VTS Week 2: Shock and Stabilization

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  1. Types of shock
    • 1. Hypovolemic
    • 2. Cardiogenic
    • 3. Distributive
    • 4. Hypoxic
    • 5. Metabolic
  2. Hypovolemic Shock
    Inadequate circulating volume. hemorrhage, v/d, decreased fluid intake, burns, third space loss
  3. Cardiogenic Shock
    Pump failure - low forward flow. Ventricular hypertrophy, myocardial infarction, dysrhythmias, valvular disease, anatomical defects, poor contractility, etc
  4. Distributive Shock
    Inappropriate distribution of blood flow. "Relative hypovolemia". Systemic inflammatory response, neurological dysfunction, caval syndrome, organomegaly, tamponade, outflow obstruction, thromboembolism
  5. Hypoxic Shock
    Improper oxygen loading or unloading. Hypoxemia, anemia, methemoglobinemia, RBC dysfunction
  6. Metabolic Shock
    Intracellular dysfunction that decreases energy production. Hypoglycemia - inadequate energy substrate for normal cellular function. Cyanide toxicity - mitochondrial dysfunction. Heatstroke - metabolic rate exceeds energy production
  7. 6 perfusion parameters
    • 1. mentation
    • 2. heart rate
    • 3. pulse quality
    • 4. MM color
    • 5. capillary refill time
    • 6. extremity-core temperature gradient
  8. earliest sign of shock
    decreased cerebral function
  9. 4 stages of shock
    • 1. initial stage
    • 2. compensatory shock
    • 3. decompensatory shock
    • 4. refractory shock
  10. Initial stage of shock
    inadequate 02 delivery causes hypoxia. Anaerobic metabolism ensues creating lactic acid and pyruvic acid build-up, causing metabolic acidosis. Liver removes these acids but requires O2 that is unavailable
  11. Compensatory shock
    Systemic acidosis = vasodilation and hyperventilation to rid body of carbon dioxide. Hyperventilation increases preload. Decreased cardiac output and hypotension cayse baroreceptor mediated reflex. Compensatory hormones released from adrenal gland. Norepinephrine and epinephrine cause and increase in heart rate contractility, and systemic vascular resistance (SVR). Cortisol enhances catecholamine effects on arterioles. Sodium and water are conserved via renin-angiotensin and aldosterone activation in an effort to increase intravascular volume. Vasopressin is also released causing vasoconstriction in kidneys, GI tract, and other organs in an effort to divert blood flow to the heart, lungs, and brain
  12. Decompensatory shock
    Proceeds to progressive stage and compensatory mechanisms begin to fail. Anaerobic metabolism continues and metabolic acidosis worsens, causing arteriolar smooth muscle and precapillary sphincter relaxation leading to peripheral pooling of blood. Hydrostatic pressure increases causing leakage of fluid and protein into the surrounding tissues. This loss of fluid increases blood viscosity which can cause a hypercoagulable state. Continued shunting of blood from intestinal tract can cause ischemia and mucosal acidosis, increasing bacterial translocation, leading to endotoxic shock. Shunting from kidneys can induce renal tubular necrosis.
  13. Refractory Shock
    Irreversible tissue death has occurred and vital organs have failed (MODS). Death is imminent.
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VTS Week 2: Shock and Stabilization
2017-05-10 13:49:32
VTS ECC veterinary

VTS Week 2: Shock and Stabilization
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