Hyperthermia is a potential factor for an unfavorable functional neurologic recovery after successful cardiopulmonary resuscitation.

Conventional cooling methods to induce mild therapeutic hypothermia seem to improve survival and neurologic outcome after cardiac arrest. Our review supports the current best medical practice as recommended by the International Resuscitation Guidelines.

We investigated the relationship between lactate clearance and outcome in patients surviving the first 48 hours after cardiac arrest. We conducted the study in the emergency department of an urban tertiary care hospital. We analyzed the data for all 48-hour survivors after successful resuscitation from cardiac arrest during a 10-year period. Serial lactate measurements, demographic data, and key cardiac arrest data were correlated to survival and best neurologic outcome within 6 months after cardiac arrest. Parameters showing significant results in univariate analysis were tested for significance in a logistic regression model. Of 1502 screened patients, 394 were analyzed. Survivors (n = 194, 49%) had lower lactate levels on admission (median, 7.8 [interquartile range, 5.4-10.8] vs 9 [6.6-11.9] mmol/L), after 24 hours (1.4 [1-2.5] vs 1.7 [1.1-3] mmol/L), and after 48 hours (1.2 [0.9-1.6] vs 1.5 [1.1-2.3] mmol/L). Patients with favorable neurologic outcome (n = 186, 47%) showed lower levels on admission (7.6 [5.4-10.3] vs 9.2 [6.7-12.1] mmol/L) and after 48 hours (1.2 [0.9-1.6] vs 1.5 [1-2.2] mmol/L). In multivariate analysis, lactate levels at 48 hours were an independent predictor for mortality (odds ratio [OR]: 1.49 increase per mmol/L, 95% confidence interval [CI]: 1.17-1.89) and unfavorable neurologic outcome (OR: 1.28 increase per mmol/L, 95% CI: 1.08-1.51). Lactate levels higher than 2 mmol/L after 48 hours predicted mortality with a specificity of 86% and poor neurologic outcome with a specificity of 87%. Sensitivity for both end points was 31%. Lactate at 48 hours after cardiac arrest is an independent predictor of mortality and unfavorable neurologic outcome. Persisting hyperlactatemia over 48 hours predicts a poor prognosis.

Evidence of moderate quality suggests that conventional cooling methods provided to induce mild therapeutic hypothermia improve neurological outcome after cardiac arrest, specifically with better outcomes than occur with no temperature management. We obtained available evidence from studies in which the target temperature was 34°C or lower. This is consistent with current best medical practice as recommended by international resuscitation guidelines for hypothermia/targeted temperature management among survivors of cardiac arrest. We found insufficient evidence to show the effects of therapeutic hypothermia on participants with in-hospital cardiac arrest, asystole or non-cardiac causes of arrest.

We found no evidence of substantial differences in total mortality between several vasopressors. Dopamine increases the risk of arrhythmia compared with norepinephrine and might increase mortality. Otherwise, evidence of any other differences between any of the six vasopressors examined is insufficient. We identified low risk of bias and high-quality evidence for the comparison of norepinephrine versus dopamine and moderate to very low-quality evidence for all other comparisons, mainly because single comparisons occasionally were based on only a few participants. Increasing evidence indicates that the treatment goals most often employed are of limited clinical value. Our findings suggest that major changes in clinical practice are not needed, but that selection of vasopressors could be better individualised and could be based on clinical variables reflecting hypoperfusion.