Answer: Thanks for the very interesting question! To be frank, we are not sure why the contraindications list hypothermia for Atropine and Transcutaneous Pacing (TCP) but do not list hypothermia as a contraindication for Dopamine administration. We will be bringing this back up this Fall when the entire ALS-PCS is opened for revision pending the 2015 AHA Guidelines release. Great pick up!
We are wondering if the reason for listing hypothermia as a contraindication in general for symptomatic bradycardia is that severely hypothermic patients tend to be bradycardic and relatively hypotensive. In these clinical scenarios, it may be a superior strategy to treat the underlying cause (hypothermia) rather than perhaps making the hypothermic myocardium more irritable with Atropine or TCP. That being said, this does not explain the exemption (if you will) of Dopamine using the same argument.
As for your point about the practice of not giving drugs to the severely hypothermic patients, the 2010 AHA Guidelines (Vanden Hoek et al, Part 12: Cardiac Arrest in Special Situations) states the following for the management of the severely hypothermic patient on page S846:
ACLS management of cardiac arrest due to hypothermia focuses on aggressive active core rewarming techniques as the primary therapeutic modality. Conventional wisdom indicates that the hypothermic heart may be unresponsive to cardiovascular drugs, pacemaker stimulation, and defibrillation; however, the data to support this are essentially theoretical. In addition, drug metabolism may be reduced, and there is a theoretical concern that medications could accumulate to toxic levels in the peripheral circulation if given repeatedly to the severely hypothermic victim. For these reasons, previous guidelines suggest withholding IV drugs if the victim’s core body temperature is <30°C (86°F).
In the last decade a number of animal investigations have been performed evaluating both vasopressors and antiarrhythmic medications that could challenge some of this conventional wisdom. In a meta-analysis of these studies, Wira et al found that vasopressor medications (ie, epinephrine or vasopressin) increased rates of return of spontaneous circulation (ROSC) when compared with placebo (62% versus 17%; P<0.0001, n=77). Coronary perfusion pressures were increased in groups that received vasopressors compared with placebo. But groups given antiarrhythmics showed no improvement in ROSC when compared with control groups, although sample sizes were relatively small (n=34 and n=40, respectively).
One small-animal investigation suggested that the application of standard normothermic ACLS algorithms using both drugs (ie, epinephrine and amiodarone) and defibrillation improved ROSC compared with a placebo arm of defibrillation only (91% versus 30%; P<0.01; n=21). Human trials of medication use in accidental hypothermia do not exist, although case reports of survival with use of intra-arrest medication have been reported.
Given the lack of human evidence and relatively small number of animal investigations, the recommendation for administration or withholding of medications is not clear. It may be reasonable to consider administration of a vasopressor during cardiac arrest according to the standard ACLS algorithm concurrent with rewarming strategies (Class IIb, LOE C).
In other words, it may be reasonable to continue giving medications to profoundly hypothermic patients in the setting of cardiac arrest or cardiovascular collapse as long as we do so along with aggressive rewarming strategies. Since invasive active core rewarming is available in-hospital, this is why there continues to be a focus of early rapid transport as well with these patients.
Thanks again for the terrific question!
The relevant references from the AHA for this section are listed below:
Winegard C. Successful treatment of severe hypothermia and prolonged cardiac arrest with closed thoracic cavity lavage. J Emerg Med. 1997;15:629–632.
Dobson JA, Burgess JJ. Resuscitation of severe hypothermia by extracorporeal rewarming in a child. J Trauma. 1996;40:483–485.
Reuler JB. Hypothermia: pathophysiology, clinical settings, and management. Ann Intern Med. 1978;89:519–527.
Elenbaas RM, Mattson K, Cole H, Steele M, Ryan J, Robinson W. Bretylium in hypothermia-induced ventricular fibrillation in dogs. Ann Emerg Med. 1984;13:994–999.
Kornberger E, Lindner KH, Mayr VD, Schwarz B, Rackwitz KS, Wenzel V, Krismer AC, Mair P. Effects of epinephrine in a pig model of hypothermic cardiac arrest and closed-chest cardiopulmonary resuscitation combined with active rewarming. Resuscitation. 2001;50:301–308.
Schwarz B, Mair P, Raedler C, Deckert D, Wenzel V, Lindner KH. Vasopressin improves survival in a pig model of hypothermic cardiopulmonary resuscitation. Crit Care Med. 2002;30:1311–1314.
Schwarz B, Mair P, Wagner-Berger H, Stadlbauer KH, Girg S, Wenzel V, Lindner KH. Neither vasopressin nor amiodarone improve CPR outcome in an animal model of hypothermic cardiac arrest. Acta Anaesthesiol Scand. 2003;47:1114–1118.
Stoner J, Martin G, O’Mara K, Ehlers J, Tomlanovich M. Amiodarone and bretylium in the treatment of hypothermic ventricular fibrillation in a canine model. Acad Emerg Med. 2003;10:187–191.
Wira C, Martin G, Stoner J, Margolis K, Donnino M. Application of normothermic cardiac arrest algorithms to hypothermic cardiac arrest in a canine model. Resuscitation. 2006;69:509–516.
Wira CR, Becker JU, Martin G, Donnino MW. Anti-arrhythmic and vasopressor medications for the treatment of ventricular fibrillation in severe hypothermia: a systematic review of the literature. Resuscitation. 2008;78:21–29.