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Cardiogenic shock in ACS. Part 1: prediction, presentation and medical therapy

Nature Reviews Cardiology volume 9, pages 158–171 (2012)Cite this article

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Abstract

Ischemic cardiogenic shock is a complex, self-perpetuating pathological process that frequently causes death irrespective of medical therapy. Early definition of coronary anatomy is a pivotal step towards survival. Those destined to develop shock are likely to have three-vessel or left main stem disease with previously impaired left ventricular function. Early reperfusion of the occluded artery can limit infarct size, but ischemia–reperfusion injury or the 'no-reflow' phenomenon can preclude improvement in myocardial contractility. Emergence of shock depends upon the volume of ischemic myocardium, stroke volume, and peripheral vascular resistance. If cytokine release triggers the systemic inflammatory response, systemic vascular resistance falls and inadequate coronary perfusion pressure heralds the downward spiral. Survival depends on early recognition of shock, followed by aggressive targeted treatment of left, right, or biventricular failure. The goal is to prevent end-organ dysfunction and severe metabolic derangement by raising mean arterial pressure, which is achieved with inotropes and vasopressors, often at the expense of tachycardia, elevated myocardial oxygen consumption, and extended ischemia. The value of intra-aortic balloon counter-pulsation is now questioned in patients with advanced shock. When mean arterial pressure is <55 mmHg with serum lactate >11 mmol/l, death is likely and mechanical circulatory support becomes the only chance for survival.

Key Points

  • Cardiogenic shock complicates 5–10% of ST-segment elevation myocardial infarctions and 2–3% of non-ST segment elevation coronary syndromes, with mortality ranging from 40% to 80%

  • Angiographic findings during primary angioplasty can predict cardiogenic shock, but early reperfusion has decreased the incidence of full thickness infarction and improved survival

  • Ventricular septal rupture occurs in up to 0.5% of patients with ST-segment elevation myocardial infarction, whereas severe mitral regurgitation occurs in 10%, and free-wall rupture in 3%

  • Cytokine release can trigger the systemic inflammatory response, causing low peripheral vascular resistance and profound refractory shock in around one-third of cases

  • Management of primary left ventricular failure involves early reperfusion and administration of adrenergic inotropes and vasopressors; right ventricular failure is treated with volume loading, inotropes, and pulmonary vasodilators

  • When mean arterial pressure is <55 mmHg, serum lactate >11 mmol/l, base deficit >12 mmol/l, and SvO2 <65% despite medical therapy, recovery is unlikely without mechanical circulatory support

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Figure 1: Self-perpetuating mechanisms of cardiogenic shock.
Figure 2: Influence of PPCI on extent of myocardial infarction and stunning.
Figure 3: Myocardial disruption after acute myocardial infarction.
Figure 4: In-hospital mortality in cardiogenic shock by stage I (clinical) severity category.
Figure 5: Medical management of acute right ventricular dysfunction after myocardial infarction.

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  1. Departments of Cardiothoracic Surgery, Headley Way, Headington, OX3 9DU, Oxford, UK

    Stephen Westaby

  2. Cardiology, John Radcliffe Hospital, Headley Way, Headington, OX3 9DU, Oxford, UK

    Rajesh Kharbanda & Adrian P. Banning

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S. Westaby is a stockholder/Director of Calon Cardio-Technology. The other authors declare no competing interests.

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Westaby, S., Kharbanda, R. & Banning, A. Cardiogenic shock in ACS. Part 1: prediction, presentation and medical therapy. Nat Rev Cardiol 9, 158–171 (2012). https://doi.org/10.1038/nrcardio.2011.194

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