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Myocardial Dysfunction and Shock after Cardiac Arrest
#MMPMID26421284
Jentzer JC
; Chonde MD
; Dezfulian C
Biomed Res Int
2015[]; 2015
(?): 314796
PMID26421284
show ga
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.