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Cardiorespiratory and metabolic effects of profound hypothermia.

At operation the body temperature of mechanically ventilated infants was initially decreased to 25--22 degrees C with surface cooling and further lowered to 16 degrees C by total body perfusion. During circulatory arrest, averaging 40 min, repair of complex intracardiac deformities was carried out. Rewarming to 36 degrees C was achieved by 35--65 min of total body perfusion. Of 29 infants, 23 under 10 kg survived their correction; normothermic ventilation without added CO2 was given throughout the cooling period. The following measurements were made: gas exchange, lung mechanics, heart rate, arterial pressure, right atrial pressure, cardiac output (Qt), ECG, core and nasopharyngeal temperature, as well as biochemical determinations. During surface cooling O2 consumption (VO2), CO2 production (VCO2), endtidal CO2 (PETCO2) and PaCO2 decreased proportionally and linearly with body temperature. Inspiratory resistance, total compliance, physiological dead space (VD/VT), and the single breath CO2 curve did not reveal disturbed lung function. Mean arterial pressure was 98, 90, and 70 mm Hg and heart rate was 141, 107, and 76 beat/min, at temperature 35, 30, and 25 degrees C, respectively. Cardiac index was 2.2 +/- 0.2 liter/min/m2 (mean +/- SEM, n = 25) 2 hours after surgery. Arterial lactate reached peak values of 4.1 +/- 0.3 mM/liter (n = 17), during rewarming but returned to normal. Respiratory alkalosis caused by hyperventilation during cooling caused no apparent harm. No neurological damage was observed. It is concluded that surface cooling performed with normothermic ventilation under guidance of core temperature, VO2, PETCO2, and VCO2, is a safe method.