• Trine Funder Pedersen, Magnus Løberg Thorbjørnsen, Pål Klepstad, Kjetil Sunde, and Ola Dale.
• Det medisinske fakultet, Norges teknisk-naturvitenskapelige universitet, Medpost 159, Olav Kyrres gate 3, 7006 Trondheim.
• Tidsskr. Nor. Laegeforen. 2007 Jan 18;127(2):163-6.

BackgroundTherapeutic hypothermia is used primarily to limit the ischemic damage following cardiac arrest. The main goal for the treatment is the brain. Therapeutic hypothermia is resource demanding and is therefore done in intensive care units with strong competence in treatment and monitoring of critically ill patients. This review focuses mainly on physiological and pharmacological aspects of therapeutic hypothermia.MethodA literature search was conducted using the PubMed database and the reference lists in relevant articles were searched manually.Results And InterpretationBiochemical changes during hypothermia lead to increased tolerance to ischemic episodes and can reduce post-ischemic reperfusion injury to the central nervous system. Knowledge of pharmacological changes during hypothermia is limited, and hypothermic patients are often given doses of drugs recommended for normothermic patients. Reduced enzyme activity during hypothermia, reduced perfusion of liver and kidney and reduced bile-production also contribute to slower elimination of drugs. For some drugs the distribution volume is altered. Consequently, the dosing of several drugs should be reduced during hypothermia. Knowledge about the influence of hypothermia on receptors is sparse. Little is also known about the effects of reheating, but one has to assume that the process will be reversed and that the dosing therefore has to be increased upon reheating. The need for additional studies of the pharmacology of therapeutic hypothermia is obvious.

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