Shock Overview A state of tissue hypoxia due to decreased or dysregulated oxygen delivery or extraction, resulting in end-organ damage and often occurring in the setting of hypotension Shock can develop in the setting of increased tissue demand, decreased O2 supply, or both. While initially reversible, it rapidly progresses: cell death -> end-organ dysfunction -> multiorgan failure -> death Common Clinical Manifestations • Neuro: altered mental status • CV: hypotension (SBP < 90 mmHg or decr > 40 mmHg from bl), wide vs. narrow pulse pressure • Pulm: resp. alterations (tachypneic / incr MV vs. somnolent/depressed) • Renal: metabolic acidosis, oliguria (< 0.5 mL/kg/hr) • Ext: warm vs. cold (feel shins and up), dry vs. wet (dependent areas, back of thigh/flank edema) Distributive Shock - Decreased SVR and altered O2 extraction • Inflammatory: infectious (sepsis) or not (pancreatitis. post-arrest) • Reactionary: anaphylaxis, toxins/meds • Other: AI, thyroid dz liver failure, neurogenic/spinal Hypovolemic Shock - Low CO and therefore inadequate O2 delivery • Hemorrhagic: bleeding out (trauma, GI, post-partum) bleeding in (trauma, hemothorax. RP bleed) • Hypovolemic: GI (vomiting/diarrhea), renal (over-diuresis, dialysis/CRRT, post-ATN, post-obstructive polyuria), surgical (burns, open abdomen/wound. drains) Cardiogenic Shock - Low CO and therefore inadequate O2 delivery • MI, Heart Failure, Severe Valve Dz, Myocarditis, Arrhythmias Obstructive Shock - Low CO and therefore inadequate O2 delivery • PE, Tension ptx, Tamponade Dr. Meredith Greer @EmmGeezee #Shock #Classification #diagnosis #management #Overview #criticalcare #differential #causes #classification
