Abstract

Rewarming from accidental hypothermia is often complicated by hypothermia-induced cardiac dysfunction, calling for immediate pharmacologic intervention. Studies show that although cardiac pharmacologic support is applied when rewarming these patients, a lack of updated treatment recommendations exist. Mainly due to lack of clinical and experimental data, neither of the international guidelines includes information about pharmacologic cardiac support at temperatures below 30 °C. However, core temperature of accidental hypothermia patients is often reduced below 30 °C. Few human studies exploring effects of adrenergic drugs during hypothermia have been published, and therefore prevailing information is collected from pre-clinical studies. The most prominent finding in these studies is an apparent depressive effect of adrenaline on cardiac function when used in doses which elevate cardiac output during normothermia. Also noradrenaline and isoprenaline largely lacked positive cardiac effects during hypothermia, while dopamine is a more promising drug for supporting cardiac function during rewarming. Data and information from these studies are in support of the prevailing notion; not to use adrenergic drugs at core temperatures below 30 °C.

Highlights

  • Rewarming victims of accidental hypothermia is often complicated by hypothermia-induced cardiac dysfunction

  • An additional study on rats from our lab showed that 1 μg/min of adrenaline given during cooling caused a maintained depression of cardiac function during rewarming [35]. These results indicate that hypothermia has a severe impact on cardiac inotropic effects mediated by the β1-receptor pathway, as β1-adrenergic stimulation during hypothermia has a negative impact on inotropic effect of β1-agonists after rewarming

  • From a combined in vitro and in vivo study in our lab, we showed that this hypothermiainduced reduction of inotropic effect via β1-receptor stimulation is seen in the presence of in vivo and in vitro β1-receptor super-sensitivity

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Summary

Introduction

Rewarming victims of accidental hypothermia is often complicated by hypothermia-induced cardiac dysfunction. In its fulminant form this condition is described as rewarming shock; an acute heart failure with a progressive fall in cardiac output (CO) where the patient terminates in a sudden and intractable fall in blood pressure [1]. This serious complication to clinical therapy adds to the virtually unchanged low survival rate of accidental hypothermia over the last decades [2, 3]. I.e. drugs that enhance force of cardiac contraction [4] could provide such pharmacologic support, but current guidelines do not support this view. Both the American Heart Association and the European Resuscitation Council advise against using

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