Introduction

Cardiogenic shock (CGS) complicates 5 – 10% of cases of acute myocardial infarction (AMI) and the most common cause of CGS is AMI (80% of cases).1 When CGS occurs after ST-segment elevation myocardial infarction (STEMI), the median time delay before the onset of shock is 5–6 hours.2 CGS complicates non-ST-segment elevation myocardial infarction (NSTEMI) less frequently (approximately 2.5% of NSTEMI cases) and tends to occur later (median time delay of 76 hours).3 Fewer than 50% of patients with CGS survive up to 1 year.4

The clinical syndrome of CGS is present when there is inadequate cardiac output and systemic tissue hypoperfusion despite adequate circulating volume and filling pressure. The haemodynamic criteria used to define CGS are a systolic blood pressure (SBP) <90 mmHg for at least 30 min, or a need for vasopressors to achieve SBP ≥90 mmHg, or a fall in mean arterial blood pressure >30 mmHg below baseline, combined with an unsupported cardiac index <1.8 L/min/m² or <2.2 L/min/m² with cardiac support, and a pulmonary capillary wedge pressure >15 mmHg indicating elevated left ventricular (LV) filling pressures.2 In patients with AMI, an acute reduction in LV contractile function is central to the process leading to CGS along with reduced coronary blood flow, increased myocardial oxygen demand, diastolic dysfunction and elevated LV end diastolic pressure. Neurohormonal compensatory mechanisms, including sympathetic stimulation promote tachycardia and vasoconstriction, both of which increase cardiac work that in turn increases LV preload. Systemic inflammatory responses also contribute to the pathophysiology,5 and metabolic derangements such as acidosis may further impair myocardial contractility.