Pathophysiology of Hypovolemic Shock

April 3, 2018 | Author: Ian Rama | Category: Shock (Circulatory), Bleeding, Intravenous Therapy, Blood, Animal Physiology


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Minor hypovolemia from a known cause that has been completely controlled (such as a blood donation from a healthypatient who is not anemic) may be countered with initial rest for up to half an hour. Oral fluids that include moderate sugars and electrolytes are needed to replenish depleted sodium ions. Furthermore the advice for the donor is to eat good solid meals with proteins for the next few days. Typically, this would involve a fluid volume of less than one liter, although this is highly dependent on body weight. Larger people can tolerate slightly more blood loss than smaller people. More serious hypovolemia should be assessed by a physician. [edit]First aid External bleeding should be controlled by direct pressure. If direct pressure fails, a tourniquet should be used in the case of hemorrhage that cannot be controlled by direct pressure. If left on for more than 8 hours, the use of a tourniquet can kill all the tissue below its application upon a limb, making amputation necessary. The US Military now suggests applying a tourniquet to a bleeding extremity first, because direct pressure does not usually stop bleeding. Other techniques such as elevation and pressure points usually fail completely. If a first-aid provider recognizes internal bleeding the life-saving measure to take is to immediately call for emergency assistance. [edit]Field care Emergency oxygen should be immediately employed to increase the efficiency of the patient's remaining blood supply[citation needed]. This intervention can be life-saving[citation needed]. The use of intravenous fluids (IVs) may help compensate for lost fluid volume, but IV fluids cannot carry oxygen in the way that blood can, however blood substitutes are being developed which can. Infusion of colloid or crystalloid IV fluids will also dilute clotting factors within the blood, increasing the risk of bleeding. It is current best practice to allow permissive hypotension in patients suffering from hypovolemic shock[13] both to ensure clotting factors are not overly diluted but also to FBC. Glucose. [edit]Hospital treatment If the hypovolemia was caused by medication.stop blood pressure being artificially raised to a point where it "blows off" clots that have formed. the administration of antidotes may be appropriate but should be carefully monitored to avoid shock or the emergence of other pre-existing conditions[citation needed]. Cross-match Central Venous Line/Blood Pressure Arterial Line/Arterial Blood Gases Urine output measurements (via urinary catheter) Blood pressure SpO2 Oxygen saturations The following interventions would be carried out:      [edit] IV access Oxygen as required Surgical repair at sites of hemorrhage Inotrope therapy (Dopamine.[12] Blood transfusions coupled with surgical repair are the definitive treatment for hypovolemia caused bytrauma[citation needed] . Fluid replacement is beneficial in hypovolemia of stage 2. For a patient presenting with hypovolemic shock in hospital the following investigations would be carried out:       Blood tests: U+Es/Chem7. and is necessary in stage 3 and 4. Noradrenaline) Fresh frozen plasma/whole blood . See also the discussion of shock and the importance of treating reversible shock while it can still be countered. third-spacing) Risk Factors:  Non.adrenaline.peritonitis .ascites .CIRCULATORY SYSTEM ETIOLOGY/CAUSE:  Loss of Blood Volume external blood loss internal blood loss  Loss of plasma Volume GI losses Renal losses  Transcutaneous Losses  Internal losses (a.dehydration .Modifiable  Modifiable such as: Fluid Losses: Internal Losses: .vomiting .a.burns . dopamine) .k.↑ SVR  ↓ tissue perfusion  ↑ Oxygen requirement  ↓ BP  ↑ Oxygen demand  Splenic discharge( disgorging stored RBC and Plasma ) Gross/Anatomical Physical Changes:     ↑ Sodium/water retention ↑ Heart Rate/Contractility ↑ Volume ↑ Cardiac Volume - if compensation fails great losses .diarrhea .trauma .hemorrhage .diuresis .diabetis Insipidus/mellitus ↓ Intravascular Volume ↓ Cardiac Output Compensatory Mechanisms Molecular Changes:    Kidneys releases Aldosterone ADH ( posterior pituary gland ) Cathecholamine released by the Adrenal Gland (norepinephrine.surgery . Pathophysiologic Manifestation on Effect on Bodily Function:     ↓ cardiac output ↓ cardiac ejection ↓ impaired cellular metabolism ↓ BP Complications:   Multiple Organ Failure Death Clinical Manifestations ( S/S ) :         poor skin turgor thirst oliguria thready pulse cool clammy skin weakness pale skin mental status deterioration (mental confusion/loss of conciousness) Laboratory Exams:       CBC CT Scan or X-Ray of suspected area Endoscopy Echocardiogram Right Heart Catheterization ( Swan-Ganz) Urine Specific Gravity HYPOVOLEMIC SHOCK .
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