Clinical meaning
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, mitochondrial dysfunction, inflammatory cascade activation), and irreversible stages (widespread cellular death, multiorgan failure, refractory hypotension). The clinician must rapidly identify the shock type through hemodynamic assessment, physical examination, point-of-care ultrasound, and targeted laboratory evaluation to initiate type-specific resuscitation.