Iaizzo P A, Kehler C H, Zink R S, Belani K G, Sessler D I
Department of Anesthesiology, University of Minnesota, Minneapolis, USA.
Anesth Analg. 1996 Apr;82(4):782-9. doi: 10.1097/00000539-199604000-00019.
This study was designed to evaluate how vital organ and skin-surface temperatures correlate with other clinical signs of a malignant hyperthermia (MH) episode. Six susceptible swine were anesthetized with thiopental and nitrous oxide and kept normothermic (approximately equal to 38 degrees C). After a 30-min control period, halothane (1 minimum alveolar anesthetic concentration) was administered, followed in 5 min by a bolus of succinylcholine (2 mg/kg intravenously). Monitoring included: 1) ETCO2; 2)PaO2, PaCO2, pHa; 3) cardiovascular function; 4) core temperatures (esophagus, pulmonary artery, and rectum); 5) organ temperatures (brain, kidney, liver, and four skeletal muscles); and 6) skin temperatures (forehead, neck, and axilla). Within 10 min after exposure to halothane and succinylcholine, all animals developed fulminant MH. Kidney, liver, and brain temperatures increased more rapidly than pulmonary artery temperature with the onset of MH. Temperatures significantly increased in the visceral organs prior to the detection of contractures within skeletal muscles. The masseter, longissimus dorsi, quadriceps, deltoid, and extensor digiti II intramuscular temperatures were 1-2 degrees C less than pulmonary artery and esophageal temperatures during the episodes, whereas those of the kidney, liver, and brain were the same or slightly greater. When it occurs, core hyperthermia during acute MH results largely from heat produced in central organs, not in skeletal muscle per se. In these swine, changes in axilla skin surface temperatures correlated well with core temperature trends, whereas those of the neck and forehead did not. Unless a skin-surface probe can be placed in close proximity to a major vessel, cutaneous temperatures should not be substituted for measurements at an appropriate core site.
