Abstract
At laboratory and clinical levels, therapeutic hypothermia has been shown to improve neurologic outcomes and mortality following cardiac arrest. We reviewed each cardiac arrest in our community-based Veterans Affairs Medical Center over a three-year period. The majority of cases were in-hospital arrests associated with initial pulseless electrical activity or asystole. Of a total of 100 patients suffering 118 cardiac arrests, 29 arrests involved comatose survivors, with eight patients completing therapeutic cooling. Cerebral performance category scores at discharge and six months were significantly better in the cooled cohort versus the noncooled cohort, and, in every case except for one, cooling was offered for appropriate reasons. Mean time to initiation of cooling protocol was 3.7 hours and mean time to goal temperature of 33°C was 8.8 hours, and few complications clearly related to cooling were noted in our case series. While in-patient hospital mortality of cardiac arrest was high at 65% mortality during hospital admission, therapeutic hypothermia was safe and feasible at our center. Our cooling times and incidence of favorable outcomes are comparable to previously published reports. This study demonstrates the feasibility of implementing, a cooling protocol a community setting, and the role of neurologists in ensuring effective hospital-wide implementation.
Highlights
Comatose survivors of cardiac arrest notoriously have poor outcomes including significant neurological deficits and persistent vegetative state
Some authors have called upon neurologists to become more active in management of these patients beyond offering prognosis and in helping create hospitalwide policies given that therapeutic hypothermia remains one of the only proven treatments for improving neurologic outcome [21], and a recent report from Prior and colleagues demonstrated the success of planning and implementing a therapeutic hypothermia protocol in a community-based hospital setting [20]. In this retrospective analysis, we report our experience with implementation of therapeutic hypothermia for comatose cardiac arrest survivors and its outcomes in an academically affiliated community-based Veterans Affairs medical center in which the majority of events were in-hospital
The mechanism of arrest involved a primary pulmonary arrest in 8 arrests (21%), primary cardiac in 12 (32%), gastrointestinal bleeding or catastrophe in 5 (13%), intraoperative event in 2 (5%), sepsis or infection in 4 (11%), and unknown or other etiology in 7 (18%). Comorbidities within this cohort included coronary artery disease (CAD) or congestive heart failure (CHF) in 17 patients (45%), cardiovascular risk factors defined as hypertension, diabetes, dyslipidemia, or tobacco use disorder in 21 (55%), cancer diagnosis in 9 (24%), pulmonary disease in 8 (21%), gastrointestinal bleeding or end-stage liver disease in 7 (18%), end-stage renal disease in 5 (13%), human immunodeficiency virus (HIV) or hepatitis infection in 2 (5%), and history or ongoing substance or alcohol abuse in 5 (13%)
Summary
Comatose survivors of cardiac arrest notoriously have poor outcomes including significant neurological deficits and persistent vegetative state. Animal and human studies have demonstrated that hypothermia reduces brain metabolism and oxygen and ATP consumption [3, 4], reduces the release of excitotoxic glutamate via regulation of transmembrane electrolyte transport [5], protects against oxidative stress and lipid peroxidation [6, 7], and alters gene expression (see reviews by Holzer [8], Liu and Yenari [9], and Yenari et al [10]) to promote brain cell survival after cerebral ischemia These physiologic effects were shown to have clinical significance with the publication in 2002 of two major clinical trials of therapeutic hypothermia in comatose survivors of cardiac arrest. These studies, by Bernard and colleagues [11] in Australia and by the Hypothermia after Cardiac Arrest Study Group [12] in Europe, showed that cooling these patients improved neurological outcomes and reduced rate of death
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