ECC1- Shock

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  1. Any condition where the metabolic demand for oxygen exceeds uptake and utilization, resulting in a measurable change in organ function.
    shock
  2. What are the determinants of tissue perfusion?
    • cardiac output and systemic vascular resistance
    • CO= SV x HR
    • SV= preload x afterload x inotropy
  3. What are the determinants of oxygen delivery to the tissues?
    arterial O2 content (CaO2) and cardiac output
  4. Describe the pathophysiology of shock.
    decreased delivery or utilization of shock--> oxygen demand outweighs supply--> O2 utilization becomes delivery dependent--> switch to anaerobic metabolism--> lactate production--> metabolic acidosis--> mitochondrial dysfunction--> worsening energy debt--> loss of cell membrane integrity--> intracellular shift of fluid, cell swelling--> oxygen free radical formation--> cell necrosis or apoptosis--> tissue injury and organ failure
  5. What are the stages of shock? (3)
    • compensated shock
    • decompensated shock
    • terminal shock
  6. Describe the physiology of compensated shock.
    physiological response to shock in which there is redistribution of fluid from the interstitium to the vascular space and release of vasoactive agents to maintain BP--> maintenances of core blood flow and oxygen delivery at the expense of the periphery
  7. What vasoactive agents play a part in compensated shock? What is the result of each? (3)
    • catecholamines--> vasoconstriction--> increase SVR and MAP; increased inotropy and HR--> maintains SV and CO
    • ADH--> vasoconstriction--> increased SVR and MAP; increased water retention--> increased blood volume and preload--> increased SV and CO
    • RAAS--> vasoconstriction--> increased SVR and MAP; increased Na+ and water retention--> increased blood volume/ preload
  8. Describe the clinical manifestations of compensated shock. (6)
    • tachy
    • pale mm's
    • prolonged crt
    • cold extremities
    • diminished peripheral pulses
    • NORMAL BP!!!
  9. What are the clinical consequences of peripheral vasoconstriction with compensated shock?(4)
    • pale MM's
    • prolonged CRT
    • cold extremities
    • diminished peripheral pulses
  10. Describe the physiology of decompensated shock.
    compensatory mechanisms are exceeded and there is inability to maintain BP and/or normal cellular metabolism--> core perfusion starts to diminish
  11. Describe the clinical manifestations of decompensated shock. (4)
    • depressed mentation
    • tachypnea
    • hypothermia
    • HYPOTENSION!!!
  12. Describe the physiology of terminal shock.
    prolonged hypotension, severe metabolic acidosis, bradycardia despite decreased CO and BP, loss of vasomotor tone and subsequent vasodilation, maldistribution of blood flow to non-essential organs and peripheral pooling of blood, cardiovascular collapse and death
  13. What is unique about feline shock patients? (3)
    • cats can manifest bradycardia at any stage of shock (rather than the expected tachycardia)
    • cats manifest hypothermia more commonly along with hypotension
  14. What are the categories of shock? (6)
    hypovolemic, obstructive, (mal)distributive, cardiogenic, anemic/ hypoxemic, metabolic
  15. What are the perfusion-related (4) and non-perfusion-related (2) categories of shock?
    • Perfusion: hypovolemic, obstructive, maldistributive, cardiogenic
    • Non-perfusion: anemic/ hypoxemic, metabolic
  16. What is hypovolemic shock?
    diminished circulating blood volume secondary to hemorrhage, GI losses, severe dehydration, cavitary effusions/ edema
  17. Describe the physiology of hypovolemic shock.
    decreased preload--> decreased SV--> decreased CO--> decreased MAP--> decreased oxygen delivery--> tissue hypoxia
  18. What are the clinical signs of hypovolemic shock? (7)
    • tachycardia
    • weak pulses
    • pale MM's
    • prolonged CRT
    • cold extremities/ hypothermia
    • tachypnea
    • altered mentation
    • [severity consistent with rate and magnitude of volume loss]
  19. What is the shock-specific treatment for hypovolemic shock?
    fluid resuscitation
  20. What is obstructive shock? (5 causes)
    impaired venous return secondary to pericardial effusion (tamponade), GDV/ mesenteric torsion, tension pneumothorax, massive PTE, caudal vena cava or portal vein thrombosis
  21. Describe the physiology of obstructive shock.
    decreased preload--> decreased SV--> decreased CO--> decreased MAP--> decreased oxygen delivery--> tissue hypoxia
  22. What are the clinical signs of obstructive shock? (7)
    • tachycardia
    • weak pulses
    • cold extremities/ hypothermia
    • pale MM's
    • prolonged CRT
    • altered mentation
    • signs associated with underlying cause (tachypnea/ dyspnea (PTE), muffled heart sounds, abdominal distension)
  23. What is the shock-specific treatment for obstructive shock?
    • shock fluid therapy administered "above" obstruction
    • relieve obstruction (surgery, pericardiocentesis, thoracocentesis, thrombolytic therapy- depends on underlying cause)
  24. What is maldistributive shock?
    inappropriate vasodilation secondary to sepsis (increased NO), anaphylaxis (histamine), neurogenic (loss of SNS innervation)
  25. Describe the physiology of maldistributive shock. (2 possibilities)
    • decreased SVR--> decreased MAP--> decreased tissue perfusion
    • venous pooling-> decreased preload--> decreased SV--> decreased CO-->decreased MAP--> decreased oxygen delivery--> tissue hypoxia
  26. What are the clinical signs of maldistributive shock? (7)
    • tachycardia
    • weak or hyperdynamic pulses
    • pale or red MMs
    • prolonged or shortened CRT
    • erythema
    • tachypnea
    • altered mentation
  27. What is the shock specific treatment for maldistributive shock?
    • IV fluids- combine crystalloids and colloids
    • vassopressors (increases SVR)- dopamine, NE, Epi, vasopressin
  28. What is cardiogenic shock?
    diminished forward flow of blood from the heart to arterial circulation caused by DCM, severe mitral regurg, myocardial dysfunction, severe tachycardia/ bradycardia
  29. Describe the physiology of cardiogenic shock.
    Decreased SV--> decreased CO--> decreased MAP--> decreased oxygen delivery--> tissue hypoxia
  30. What are the clinical signs of cardiogenic shock? (7)
    • tachycardia
    • weak pulses
    • pale or cyanotic MMs
    • prolonged CRT
    • cold extremities, hypothermia
    • tachypnea/ dyspnea
    • altered mentation
    • [consistent with severity of forward failure and pulmonary congestion]
  31. What is the shock specific treatment for cardiogenic shock?
    • positive inotropes (to increase contractility)- dobutamine, dopamine, pimobendan
    • anti-arrhythmics (to decrease HR)- lidocaine, procainamide(ventricular), esmolol, diltiazem (atrial)
    • anti-cholinergics (to increase rate)- atropine, glycopyrolate
  32. What is anemic/ hypoxemic shock?
    decreased arterial oxygen caused by loss of hemoglobin secondary to blood loss, hemolysis, or diminished RBCs production or caused by decreased saturation of hemoglobin secondary to VQ mismatch, hypoventilation, anatomical shunt, decreased inhaled oxygen tension, diffusion impairment
  33. How can you often distinguish maldistributive shock from anemic shock?
    • red MMs and snappy pulses- maldistributive
    • pale MMs and snappy pulses- anemia
  34. What are the clinical signs of anemic shock? (6)
    • tachycardia
    • snappy pulses
    • pale/ icteric MMs
    • normal CRT
    • tachypnea
    • altered mentation
  35. What are the clinical signs of hypoxemic shock? (7)
    • tachycardia
    • strong pulses
    • cyanotic MMs
    • normal CRT
    • tachypnea/dyspnea
    • wheezing/ stridor
    • altered mentation
  36. What is the shock specific treatment for anemic shock?
    transfusion
  37. What is the shock specific treatment for hypoxemic shock?
    supplemental oxygen, mechanical ventilation
  38. What are "snappy" pulses?
    tall/ narrow pulses
  39. Describe metabolic shock.
    cellular dysmetabolism independent of tissue perfusion and oxygen delivery; inability to make cellular energy
  40. What are potential causes of metabolic shock? (3)
    • hypoglycemia (no substrate for energy production)
    • cyanide toxicity (uncoupling of oxidative phosphorylation)
    • mitochondrial dysfunction
  41. What are the clinical signs of metabolic shock? (7)
    • maybe none
    • tachycardia
    • normal to strong pulses early, weak pulses late
    • normal or red MMs
    • normal CRT
    • tachypnea
    • altered mentation
  42. What is the shock specific treatment for metabolic shock?
    • dextrose (if hypoglycemia)
    • supportive care

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Author:
Mawad
ID:
322618
Filename:
ECC1- Shock
Updated:
2016-08-25 17:07:33
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vetmed ECC1
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vetmed ECC1
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