Michael N Young1, Ryan D Hollenbeck2, Jeremy S Pollock3, Jennifer L Giuseffi4, Li Wang5, Frank E Harrell5, John A McPherson6. 1. Division of Cardiovascular Medicine (MNY, JAM), Vanderbilt University Medical Center, Nashville, TN, USA. Electronic address: michael.young@vanderbilt.edu. 2. Mercy Cardiology Clinic (RDH), Mercy Medical Center-Cedar Rapids, Cedar Rapids, IA, USA. 3. Division of Cardiovascular Medicine (JSP), University of Maryland Medical Center, Baltimore, MD, USA. 4. Cardiovascular Division (JLG), WellStar Medical Group, Marietta, GA, USA. 5. Department of Biostatistics (LW, FEH), Vanderbilt University Medical Center, Nashville, TN, USA. 6. Division of Cardiovascular Medicine (MNY, JAM), Vanderbilt University Medical Center, Nashville, TN, USA.
Abstract
INTRODUCTION: To determine if higher achieved mean arterial blood pressure (MAP) during treatment with therapeutic hypothermia (TH) is associated with neurologically intact survival following cardiac arrest. METHODS: Retrospective analysis of a prospectively collected cohort of 188 consecutive patients treated with TH in the cardiovascular intensive care unit of an academic tertiary care hospital. RESULTS: Neurologically intact survival was observed in 73/188 (38.8%) patients at hospital discharge and in 48/162 (29.6%) patients at a median follow up interval of 3 months. Patients in shock at the time of admission had lower baseline MAP at the initiation of TH (81 versus 87mmHg; p=0.002), but had similar achieved MAP during TH (80.3 versus 83.7mmHg; p=0.11). Shock on admission was associated with poor survival (18% versus 52%; p<0.001). Vasopressor use among all patients was common (84.6%) and was not associated with increased mortality. A multivariable analysis including age, initial rhythm, time to return of spontaneous circulation, baseline MAP and achieved MAP did not demonstrate a relationship between MAP achieved during TH and poor neurological outcome at hospital discharge (OR 1.28, 95% CI 0.40-4.06; p=0.87) or at outpatient follow up (OR 1.09, 95% CI 0.32-3.75; p=0.976). CONCLUSION: We did not observe a relationship between higher achieved MAP during TH and neurologically intact survival. However, shock at the time of admission was clearly associated with poor outcomes in our study population. These data do not support the use of vasopressors to artificially increase MAP in the absence of shock. There is a need for prospective, randomized trials to further define the optimum blood pressure target during treatment with TH.
INTRODUCTION: To determine if higher achieved mean arterial blood pressure (MAP) during treatment with therapeutic hypothermia (TH) is associated with neurologically intact survival following cardiac arrest. METHODS: Retrospective analysis of a prospectively collected cohort of 188 consecutive patients treated with TH in the cardiovascular intensive care unit of an academic tertiary care hospital. RESULTS: Neurologically intact survival was observed in 73/188 (38.8%) patients at hospital discharge and in 48/162 (29.6%) patients at a median follow up interval of 3 months. Patients in shock at the time of admission had lower baseline MAP at the initiation of TH (81 versus 87mmHg; p=0.002), but had similar achieved MAP during TH (80.3 versus 83.7mmHg; p=0.11). Shock on admission was associated with poor survival (18% versus 52%; p<0.001). Vasopressor use among all patients was common (84.6%) and was not associated with increased mortality. A multivariable analysis including age, initial rhythm, time to return of spontaneous circulation, baseline MAP and achieved MAP did not demonstrate a relationship between MAP achieved during TH and poor neurological outcome at hospital discharge (OR 1.28, 95% CI 0.40-4.06; p=0.87) or at outpatient follow up (OR 1.09, 95% CI 0.32-3.75; p=0.976). CONCLUSION: We did not observe a relationship between higher achieved MAP during TH and neurologically intact survival. However, shock at the time of admission was clearly associated with poor outcomes in our study population. These data do not support the use of vasopressors to artificially increase MAP in the absence of shock. There is a need for prospective, randomized trials to further define the optimum blood pressure target during treatment with TH.
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