The Comparative Epidemiology, Pathophysiology and Management of Cardiogenic Shock Associated With Acute Myocardial Infarction and Advanced Heart Failure

Cardiogenic shock (CS) results from low cardiac output caused by myocardial dysfunction, coupled with systemic end-organ tissue hypoperfusion and elevated ventricular filling pressures, along a spectrum of shock severity. This narrative review aims to compare the epidemiology, pathophysiology, and contemporary management of 2 common etiologies of CS caused by acute myocardial infarction (AMI-CS) and advanced heart failure (HF-CS). CS complicates up to 14% of AMI and 5% of HF admissions. Rapid therapeutic intervention after prompt recognition of CS etiology is the mainstay toward improving clinical outcomes and mitigating end-organ sequelae and death. In AMI-CS, persistent hypotension often leads to subsequent hypoperfusion and congestion, and early culprit coronary artery lesion revascularization is critical. In HF-CS, congestion often precedes hypoperfusion and hypotension, and targeting the underlying nonischemic cause of myocardial dysfunction is key. Tailoring of hemodynamic strategies with vasoactive agents and temporary mechanical circulatory and end-organ support to manage the predominant ventricular failure, hemometabolic phenotypes, and shock severity associated with each etiology is discussed. Given the limited evidence-base in CS care, we also highlight potential knowledge gaps ripe for future exploration.