DOI: 10.1097/01.CCM.0000226836.72913.C4

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PMID: 16801865

Issn Print: 0090-3493

Publication Date: 2006/07/01


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Therapeutic hypothermia for anoxic brain injury following cardiac arrest: A “cool” transition toward cardiopulmonary cerebral resuscitation*

Alain Broccard

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Excerpt

Over the past decades, substantial efforts have been made to reduce the time needed to restore effective circulation after out-of-hospital cardiac arrest (1). These efforts have resulted in the development of public alarm systems (e.g., 911), the deployment of ambulances operated by trained personnel, and the availability of automatic external defibrillators in many public areas. Awareness campaigns and basic life support training for the layperson have been launched; resuscitation guidelines that incorporate the latest advances in research are regularly published. Despite encouraging progress, victims of out-of-hospital cardiac arrests still experience anoxic brain injury and not uncommonly remain comatose after arrival to the emergency department, where a work-up for possible causes of the arrest is rapidly initiated. When an ST-elevation myocardial infarction is suspected, β-blockers, aspirin, clopidogrel, heparin, and reperfusion strategies including fibrinolysis or rapid transfer to a catheterization laboratory are considered (2): We have learned that “time is muscle.” This concept has and will continue to save myocardium but is ultimately doomed to fail if subsequently these patients do not recover acceptable brain function.
Until relatively recently, the main clinical focus on postresuscitation care was the heart and circulation. It is not rare, for instance, to see cardiac medications prescribed for perfectly sound “cardiac reasons” without much consideration for their potential effects on cerebral perfusion and recovery. Such a state of mind can be partially explained by the following: a) the absence of pharmacologic interventions proven to limit or improve anoxic brain injury; b) the multitude of therapeutic options available to manage arrhythmias, myocardial infarction, and shock; c) the perception that the fate of brain is sealed on admission by the circumstances of the cardiac arrest and the time required to restore a spontaneous circulation; and d) the concept of cardiopulmonary resuscitation itself, which omits the mention of the brain as a key resuscitation target. With the advent of new effective therapy for the anoxic brain, however, resignation and a wait-and-see attitude toward anoxic brain injury must change.
In this issue of Critical Care Medicine, Dr. Oddo and colleagues (3) report the results of an interesting and well-conducted retrospective study. They evaluated the impact of a therapeutic hypothermia protocol in consecutive comatose patients who had sustained an out-of-hospital cardiac arrest. Their results show that therapeutic hypothermia can be applied successfully and safely to this population. The implementation of their protocol was associated with two-fold increase in the number of patients with a good neurologic recovery: 24 of 43 with the hypothermia protocol vs. 11 of 43 with standard treatment. These positive results are in line with two previous landmark randomized studies that clearly demonstrated improved neurologic outcome in victims of ventricular fibrillation cardiac arrest using external cooling (32–34°C) (4, 5). In contrast to the preceding two trials, in which only carefully selected patients were enrolled (up to 92% of out-of-hospital cardiac arrests initially assessed for eligibility were excluded) (3), the study by Dr. Oddo and colleagues (3) included all out-of-hospital cardiac arrests during a 2-yr period. In addition, patients with hemodynamic instability, shock, or causes of cardiac arrest other than ventricular fibrillation (pulseless electrical activity or asystole) were also included. Overall, this study shows that the benefit of hypothermia can be safely achieved in “real life,” outside the artificial settings of randomized trials, in a broad patient population. Does this mean we should be cooling down all persistently comatose victims of cardiac arrest?
Although the present retrospective study does not answer this question, it does provide some important clues. Circulatory arrest caused by pulseless electrical activity, asystole, or associated with a prolonged period of no or limited perfusion (e.g.

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