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The sympathetic response to profound hypothermia and circulatory arrest in infants

1980; Springer Nature; Volume: 27; Issue: 2 Linguagem: Inglês

10.1007/bf03007773

0008-2856

Margaret Wood, David G. Shand, Andrew J. Wood,

Neuroscience of respiration and sleep

It has been suggested that the increased incidence of ventricular arrhythmias recognized below 30°C might be catecholamine mediated. Elevated catecholamine concentrations have been reported in experimentally induced hypothermia in animals. Plasma concentrations of epinephrine and norepinephrine were measured during profound hypothermia and total circulatory arrest in infants under one year of age undergoing surgical correction of congenital cardiac defects. There was no significant change in either epinephrine or norepinephrine levels during surface cooling to 28° C. Circulatory arrest and exsanguination at 18° C were not associated with a rise in catecholamine levels. However, there was a striking rise in the levels of both epinephrine and norepinephrine with the recommencement of bypass and rewarming. The mean plasma norepinephrine concentration rose from 466 pg/ml (SE ± 81) at circulatory arrest to 4543 pg/ml (SE ± 2058) on rewarming bypass (p < 0.02), while the mean plasma epinephrine concentration rose from 218 pg/ml (SE ± 54) at circulatory arrest to 3724 pg/ml (SE ± 1064) on rewarming bypass (p < 0.02). The plasma catecholamine concentrations fell once cardiopulmonary bypass was discontinued, when the infant's temperature was 37° C. It would, therefore, appear unlikely that the ventricular irritability recognized below 30° C is due to catecholamine excess. The accumulation of catecholamines and/or metabolic products in the infants during circulatory arrest with their subsequent release into the circulation during rewarming may account for the elevation of catecholamine levels during rewarming bypass.