25c The lowered heart rate results from a de crease in the spontaneous depolarization of pace- maker cells and is refractory to atropine. At core temperatures below 32°C, atrial dysrhythmia oc curs, secondary to atrial distension." Ventricular arrhythmias are commonly observed below 32.2°C but primary ventricular fibrillation is rare at 32.2 C with maximal susceptibility occurring between 28°C and 30°C. 70 At core temperatures lower than 30°C, the heart is very sensitive to mechanical ef stimulation, and cardiopulmonary resuscitation forts may convert a very slow sinus bradycardia to ventricular fibrillation. As the core temperature ap- proaches 25°C, fluid shifts out of the vascular space which may increase the hematocrit by 150% The ensuing hypovolemia and increased blood viscos- further compromise the cardiac output ity An electrocardiogram demonstrates significant changes with hypothermia. These electrical changes are indicative of specific myocardial ionic activities that are influenced by the cold. Membrane currents are controlled by multiple processes that control the membrane channels, which are composed of lipo- protein and other chemicals whose activities are temperature-dependent. Thus, low temperatures result in both a slower activation and inactivation of different membrane currents, and they contrib ute to various electrophysiological changes. Dur ing hypothermia there is a prolongation of the PR and Q-T intervals and widening of the QRS com plex. A significant drop in core temperature results in the reduction of the rate of depolarization, which in turn results in a widening of the QRS complex. The explanation for this phenomenon is that dur- ing hypothermia, the rate of the opening and clos- ing of the sodium channels is decreased, and so-