Definition and aetiology

 Cardiogenic shock is defined as hypoperfusion due to inadequate cardiac output or, more technically, a cardiac index of < 2.2 L/min/m (. While cardiogenic shock is the final common pathway of many disease processes (e.g. sepsis, anaphylaxis, haemorrhage), the important primary causes of acute heart failure or cardiogenic shock (Fig. 1) are described here.

Fig1. Some common causes of cardiogenic shock. (LA = left atrium; LV = left ventricle; PA = pulmonary artery; RA = right atrium; RV = right ventricle)

 Myocardial infarction

 In the majority of cases, cardiogenic shock following acute MI is due to left ventricular dysfunction. However, it may also be due to infarction of the right ventricle, or a variety of mechanical complications, including tamponade (due to infarction and rupture of the free wall), an acquired ventricular septal defect (due to infarction and rupture of the septum) and acute mitral regurgitation (due to infarction or rupture of the papillary muscles).

 Severe myocardial systolic dysfunction causes a fall in cardiac output, BP and coronary perfusion pressure. Diastolic dysfunction causes a rise in left ventricular end-diastolic pressure, pulmonary congestion and oedema, leading to hypoxaemia that worsens myocardial ischaemia. This is further exacerbated by peripheral vasoconstriction. These factors combine to create the ‘downward spiral’ of cardiogenic shock (Fig. 2). Hypotension, oliguria, delirium and cold, clammy peripheries are the manifestations of a low cardiac output, whereas breathlessness, hypoxaemia, cyanosis and inspiratory crackles at the lung bases are typical features of pulmonary oedema. If necessary, a Swan–Ganz catheter can be used to measure the pulmonary artery pressures and cardiac output ( Fig. 3). These findings can be used to categorise patients with acute MI into four haemodynamic subsets (Box1) and titrate therapy accordingly.

 In cardiogenic shock associated with acute MI, immediate percutaneous coronary intervention should be performed. The viable myocardium surrounding a fresh infarct may contract poorly for a few days and then recover. This phenomenon is known as myocardial stunning and means that acute heart failure should be treated intensively because overall cardiac function may subsequently improve.

Fig2. The downward spiral of cardiogenic shock.

Fig3. A pulmonary artery (Swan–Ganz) catheter

Box1. Acute myocardial infarction: haemodynamic subsets

 Acute massive pulmonary embolism

 Massive PE may complicate leg or pelvic vein thrombosis and usually presents with sudden collapse. Bedside echocardiography may demonstrate a small, under-filed, vigorous left ventricle with a dilated right ventricle; it is sometimes possible to see thrombus in the right ventricular outflow tract or main pulmonary artery. In practice, it can be difficult to distinguish massive PE from a right ventricular infarct on transthoracic echocardio gram. CT pulmonary angiography usually provides a definitive diagnosis. Acute valvular pathology, aortic dissection and cardiac tamponade These conditions should be considered in an undifferentiated presentation of shock.