Hemodynamic & Shock Physiology

Shock is a state of inadequate tissue perfusion resulting in cellular hypoxia, anaerobic metabolism, lactic acidosis, and progressive organ dysfunction. Hemodynamic parameters — cardiac output (CO = stroke volume × heart rate), systemic vascular resistance (SVR), and preload (central venous pressure/pulmonary capillary wedge pressure) — define four shock categories. Hypovolemic shock results from decreased preload due to volume loss (hemorrhage, dehydration): low CO, low CVP/PCWP, high SVR (compensatory vasoconstriction). Cardiogenic shock results from pump failure (massive MI, severe valvular disease): low CO, high CVP/PCWP (fluid backs up), high SVR. Distributive shock results from pathological vasodilation (sepsis, anaphylaxis, neurogenic): low SVR is the hallmark, with initially high CO in warm septic shock (hyperdynamic phase) that progresses to low CO in cold septic shock (hypodynamic/decompensated phase); CVP/PCWP may be low (relative hypovolemia). Obstructive shock results from mechanical obstruction to blood flow (tension pneumothorax, cardiac tamponade, massive PE): low CO with elevated CVP (fluid cannot enter or exit the heart). The cellular response to shock progresses through compensated (baroreceptor-mediated tachycardia, vasoconstriction, RAAS activation maintaining blood pressure), progressive (cellular hypoxia, anaerobic metabolism, lactic acidosis,...