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Aims: Partial pressure of arterial carbon dioxide (PaCO 2 ) is a regulator of cerebral blood flow after brain injury. We sought to test the association between PaCO 2 after resuscitation from cardiac arrest and neurological outcome., Methods: A prospective protocol-directed cohort study across six hospitals., Inclusion Criteria: age ≥18, non-traumatic cardiac arrest, mechanically ventilated after return of spontaneous circulation (ROSC), and receipt of targeted temperature management. Per protocol, PaCO 2 was measured by arterial blood gas analyses at one and six hours after ROSC. We determined the mean PaCO 2 over this initial six hours after ROSC. The primary outcome was good neurological function at hospital discharge, defined a priori as a modified Rankin Scale ≤3. Multivariable Poisson regression analysis was used to test the association between PaCO 2 and neurological outcome., Results: Of the 280 patients included, the median (interquartile range) PaCO 2 was 44 (37-52) mmHg and 30% had good neurological function. We found mean PaCO 2 had a quadratic (inverted "U" shaped) association with good neurological outcome, with a mean PaCO 2 of 68 mmHg having the highest predictive probability of good neurological outcome, and worse neurological outcome at higher and lower PaCO 2 . Presence of metabolic acidosis attenuated the association between PaCO 2 and good neurological outcome, with a PaCO 2 of 51 mmHg having the highest predictive probability of good neurological outcome among patients with metabolic acidosis., Conclusion: PaCO 2 has a "U" shaped association with neurological outcome, with mild to moderate hypercapnia having the highest probability of good neurological outcome., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Objectives: Laboratory studies suggest elevated blood pressure after resuscitation from cardiac arrest may be protective; however, clinical data are limited. We sought to test the hypothesis that elevated postresuscitation mean arterial blood pressure is associated with neurologic outcome., Design: Preplanned analysis of a prospective cohort study., Setting: Six academic hospitals in the United States., Patients: Adult, nontraumatic cardiac arrest patients treated with targeted temperature management after return of spontaneous circulation., Interventions: Mean arterial blood pressure was measured noninvasively after return of spontaneous circulation and every hour during the initial 6 hours after return of spontaneous circulation., Measures and Main Results: We calculated the mean arterial blood pressure and a priori dichotomized subjects into two groups: mean arterial blood pressure 70-90 and greater than 90 mm Hg. The primary outcome was good neurologic function, defined as a modified Rankin Scale less than or equal to 3. The modified Rankin Scale was prospectively determined at hospital discharge. Of the 269 patients included, 159 (59%) had a mean arterial blood pressure greater than 90 mm Hg. Good neurologic function at hospital discharge occurred in 30% of patients in the entire cohort and was significantly higher in patients with a mean arterial blood pressure greater than 90 mm Hg (42%) as compared with mean arterial blood pressure 70-90 mm Hg (15%) (absolute risk difference, 27%; 95% CI, 17-37%). In a multivariable Poisson regression model adjusting for potential confounders, mean arterial blood pressure greater than 90 mm Hg was associated with good neurologic function (adjusted relative risk, 2.46; 95% CI; 2.09-2.88). Over ascending ranges of mean arterial blood pressure, there was a dose-response increase in probability of good neurologic outcome, with mean arterial blood pressure greater than 110 mm Hg having the strongest association (adjusted relative risk, 2.97; 95% CI, 1.86-4.76)., Conclusions: Elevated blood pressure during the initial 6 hours after resuscitation from cardiac arrest was independently associated with good neurologic function at hospital discharge. Further investigation is warranted to determine if targeting an elevated mean arterial blood pressure would improve neurologic outcome after cardiac arrest.

Background: Studies examining the association between hyperoxia exposure after resuscitation from cardiac arrest and clinical outcomes have reported conflicting results. Our objective was to test the hypothesis that early postresuscitation hyperoxia is associated with poor neurological outcome., Methods: This was a multicenter prospective cohort study. We included adult patients with cardiac arrest who were mechanically ventilated and received targeted temperature management after return of spontaneous circulation. We excluded patients with cardiac arrest caused by trauma or sepsis. Per protocol, partial pressure of arterial oxygen (Pao 2 ) was measured at 1 and 6 hours after return of spontaneous circulation. Hyperoxia was defined as a Pao 2 >300 mm Hg during the initial 6 hours after return of spontaneous circulation. The primary outcome was poor neurological function at hospital discharge, defined as a modified Rankin Scale score >3. Multivariable generalized linear regression with a log link was used to test the association between Pao 2 and poor neurological outcome. To assess whether there was an association between other supranormal Pao 2 levels and poor neurological outcome, we used other Pao 2 cut points to define hyperoxia (ie, 100, 150, 200, 250, 350, 400 mm Hg)., Results: Of the 280 patients included, 105 (38%) had exposure to hyperoxia. Poor neurological function at hospital discharge occurred in 70% of patients in the entire cohort and in 77% versus 65% among patients with versus without exposure to hyperoxia respectively (absolute risk difference, 12%; 95% confidence interval, 1-23). Hyperoxia was independently associated with poor neurological function (relative risk, 1.23; 95% confidence interval, 1.11-1.35). On multivariable analysis, a 1-hour-longer duration of hyperoxia exposure was associated with a 3% increase in risk of poor neurological outcome (relative risk, 1.03; 95% confidence interval, 1.02-1.05). We found that the association with poor neurological outcome began at ≥300 mm Hg., Conclusions: Early hyperoxia exposure after resuscitation from cardiac arrest was independently associated with poor neurological function at hospital discharge., (© 2018 American Heart Association, Inc.)

Aims: Recent guidelines for management of cardiac arrest recommend chest compression rates of 100-120 compressions/min. However, animal studies have found cardiac output to increase with rates up to 150 compressions/min. The objective of this study was to test the association between chest compression rates during cardiopulmonary resuscitation for in-hospital cardiac arrest (IHCA) and outcome., Methods: We conducted a prospective observational study at a single academic medical center., Inclusion Criteria: age≥18, IHCA, cardiopulmonary resuscitation performed. We analyzed chest compression rates measured by defibrillation electrodes, which recorded changes in thoracic impedance. The primary outcome was return of spontaneous circulation (ROSC). We used multivariable logistic regression to determine odds ratios for ROSC by chest compression rate categories (100-120, 121-140, >140 compressions/min), adjusted for chest compression fraction (proportion of time chest compressions provided) and other known predictors of outcome. We set 100-120 compressions/min as the reference category for the multivariable model., Results: We enrolled 222 consecutive patients and found a mean chest compression rate of 139±15. Overall 53% achieved ROSC; among 100-120, 121-140, and >140 compressions/min, ROSC was 29%, 64%, and 49% respectively. A chest compression rate of 121-140 compressions/min had the greatest likelihood of ROSC, odds ratio 4.48 (95% CI 1.42-14.14)., Conclusions: In this sample of adult IHCA patients, a chest compression rate of 121-140 compressions/min had the highest odds ratio of ROSC. Rates above the currently recommended 100-120 compressions/min may improve the chances of ROSC among IHCA patients., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)

Objectives: Guidelines for post-cardiac arrest care recommend blood pressure optimization as one component of neuroprotection. Although some retrospective clinical studies suggest that postresuscitation hypotension may be harmful, and laboratory studies suggest that a postresuscitation hypertensive surge may be protective, empirical data are few. In this study, we prospectively measured blood pressure over time during the postresuscitation period and tested its association with neurologic outcome., Design: Single center, prospective observational study from 2009 to 2012., Patients: Inclusion criteria were age 18 years old or older, prearrest independent functional status, resuscitation from cardiac arrest, and comatose immediately after resuscitation., Measurements and Main Results: Our research protocol measured blood pressure noninvasively every 15 minutes for the first 6 hours after resuscitation. We calculated the 0- to 6-hour time-weighted average mean arterial pressure and used multivariable logistic regression to test the association between increasing time-weighted average mean arterial pressures and good neurologic outcome, defined as Cerebral Performance Category 1 or 2 at hospital discharge. Among 151 patients, 44 (29%) experienced good neurologic outcome. The association between blood pressure and outcome appears to have a threshold effect at time-weighted average mean arterial pressure value of 70 mm Hg. This threshold (mean arterial pressure > 70 mm Hg) had the strongest association with good neurologic outcome (odds ratio, 4.11; 95% CI, 1.34-12.66; p = 0.014). A sustained intrinsic hypertensive surge was relatively uncommon and was not associated with neurologic outcome., Conclusions: We found that time-weighted average mean arterial pressure was associated with good neurologic outcome at a threshold of mean arterial pressure greater than 70 mm Hg.

Objectives: Recent guidelines for the treatment of postcardiac arrest syndrome recommend optimization of vital organ perfusion after return of spontaneous circulation to reduce the risk of postresuscitation multiple organ injury. However, the prevalence of extracerebral multiple organ dysfunction in postcardiac arrest patients and its association with in-hospital mortality remain unclear., Design: Single-center, prospective observational study., Setting: Urban academic medical center., Patients: Postcardiac arrest patients. Inclusion criteria were as follows: age older than 17 years, nontrauma cardiac arrest, and comatose after return of spontaneous circulation., Interventions: We prospectively captured all extracerebral components of the Sequential Organ Failure Assessment score over the first 72 hours after return of spontaneous circulation. The primary outcome measure was in-hospital mortality. We used multivariate logistic regression to determine if multiple organ dysfunction (defined as the highest extracerebral Sequential Organ Failure Assessment score) was an independent predictor of death, after adjustment for the presence of cerebral injury (defined as not following commands at any point over 0-72 hr)., Measurements and Main Results: We enrolled 203 postcardiac arrest patients; 96% had some degree of extracerebral organ dysfunction and 66% had severe dysfunction in two or more extracerebral organ systems. The most common extracerebral organ failures were cardiovascular (i.e., vasopressor dependence) and respiratory (i.e., oxygenation impairment). The highest extracerebral Sequential Organ Failure Assessment score over 72 hours had an independent association with in-hospital mortality (odds ratio 1.95 [95% CI, 1.15-3.29]). Of the individual organ systems, only the cardiovascular and respiratory Sequential Organ Failure Assessment scores had an independent association with in-hospital mortality., Conclusions: The results of this study support the hypothesis that extracerebral organ dysfunction is common and associated with mortality in postcardiac arrest syndrome. This association appears to be driven by postresuscitation hemodynamic dysfunction and oxygenation impairment. Further research is needed to determine the value of hemodynamic and oxygenation optimization as a part of treatment strategies for patients with postcardiac arrest syndrome.

Background: Partial pressure of arterial CO2 (Paco(2)) is a regulator of cerebral blood flow after brain injury. Recent guidelines for the management of cardiac arrest recommend maintaining Paco(2) at 40 to 45 mm Hg after successful resuscitation; however, there is a paucity of data on the prevalence of Paco(2) derangements during the post-cardiac arrest period and its association with outcome., Methods and Results: We analyzed a prospectively compiled and maintained cardiac arrest registry at a single academic medical center. Inclusion criteria are as follows: age ≥18, nontrauma arrest, and comatose after return of spontaneous circulation. We analyzed arterial blood gas data during 0 to 24 hours after the return of spontaneous circulation and determined whether patients had exposure to hypocapnia and hypercapnia (defined as Paco(2) ≤30 mm Hg and Paco(2) ≥50 mm Hg, respectively, based on previous literature). The primary outcome was poor neurological function at hospital discharge, defined as Cerebral Performance Category ≥3. We used multivariable logistic regression, with multiple sensitivity analyses, adjusted for factors known to predict poor outcome, to determine whether post-return of spontaneous circulation hypocapnia and hypercapnia were independent predictors of poor neurological function. Of 193 patients, 52 (27%) had hypocapnia only, 63 (33%) had hypercapnia only, 18 (9%) had both hypocapnia and hypercapnia exposure, and 60 (31%) had no exposure; 74% of patients had poor neurological outcome. Hypocapnia and hypercapnia were independently associated with poor neurological function, odds ratio 2.43 (95% confidence interval, 1.04-5.65) and 2.20 (95% confidence interval, 1.03-4.71), respectively., Conclusions: Hypocapnia and hypercapnia were common after cardiac arrest and were independently associated with poor neurological outcome. These data suggest that Paco(2) derangements could be potentially harmful for patients after resuscitation from cardiac arrest.

Objective: Clinical trials of therapeutic hypothermia (TH) after cardiac arrest excluded patients with persistent hemodynamic instability after return of spontaneous circulation (ROSC), and thus equipoise may exist regarding use of TH in these patients. Our objective was to determine if TH is associated with worsening hemodynamic instability among patients who are vasopressor-dependent after ROSC., Methods: We performed a prospective observational study in vasopressor-dependent post-cardiac arrest patients. Inclusion criteria were age >17, non-trauma cardiac arrest, comatose after ROSC, and persistent vasopressor dependence. The decision to initiate TH (33-34 ° C) was made by the treating physician. We measured cumulative vasopressor index (CVI) and mean arterial pressure (MAP) every 15 min during the first 6h after ROSC. The outcome measures were change in CVI (primary outcome) and MAP (secondary outcome) over time. We graphed median CVI and MAP over time for the treated and not treated cohorts, and used propensity adjusted repeated measures mixed models to test for an association between TH induction and change in CVI or MAP over time., Results: Seventy-five post-cardiac arrest patients were included (35 treated; 40 not treated). We observed no major differences in CVI or MAP over time between the treated and not treated cohorts. In the mixed models we found no statistically significant association between TH induction and changes in CVI or MAP., Conclusion: In patients with vasopressor-dependency after cardiac arrest, the induction of hypothermia was not associated with a decrease in mean arterial pressure or increase in vasopressor requirement., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

Background: The post-cardiac arrest syndrome (period of critical illness following return of spontaneous circulation [ROSC]) is a promising window of opportunity for clinical trials of therapeutic interventions to improve outcome from cardiac arrest. However, the methodological rigor of post-ROSC trials and the ability to compare or pool data on treatment effects across studies requires consistent and appropriate outcome measures. We aimed to determine the current degree of uniformity of outcome measures in clinical trials of post-ROSC interventions., Methods: We conducted a systematic review of Cochrane Library, MEDLINE, EMBASE, CINAHL, conference proceedings, and clinical trial registrations using a comprehensive strategy. We identified experimental or quasi-experimental trials testing post-ROSC interventions in adults. Four authors independently extracted data and assessed study quality using standardized instruments., Results: The search yielded 33 potential studies, of which 13 randomized controlled trials (n=1937) were included in the final analysis. Seven trials tested pharmacologic therapies and six tested non-pharmacologic therapies. Our main finding is that heterogeneity in the selection and reporting of outcomes limited comparability of results across studies. No two trials used exactly the same primary outcome, and timing of measurement varied widely. We found only two commonalities: (1) indices of functional survival were used rather than survival alone, and (2) ordinal scales of neurological function were collapsed into clinically meaningful groups ("good" versus "bad" outcome)., Conclusion: Currently there is a lack of uniformity in selection and reporting of outcome measures among trials of post-ROSC interventions. Achieving consensus would be an important advance for resuscitation science.

Aim: After return of spontaneous circulation (ROSC) from cardiac arrest, profound myocardial stunning and systemic inflammation may cause hemodynamic alterations; however, the prevalence of post-ROSC hemodynamic instability and the strength of association with outcome have not been established. We tested the hypothesis that exposure to arterial hypotension after ROSC occurs commonly (>50%) and is an independent predictor of death., Methods: Single-center retrospective cohort study of all post-cardiac arrest patients over 1 year., Inclusion Criteria: (1) age >17; (2) non-trauma; (3) sustained ROSC after cardiac arrest. Using the Jones criteria, subjects were assigned to one of two groups based on the presence of hypotension within 6h after ROSC: (1) exposures-two or more systolic blood pressures (SBPs) <100mmHg or (2) non-exposures-less than two SBP <100mmHg. The primary outcome was in-hospital mortality. We compared mortality rates between groups and used multivariate logistic regression to determine if post-ROSC hypotension independently predicted death., Results: 102 subjects met inclusion criteria. In-hospital mortality was 75%. Exposure to hypotension occurred in 66/102 (65%) and was associated with significantly higher mortality (83%) compared to non-exposures (58%, p=0.01). In a model controlling for common confounding variables (age, pre-arrest functional status, arrest rhythm, and provision of therapeutic hypothermia (HT)), early exposure to hypotension was a strong independent predictor of death (OR 3.5 [95% CI 1.3-9.6])., Conclusions: Early exposure to arterial hypotension after ROSC was common and an independent predictor of death. These data suggest that post-ROSC hypotension could potentially represent a therapeutic target in post-cardiac arrest care.

Objectives: Induced hypothermia (HT) after cardiac arrest improved outcomes in randomized trials. Current post-cardiac arrest treatment guidelines advocate HT; however, utilization in practice remains low. One reported barrier to adoption is clinician concern over potential technical difficulty of HT. We hypothesized that using a standardized order set, clinicians could achieve HT target temperature in routine practice with equal or better efficiency than that observed in randomized trials., Methods: After a multidisciplinary HT education program, we implemented a standardized order set for HT induction and maintenance including sedation and paralysis, intravenous cold saline infusion, and an external cooling apparatus, with a target temperature range of 33-34 degrees C. We performed a retrospective analysis of a prospectively compiled and maintained registry of cardiac arrest patients with HT attempted (intent-to-treat) over the first year of implementation. The primary outcome measures were defined a priori by extrapolating treatment arm data from the largest and most efficacious randomized trial: 1) successful achievement of target temperature for >or=85% of patients in the cohort and 2) median time from return of spontaneous circulation (ROSC) to achieving target temperature <8 hours., Results: Clinicians attempted HT on 23 post-cardiac arrest patients (arrest location: 78% out-of-hospital, 22% in-hospital; initial rhythm: 26% ventricular fibrillation/tachycardia, 70% pulseless electrical activity or asystole) and achieved the target temperature in 22/23 (96%) cases. Median time from ROSC to target temperature was 4.4 (interquartile range 2.8-7.2) hours. Complication rates were low., Conclusions: Using a standardized order set, clinicians can achieve HT target temperature in routine practice.