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BioMed Research International
Volume 2015, Article ID 314796, 14 pages
http://dx.doi.org/10.1155/2015/314796
Review Article

Myocardial Dysfunction and Shock after Cardiac Arrest

1Division of Cardiology, UPMC Heart and Vascular Institute, University of Pittsburgh Presbyterian Hospital, 200 Lothrop Street, Pittsburgh, PA 15213, USA
2Department of Critical Care Medicine, University of Pittsburgh Presbyterian Hospital, 200 Lothrop Street, Pittsburgh, PA 15213, USA
3Safar Center for Resuscitation Research, University of Pittsburgh Presbyterian Hospital, 200 Lothrop Street, Pittsburgh, PA 15213, USA

Received 22 May 2015; Accepted 28 June 2015

Academic Editor: Spyros Mentzelopoulos

Copyright © 2015 Jacob C. Jentzer et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Postarrest myocardial dysfunction includes the development of low cardiac output or ventricular systolic or diastolic dysfunction after cardiac arrest. Impaired left ventricular systolic function is reported in nearly two-thirds of patients resuscitated after cardiac arrest. Hypotension and shock requiring vasopressor support are similarly common after cardiac arrest. Whereas shock requiring vasopressor support is consistently associated with an adverse outcome after cardiac arrest, the association between myocardial dysfunction and outcomes is less clear. Myocardial dysfunction and shock after cardiac arrest develop as the result of preexisting cardiac pathology with multiple superimposed insults from resuscitation. The pathophysiology involves cardiovascular ischemia/reperfusion injury and cardiovascular toxicity from excessive levels of inflammatory cytokine activation and catecholamines, among other contributing factors. Similar mechanisms occur in myocardial dysfunction after cardiopulmonary bypass, in sepsis, and in stress-induced cardiomyopathy. Hemodynamic stabilization after resuscitation from cardiac arrest involves restoration of preload, vasopressors to support arterial pressure, and inotropic support if needed to reverse the effects of myocardial dysfunction and improve systemic perfusion. Further research is needed to define the role of postarrest myocardial dysfunction on cardiac arrest outcomes and identify therapeutic strategies.