Editorial

Therapeutic hypothermia and the need for defibrillation: wet or dry?

Joseph Varon MD*

The University of Texas Health Science Center Houston, St Luke’s Episcopal Hospital, Houston, TX 77030, USA The University of Texas Medical Branch at Galveston, St Luke’s Episcopal Hospital, Galveston, TX 77030, USA

Received 19 March 2007; accepted 20 March 2007

Therapeutic hypothermia has been used for millennia for a variety of reasons. However, the use of cold temperatures in modern clinical medicine is probably only

200 years old. The Russian method of resuscitation, described in 1803, consisted in covering a patient with snow, hoping for return of spontaneous circulation [1]. Therapeutic hypothermia was used during Napoleon’s Russian campaign in 1812, by the surgeon Baron de Larrey, in an attempt to preserve injured limbs as well as for its anesthetic effects during amputation [2]. However, the first actual recorded clinical use of TH was in 1937, when Dr Temple Fay bcooledQ a lady to 328C for 24 hours, in a desperate attempt to prevent cancer cells from further multiplying and progressing at lower temperatures [3,4]. The use of TH after cardiac arrest in humans in modern medicine was first reported in 1957 by Benson and colleagues [5]. They cooled 4 patients (to 308C-338C) after in-hospital cardiac arrest for periods of 24 to 72 hours. All 4 patients recovered. Interest in the use of mild to moderate induced TH (328C-348C) after cardiac arrest was spurred by the pioneering work of the late Dr Peter Safar.

After 2 landmark randomized controlled studies pub- lished in 2002, in which moderate hypothermia was

* The University of Texas Health Science Center Houston, St Luke’s Episcopal Hospital, Houston, TX, USA. Tel.: +1 713 669 1670; fax: +1 713 669 1671.

E-mail address: [email protected].

demonstrated to improve the outcome in patients with coma after resuscitation from out-of-hospital cardiac arrest, this intervention is now endorsed by the International Liaison Committee on Resuscitation, the European Resus- citation Council, and the American Heart Association [6- 8]. Indeed, these organizations now recommend the use of induced Mild hypothermia in comatose survivors of out-of- hospital cardiac arrest caused by ventricular fibrillation. Evidence-based medicine compels that a moderate degree of selective brain cooling, if instituted promptly, may protect against ischemic neuronal injury of the type that occurs commonly after a cardiac arrest (class IIa recom- mendation) [9].

During TH, some patients may have recurrent ven- tricular fibrillation requiring cardiac defibrillation. If the patient is being cooled using Surface cooling, con- cerns arise regarding safety for the operator and the patient as well as efficacy. Theoretically, TH could impair defibrillation by reducing sodium channel conductance and increasing electrical heterogeneity via dispersion in the action potential duration [10]. In this issue of The American Journal of Emergency Medicine, Schratter and associates [11] report the results of an animal model of cardiac arrest in which they assessed the safety and effectiveness of transthoracic defibrillation during surface cooling with cold water as compared with dry conditions. These investigators demonstrate that transthoracic defibril- lation is feasible and safe during TH in wet conditions and

0735-6757/$ - see front matter D 2007 doi:10.1016/j.ajem.2007.03.022

480 Editorial

that the energy delivered to the victims is the same as in dry conditions.

Therapeutic hypothermia is now seen as a new neuro- protective strategy and is gaining ground as an emergency therapy. The best cooling technique is one that is easy to use and at the same time effective. In the future, TH trials to lower temperatures may produce an unstable electrophysi- ologic state. However, data such as those presented by Schratter and colleagues [11] suggest that TH may be used to slow metabolic processes without concerns over the ability to successfully and safely defibrillate and treat hypothermia-induced dysrhythmias. It is clear that, based on this study, in surface cooling with ice conditions, electrical defibrillation is safe and efficacious.

References

1. Varon J, Sternbach GL. Cardiopulmonary resuscitation: lessons from the past. J Emerg Med 1991;9:503 - 7.
2. Mordecai Y, Globus RB, Dietrich WD, Sternau L, Morikawa E, Ginsberg MD. Temperature modulation of neuronal injury. In:

Harbans L, Harbans L, editors. Emerging strategies in neuroprotec- tion. Boston7 Birkhauser; 1992. p. 289 - 306.

1. Fay T. Observations on prolonged human refrigeration. N Y State J Med 1940;40:1351 - 4.
2. Alzaga AG, Salazar G, Varon J. Breaking the thermal barrier: Dr Temple Fay. Resuscitation 2006;69:359 - 64.
3. Benson DW, Williams GR, Spencer FC. The use of hypothermia after cardiac arrest. Anesth Analg 1958;38:423 - 8.
4. Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 2002;346:549 - 56.
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7. Alzaga A, Cerdan M, Varon J. Therapeutic hypothermia. Resuscita- tion 2006;70:369 - 80.
8. Sprung J, Laszlo A, Turner LA, et al. Effects of hypothermia, potassium and verapamil on the action potential characteristics of canine cardiac Purkinje fibers. Anesthesiology 1995;82:713 - 22.
9. Schratter A, Weihs W, Holzer M, et al. External cardiac defibrillation during wet surface cooling in pigs. Am J Emerg Med 2007;25:420 - 4.