Characteristics of circulatory failure after out-of-hospital cardiac arrest: a prospective cohort study

Abstract

BackgroundCirculatory failure after out-of-hospital cardiac arrest (OHCA) as part of the postcardiac arrest syndrome (PCAS) is believed to be caused by an initial myocardial depression that later subsides into a superimposed vasodilatation. However, the relative contribution of myocardial dysfunction and systemic inflammation has not been established. Our objective was to describe the macrocirculatory and microcirculatory failure in PCAS in more detail.MethodsWe included 42 comatose patients after OHCA where circulatory variables were invasively monitored from admission until day 5. We measured the development in cardiac power output (CPO), stroke work (SW), aortic elastance, microcirculatory metabolism, inflammatory and cardiac biomarkers and need for vasoactive medications. We used survival analysis and Cox regression to assess time to norepinephrine discontinuation and negative fluid balance, stratified by inflammatory and cardiac biomarkers.ResultsCPO, SW and oxygen delivery increased during the first 48 hours. Although the estimated afterload fell, the blood pressure was kept above 65 mmHg with a diminishing need for norepinephrine, indicating a gradually re-established macrocirculatory homoeostasis. Time to norepinephrine discontinuation was longer for patients with higher pro-brain natriuretic peptide concentration (HR 0.45, 95% CI 0.21 to 0.96), while inflammatory biomarkers and other cardiac biomarkers did not predict the duration of vasoactive pressure support. Markers of microcirculatory distress, such as lactate and venous-to-arterial carbon dioxide difference, were normalised within 24 hours.ConclusionThe circulatory failure was initially characterised by reduced CPO and SW, however, microcirculatory and macrocirculatory homoeostasis was restored within 48 hours. We found that biomarkers indicating acute heart failure, and not inflammation, predicted longer circulatory support with norepinephrine. Taken together, this indicates an early and resolving, rather than a late and emerging vasodilatation.Trial registrationNCT02648061.

Veno‐arterial CO2 difference and lactate for prediction of early mortality after cardiac arrest

“…Although cardiac output was not systematically recorded in our study, we observed a decrease in ∆pCO 2 during the initial 24 h in both survivors and non‐survivors. This is in line with previous findings that low cardiac output typically improves within 24 h after ROSC 4,5,35 . Shock at admission was associated with a higher initial ∆pCO 2 but a ∆pCO 2 above 0.8 kPa was not linked to higher vasopressor requirement.…”

“…This is in line with previous findings that low cardiac output typically improves within 24 h after ROSC. 4,5,35 Shock at admission was associated with a higher initial ΔpCO 2 but a ΔpCO 2 above 0.8 kPa was not linked to higher vasopressor requirement. Furthermore, ΔpCO 2 was not a good predictor of early death in the subgroup of patients with shock at admission.…”

“…1 Although most deaths are secondary to hypoxic-ischemic brain injury and subsequent withdrawal of life-sustaining therapy (WLST), a significant number of patients die due to cardiovascular and/or multiorgan failure. 2,3 After return of spontaneous circulation (ROSC), patients are at risk of myocardial depression, 4 systemic inflammatory response syndrome with endothelial dysfunction and vasodilatation 5 and microcirculatory dysfunction 6,7 that may result in occult or overt circulatory shock with organ failure and an increased risk of in-hospital death. 5,[8][9][10] Early, non-neurologic death typically occurs earlier than death secondary to hypoxicischemic brain injury, often within the first 48 h after ROSC.…”

Inflammatory response after out‐of‐hospital cardiac arrest—Impact on outcome and organ failure development

“…10 Our search terms yielded 15 individual studies with 2778 patients that evaluated IL-6 as a prognostic marker. 4,[11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27] In eight of the 11 studies where AUC for the association of IL-6 with poor outcome was available, the highest AUC was recorded at admission with a median of 0.78 and values ranging between 0.71 and 0.98 (Table 1). Peak concentrations of IL-6 were consistently recorded at admission (Figure 2).…”

“…17 Elevated IL-6 levels were not associated with prolonged need for circulatory support during the first 5 days of post-resuscitation care. 27 A study by Akin et al showed that IL-6 at admission combined with NSE on day three improved prognostic performance for sixmonth neurological outcomes compared to NSE on day three in a multivariable model. 25 Admission IL-6 was also superior to admission NSE for predicting 30-day neurological outcome.…”