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Electronic letters published:
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IN RESPONSE:
Therapeutic Hypothermia after Cardiac Arrest, slow to catch on
Correction
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A. Maziar Zafari, MD/PhD Emory University, Bakhtiar Ali
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azafari{at}emory.edu A. Maziar Zafari, et al.
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We thank Dr. Rincon for his comments about the role of induced hypothermia in the management of cardiac arrest. Our narrative review focused on the key modifications in the updated American Heart Association (AHA) guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiovascular care (ECC) to highlight the most important practical changes to CPR and ECC. (1) In all forms of cardiac arrest availability of high-quality basic life support skills has the highest impact on survival. Thus, the most critical determinant of survival from cardiac arrest is the presence of rescuers who are trained to push hard and fast allowing full chest recoil while minimizing interruptions in compressions, and defibrillating promptly when appropriate. (2) Induced hypothermia has the potential to play a critical role in the postresuscitative care of a small subset of cardiac arrest victims. We concur with Dr. Rincon’s comment that increased awareness about and induction of therapeutic hypothermia in select patients could translate into better outcomes with advanced cardiovascular life support. In the updated 2005 guidelines, the AHA identified induced hypothermia as one of several beneficial therapies in the postresuscitative care of cardiac arrest. (3) Benefit of induced hypothermia was observed in a select subset of patients who were initially comatose but hemodynamically stable after a witnessed arrest with ventricular fibrillation (VF). (3, 4) In the hypothermia after cardiac arrest (HACA) study only 8% of cardiac arrest victims were eligible to receive induced hypothermia. (4) Similar therapy may be beneficial for patients with non-VF arrest out of hospital or for in-hospital arrest. (3) Further experimental studies and clinical trials are required to determine optimal methods of cooling and optimal timing, duration, and intensity of cooling in order to achieve a measurable impact on CPR outcomes. (2, 5) Finally, we would like to thank several readers, particularly Dr. Smith, for pointing out our error about the mechanism of action of atropine, an acetylcholine receptor antagonist of the muscarinic type. REFERENCES: 1. Ali B, Zafari AM. Narrative review: cardiopulmonary resuscitation and emergency cardiovascular care: review of the current guidelines. Ann Intern Med 2007;147:171-179. 2. Hazinski MF, Nadkarni VM, Hickey RW, O'Connor R, Becker LB, Zaritsky A. Editorial: major changes in the 2005 AHA Guidelines for CPR and ECC: reaching the tipping point for change. Circulation 2005;112(suppl IV):IV- 206-IV-211. 3. 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care, Part 7.5: Postresuscitation Support. Circulation 2005;112(suppl IV):IV-84-IV-88. 4. The Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurological outcome after cardiac arrest. N Eng J Med 2002;346:549-556. 5. Safar PJ, Kochanek PM. Editorial: therapeutic hypothermia after cardiac arrest. N Eng J Med 2002;346:612-613. Conflict of Interest:None declared |
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Fred Rincon, MD Columbia University
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doc{at}fredrincon.com Fred Rincon
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Ali and colleagues (1) review recent advances on cardiopulmonary resuscitation and emergency cardiovascular care. Though this is an excellent review of the most recent updates in resuscitation medicine, the authors ignored the latest therapeutic tool for the amelioration of neurological damage after cardiac arrest: therapeutic hypothermia. Based on overwhelming evidence from clinical trials, the American Heart Association incorporated therapeutic hypothermia into its Advanced Cardiac Life Support guidelines as the last link of the chain of survival (2). Recently, three trials demonstrated the neuroprotective effects of hypothermia after cardiac arrest. In the largest, the Hypothermia after cardiac Arrest (HACA) trial, 275 comatose survivors of ventricular fibrillation (VF) arrest were randomized to mild hypothermia to a target bladder temperature of 32-34 °C for 24 hours using a whole body blanket that delivered cooled air (3). A favorable outcome at six months, defined as independence with moderate-to-no disability, was seen in 55% of patients in the hypothermia group vs. 39% in the control group (relative risk 1.40; 95% CI, 1.08-1.81, P=0.009). Mortality was also reduced with hypothermia from 55% in the control group vs. 41% in hypothermia group (relative risk 0.74, 95%, CI, 0.58-0.85, p=0.02). In a second study, 75 comatose survivors of VF cardiac arrest were randomized to therapeutic hypothermia to a target pulmonary artery (PA) temperature of 33°C for 12 hrs using cold ice packs to the head and torso (4). A favorable neurological outcome occurred nearly twice as frequently in the hypothermia group (49% vs. 26%, p=0.046). In the third trial, 30 comatose survivors of primarily asystole and pulseless electrical activity (PEA) cardiac arrest were randomized to mild hypothermia to a target bladder temperature of 34 C? for a maximum of 4 hours using a helmet device placed around the head and neck which contained a solution of aqueous glycerol (5).The results of these three trials have been summarized in a recent meta-analysis (6). All three studies followed patients until death or hospital discharge. Patients in hypothermia group were more likely to be discharged with no or minimal neurological damage (RR, 1.68; 95% CI, 1.29-2.07) which translates into a number-needed to treat of 6 patients even when controlling for several variables such as age, gender, time from collapse to ROSC, and technique, the short term effect of hypothermia was maintained. As we know, morbidity and mortality of patients successfully resuscitated from cardiac arrest primarily depends on neurological outcome. Unfortunately, clinical trials of therapies directed towards reducing the extent of neuronal damage by means of pharmacologic interventions with barbiturates (7), calcium channel antagonists (8), benzodiazepines, magnesium, and steroids (9) have been discouraging. To date, the only clinically effective tool for amelioration of brain damage by ischemia and reperfusion is mild to moderate induced hypothermia. Nevertheless, for a variety of reasons, therapeutic hypothermia for cardiac arrest has been slow to catch on. In an a recently international internet- based survey to learn more about current practices and attitudes regarding hypothermia, the vast majority of cardiology and emergency medicine specialists (74% of US respondents) who care for cardiac arrest victims had never used hypothermia for this indication (10). The most frequently cited reasons for non-use by respondents were "not enough data," "not part of Advanced Cardiac Life Support guidelines," and "too technically difficult to use". All of these responses clearly contradict the current evidence. I agree that based on our better understanding of the pathophysiology of cardiac arrest and brain ischemia, clinicians must tailor their care to incorporate recent intra-cardiac arrest and post-cardiac arrest interventions aimed to improve neurological outcome and survival but we should not forget about the last link in the chain of survival. This is the only effective therapeutic tool for the amelioration of neurological damage after cardiac arrest. Fred Rincon, MD Department of Neurology, Division of Neurocritical Care Columbia University College of Physicians and Surgeons, New York, NY 10034 REFERENCES 1. Ali B, Zafari AM. Narrative Review: Cardiopulmonary Resuscitation and Emergency Cardiovascular Care: Review of the Current Guidelines. Ann Intern Med. 2007;147:171-179. 2. 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2005;112(24 Suppl):IV1-203. 3. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med. 2002;346(8):549-56. 4. Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med. 2002;346(8):557-63. 5. Hachimi-Idrissi S, Corne L, Ebinger G, Michotte Y, Huyghens L. Mild hypothermia induced by a helmet device: a clinical feasibility study. Resuscitation. 2001;51(3):275-81. 6. Eisenburger P, Sterz F, Holzer M, et al. Therapeutic hypothermia after cardiac arrest. Curr Opin Crit Care. 2001;7(3):184-8. 7. Randomized clinical study of thiopental loading in comatose survivors of cardiac arrest. Brain Resuscitation Clinical Trial I Study Group. N Engl J Med. 1986;314(7):397-403. 8. A randomized clinical study of a calcium-entry blocker (lidoflazine) in the treatment of comatose survivors of cardiac arrest. Brain Resuscitation Clinical Trial II Study Group. N Engl J Med. 1991;324(18):1225-31. 9. Jastremski M, Sutton-Tyrrell K, Vaagenes P, Abramson N, Heiselman D, Safar P. Glucocorticoid treatment does not improve neurological recovery following cardiac arrest. Brain Resuscitation Clinical Trial I Study Group. Jama. 1989;262(24):3427-30. 10. Merchant RM, Soar J, Skrifvars MB, et al. Therapeutic hypothermia utilization among physicians after resuscitation from cardiac arrest. Crit Care Med. 2006;34(7):1935-40. Conflict of Interest:None declared |
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Jeffrey Smith, MD, MPH N/A
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smithje{at}battelle.org Jeffrey Smith
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Regarding the Narrative Review: Cardiopulmonary Resuscitation and Emergency Cardiovascular Care: review of the Current Guidelines in the August 7, 2007 issue of the Annals of Internal Medicine, page 175 under the subheading "Atropine", it is stated that "Atropine is a cholinesterase inhibitor", however atropine is an acetylcholine receptor blocker (though it is used to treat cholinesterase inhibitor toxicity, e.g., from organophosphates) and thus acts as a parasympathetic inhibitor by that mechanism. Conflict of Interest:None declared |
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