CONTEXT Laboratory investigations suggest that exposure to hyperoxia after resuscitation from cardiac arrest may worsen anoxic brain injury; however, clinical data are lacking. OBJECTIVE To test the ...hypothesis that postresuscitation hyperoxia is associated with increased mortality. DESIGN, SETTING, AND PATIENTS Multicenter cohort study using the Project IMPACT critical care database of intensive care units (ICUs) at 120 US hospitals between 2001 and 2005. Patient inclusion criteria were age older than 17 years, nontraumatic cardiac arrest, cardiopulmonary resuscitation within 24 hours prior to ICU arrival, and arterial blood gas analysis performed within 24 hours following ICU arrival. Patients were divided into 3 groups defined a priori based on PaO2 on the first arterial blood gas values obtained in the ICU. Hyperoxia was defined as PaO2 of 300 mm Hg or greater; hypoxia, PaO2 of less than 60 mm Hg (or ratio of PaO2 to fraction of inspired oxygen <300); and normoxia, not classified as hyperoxia or hypoxia. MAIN OUTCOME MEASURE In-hospital mortality. RESULTS Of 6326 patients, 1156 had hyperoxia (18%), 3999 had hypoxia (63%), and 1171 had normoxia (19%). The hyperoxia group had significantly higher in-hospital mortality (732/1156 63%; 95% confidence interval {CI}, 60%-66%) compared with the normoxia group (532/1171 45%; 95% CI, 43%-48%; proportion difference, 18% 95% CI, 14%-22%) and the hypoxia group (2297/3999 57%; 95% CI, 56%-59%; proportion difference, 6% 95% CI, 3%-9%). In a model controlling for potential confounders (eg, age, preadmission functional status, comorbid conditions, vital signs, and other physiological indices), hyperoxia exposure had an odds ratio for death of 1.8 (95% CI, 1.5-2.2). CONCLUSION Among patients admitted to the ICU following resuscitation from cardiac arrest, arterial hyperoxia was independently associated with increased in-hospital mortality compared with either hypoxia or normoxia.
Laboratory and recent clinical data suggest that hyperoxemia after resuscitation from cardiac arrest is harmful; however, it remains unclear if the risk of adverse outcome is a threshold effect at a ...specific supranormal oxygen tension, or is a dose-dependent association. We aimed to define the relationship between supranormal oxygen tension and outcome in postresuscitation patients.
This was a multicenter cohort study using the Project IMPACT database (intensive care units at 120 US hospitals). Inclusion criteria were age >17 years, nontrauma, cardiopulmonary resuscitation preceding intensive care unit arrival, and postresuscitation arterial blood gas obtained. We excluded patients with hypoxia or severe oxygenation impairment. We defined the exposure by the highest partial pressure of arterial oxygen (PaO(2)) over the first 24 hours in the ICU. The primary outcome measure was in-hospital mortality. We tested the association between PaO(2) (continuous variable) and mortality using multivariable logistic regression adjusted for patient-oriented covariates and potential hospital effects. Of 4459 patients, 54% died. The median postresuscitation PaO(2) was 231 (interquartile range 149 to 349) mm Hg. Over ascending ranges of oxygen tension, we found significant linear trends of increasing in-hospital mortality and decreasing survival as functionally independent. On multivariable analysis, a 100 mm Hg increase in PaO(2) was associated with a 24% increase in mortality risk (odds ratio 1.24 95% confidence interval 1.18 to 1.31. We observed no evidence supporting a single threshold for harm from supranormal oxygen tension.
In this large sample of postresuscitation patients, we found a dose-dependent association between supranormal oxygen tension and risk of in-hospital death.
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 (PaO2) was measured at 1 and 6 hours after return of spontaneous circulation. Hyperoxia was defined as a PaO2 >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 PaO2 and poor neurological outcome. To assess whether there was an association between other supranormal PaO2 levels and poor neurological outcome, we used other PaO2 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.
Successful resuscitation from cardiac arrest results in a post–cardiac arrest syndrome, which can evolve in the days to weeks after return of sustained circulation. The components of post–cardiac ...arrest syndrome are brain injury, myocardial dysfunction, systemic ischemia/reperfusion response, and persistent precipitating pathophysiology. Pediatric post–cardiac arrest care focuses on anticipating, identifying, and treating this complex physiology to improve survival and neurological outcomes. This scientific statement on post–cardiac arrest care is the result of a consensus process that included pediatric and adult emergency medicine, critical care, cardiac critical care, cardiology, neurology, and nursing specialists who analyzed the past 20 years of pediatric cardiac arrest, adult cardiac arrest, and pediatric critical illness peer-reviewed published literature. The statement summarizes the epidemiology, pathophysiology, management, and prognostication after return of sustained circulation after cardiac arrest, and it provides consensus on the current evidence supporting elements of pediatric post–cardiac arrest care.
Partial pressure of arterial carbon dioxide (PaCO2) is a regulator of cerebral blood flow after brain injury. We sought to test the association between PaCO2 after resuscitation from cardiac arrest ...and neurological outcome.
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, PaCO2 was measured by arterial blood gas analyses at one and six hours after ROSC. We determined the mean PaCO2 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 PaCO2 and neurological outcome.
Of the 280 patients included, the median (interquartile range) PaCO2 was 44 (37–52) mmHg and 30% had good neurological function. We found mean PaCO2 had a quadratic (inverted “U” shaped) association with good neurological outcome, with a mean PaCO2 of 68 mmHg having the highest predictive probability of good neurological outcome, and worse neurological outcome at higher and lower PaCO2. Presence of metabolic acidosis attenuated the association between PaCO2 and good neurological outcome, with a PaCO2 of 51 mmHg having the highest predictive probability of good neurological outcome among patients with metabolic acidosis.
PaCO2 has a “U” shaped association with neurological outcome, with mild to moderate hypercapnia having the highest probability of good neurological outcome.
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 followsage 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 (PaCO2) is a regulator of cerebral blood flow after brain injury. Recent guidelines for the management of cardiac arrest recommend maintaining PaCO2 at 40 ...to 45 mm Hg after successful resuscitation; however, there is a paucity of data on the prevalence of PaCO2 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 followsage ≥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 PaCO2 ≤30 mm Hg and PaCO2 ≥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 PaCO2 derangements could be potentially harmful for patients after resuscitation from cardiac arrest.
Abstract 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.
OBJECTIVE:Expert guidelines advocate hemodynamic optimization after return of spontaneous circulation (ROSC) from cardiac arrest despite a lack of empirical data on prevalence of post-ROSC ...hemodynamic abnormalities and their relationship with outcome. Our objective was to determine whether post-ROSC arterial hypotension predicts outcome among postcardiac arrest patients who survive to intensive care unit admission.
DESIGN:Cohort study utilizing the Project IMPACT database (intensive care unit admissions from 120 U.S. hospitals) from 2001–2005.
SETTING:One hundred twenty intensive care units.
PATIENTS:Inclusion criteria were1) age ≥18 yrs; 2) nontrauma; and 3) received cardiopulmonary resuscitation before intensive care unit arrival.
INTERVENTIONS:None.
MEASUREMENTS AND MAIN RESULTS:Subjects were divided into two groups1) Hypotension Present—one or more documented systolic blood pressure <90 mm Hg within 1 hr of intensive care unit arrival; or 2) Hypotension Absent—all systolic blood pressure ≥90 mm Hg. The primary outcome was in-hospital mortality. The secondary outcome was functional status at hospital discharge among survivors. A total of 8736 subjects met the inclusion criteria. Overall mortality was 50%. Post-ROSC hypotension was present in 47% and was associated with significantly higher rates of mortality (65% vs. 37%) and diminished discharge functional status among survivors (49% vs. 38%), p < .001 for both. On multivariable analysis, post-ROSC hypotension had an odds ratio for death of 2.7 (95% confidence interval, 2.5–3.0).
CONCLUSIONS:Half of postcardiac arrest patients who survive to intensive care unit admission die in the hospital. Post-ROSC hypotension is common, is a predictor of in-hospital death, and is associated with diminished functional status among survivors. These associations indicate that arterial hypotension after ROSC may represent a potentially treatable target to improve outcomes from cardiac arrest.
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