Clinical Review ABC of interventional cardiology

Percutaneous coronary intervention: cardiogenic shock

BMJ 2003; 326 doi: (Published 26 June 2003) Cite this as: BMJ 2003;326:1450

This article has a correction. Please see:

  1. John Ducas, consultant cardiologist, associate professor,
  2. Ever D Grech, consultant cardiologist, assistant professor
  1. Health Sciences Centre and St Boniface Hospital, Winnipeg, Manitoba, Canada, University of Manitoba, Winnipeg.
  2. Health Sciences Centre and St Boniface Hospital, University of Manitoba.


    Cardiogenic shock is the commonest cause of death after acute myocardial infarction. It occurs in 7% of patients with ST segment elevation myocardial infarction and 3% with non-ST segment elevation myocardial infarction.

    Cardiogenic shock is a progressive state of hypotension (systolic blood pressure < 90 mm Hg) lasting at least 30 minutes, despite adequate preload and heart rate, which leads to systemic hypoperfusion. It is usually caused by left ventricular systolic dysfunction. A patient requiring drug or mechanical support to maintain a systolic blood pressure over 90 mm Hg can also be considered as manifesting cardiogenic shock. As cardiac output and blood pressure fall, there is an increase in sympathetic tone, with subsequent cardiac and systemic effects—such as altered mental state, cold extremities, peripheral cyanosis, and urine output < 30 ml/hour.

    Effects of cardiogenic shock

    Cardiac effects

    In an attempt to maintain cardiac output, the remaining non-ischaemic myocardium becomes hypercontractile, and its oxygen consumption increases. The effectiveness of this response depends on the extent of current and previous left ventricular damage, the severity of coexisting coronary artery disease, and the presence of other cardiac pathology such as valve disease.

    A 65 year old man with a 3–4 hour history of acute anterior myocardial infarction had cardiogenic shock and acute pulmonary oedema, requiring mechanical ventilation and inotropic support. He underwent emergency angiography (top), which showed a totally occluded proximal left anterior descending artery (arrow). A soft tipped guidewire was passed across the occlusive thrombotic lesion, which was successfully stented (middle). Restoration of brisk antegrade flow down this artery (bottom) followed by insertion of an intra-aortic balloon pump markedly improved blood pressure and organ perfusion. The next day he was extubated and weaned off all inotropic drugs, and the intra-aortic balloon pump was removed

    Three possible outcomes may occur:

    • Compensation—which restores normal blood pressure and …

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