Cardiogenic shock (CS) is associated with significant mortality. Advances in pharmacological therapies and mechanical circulatory support (MCS) devices have markedly improved the therapeutic approach to CS, though treatment efficacy and safety vary. The recent DanGer shock trial showed a significant reduction in 6-month mortality for CS patients due to acute myocardial infarction. Future randomised trials should evaluate a phenotype-guided pharmaco-MCS approach to the management of CS. This paper summarises contemporary pharmacological and MCS treatments for patients with CS.

Introduction

Etiology and Pathophysiology of Cardiogenic Shock (CS)

Cardiogenic shock (CS) is a life-threatening condition with short-term (in-hospital or 30-day) mortality exceeding 30% across the literature (Chioncel et al, 2011; Chioncel et al, 2020; Maggioni et al, 2010). There are three components to the diagnosis of CS: an underlying cardiac pathology, circulatory failure related to the cardiac pathology and evidence of hypoperfusion due to circulatory failure.

The acute coronary syndrome is the archetypal cause of CS, but recent studies have increasingly recognised other causes of CS, including end-stage heart failure due to non-ischaemic cardiomyopathy, fulminant and other inflammatory myocarditis, and valvular heart disease. The underlying etiology is a major determinant of the CS phenotype, indication for treatment, clinical course and potential outcomes. For example, revascularization is indicated in CS due to acute myocardial infarction. Full recovery is likely in acute fulminant myocarditis if the patient survives CS, but ‘heart replacement therapy’ may be indicated in CS due to end-stage cardiomyopathy.

Irrespective of the underlying etiology, reduction in cardiac output is the dominant pathophysiology of circulatory failure in CS. Global oxygen delivery is a function of cardiac output of blood oxygen content. Global oxygen delivery diminishes due to the compromised cardiac output and may become inadequate to maintain tissue/organ perfusion, leading to clinical and metabolic features of hypoperfusion. Prompt correction of low cardiac output and improved oxygen delivery is necessary to avoid multi-organ failure and death from CS.