Abstract
Out-of-hospital cardiac arrest (CA) remains a leading cause of sudden morbidity and mortality; however, outcomes have continued to improve in the era of targeted temperature management (TTM). In this review, we highlight the clinical use of TTM, and provide an updated summary of multimodality monitoring possible in a modern ICU. TTM is neuroprotective for survivors of CA by inhibiting multiple pathophysiologic processes caused by anoxic brain injury, with a final common pathway of neuronal death. Current guidelines recommend the use of TTM for out-of-hospital CA survivors who present with a shockable rhythm. Further studies are being completed to determine the optimal timing, depth and duration of hypothermia to optimize patient outcomes. Although a multidisciplinary approach is necessary in the CA population, neurologists and neurointensivists are central in selecting TTM candidates and guiding patient care and prognostic evaluation. Established prognostic tools include clinal exam, SSEP, EEG and MR imaging, while functional MRI and invasive monitoring is not validated to improve outcomes in CA or aid in prognosis. We recommend that an evidence-based TTM and prognostication algorithm be locally implemented, based on each institution's resources and limitations. Given the high incidence of CA and difficulty in predicting outcomes, further study is urgently needed to determine the utility of more recent multimodality devices and studies.
Highlights
Out-of-hospital cardiac arrest (CA) remains a leading cause of sudden morbidity and mortality
We suggest that paralytics be used during induction and rewarming phases of temperature management (TTM), to facilitate tight temperature control and to prevent shivering
Clinical seizures are reported from TTM trials to occur in over 25% of patients [32], while malignant EEG features are recorded in up to 86% of patients who remain comatose after resuscitation and re-warming [43]
Summary
Out-of-hospital cardiac arrest (CA) remains a leading cause of sudden morbidity and mortality. Neuronal injury occurs when the severity and duration of ischemia is sufficient to cause depolarization of the neuronal plasma membrane In animal models, this has been demonstrated to occur when blood flow falls below 10 mL/100 g per minute [5, 6]. Global ischemia causes a depletion of intracellular ATP, with subsequent failure of ATP-dependent ionic channels This results in accumulation of interstitial potassium with subsequent cell membrane depolarization. In vivo measurements of calcium demonstrate that in the acute ischemic period, cytosolic levels increase exponentially within 8 min of ischemia in vulnerable brain regions, levels can return to baseline within 30–60 min if reperfusion occurs [5, 10]. Animal models have demonstrated that rapid infiltration of neutrophil and pro-inflammatory T-lymphocytes into the brain occur as early as 3 h following ROSC, and last up to 3 days [11]
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