The use of hypothermia in cardiac and neurologic surgery is well established, but its use in treating hemorrhagic shock is controversial. Using a modified Wiggers hemorrhagic shock model, we examined the effects of hypothermia (group 1, 33°C, N = 7; group 2, 28°C, N = 12) after inducing hemorrhagic shock. In group 3, N = 6, dogs were maintained at body temperature in hemorrhagic shock and throughout resuscitation (normothermic shock). Sixty minutes after resuscitation (shed blood and lactated Ringer's solution, 50 ml/kg body wt), all hypothermic dogs were rewarmed and studied for an additional 120 min. Comparison of moderately hypothermic, severely hypothermic, and normothermic dogs showed a lower heart rate (80.6 ± 3.3, 62.5 ± 4.1, and 136.7 ± 4.2 beats/min, P < 0.05), reduced rate of left ventricular pressure fall (938 ± 125, 700 ± 75, and 1550 ± 275 mm Hg/sec, P < 0.05), a lower arterial pH (7.15 ± 0.02, 7.10 ± 0.03, and 7.24 ± 0.02, P < 0.05), a lower respiratory rate (18 ± 1, 14 ± 1, and 24 ± 2 breaths/min, P < 0.05), and a higher arterial pCO2 (36.6 ± 1.6, 46.9 ± 4.6, and 20.3 ± 2.0 mm Hg, P < 0.05). Left ventricular end-diastolic pressure was lower in the severely hypothermic dogs while stroke volume was higher in this group. Rewarming ablated all differences in cardiovascular performance and acid-base balance. Our data show that moderate hypothermia during hemorrhagic shock increased coronary perfusion, enhanced cardiac contractile performance, and significantly reduced myocardial oxygen requirements. Severe hypothermia (body temperature, 28°C) was associated with increased ventricular irritability, often leading to fatal arrhythmias. The increased evidence of arrhythmias and increased mortality associated with severe reduction in body temperature preclude the clinical use of this level of hypothermia.
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