Management of shock phenotypes after cardiac arrest: beyond cardiogenic shock

Postcardiac-arrest circulatory failure is commonly labeled cardiogenic shock, although its physiology is heterogeneous, dynamic, and frequently mixed. This review examines recent evidence and proposes a treatment-oriented framework.

Hypotension, hyperlactatemia, vasopressor dependence, and myocardial dysfunction do not establish ongoing shock after cardiac arrest or identify its mechanism. Recent studies demonstrate clinically important discordance between arterial pressure, cardiac output, filling pressures, oxygen transport, metabolic recovery, and prognosis. Four primary hemodynamic phenotypes are proposed: vasoplegic-inflammatory shock; myocardial dysfunction and low-flow shock; hypovolemia; and right ventricular and pulmonary vascular dysfunction. Mixed shock is an overlap group, whereas reversible metabolic pseudoshock describes arrest-related hyperlactatemia that resolves without persistent hemodynamic compromise.

Repeated multimodal assessment should determine whether circulatory dysfunction is resolving or persisting and identify the dominant mechanism. Treatment, advanced monitoring, and mechanical circulatory support should then be individualized, with neurological uncertainty incorporated into escalation decisions.