Abstract

Despite the availability of invasive circulatory monitoring, inotropes and thrombolysis, mortality from cardiogenic shock remains in excess of 50%, and continues to account for the deaths of between 7% and 11% of patients admitted with myocardial infarction.1–,3 In the majority of these patients, the problem is one of overwhelming left ventricular damage and, intuitively, revascularization should be the primary therapeutic strategy. However, attempts to prove this have been fraught with difficulty, and the randomized trial paradigm that revolutionized our approach to acute cardiology appears to have faltered. This review examines the features of cardiogenic shock that have hindered attempts to improve its outcome, discusses whether current evidence is sufficient to support a policy of revascularization and explores the potential value of approaches aimed at minimizing reperfusion damage. The development of cardiogenic shock is rarely unexpected, most patients who develop shock do so within 48 hours of admission, with only 10% shocked on arrival.2 As would be expected, shock is associated with larger infarcts, prior infarction, diabetes and infarct extension.4,,5 The diagnosis itself is straightforward, with a systolic blood pressure <90 mmHg for more than 30 min in the absence of hypovolaemia or other potential causes of hypotension. Additional features such as oliguria and impaired peripheral perfusion identify those at particularly high risk of death.6 The widespread availability of bedside echocardiography has rendered the use of invasive haemodynamics, and in particular a requirement for a cardiac index of less than 2.2 l/min/m2, virtually obsolete in the decision‐making process. Echocardiography readily identifies the mechanism of shock and those patients that might benefit from surgery for intra‐ or extra‐myocardial rupture (Figure 1).4,7,,8 Figure 1. Apical four‐chamber echo view with relative incidence of the mechanisms responsible for cardiogenic shock in the SHOCK 8 and MILIS 4 …

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