Myocardial Dysfunction and Shock after Cardiac Arrest

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.

Improving Survival From Cardiac Arrest: A Review of Contemporary Practice and Challenges

“…It also produces strong cardiac badrenergic receptor activation, which may trigger recurrent ventricular arrhythmias and produce reversible myocardial dysfunction, leading to impaired cardiac function after return of spontaneous circulation. [50][51][52] Because of these concerns, norepinephrine, an a-agonist vasopressor with weaker b-adrenergic effects than epinephrine, was compared with epinephrine in a randomized trial but failed to improve survival after cardiac arrest when used in high doses. 29 Vasopressin increases organ perfusion pressure without harmful b-adrenergic effects and may have greater efficacy during acidemic conditions that impair adrenergic receptor responses.…”

“…52,78 The shock state that follows return of spontaneous circulation is dynamic, progressing from lowoutput cardiogenic shock caused by postarrest myocardial dysfunction to vasodilated distributive shock with capillary leak caused by a systemic inflammatory response that mimics sepsis. 51,52 Observational studies suggest that early 75 Sutherasan et al, 77 and Geri et al 86 hemodynamic optimization as part of a postarrest care bundle can improve outcomes, analogous to management of septic shock ( Figure 4). 52,[79][80][81] Patients often require fluid resuscitation after return of spontaneous circulation, although this should be guided by measures of preload responsiveness and intravascular volume status to avoid volume overload.…”

“…51,52 Observational studies suggest that early 75 Sutherasan et al, 77 and Geri et al 86 hemodynamic optimization as part of a postarrest care bundle can improve outcomes, analogous to management of septic shock ( Figure 4). 52,[79][80][81] Patients often require fluid resuscitation after return of spontaneous circulation, although this should be guided by measures of preload responsiveness and intravascular volume status to avoid volume overload. 51,52,76 Hypotension refractory to fluids typically responds to vasopressors.…”

“…52,[79][80][81] Patients often require fluid resuscitation after return of spontaneous circulation, although this should be guided by measures of preload responsiveness and intravascular volume status to avoid volume overload. 51,52,76 Hypotension refractory to fluids typically responds to vasopressors. Norepinephrine is the first-line vasopressor for shock after return of spontaneous circulation; epinephrine is a useful alternative, but dopamine is more proarrhythmic and therefore not recommended ( Figure 4).…”

“…Norepinephrine is the first-line vasopressor for shock after return of spontaneous circulation; epinephrine is a useful alternative, but dopamine is more proarrhythmic and therefore not recommended ( Figure 4). 52,75,76,82 Guidelines recommend maintaining a systolic blood pressure greater than 90 to 100 mm Hg and a mean arterial pressure greater than 65 mm Hg. 75,76 Observational studies have found that a higher mean arterial pressure early after return of spontaneous circulation is associated with better neurologic outcomes, up to 80 to 100 mm Hg; there is no evidence that increasing vasopressor doses to achieve a higher mean arterial pressure is beneficial.…”