Therapeutic Hypothermia after Cardiac Arrest: Experience at an Academically Affiliated Community-Based Veterans Affairs Medical Center

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.

Hypothermia and Pharmacological Regimens that Prevent Overexpression and Overactivity of the Extracellular Calcium-Sensing Receptor Protect Neurons against Traumatic Brain Injury

“…One approach for such investigations is to delineate mechanisms rendering the effects of the already known neuroprotective regimens, such as hypothermia. 6,26,27 In this study, we confirmed the neuroprotective action of hypothermia in TBI by demonstrating its ability to reduce brain lesion size and to facilitate the recovery of motor function in an established CCI injury model. We further showed that CCI-induced CaSR overexpression and concurrent down-regulation of GABA-B-R1 occurred before apparent neurodegeneration and that these effects were partially averted by hypothermia, suggesting that alterations in CaSR and GABA-B-R1 expression may be a part of brain injury response after TBI.…”

Urban and Suburban Hospital System Implementation of Multipoint Access Targeted Temperature Management in Postcardiac Arrest Patients

“…This eliminated the delay of staff checking with one individual before implementing the process. Time metrics for the induction phase improved with increased Code ICE experiences ( Jimmink et al, 2008;Kilgannon et al, 2008;Prior et al, 2010;Shah et al, 2011;Gessner et al, 2012). This pattern is consistent with better provider and patient outcomes with increased patient volumes (Nichol et al, 2010).…”