Cardiogenic Shock

C ardiogenic shock (CS) is a common cause of mortality, and management remains challenging despite advances in therapeutic options. CS is caused by severe impairment of myocardial performance that results in diminished cardiac output, end-organ hypoperfusion, and hypoxia. Clinically this presents as hypotension refractory to volume resuscitation with features of end-organ hypoperfusion requiring pharmacological or mechanical intervention. Acute myocardial infarction (MI) accounts for 81% of patient in CS. Contemporary trials and guidelines (Table 1) outline clinical criteria for defining CS and are limited by lack of uniformity. The SHOCK (Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock) and intra-aortic balloon pump (IABP)-SHOCK II trials used systolic blood pressure (SBP) measurements of <90 mm Hg for ≥30 minutes or use of pharmacological and/or mechanical support to maintain an SBP ≥90 mm Hg. Evidence of end-organ hypoperfusion varied between the trials but typically included urine output of <30 mL/h, cool extremities, altered mental status, and/or serum lactate >2.0 mmol/L. The SHOCK Trial included cardiac index (CI) of ≤2.2 L/min per m and a pulmonary capillary wedge pressure (PCWP) of ≥15 mm Hg. An SBP <90 mm Hg that is refractory to fluid resuscitation with clinical and laboratory evidence of end-organ dysfunction, in the setting of suspected cardiac dysfunction, is essential to the definition of CS. However, CS is a continuum that extends from pre-shock to refractory shock states, which influence the timely considerations of various interventions. Acknowledging this continuum in future trials would likely facilitate the unification of clinical and hemodynamic criteria in defining CS. Epidemiology