Abstract
BackgroundWhole body ischemia and reperfusion injury after cardiac arrest leads to the massive inflammation clinically manifested in the post-cardiac arrest syndrome. Previous studies on the inflammatory effect on circulatory failure after cardiac arrest have either investigated a selected patient group or a limited part of the inflammatory mechanisms. We examined the association between cardiac arrest characteristics and inflammatory biomarkers, and between inflammatory biomarkers and circulatory failure after cardiac arrest, in an unselected patient cohort. MethodsThis was a prospective study of 50 consecutive patients with out-of-hospital cardiac arrest. Circulation was invasively monitored from admission until day five, whereas inflammatory biomarkers, i.e. complement activation, cytokines and endothelial injury, were measured daily. We identified predictors for an increased inflammatory response, and associations between the inflammatory response and circulatory failure. ResultsWe found a marked and broad inflammatory response in patients after cardiac arrest, which was associated with clinical outcome. Long time to return of spontaneous circulation and high lactate level at admission were associated with increased complement activation (TCC and C3bc), pro-inflammatory cytokines (IL-6, IL-8) and endothelial injury (syndecan-1) at admission. These biomarkers were in turn significantly associated with lower mean arterial blood pressure, lower cardiac output and lower systemic vascular resistance, and increased need of circulatory support in the initial phase. High levels of TCC and IL-6 at admission were significantly associated with increased 30-days mortality. ConclusionInflammatory biomarkers, including complement activation, cytokines and endothelial injury, were associated with increased circulatory failure in the initial period after cardiac arrest.
Highlights
MethodsThe inflammatory response after out-of-hospital cardiac arrest (OHCA) share many characteristics with sepsis, and is described as a “sepsis-like syndrome”.1 Whole body ischemia and subsequent reperfusion injury leads to a systemic inflammation, which is, together with anoxic brain injury and myocardial dysfunction, the main elements of the post-cardiac arrest syndrome (PCAS).[2]The balance between pro- and anti-inflammatory cytokine signalling is important for the effect of the immune system on the development of organ failure.[3]
Long time to return of spontaneous circulation and high lactate level at admission were associated with increased complement activation (TCC and complement 3 activation product (C3bc)), pro-inflammatory cytokines (IL-6, IL-8) and endothelial injury at admission
Findings so far indicate that high levels of interleukin 6 (IL-6) and complement factor 3 were associated with mortality, whereas high levels of IL-6 and IL-10 were associated with organ failure.[1,5,6,7,8,9]
Summary
MethodsThe inflammatory response after out-of-hospital cardiac arrest (OHCA) share many characteristics with sepsis, and is described as a “sepsis-like syndrome”.1 Whole body ischemia and subsequent reperfusion injury leads to a systemic inflammation, which is, together with anoxic brain injury and myocardial dysfunction, the main elements of the post-cardiac arrest syndrome (PCAS).[2]The balance between pro- and anti-inflammatory cytokine signalling is important for the effect of the immune system on the development of organ failure.[3]. Whole body ischemia and reperfusion injury after cardiac arrest leads to the massive inflammation clinically manifested in the postcardiac arrest syndrome. Long time to return of spontaneous circulation and high lactate level at admission were associated with increased complement activation (TCC and C3bc), pro-inflammatory cytokines (IL-6, IL-8) and endothelial injury (syndecan-1) at admission. These biomarkers were in turn significantly associated with lower mean arterial blood pressure, lower cardiac output and lower systemic vascular resistance, and increased need of circulatory support in the initial phase. Conclusion: Inflammatory biomarkers, including complement activation, cytokines and endothelial injury, were associated with increased circulatory failure in the initial period after cardiac arrest.
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