Practical Pharmacologic Aspects of Therapeutic Hypothermia After Cardiac Arrest

Paul A. Arpino, Pharm.D.; David M. Greer, M.D.


Pharmacotherapy. 2008;28(1):102-111. 

In This Article

Abstract and Introduction

Therapeutic hypothermia has emerged as an effective means of improving neurologic outcomes among cardiac arrest survivors. To achieve optimal results, clinicians must understand and anticipate potential adverse effects of cooling and provide rigorous monitoring and/or pharmacologic interventions as appropriate. Using pharmacotherapy to counter adverse effects of cooling or to treat an intrinsic process under hypothermic conditions requires understanding how hypothermia will influence the clinical effects of the drug, including the drug's pharmacokinetics and pharmacodynamics. The pharmacologic aspects of therapeutic hypothermia in relation to physiology and adverse effects are reviewed.

Therapeutic hypothermia to prevent ischemic brain injury during cardiac surgery was introduced in the 1950s.[1] Since then, cooling to mild hypothermia (32–34B0C) has been used for many neurologic conditions, including traumatic brain injury, stroke, and anoxic brain injury resulting from cardiac arrest.[2,3] It was not until the technique was applied in a more controlled fashion that its merit was formally established. Publication of two large randomized trials of controlled therapeutic hypothermia in sudden cardiac arrest resulted in international recom-mendations for its use.[4–6]

We review the pharmacologic aspects of hypothermia as they relate to physiology and the adverse effects of mild therapeutic cooling, focusing on patients with sudden cardiac arrest. However, much of this review is applicable to clinicians who use therapeutic hypothermia for stroke, anoxic injury, and traumatic brain injury.


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