Background: Cardiac arrest in hospitalized children is associated with poor outcomes, but no contemporary study has reported whether the trends in survival have changed over time. In this study, we examined temporal trends in survival for pediatric patients with an in-hospital pulseless cardiac arrest and pediatric patients with a nonpulseless cardiopulmonary resuscitation event from 2000 to 2018. Methods: This was an observational study of hospitalized pediatric patients (≤18 years of age) who received cardiopulmonary resuscitation from January 2000 to December 2018 and were included in the Get With The Guidelines-Resuscitation registry, a United States–based in-hospital cardiac arrest registry. The primary outcome was survival to hospital discharge, and the secondary outcome was return of spontaneous circulation (binary outcomes). Generalized estimation equations were used to obtain unadjusted trends in outcomes over time. Separate analyses were performed for patients with a pulseless cardiac arrest and patients with a nonpulseless event (bradycardia with poor perfusion) requiring cardiopulmonary resuscitation. A subgroup analysis was conducted for shockable versus nonshockable initial rhythms in pulseless events. Results: A total of 7433 patients with a pulseless cardiac arrest and 5751 patients with a nonpulseless event were included for the analyses. For pulseless cardiac arrests, survival was 19% (95% CI, 11%–29%) in 2000 and 38% (95% CI, 34%–43%) in 2018, with an absolute change of 0.67% (95% CI, 0.40%–0.95%; P <0.001) per year, although the increase in survival appeared to stagnate following 2010. Return of spontaneous circulation also increased over time, with an absolute change of 0.83% (95% CI, 0.53%–1.14%; P <0.001) per year. We found no interaction between survival to hospital discharge and the initial rhythm. For nonpulseless events, survival was 57% (95% CI, 39%–75%) in 2000 and 66% (95% CI, 61%–72%) in 2018, with an absolute change of 0.80% (95% CI, 0.32%–1.27%; P =0.001) per year. Conclusions: Survival has improved for pediatric events requiring cardiopulmonary resuscitation in the United States, with a 19% absolute increase in survival for in-hospital pulseless cardiac arrests and a 9% absolute increase in survival for nonpulseless events between 2000 and 2018. However, survival from pulseless cardiac arrests appeared to have reached a plateau following 2010.

Introduction: Mitochondrial dysfunction leading to impairment of oxygen extraction, referred to as cytopathic hypoxia, contributes to morbidity in sepsis. Oxygen consumption (VO 2 ) may be a useful measure of the severity of cytopathic hypoxia. We monitored VO 2 and carbon dioxide production (VCO 2 ) in septic patients and investigated the association with hospital survival. Methods: We retrospectively identified adult (!18 years) septic patients from a larger prospective observational cohort of critically ill patients on mechanical ventilation. A gas-exchange monitor recorded continuous VO 2 and VCO 2 for up to 48 h. We then tested the association of median VO 2 , VCO 2 , respiratory quotient (RQ), and the VO 2 :lactate ratio with survival. Results: A total of 46 septic patients were included in the analysis, of whom 28 (61%) survived. Overall median VO 2 was not associated with survival (3.72 mL/kg/min [IQR: 3.39, 4.92] in survivors and 3.42 mL/ kg/min [IQR: 2.97, 5.26] in non-survivors, P ¼ 0.12). The overall median VCO 2 and RQ were also not associated with survival. Adjusting for age and the presence of shock did not change these results. The VO 2 :lactate ratio was associated with survival (adjusted OR 2.17 [95% CI 1.12, 4.22] per unit increase in ratio, P ¼ 0.03). The percent change in median VCO 2 was 11.6% [IQR: À8.2, 28.7] in survivors compared with À8.3% [IQR: À18.0, 4.7] in non-survivors (P ¼ 0.03). The percent changes in median VO 2 and RQ were not different between groups. Conclusion: The VO 2 :lactate ratio was significantly higher in survivors, while there was no association between median VO 2 alone and survival. There was a significant difference in change in VCO 2 over time between survivors and non-survivors.

Introduction: Ubiquinol (reduced coenzyme Q10) is essential for adequate aerobic metabolism. The objective of this trial was to determine whether ubiquinol administration in patients resuscitated from cardiac arrest could increase physiological coenzyme Q10 levels, improve oxygen consumption, and reduce neurological biomarkers of injury.Materials and methods: This was a randomized, double-blind, placebo-controlled trial in patients successfully resuscitated from cardiac arrest.Patients were randomized to receive enteral ubiquinol (300 mg) or placebo every 12 h for up to 7 days. The primary endpoint was total coenzyme Q10 plasma levels at 24 h after enrollment. Secondary endpoints included neuron specific enolase, S100B, lactate, cellular and global oxygen consumption, neurological status, and in-hospital mortality.Results: Forty-three patients were included in the modified intention-to-treat analysis. Median coenzyme Q10 levels were significantly higher in the ubiquinol group as compared to the placebo group at 24 h (441 [IQR, 215À510] hg/mL vs. 113 [IQR, 94À208] hg/mL, P < 0.001). Similar results were observed at 48 and 72 h. There were no differences between the two groups in any of the secondary endpoints. Median neuron specific enolase levels were not different between the two groups at 24 h (16.8 [IQR, 9.5À19.8] hg/mL vs. 8.2 [IQR, 4.3À19.1] hg/mL, P = 0.61).Conclusions: Administration of enteral ubiquinol increased plasma coenzyme Q10 levels in post-cardiac arrest patients as compared to placebo. There were no differences in neurological biomarkers and oxygen consumption between the two groups.