PHTY300 Study Guide - Final Guide: Vascular Resistance, Antihypotensive Agent, Sofa Score
Document Summary
Life-threatening organ dysfunction caused by a dysregulated host response to infection. Early sepsis = increase co, decrease systemic vascular resistance, vasodilated circulation with hyperdynamic state qsofa: rr >/= 22/min; gcs=13; systolic blood pressure =100mmhg. Subset of sepsis with persistent hypotension requiring vasopressors to maintain >/= map. Early haemodynamic resuscitation and continued support with fluids resuscitation antibiotics & vasopressors (noradrenaline) - risk of symmetrical peripheral gangrene. Early and adequate antibiotic therapy increase survival rate. Secondary impact of sepsis (resolve by exercise training) Muscle weakness & sepsis-induced myopathy: infection circulating mediators (endotoxin, cytokines, chemokines promote inflammation & increase catabolism) intracellular mediators dysfunction (decrease force) & catabolism (decrease muscle mass) muscle weakness. Immobility: develops proinflammatory state with bed rest increase production of reactive oxygen species and decrease in anti-oxidative defenses. Effect of stoma & open wound decrease nitrogen and hco3 metabolic acidosis increase protein degradation muscle wasting. Muscle strength & passive movement: decrease pro-inflammatory cytokine, increase anti-inflammatory cytokine.
