Relative adrenal insufficiency in post-cardiac arrest shock is under-recognized

Miller, Joseph; Donnino, Michael W.; Rogan, Michael; Goyal, Nikhil

doi:10.1016/j.resuscitation.2007.07.034

Cited by 37 publications

(19 citation statements)

References 22 publications

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“…In the post-arrest period, tissue hypoperfusion may persist for multiple reasons including the lack of resolution of the underlying insult, a post-arrest systemic inflammatory response (20, 21), myocardial depression with resultant cardiogenic shock (22), microcirculatory dysfunction (23–25), and mitochondrial injury(26, 27). The development of other complications such as sepsis (28), bowel ischemia (29, 30), seizures (31), and/or adrenal insufficiency causing shock (32) could play a role if present. Another potential cause of elevated lactate levels in the post-arrest period may be the presence of a hyper metabolic state with accelerated aerobic glycolysis potentially caused by activation of the Na+ K+ ATPase by endogenous epinephrine (33, 34).…”

Section: Discussionmentioning

confidence: 99%

Initial Lactate and Lactate Change in Post–Cardiac Arrest

Donnino

Andersen

Giberson

et al. 2014

Critical Care Medicine

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132

101

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Introduction Rate of lactate change is associated with in-hospital mortality in post-cardiac arrest patients. This association has not been validated in a prospective multicenter study. Objective To determine the association between percent lactate change and outcomes in post-cardiac arrest patients. Methods Four-center prospective observational study conducted from June 2011 to March 2012. Inclusion criteria consisted of adult out-of-hospital non-traumatic cardiac arrest patients who were comatose after return of spontaneous circulation. The primary outcome was survival to hospital discharge, and secondary outcome was good neurological outcome. We compared the absolute lactate levels and the differences in the percent lactate change over 24-hrs between survivors and non-survivors and between subjects with good and bad neurological outcomes. Results 100 patients were analyzed. The median age was 63 years (IQR: 50 – 75) and 40% were female. 97% received therapeutic hypothermia and overall survival was 46%. Survivors and patients with good neurological outcome had lower lactate levels at 0, 12 and 24 hours (p < 0.01). In adjusted models percent lactate decrease at 12 hours was greater in survivors (OR 2.2 [95% CI 1.1 – 6.2]) and in those with good neurological outcome (OR 2.2 [95% CI 1.1 – 4.4]). Conclusion Lower lactate levels at 0, 12 and 24 hours as well as greater percent decrease in lactate over the first 12-hours post-cardiac arrest are associated with survival and good neurologic outcome.

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Section: Discussionmentioning

confidence: 99%

Initial Lactate and Lactate Change in Post–Cardiac Arrest

Donnino

Andersen

Giberson

et al. 2014

Critical Care Medicine

Self Cite

132

101

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“…In the post-resuscitation phase adrenal insufficiency induces hypotension and reduces the effectiveness of vasopressors [73]. These hemodynamic alterations [74] render patients at high risk for acute organ hypo-perfusion and multiorgan system dysfunction [75]. The relationship between adrenal dysfunction and post-resuscitation shock was analyzed in several studies.…”

Section: Post-cardiac Arrest Syndromementioning

confidence: 99%

Glucocorticoids as an Emerging Pharmacologic Agent for Cardiopulmonary Resuscitation

Varvarousi

Stefaniotou

Varvaroussis

et al. 2014

Cardiovasc Drugs Ther

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Although cardiac arrest (CA) constitutes a major health problem with dismal prognosis, no specific drug therapy has been shown to improve survival to hospital discharge. CA causes adrenal insufficiency which is associated with poor outcome and increased mortality. Adrenal insufficiency may manifest as an inability to increase cortisol secretion during and after cardiopulmonary resuscitation (CPR). Several studies suggest that glucocorticoids during and after CPR seem to confer benefits with respect to return of spontaneous circulation (ROSC) rates and long term survival. They have beneficial hemodynamic effects that may favor their use during CPR and in the early post-resuscitation period. Moreover, they have anti-inflammatory and anti-apoptotic properties that improve organ function by reducing ischemia/reperfusion (I/R) injury. However, glucocorticoid supplementation has shown conflicting results with regard to survival to hospital discharge and neurological outcome. The purpose of this article is to review the pathophysiology of hypothalamic-pituitary-adrenal (HPA) axis during CPR. Furthermore, this article reviews the effects of glucocorticoids use during CRP and the post-resuscitation phase.

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“…[44][45][46][47][48][49] Low-dose steroid administration for septic shock remains controversial, 50 and direct evidence supporting corticosteroid administration during PCA care is lacking. CIRCI, or relative adrenal insufficiency (RAI), after ROSC was identified in several human clinical studies and has been associated with increased mortality.…”

Section: Adrenal Dysfunctionmentioning

confidence: 99%