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.
Preplanned analysis of a prospective cohort study.
Six academic hospitals in the United States.
Adult, nontraumatic cardiac arrest patients treated with targeted temperature management after return of spontaneous circulation.
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.
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).
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.
1Department of Emergency Medicine, Cooper University Hospital, Cooper Medical School of Rowan University, Camden, NJ.
2Department of Emergency Medicine, Indiana University School of Medicine, Indianapolis, IN.
3Department of Emergency Medicine, University of Mississippi Medical Center, Jackson, MS.
4Division of Critical Care Medicine, Department of Medicine, Cooper University Hospital, Cooper Medical School of Rowan University, Camden, NJ.
5Department of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA.
6Division of Critical Care Medicine, Departments of Emergency Medicine and Anesthesiology, Washington University School of Medicine, St. Louis, MO.
7Center for Resuscitation Science and Department of Emergency Medicine, University of Pennsylvania, Philadelphia, PA.
*See also p. 138.
All authors have made substantial contributions to this article: Dr. Trzeciak supervised all aspects of the study and takes responsibility for the article as a whole. Drs. Roberts, Kilgannon, and Trzeciak conceived this study. Dr. Roberts, Dr. Kilgannon, and Ms. Shea managed the data. Drs. Roberts and Trzeciak analyzed the data and interpreted results. Drs. Roberts and Trzeciak drafted the article, and all authors contributed substantially to its revision. All authors took part in acquiring the data and approved the article in its final form.
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Supported, in part, by the National Heart, Lung, and Blood Institute (United States), R01HL112815 and K23HL126979.
Dr. Roberts’ institution received funding from National Heart, Lung, and Blood Institute (NHLBI). Dr. Kilgannon’s institution received funding from NHLBI R01HL112815 and K23HL126979. Drs. Hunter’s, Donnino’s, Shapiro’s institution received funding from the National Institutes of Health (NIH). Dr. Puskarich’s institution received funding from NHLBI, K23GM113041, National Institute for General Medical Sciences for salary support, and he received funding from NIH Loan Repayment Program. Dr. Shea’s institution received funding from NIH R01, NIH K23. Dr. Jones’ institution received funding from Roche, AstraZeneca, and Hologic, and he disclosed he is an investigator on studies for which his department has received research grants from Roche, AstraZeneca, Janssen, and Hologic. Dr. Abella’s institution received funding from NHLBI, Medtronic Foundation, Patient-Centered Outcomes Research Institute, American Heart Association, and Physio-Control, and he received funding from Physio-Control, CardioReady, and CR Bard. Drs. Roberts, Kilgannon, Hunter, Puskarich, Shea, Donnino, Shapiro, and Trzeciak received support for article research from the NIH. The remaining authors have disclosed that they do not have any potential conflicts of interest.
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