Background This study aimed to investigate bradycardia as an adverse effect after administration of dexmedetomidine during 33℃ target temperature management.
Methods A retrospective study was conducted on patients who underwent 33℃ target temperature management in the emergency department during a 49-month study period. We collected data including age, sex, weight, diagnosis, bradycardia occurrence, target temperature management duration, sedative drug, and several clinical and laboratory results. We conducted logistic regression for an analysis of factors associated with bradycardia.
Results A total of 68 patients were selected. Among them, 39 (57.4%) showed bradycardia, and 56 (82.4%) were treated with dexmedetomidine. The odds ratio for bradycardia in the carbon monoxide poisoning group compared to the cardiac arrest group and in patients with higher body weight were 7.448 (95% confidence interval [CI] 1.834-30.244, p = 0.005) and 1.058 (95% CI 1.002-1.123, p = 0.044), respectively. In the bradycardia with dexmedetomidine group, the infusion rate of dexmedetomidine was 0.41 ± 0.15 μg/kg/h. Decisions of charged doctor’s were 1) slowing infusion rate and 2) stopping infusion or administering atropine for bradycardia. No cases required cardiac pacing or worsened to asystole.
Conclusions Despite the frequent occurrence of bradycardia after administration of dexmedetomidine during 33℃ target temperature management, bradycardia was completely recovered after reducing infusion rate or stopping infusion. However, reducing the infusion rate of dexmedetomidine lower than the standard maintenance dose could be necessary to prevent bradycardia from developing in patients with higher body weight or carbon monoxide poisoning during 33℃ targeted temperature management.
BACKGROUND The aim of this study was to assess the relationship between acute physiologic and chronic health examination (APACHE) II and sequential organ failure assessment (SOFA) scores and outcomes of post-cardiac arrest patients treated with therapeutic hypothermia (TH). METHODS Out-of-hospital cardiac arrest (OHCA) survivors treated with TH between January 2010 and December 2012 were retrospectively evaluated. We captured all components of the APACHE II and SOFA scores over the first 48 hours after intensive care unit (ICU) admission (0 h). The primary outcome measure was in-hospital mortality and the secondary outcome measure was neurologic outcomes at the time of hospital discharge. Receiver-operating characteristic and logistic regression analysis were used to determine the predictability of outcomes with serial APACHE II and SOFA scores. RESULTS A total of 138 patients were enrolled in this study. The area under the curve (AUC) for APACHE II scores at 0 h for predicting in-hospital mortality and poor neurologic outcomes (cerebral performance category: 3-5) was more than 0.7, and for SOFA scores from 0 h to 48 h the AUC was less than 0.7. Odds ratios used to determine associations between APACHE II scores from 0 h to 48 h and in-hospital mortality were 1.12 (95% confidence interval [CI], 1.03-1.23), 1.13 (95% CI, 1.04-1.23), and 1.18 (95% CI, 1.07-1.30). CONCLUSIONS APACHE II, but not SOFA score, at the time of ICU admission is a modest predictor of in-hospital mortality and poor neurologic outcomes at the time of hospital discharge for patients who have undergone TH after return of spontaneous circulation following OHCA.
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