TEST 3: Shock Flashcards
Basic principles of shock
(Lecture, p. 1557)
-Inadequate tissue perfusion—> decreased oxygen and nutrient delivery —> impaired cellular metabolism
-Can have increased oxygen demand and nutrients (hyper metabolic state)
-Can have decreased removal of cellular waste
Cellular changes in shock
(Lecture, p.1558)
Main problem of shock at the cellular level:
-We switch from aerobic to anaerobic metabolism (d/t overconsumption of oxygen)
When anaerobic metabolism starts:
-Increased lactate, metabolic acidosis, increase in the oxy-hgb dissociation
-Next, protein metabolism increases, causing increased muscle wasting( decreased real and cardiac muscle strength) decrease immunoglobulin (will decrease your immune response) and increased cellular edema (inflammatory response that activates the clotting cascade)
-Lastly, decreased ATP, which increase intracellular Na/ water, decreased circulating volume, and can also trigger the clotting cascade
Metabolic changes in shock
(Lecture)
- Increased glucose, which causes:
Increased protein breakdown, increased pyruvate, increased lactate (also increases insulin resistance) - Increases catecholamines, cortisol, and growth hormone, which causes:
Increased gluconeogensis and glycogenolysis (which deplete energy store and increase cell failure), also increase Lipolysis (so you increase the amount of free fatty acids and triglycerides) this can also increase insulin resistance
General shock management
(Lecture)
-Consider patient history, risk factors, clinical situation
-Tx: address under lying cause, improve tissue perfusion, improve oxygen delivery, and manage hyperglycemia
Stages of shock
(Lecture)
- Compensated:
Where the body is still able to compensate for relative or absolute fluid loss (patient is able to maintain adequate BP and cerebral perfusion) - Decompensated:
Late phase of shock where body’s compensatory mechanisms are unable to maintain adequate perfusion to the brain and vital organs - Irreversible:
Rapid deterioration of the cardiovascular system and the compensatory mechanisms have failed—> DEATH
Cardiogenic shock
(Lecture, p. 1567)