocal atrial tachycardia or MAT and is often seen among people with severe COPD. vagal stimulation or MI. Quick Check: Wandering Atrial Pacemaker Ventricular Rate QRS complex Atrial Rate P wave PRI (PR interval) *Rates >100 for MAT Rhythm Irregular 60 to 100. premature atrial contractions. atrial tachycardia and wandering atrial pacemaker.Chapter Review Atrial dysrhythmias include atrial fibrillation. atrial flutter. precipitated by a PAC and resulting in hemodynamic compromise if it is sustained or the patient's pre-existing clinical condition is compromised. Atrial fibrillation is typically irregularly irregular and may result in a drop in cardiac output because of loss of “atrial kick. or sawtooth-shaped P waves. Heart rates may range from 150 bpm to 250 bpm. List the following rhythm strips as • Atrial fibrillation • Atrial flutter • Premature atrial contractions • Paroxysmal atrial tachycardia • Wandering atrial pacemaker Answer: Atrial Flutter 39 . They are often benign and may result from CNS stimulation or stimulating medications or products. WAP and MAT differ with respect to rate. Premature atrial contractions refer to a premature beat arising from an irritable focus within the atrium. Treatment depends on symptom presentation. Paroxysmal atrial tachycardia starts and stops suddenly.” Atrial flutter may result in a variable ventricular response and is associated with characteristic flutter. Answer: Atrial fibrillation Answer: Sinus rhythm with PAC 40 . They are also referred to as nodal rhythms and may arise when the SA node fails or is suppressed. which results in a variable PR interval. resulting in a P wave of an alternate shape or morphology when compared with an impulse arising from the SA node. as the impulse originates from a single site in the nodal or junctional region. or follow the QRS. initiation of impulses in the SA node less than 40 bpm. reserving the term junctional tachycardia for those junctional origin rates greater than 100 bpm.1 As a result. which may spread backward (retrograde) into the atria or forward (antegrade) into the ventricles. The inherent rate of the AV nodal region is 40 bpm to 60 bpm.2 (See Tracing 16.12 second) because the impulse originates at a location that is closer to the ventricle (nodal region). requiring less time for conduction to the ventricles. Junctional rhythms occur when there is failure of SA node firing. the P wave will be inverted. P waves may be absent. Depending on where in the AV junction the impulse originates (high.1-3 For example. heart rates in true junctional (nodal) rhythms are also between 40 bpm to 60 bpm. resulting in an inverted P wave. 41 . it may even occur after the QRS if the junctional impulse reaches the ventricles before the atria or if the atria and ventricles are depolarized at the same time.) A normal-appearing QRS is usually produced as the impulse is propagated into the ventricles following the normal conduction pathway.1 Rhythms arising from the junctional region are categorized as: • • • • Junctional rhythm Premature junctional contraction or complex Accelerated junctional rhythm Junctional tachycardia Junctional rhythm: This is a very regular rhythm.CHAPTER 5: Junctional (Nodal) Rhythms Junctional rhythms come from an impulse that arises in the area surrounding the AV node at the AV junction and include the bundle of His. or forward (antegrade). The PR interval is short (< 0. an electrical impulse may spread backward (retrograde) into the atria. The junctional impulse follows an alternate conduction pathway. usually shortened. Sometimes the P wave is buried within the QRS and not seen at all if the atria and ventricles are depolarized at the same time. Junctional rhythms with heart rates from 60 bpm to 100 bpm are referred to as accelerated junctional rhythms. buried or follow the QRS. Impulses firing at the AV junction located in the middle of the heart results in abnormal depolarization. or when there is blockage of a beat originating in the SA node. The P wave may be completely undetected or be “buried” within the QRS. mid or low region). because the impulse originates at a location that is closer to the ventricle (nodal region). inverted.2 Therefore. thus requiring less time for conduction. The P wave may be absent.2 Because the ventricles usually depolarize normally. Causes and treatment modalities are the same as that described for junctional rhythms. myocardial ischemia.3 The characteristics of the waveforms: P wave. Removal of the underlying cause may be the only remedy indicated.12 second). caffeine or digoxin toxicity.) A premature junctional (nodal) contraction (PJC/PNC) is distinct in that the P wave is of a different shape (often inverted) from that of the underlying rhythm. the P-R interval is shortened (<0. valvular heart disease.4 Treatment may not be necessary if the heart rate is within normal limits and there are no adverse physiological effects noted (stable blood pressure and mental status).Tracing 16: Junctional Rhythm P waves are absent in this junctional rhythm. inverted or following the QRS.12 sec.12 sec if P wave present Rhythm Regular Irregular Premature junctional (nodal) contraction (PJC/PNC): A premature beat arising from the AV nodal or junctional area that comes before a normal beat and is followed by a pause before the underlying rhythm resumes. the QRS complex has a normal duration of less than 0.2. PR interval and QRS complex are identical to that described in the section on junctional rhythms. The distinguishing feature is that the PJC/PNC occurs prematurely in the cardiac cycle. stimulant drugs.2. The heart rate is approximating 60 bpm. Potential causes of junctional rhythms include an electrolyte abnormality. 42 .1. Quick Check: Junctional Rhythm Ventricular Rate QRS complex Atrial Rate P wave PRI (PR interval) 40 to 60 Normal Same as ventricular Inverted. absent. or following the QRS None or <0. If the P wave occurs before the QRS. (See Tracing 17. PR interval and QRS complex are identical to that described in the section on junctional rhythm. The characteristics of the waveforms: P wave. Tracing 18: Accelerated Junctional Rhythm Junctional tachycardia: This is a rhythm originating from the AV junctional region with a rate >100 bpm. This rhythm may be caused by digitalis toxicity. 43 .2 (See Tracing 18. Treatment may consist of medications to decrease the rate: beta-blockers. The characteristics of the waveforms: P wave. Causes and treatment modalities are the same as that described for junctional rhythms. so a junctional rhythm with a HR greater than >60 and <100 bpm qualifies as an accelerated junctional rhythm. Causes and treatment modalities are the same as that described for junctional rhythms. It may be paroxysmal. The distinguishing feature is based on the heart rate only. an increase in myocardial oxygen demand. calcium antagonists or adenosine.) Remember that the inherent junctional rate is normally 40 to 60 bpm. Adverse effects include a decrease in cardiac output and corresponding drop in blood pressure as the increased heart rate results in incomplete ventricular filling. The distinguishing feature is based on the heart rate only.1 It is usually a result of the firing of an irritable focus in the AV junction that takes over as the pacemaker of the heart.3. heart disease. stimulants or anything else that may provoke the sympathetic nervous system.4 Attempts should be made to treat the underlying cause.Tracing 17: Premature Junctional Contraction Accelerated junctional rhythm: This rhythm is a junctional rhythm with a ventricular rate >60 and <100 bpm. as is the case in Tracing 19. PR interval and QRS complex are identical to that described in the section on junctional rhythms. Morphology of the P and QRS are the same as those in the already described junctional rhythms. Label each of the following strips as • Junctional rhythm • Premature junctional contraction • Accelerated junctional rhythm • Junctional tachycardia Answer: Premature junctional contraction (2) 44 . Accelerated junctional rhythm is characterized as a junctional rhythm with a rate of 60 to 100 bpm. absent (buried within) or follow the QRS. QRS intervals and morphology are normal. Junctional tachycardia is characterized as a junctional rhythm with a rate >100 bpm.12 second in junctional rhythms. PR intervals are <0.Tracing 19: Junctional Tachycardia Chapter Review The inherent rate of the AV nodal/junctional region is 40 to 60 bpm. P waves in junctional rhythms may be inverted. A premature junctional contraction (PJC) comes early in the R-to-R interval and is followed by a pause. Answer: Junctional rhythm Answer: Junctional tachycardia 45 . 46 . larger than normal QRS complexes >0.12 second. 47 . The P waves are usually upright and normally appearing. well-traveled conduction system. The T wave slopes off in the opposite direction to the QRS.CHAPTER 6: Ventricular Rhythms Ventricular rhythms originate from an irritable focus in the ventricle. The P waves represent atrial depolarization without conduction or initiation of a cardiac cycle. As with all ventricular beats. because they do not follow the normal. Anything that disrupts normal electrolyte shifts during depolarization and repolarization may case ventricular irritability and PVCs. There is no measurable PR interval. because the impulse is initiated in the ventricle. but they are not related to the PVC. The inherent rate of the ventricle is 20 bpm to 40 bpm.1-5 Some are potentially life-threatening. There’s no preceding P wave. PVCs usually signal electrical irritability within the heart. P waves generated from the sinus node may be noted on the ECG recording. the serious nature of these dysrhythmias and the importance of recognizing them and intervening quickly.12 second) and bizarre. A change in repolarization follows. T waves associated with the ventricular beat occur in the opposite direction of the QRS as the impulse follows an alternate pathway with depolarization. There may be a “compensatory pause” that follows the PVC. if they are seen. bizarre. there is no preceding P wave. thus.1-3 In some cases.1-3 They can occur at any rate.” which may contribute up to 30% to cardiac output. ventricular dysrhythmias may achieve rates up to 250 bpm or higher. Ventricular beats have wide. The ventricular rhythms discussed in this section are: • Premature ventricular complexes (PVCs) • Ventricular tachycardia • Torsades de pointes • Ventricular fibrillation • Idioventricular rhythm Premature ventricular contractions (PVCs): These beats are similar to all other premature beats in that they interrupt the normal cardiac cycle by coming before the next sinus beat is due. This accelerated ventricular rate causes cardiac output to drop and results in acute hemodynamic instability and eventual cardiovascular collapse in a short time. The QRS is wide (>0. Impulses originating in the ventricle are very slow. This pause exceeds the usual RR interval associated with the underlying sinus rhythm. Most of these rhythms are problematic in that they result in a drop in cardiac output. Cardiac output is decreased because of the slower rate and the loss of atrial “kick. This indicates a much more unstable rhythm that has an increased likelihood of degenerating into a lethal dysrhythmia. the PVC may lead to lethal dysrhythmias such as ventricular tachycardia. Persons with weakened hearts or underlying coronary heart disease with PVCs are at risk for symptoms of lightheadedness or hemodynamic instability. or Torsades de pointes. the conduction cells will assume the ventricular rhythm as the dominant one. which can lead to significant hemodynamic instability.1 (See Tracing 24. see Tracing 21) it indicates there are multiple irritable foci conducting these impulses from the ventricle. it is called “R-on-T” phenomenon. stimulants. Frequent PVCs (six or more per minute) and PVCs that are very close to the preceding T wave warrant concern.) The R wave of the PVC occurs at the same time as the T wave of the preceding beat. it can be assumed they are arising from the same single focus. Tracing 20: Unifocal PVCs Tracing 21: Multifocal PVCs When a PVC occurs close to or at the same time as the T wave. When there are multiple-appearing PVCs (multifocal. pain or anxiety. ventricular fibrillation. Infrequent PVCs may occur in healthy people without an identifiable cause or symptoms. stress. caffeine. When the PVCs all look similar (unifocal. At this time of ventricular repolarization.4 In these situations. posing no risk to the patient. Other causes include digoxin toxicity. Each of these etiological factors may cause the heart to become “irritable” and the ventricle to fire off an early beat. Occasional or rare PVCs are usually benign. 48 . see Tracing 20). heart disease (coronary artery disease or heart failure) and hypoxia. If the PVC occurs at this vulnerable time.Three usual etiologies for PVCs are hypokalemia. the ions are lining up on either side of the cell membrane waiting for the next signal to stimulate ion movement and cardiac contraction. 12 sec Depends on underlying rhythm Normal or inverted No relationship to the PVC Rhythm Irregular PVCs may occur singly. If the patient does have symptoms and a history of heart disease. In this case. it is may be tolerated and does not necessitate immediate treatment. they are not related to the QRS complex. in clusters of two or more or in repeating patterns. for example. The QRS is wide (>0. The QRS complexes appear as large 49 . this rhythm is poorly tolerated and often life threatening. Oxygen should be administered. PVCs that occur in pairs are called couplets. and any electrolyte imbalances should be corrected. commonly called “V tach. If it is short lasting (< 30 seconds). There’s no measurable PR interval. PVCs that occur every other beat are known as bigeminy. depending on whether there is any structural heart disease. If P waves are seen. indicating that the impulse originates from the same location in the ventricle.4 Ventricular tachycardia (VT): In this rhythm. If the patient is without symptoms or history of heart disease. the rhythm may be described as monomorphic (similar shape) ventricular tachycardia. Pain should be treated. the dysrhythmia likely won’t require treatment.” three or more PVCs occur in a row and the ventricular rate exceeds 100 bpm.12). If sustained > 30 seconds.Tracing 22: R-on-T phenomenon Quick Check: Premature Ventricular Contraction Ventricular Rate QRS complex Atrial Rate P wave PRI (PR interval) Variable. Infrequent PVCs should be approached based on symptoms and cardiac history with an attempt to first find out the cause and correct it. it needs to be repleted. which is superseded by the ventricle.) It may be paroxysmal or sustained. This in an extremely unstable rhythm and may precede sudden cardiac death (SCD). If the potassium is low. bizarre and uniform.1-5 (See Tracing 23. The rhythm is regular. V tach requires immediate recognition and treatment. the physician may choose to treat the PVCs with IV medications such as beta-blockers or antiarrhythmic agents. those that occur every third beat are known as trigeminy. There’s usually no P wave due to the lack of atrial activity. depends on underlying rhythm Bizarre >0. wide complex tachycardia is regular and monomorphic as both a form of treatment and as a diagnostic aid.1 Tracing 23: Ventricular Tachycardia Quick Check: Ventricular Tachycardia Ventricular Rate QRS complex Atrial Rate P wave PRI (PR interval) Rhythm Regular > 100 bpm Bizarre >0. the first step in patient evaluation is to determine how it is affecting the patient’s clinical signs and symptoms. Adenosine may be considered initially if the stable. Continuous. of the complex is increased. or size. initiation of ACLS protocol for pulseless arrest is required: unsynchronized defibrillation accompanied by CPR. amiodarone or sotalol. The T wave slopes off in the opposite direction as the QRS and is often obscured by the preceding QRS when the rate exceeds 100 bpm. If the patient becomes unstable with signs of cardiac instability. The amplitude.6 If the patient deteriorates and a pulse is undetected. and antiarrhythmic therapy (amiodarone). close monitoring is essential. The R-on-T phenomenon can precipitate ventricular tachycardia. initial treatment consists of administering supplemental oxygen. immediate synchronized cardioversion is indicated. the initial approach for stable wide complex tachycardias calls for obtaining prompt IV access and a 12 lead ECG if the patient’s condition will allow for this added diagnostic step. digoxin toxicity and stimulants. antiarrhythmic agents or rate-controlling medications may be ordered. such as epinephrine and/or vasopressin. Protocols follow for antiarrhythmic boluses and infusions for either procainamide. When this dysrhythmia is seen. In the presence of a pulse. all with guidance from expert consultation. If the patient is without signs of cardiac instability (hypotension. hypoxia. change in mental status.4.“sawtooth” waves.6 Per the 2011 American Heart Association ACLS Guidelines. electrolyte abnormalities.6 50 . a vasopressor medication. Ventricular rates may reach up to 200 bpm. syncope.12 sec Unable to determine Usually not seen Immeasurable Ventricular tachycardia is caused by many of the same factors causing PVCs: heart disease. shortness of breath). and a pulse is undetected. Treatment of Torsades de pointes is aimed at correcting the underlying cause. Magnesium sulfate or overdrive pacing may also be ordered by the physician in an attempt to break the triggered mechanism for the rhythm. Particular emphasis is placed on medical conditions and medications known to be risk factors. starting and stopping suddenly. Tracing 24: Torsade de Pointes The cause of this form of ventricular tachycardia is often reversible.Some ventricular tachycardias can be treated with radiofrequency ablation (RFA) to abolish the ectopic focus within the ventricle.2 There are no discernable P waves. which includes unsynchronized defibrillation accompanied by CPR.3 Torsade de pointes: A special form of VT. T waves slope off in the opposite direction of the QRS but are often indiscernible due to the increased rate. and has the potential to deteriorate into ventricular fibrillation at any time. A metabolic derangement (hypokalemia. If the patient deteriorates. especially if the cause is due to a specific drug therapy.1-3 This rhythm is characterized by a prolonged QT interval that precedes its onset. hypomagnesemia or hypocalcemia) or drug toxicity (particularly drugs that prolong the QT interval) may precipitate Torsades.” which describes the QRS complexes that appear to rotate or twist about the isoelectric baseline. epinephrine and/or vasopressin. close monitoring of the patient with this rhythm is necessary. Other causes include all of those that may precipitate PVCs or ventricular tachycardia.6 Prevention of Torsade de Pointes in the hospital setting was released as a Scientific Statement from the AHA in 2010. QRS complexes are wide and bizarre (>0. This may be paroxysmal.2 Continuous. This may be performed by a cardiologist specializing in the treatment of cardiac dysrhythmias or electrophysiology (EP).12 second) with increased amplitude. Healthcare providers are also guided on the discernment of this potentially lethal rhythm and ECG/telemetry monitoring methods. Torsade de pointes means “twisting about the points. Ventricular rates may range from 150 to 250 bpm. is a ventricular dysrhythmia that arises from multiple ectopic foci within the ventricle and may also be called “polymorphic” VT. initiation of ACLS protocol for pulseless arrest is required.11 (Level ML) 51 . Torsade de pointes. An automatic implantable cardiodefibrillator (AICD) is used for patients with recurrent VT or those at risk for VT due to reduced cardiac output or heart failure. (See Tracing 25. 52 . Markedly reduced cardiac output results in a lack of tissue and organ perfusion and an undetectable pulse. The ventricular rhythm is usually regular. patients are never stable. fails or is blocked. There are no discernable P waves. P waves are either absent or totally unrelated to the QRS complex. Treatment consist of immediate defibrillation and CPR following the ACLS protocol for pulseless arrest.”1 It is a ventricular escape rhythm with rates ranging from 20 bpm to 40 bpm.) An idioventricular rhythm (“idio” in this context means “all on its own” or “spontaneously”) results when the electrical impulse initiating a cardiac cycle. (See tracing 27. atrial tissue or AV node.12 sec). then it is referred to as an accelerated idioventricular rhythm (AIVR). Therefore. The patient rapidly loses consciousness. whether at the SA node. QRS complexes or T waves. Tracing 25: Ventricular Fibrillation Ventricular fibrillation represents completely disorganized and chaotic electrical activity. Hemodynamic instability is certain due to the slow heart rate and subsequent decreased cardiac output. the PR interval is indiscernible. the ventricles are quivering or fibrillating (as in atrial fibrillation) and as a result. In this rhythm.) If the rate ranges from 40 bpm to 60 bpm. (See Tracing 26. The ventricles beat to provide a heartbeat and save the patient’s life.Ventricular fibrillation: Also referred to as “V-fib. Symptoms of decreased perfusion to tissues and organs are obvious and noted by decreased levels of consciousness and severe hypotension.” this rhythm is a chaotic pattern of electrical activity arising from multiple ectopic foci in the ventricles. Possible causes of this dysrhythmia include all of those discussed for VT and Torsades de pointes. The QRS complex is wide (> 0.) It is a lethal dysrhythmia often responsible for sudden cardiac death.6 Idioventricular rhythm: This rhythm has been referred to as a “rhythm of last resort. cardiac out and blood pressure fall quickly. The automaticity or inherent rate of the ventricle takes over as the main pacemaker of the heart. T waves slope off in the opposite direction from the QRS. and it must be treated quickly to avoid death.1-4 V-fib is always an emergency. PVCs may occur in healthy people without an identifiable cause or symptoms.12 sec None None or if present unrelated to QRS Absent Rhythm Regular The cause of IVR is usually serious cardiac disease: myocardial infarction.Tracing 26: Idioventricular Rhythm Tracing 27: Accelerated Idioventricular Rhythm Quick Check: Idioventricular Rhythm Ventricular Rate QRS complex Atrial Rate P wave PRI (PR interval) 20 to 40 >0. digoxin toxicity. Placement of a temporary pacemaker may be considered based on expert consultation. In this setting. hypoxia. Accelerated IVR is seen frequently following a myocardial infarction or when blood flow to the coronary arteries is re-established with thrombolytics or percutaneous intervention. Ventricular dysrhythmias often result in hemodynamic instability and are considered life threatening of they occur frequently or are allowed to persist. acute myocardial ischemia. digoxin toxicity. AIVR may be referred to as a reperfusion dysrhythmia. Treatment includes initiation of ACLS protocol for severe bradycardia or pulseless arrest should a pulse become undetectable. Chapter Review The inherent rate of the ventricle is 20 bpm to 40 bpm. hypoxia or metabolic imbalances. stimulants or pain. heart disease. Usual etiologies for ventricular dysrhythmias are similar and include electrolyte abnormalities. 53 . Accelerated idioventricular rhythms are serious and unstable. such as drug toxicity or metabolic derangement (hypokalemia. resulting in sudden cardiac death. Torsade de pointes is a potentially life-threatening dysrhythmia that is usually reversible and most often caused by an agent that causes QT prolongation preceding its onset.Ventricular tachycardia may be monomorphic or polymorphic and degenerate into ventricular fibrillation. Label each of the following strips as: • Premature ventricular complexes (PVCs) • Ventricular tachycardia • Torsades de pointes • Ventricular fibrillation • Idioventricular rhythm Answer: Ventricular tachycardia Answer: Premature ventricular complexes (unifocal) Answer: Torsade de Pointes 54 . Ventricular fibrillation is unmistakable and always results in severe cardiovascular collapse. and may be seen after administration of thrombolytics or coronary revascularization and may be referred to as reperfusion dysrhythmias. hypomagnesemia or hypocalcemia). thereby requiring early defibrillation and initiation of ACLS. 20 second) and is 55 . Heart rates can be normal or slowed. These rhythms may also be referred to as a SA exit block. resulting in either a delay or interruption of conduction to the ventricles. Tracing 28: First-Degree AV Block Quick Check: First-Degree AV Block Ventricular Rate QRS complex Atrial Rate P wave PRI (PR interval) Rhythm Regular Usually 60 to 100 < 0.) All impulses arriving at the AV node get through. they just take longer.12 sec Same as ventricular Normal Prolonged. it is either delayed or completely blocked. The delay in transmission is seen on the ECG as a prolonged PR interval of >0. > 0. The underlying rhythm is sinus. The clinical effect. bundle of His (AV bundle) or bundle branches.20 sec The heart rate associated with this rhythm may vary from bradycardic to tachycardic but is usually normal.1-4 (See Tracing 28.CHAPTER 7: Atrioventricular (AV) Blocks Atrioventricular (AV) blocks are dysrhythmias that represent a disruption or delay in the normal pathway of conduction. The types of AV blocks to be discussed are: • First-degree • Second-degree (Type I and II) • Third-degree First-degree AV block: This type of AV block occurs when impulses from the SA node are consistently delayed through the AV node. is aimed at increasing the heart rate and improving conduction of the impulse. P waves are normal appearing. The site of block may occur at the AV node.20 sec. which identifies a conduction delay distal to the pacemaker (SA node) site. Treatment. All P waves conduct to the AV node. The P-R interval is prolonged (>0. The rhythm originates at the SA node and follows the normal conduction pathway to the AV node.12 Once the impulse reaches the AV node. depend on how many impulses are blocked and how slow the ventricular rate is. or symptoms. if indicated. uniform Progressively lengthens Rhythm Irregular Regular Patients with this rhythm are usually asymptomatic. is usually transient. the QRS complexes seem to appear as though they are grouped. a transcutaneous pacemaker can be used if atropine does not increase the heart rate. It may also occur in association with inferior wall myocardial infarction. is to determine and remove the underlying cause. If symptoms are progressive. hyperkalemia. therefore prolonging the amount of time required to conduct through the ventricles.3 This block retains the potential to progress to a more advanced AV block. The atrial rate is regular. ranging between 60 bpm to 100 bpm. or block. vagal stimulation or administration of medications that slow the conduction time through the AV node. if needed. Possible causes include heart disease.12 second) because the conduction disturbance occurs lower in the conduction system. The P waves are normal in configuration. digitalis toxicity and heart rate-lowering medications. The PR intervals grow progressively longer until there is a P wave with no QRS to follow. The QRS is usually of normal configuration and duration but may be prolonged (>0. Progression of this rhythm into a higher degree of atrioventricular block is possible and therefore requires periodic evaluation for symptoms and monitoring. the patient with first-degree AV block is usually asymptomatic. Tracing 29: Second-Degree AV Block Type I Quick Check: Second-Degree AV Block Type I Ventricular Rate QRS complex Atrial Rate P wave PRI (PR interval) Irregular or a grouped pattern Usually < 0. Most patients with second-degree AV block type I require nothing more than careful observation.constant. Atropine can be given if the heart rate is slow and the patient becomes symptomatic. The PR interval gradually prolongs until a QRS is dropped.12 Collectively. and exceeds the ventricular rate. QRS complexes are normal appearing unless associated with a bundle branch block. This rhythm may be seen in healthy people.) It occurs when the AV node becomes progressively sicker. Second-degree AV block type I (Mobitz I or Wenckebach): This dysrhythmia. With normal heart rates. Treatment consists of determining and treating or removing the underlying cause.2 The treatment. It may occur normally among athletes and children. (See Tracing 29.12 sec Usually 60 to 100 Upright. The ventricular rate is irregular due to successive PR prolongation.1-3 56 . slowing the conduction of impulses it receives until complete conduction fails. 6 57 . transcutaneous or transvenous pacing. ranging from 60 to 100 bpm.1-3 The number of P waves to QRS complexes is referred to as a ratio. uniform Normal and consistent Regular The atrial rhythm is regular. the conduction disturbance is called “high-grade” AV block..) Second-degree AV block type II is more rarely seen than type I and much more dangerous due to its potential to deteriorate into a more advanced AV block such as third-degree or complete heart block (CHB). The impulse is intermittently blocked. The QRS may be narrow if the block is around the AV juncture and widened if the block is at the bundle branch/Purkinje region. As the number of P waves compared with QRS complexes increases. Causes of type II second-degree block include heart disease and degenerative changes in the conduction system. The P waves are normal appearing.1-5 Treatment for this rhythm includes supplemental oxygen and prompt initiation of either a positive chronotropic (heart rate-increasing) medication: atropine. creating a rhythm where two or more P waves are conducted for each QRS complex or ventricular beat. syncope or hypotension. 2:1. e.g. When two or more successive atrial impulses are blocked. The ventricular rate is irregular and less than the atrial rate due to dropped beats. The PR intervals are constant and of normal duration. the patient may have signs of decreased cardiac output such as light-headedness. If the ventricular rate (heart rate) is slow. Tracing 30: Second-Degree AV Block Type II Quick Check: Second-Degree AV Block Type II Ventricular Rate QRS complex Atrial Rate P wave PRI (PR interval) Rhythm Irregular Variable and slow Normal or >0.Second-degree AV block type II (Mobitz II): In this type of block an electrical impulse generated from the SA node is blocked at the bundle of His.12sec Usually 60 to 100 Upright. the amount of blockage increases and becomes more ominous. dopamine or epinephrine as per ACLS protocol. 3:1. (See Tracing 30. The ventricular response (QRS complex) may have a variable conduction rate in comparison with atrial contraction (P waves). 12sec Usually 60 to 100 Upright. so the P-R interval varies. the sinus and AV node are not working in coordination with each other. Tracing 32: Third-Degree AV Block Quick Check: Third-Degree AV Block Ventricular Rate QRS complex Atrial Rate P wave PRI (PR interval) 20 to 60 Normal or >0. the ventricular rate may be higher than 60 bpm. In some cases. If conduction occurs lower in the system into the ventricle. Atrial rates are usually normal. If the AV node takes over as pacemaker.) The junctional tissue at the AV node or the ventricles starts initiating beats at their inherent rates to initiate a cardiac cycle. Analysis of the ECG reveals no relationship whatsoever between the P wave and QRS complex. the inherent rate will be between 40 to 60 bpm.12 second) if the resultant heartbeat is from a junctional focus near the AV node.12 second) if from a ventricular focus. or wide (>0. ranging from 20 to 60 bpm. which would be referred to as third-degree AV block with an accelerated junctional or ventricular response. the rate may be as low as 20 to 40 bpm. ranging from 60 to 100 bpm. but the transmission to the AV node is completely blocked.Tracing 31: 2:1 and 3:1 (Variable) Second-Degree AV Block Third-degree AV block: This type of block (also called complete heart block) occurs when the sinus node sends out an electrical impulse as usual. uniform Varies (No consistent relationship between P waves and QRS complexes) 58 Rhythm Regular Regular . The QRS complex may be of normal duration (<0. Some P waves may be hidden inside the QRS complex or T waves. (See Tracing 31.3 P waves will be present with a consistent P-P interval. The QRS complexes march out in a regular pattern. It is generally a life-threatening rhythm requiring prompt recognition and treatment. In this rhythm. These beats from junctional or ventricular origin are referred to as “escape” beats. The P waves are not associated with any of the QRS complexes. the ventricular rate is typically slow. how slow the ventricular rate is and how the block affects the heart. also called “complete heart block. but it can degenerate into a more severe block. medication side effects (digoxin toxicity. it can occur without significant symptoms. First-degree. Second-degree AV block Type II is more serious than Type I AV block and may require placement of a pacemaker. treatment for third-degree AV block includes urgent external pacing. In some rare cases.This is the most serious form of heart block and may result in signs of significantly compromised cardiac output (hypotension.6 Chapter Review The underlying rhythm is sinus. Causes of this rhythm include significant heart disease. including the initiation of ACLS treatment protocols. With AV blocks. First-degree AV block is the least dangerous. syncope). Label each of the following strips as: • First-degree • Second-degree type I • Second-degree type II • Third-degree 59 . often requiring immediate treatment. the clinical effect depends on how many impulses are blocked. dopamine or epinephrine) until transvenous pacing can be initiated. or an ACLS directed administration of positive chronotropic (or heart rate-increasing) medications (atropine. The site of conduction blockage may be at the AV node. hypoxia and congenital heart defects. Third-degree AV block.” is the most serious of AV blocks.2-5 When symptomatic. calcium antagonists). bundle of His (AV bundle) or bundle branches. if this rhythm occurs gradually and the heart has time to compensate for the slow ventricular rate. All P waves are conducted with the site of blockage distal to the SA node. second-degree (types I and II) and third-degree are all types of AV block rhythms. beta-blockers. Answer: Second-degree AV block type I Answer: Third-degree AV block Answer: First-degree AV block 60 . CHAPTER 8: Myocardial Infarction and Coronary Vessels In general. the three coronary vessels that cause myocardial infarction/ischemia include the left anterior descending. Diagram 12 ECG and Myocardial Infarction The diagnosis of an MI is noted with accompanying characteristic 12-lead ECG changes. the ECG will show changes that are often quite 61 . patients develop an inferior wall MI. it gives rise to a lateral wall MI. When occluded. a lateral wall MI develops. circumflex and right coronary artery. The circumflex coronary artery (not shown) also comes off the left main coronary artery and at the back of the heart. When the circumflex coronary artery is occluded. Diagram 12 below shows the right coronary artery and its course to the inferior aspect of the heart. When the right coronary artery is occluded. Within hours of an MI. an anterolateral MI develops. When the left anterior descending coronary artery is occluded. Abnormal (elevated) serum cardiac enzymes often are measured in the setting of myocardial infarction as well. which when occluded causes an anterolateral MI. The left main coronary artery gives rise to the left anterior descending coronary artery. The first changes after an MI may be noted on the ECG as abnormal appearing T waves. Diagram 13 62 . You may instead note T wave flattening or inversion. The T wave is often prominent or accentuated.prominent. signaling a lack of adequate coronary blood flow leading to an MI if left untreated. This is followed by Q waves and return of the ST segment to baseline (Diagrams 13 and 14). aVL. one should look at the following leads for specific infarct locations: MI Anterior Lateral Inferior Leads V3 to V6 I. aVL and precordial leads overlying the anterior and lateral surface of the heart (V3 to V6). This type of MI is recognized by observing ST segment changes in leads I. 63 .V6 II. In general.Diagram 14 Another simplified view of the progressive ECG changes that occur following an MI Localization of an MI on the ECG The ECG can also help localize the myocardial infarct by assessing changes in particular leads. or type II second-degree heart block. such as occurs with anterolateral MI. Dysrhythmias that may be seen with this MI include right or left bundle branch blocks. V5. Anterolateral wall MI occurs because of coronary artery disease in the left anterior descending or circumflex coronary artery. Anterolateral MI Sometimes a myocardial infarction will involve more than one coronary artery. Image below is from a patient with an anterolateral MI. III. aVF Blood vessel LAD Circumflex/obtuse marginal RCA To confirm the MI and occlusion of the coronary artery requires an angiogram. As a result.V5 and V6 alone. Diagram 16 64 . the left anterior descending artery is often involved as well with associated ECG changes noted V3. Due to the coronary anatomy it is much more common to note changes consistent with anterolateral MI because the circumflex artery is a branch of the left main coronary artery. V4. aVL.Diagram 15 Lateral Wall MI A lateral wall MI occurs when there is occlusion of the left circumflex or the obtuse marginal coronary artery with ECG changes seen in leads I. Diagram 17 Chapter Review Occlusion of one of the three coronary vessels will result in myocardial infarction/ischemia. This results in damage to the area of the heart supplied by the corresponding coronary artery. III and aVF. On the ECG. avL. aVF. T wave changes may be one of the first ECG changes noted after a myocardial infarction.6. Lateral wall MI is associated with ECG changes in leads I. An anterolateral MI is associated with ECG changes in leads I. 65 . V5. The 12-lead ECG can help to localize the MI by associated changes in specific leads. Circumflex artery occlusion results in a lateral wall myocardial infarction Characteristic ECG changes occur with myocardial infarction. The Q waves are often largest in lead III and smallest in lead II. Left anterior descending artery occlusion results in an anterolateral wall myocardial infarction. Right coronary artery occlusion results in an inferior wall myocardial infarction.Inferior Wall MI Inferior wall MI occurs when there is occlusion of the right coronary artery (image 10). or V3-6. avL. III. Cardiac enzymes will be elevated in the setting of myocardial infarction. Inferior wall MI is associated with ECG changes in II. inferior wall MI will present with changes in leads II. Label each of the following strips as: • Anterolateral wall MI • Lateral wall MI • Inferior wall MI Answer: Inferior wall MI Conclusion With progressively increased acuity among hospitalized patients. In support of these needs. this continuing education course has been developed to allow nurses to update their clinical skills and competencies in ECG rhythm analysis with the intended ultimate result of improved patient outcomes. requiring nurses to hone their skills and gain competency in ECG interpretation. 66 . practice guidelines were issued from the AHA on electrographic monitoring in hospital settings and this has set the standard for continuous cardiac dysrhythmia telemetry monitoring. in 2004. bedside ECG monitoring is more common.13 In closure. Soderberg ES. Practice standards for electrocardiographic monitoring in hospital settings: an American Heart Association scientific statement from the Councils on Cardiovascular Nursing.long. http://ecg. Circulation. 3. et al. 2011 ACCF/AHA/HRS focused update on the management of patients with atrial fibrillation (Updating the 2006 guideline). You JJ.14(10):385-1413. 10. Advanced Cardiac Life Support. TX: American Heart Association.121(8):1047-1060. Provider Manual. Ackerman MJ. Camm AJ. http://circ. 2010. Antithrombotic therapy for atrial fibrillation: Antithrombotic therapy and prevention of thrombosis. 2010. 2012. Cardiovascular Care Made Incredibly Easy. 2011. 8. Califf RM. eds. Published 2006. http://journal. Philadelphia. 5. Prevention of Torsade de pointes in hospital settings: a scientific statement from the American Heart Association and the American College of Cardiology Foundation.110(17):2721-2746. Jenkins P. 12. Circulation. An introduction to electrocardiogram interpretation: part I. NY: McGraw-Hill Cos.jsp. 7. Clinical Cardiology. Accessed February 10.18(1):28-35. Funk M. Accessed February 10. 2010. 2. http://circ.edu. New York.ahajournals. Funk M. January C. Drew BJ. et al. 2014. 2012 focused update of the ESC guidelines for the management of atrial fibrillation: an update of the 2010 ESC guidelines for the management of atrial fibrillation — developed with the special contribution of the European Heart Rhythm Association. Published February 2012. EKGs for the Nurse Practitioner and Physician Assistant. 2nd ed. 9th ed.. http://circ. Knechtel MA. 67 . 2010. Accessed February 10.123:104-123.publications.utah.141(2 Suppl):e531S-575S. New York.chestnet. DeCatarina R. Drew BJ. et al. Singer DE. et al. 2014. New York. Accessed February 10. 6. Chulay M. ECG learning center Web site. et al. PA: Lippincott Williams & Wilkins. Circulation. 2010.REFERENCES 1. National Library of Medicine Web site. 2013.org/article. 2004. 2014.full. Chest.org/content/121/8/1047. Published October 2004. A Report of the American College of Cardiology Foundation / American Heart Association Task Force on Practice Guidelines. AACN Essentials of Critical Care Nursing. 2014. Emerg Nurse. NY: Springer Publishing Co. Accessed February 10.nlm. 2010. Burns SM. 2014. Sinz E. http://druginfo. 2014. Published February 8. 2012.org/content/123/1/104.long.. Dallas. 4. Nurse to Nurse ECG Interpretation. Lip GYH. American College of Chest Physicians evidenced-based clinical practice guidelines.aspx?articleid=1159549. Accessed February 10. 11..nih. and Cardiovascular Disease in the Young: endorsed by the International Society of Computerized Electrocardiology and the American Association of Critical-Care Nurses. 2011. Published December 20. Howard PA. Woodrow P. Inc. National Institute of Health Drug Information Portal.gov/drugportal/drugportal. 9. Curtis A.ahajournals. Wann LS.ahajournals. NY: McGraw-Hill Co. Navarro K. 13. 2009.org/content/110/17/2721. Yanowitz FG. Europace. 68 . Sinus bradycardia First-degree heart block Third-degree heart block Atrial fibrillation 69 . through the AV node. Return of the myocardial cell to its resting state (repolarization) d. The ECG is from a 71-year-old in the CCU.Test 1. and finally through the Purkinje system e. b. Serves as a gatekeeper. Propagation of the electrical impulse from the SA. All of the above 2. Located near the interatrial septum. d. the SA node c. Is capable of spontaneously generating an electrical impulse c. i. It shows: a..e. delaying impulses to allow time for the ventricles to fill 3. Spontaneous generation of an impulse in the pacemaker cells. or junction d. The following is characteristic of the sinoatrial (SA) node: a. Exchange of ions across the cell membrane resulting in myocardial depolarization b. c. The electrical events associated with each cardiac contraction or heartbeat include: a. Intrinsic rate of 40 bpm to 60 bpm b. 5. she is worried because the palpitations have now been going on for at least 60 minutes. She most likely has: a. b. Her vitals are stable and her ECG strip is shown below. A 67-year-old was admitted to the ICU because of chest pain. vague chest pain and diaphoresis. c. She claims that she got scared when a man approached her on the street and demanded her purse. b. Ventricular fibrillation Ventricular tachycardia Atrial flutter Torsades de pointes A 29-year-old female presents to the ED with complaints of palpitations. The resulting panic attack led to these symptoms. c. The patient most likely developed: a. However. d.4. The night nurse printed out the ECG strips from four different leads and they are shown below. d. Atrial tachycardia Ventricular tachycardia MI Atrial flutter 70 . aVF c. Used for diagnosis and recognition of acute coronary syndrome e. She most likely has developed: a. Blood work reveals hypokalemia. III. His BP is 65/35. 7. Chest leads: V1 through V6 d. aVL. Limb leads I. The ECG done is shown below. d. c. A 67-year-old female treated with hydrochlorothiazide for her hypertension presents to the ED with dizziness. II. Peaked T waves Torsades de pointes Atrial tachycardia Ventricular tachycardia Start amiodarone Administer 2 liters NS fluid bolus Start lidocaine Defibrillation The following are typical characteristics of the 12-lead ECG recording: a. c. aVR. Six “limb” leads and six “chest” leads b. The next step in his management is: a. d. 8. b. pulse is barely palpable and his pulse oximetry is 86% on 100% oxygen facemask.6. b. A 57-year-old male in the ICU has the following rhythm. All of the above 71 . Comprised of small boxes that are 2 millimeters (mm) in height and width d.12 to 0.20 second b. QRS complex.10 second c. All of the above 12. PR interval 0. None of the above 10. Heart rate d. Evaluation of waveforms and complexes: P wave. T wave denoted as a negative deflection from the isoelectric line 11. The following characterize the standard ECG paper used for recording: a. the rhythm is called: a. Sinus arrest d. Intervals and segments: PR interval.12 second c. Rhythm/regularity e. 60 100 125 80 13. QRS duration. If a rhythm is irregular. Sinus bradycardia b. A systematic approach to ECG analysis includes: a. What is the heart rate of this patient? a. c.05 second b. and a rate of 60 bpm to 100 bpm. QT interval c. Sinus dysrhythmia c. ST segment. b. QT interval variable and greater than or equal to one-half the distance between successive QRS complexes d. Sinus tachycardia 72 .9. yet of sinoatrial node origin (sinus) with similar looking P waves preceding each QRS. T wave and U wave (if present) b. d. Comprised of large boxes measuring 0. All of the above e. The normal values for the ECG waves and complexes are: a. Comprised of small boxes measuring 0. QRS duration greater than 0. Sinus tachycardia is identified as or associated with: a. Atrial Atrial Atrial Sinus flutter tachycardia fibrillation rhythm 18. A prolonged PR interval d. fever b. b. Exercise capacity c. fear. Blood sugar d. Heart rate less than 60 bpm b. Body mass index (BMI) 15. but the impulse’s exit from the sinus node to the atrial tissue is not conducted. Inverted P waves c. Potential hemodynamic compromise due to inadequate time for cardiac filling d. All of the above 17. Sinus bradycardia b. Sinus bradycardia is associated with: a. Heart rates in excess of 100 bpm e. pain. Sinus block 73 .14. Sinus dysrhythmia c. To determine whether a patient is “tolerating” a rhythm. This rhythm is noted on the ECG as a pause that occurs when the sinus node fires an impulse on time. Blood pressure and level of consciousness b. This rhythm is: a. the following should be evaluated/assessed: a. Anxiety. What is the rhythm of this patient? a. All of the above 16. c. d. b. Wandering atrial pacemaker d. Hyperthyroidism and/or hypovolemia c. c. Atropine b. b. Beta-blockers c. Isoproterenol d. Potential causes of PVCs include: a. A normal variant Lateral wall infarction Anterolateral wall myocardial infarction Inferior wall myocardial infarction 22. stress e. The treatment of atrial tachycardia may include: a. Lidocaine 21. Digoxin d. Electrical cardioversion b. Heart disease b. A 62-year-old male admits to the ED with a complaint of chest pain. d. Blood tests reveal an elevated cardiac enzyme and a 12-lead ECG is done with abnormal findings. pain. Hypoxia c. Anxiety. Occur after the T wave d. Multifocal b.19. These ECG changes reflect: a. Calcium channel blockers e. Adenosine c. Atrial tachycardias (paroxysmal atrial tachycardia/PAT or supraventricular tachycardia/SVT) may be treated with the following: a. All of above 20. All of the above 74 . Occur every third beat 23. Hypokalemia d. Appear wide and bizarre c. Premature ventricular contractions (PVCs) are most dangerous if they are: a. Second-degree type II c. Idioventricular rhythm e. Third-degree d. Ventricular tachycardia d. What type of AV block is associated with progressively longer PR intervals and an eventual “dropped” QRS complex? a. First-degree b. Second-degree type I (Wenckebach) 75 . Ventricular fibrillation c. All of the rhythms 25.24. The following dysrhythmias are potentially life threatening and require initiation of ACLS protocol: a. Supraventricular tachycardia with a rate of greater than 150 bpm b.