Stress response
"Ebb" (first 24 hours)
[edit | edit source]- Surges in catecholamine, cortisol and aldosterone
- Tachycardia
- Tachypnoea
- Vasoconstriction
- Decreased cardiac output
- Decreased oxygen consumption
- Lower basal metabolic rate
- Increased sodium and water retention
- Shunting of blood from periphery to vital organs
- Acute phase protein production
"Flow" (peaks at 48-72 hours)
[edit | edit source]- Secretion of catecholamines, ADH, cortisol, insulin, glucagon, growth hormone
- Enhanced proteolysis and lipolysis mobilises carbon sources for gluconeogenesis (catabolism)
- Skeletal muscle not spared
- Explosive metabolic and immune activity
- Tissue repair
- Enhanced enzymatic function
- Tachycardia and tachypnoea
- Peripheral oedema
- Fever
- Hyperglycaemia
- Leucocytosis
- Increased oxygen consumption
- Increased CO2 production
- Increased minute ventilation
- Elevated metabolic rate
- Negative nitrogen balance
Then anabolic state
[edit | edit source]- High insulin, growth hormone etc
- Oedema reabsorbed, brisk diuresis
- Decrease in serum ions as they move into cells, and therefore need replacement
Other points to note
[edit | edit source]- Liver hypoperfusion (often see cholestasis of critical illness as a marker of secondary liver hypoperfusion)
- Gut translocation (secondary to reduced splanchnic blood flow causing ischaemia-reperfusion-mediated gut injury)
- Enteral feeding supports gut integrity (maintains mucosal mass, stimulates epithelial cell proliferation, maintains villus height, promotes production of brush border enzymes, stimulates blood flow)
- Opioids likely impact stress response - immune cells express opioid receptors!
- Influence of neuroimmune axis is pretty poorly understood
- Muscle wasting - mediated by lack of anabolic factors, and increase in catabolic factors e.g. cortisol, combined with critical illness. Particularly bad in ventilated/septic patients. Strategies for prevention: