Abstract
Haemodynamic responses to the apnoea test jor the diagnosis of brain death were investigated in nine patients with severe head injury or cerebrovascular disease. To prove apnoea, the ventilator was disconnected for ten minutes and oxygen was insufflated to avoid hypoxaemia. No respiratory movement was séen in any patient. Ten minutes after disconnecting the ventilator, PaCO2 was increased to 78 ± 3 mmHg and pH was reduced to 7.17 ± 0.02. Adequate oxygenation was maintained in all patients. Cardiac output increased from 4.8 ± 0.7 to 5.7 ± 0.8 L · min− 1 (P < 0.05), and mean pulmonary artery pressure increased from 11 ± I to 17 ± 2 mmHg (P < 0.01). However, mean arterial pressure, heart rate, pulmonary artery wedge pressure and right a trial pressure did not change. Plasma catecholamines were measured in three patients. Plasma norepinephrine concentrations increased in all three patients but the changes in plasma epinephrine were minimal. These circulatory responses to acute hypercapnia were less than those reported in awake volunteers and in patients during general anaesthesia. However, since plasma norepinephrine concentration increased during the test, some sympathoadrenal response, probably of spinal origin, was present, and may have prevented the direct depressant circulatory effects of acute hypercapnia. In conclusion, the apnoea test did not produce haemodynamic disturbances when respiratory acidosis was limited toapH 7.17±0.02 and PaCO2 60–80 mmHg.
Résumé
Lors de l’établissement du diagnostic de mon cérébrale chez neuf patients victimes de traumatisme on de maladie cérébrovasculaire, nous avans mesuré la réponse hémodynamique an test d’apnée. Le ventilateur était débranché pendant dix minutes alors qu’on insujflait de l’oxygène afin d’éviter l’ hypoxémie. Aucun patient tie fit de mouvement respiratoire el an bout de dix minutes la PaCO2 était de 78 ± 3 mmHg alors que le pH était de 7,17 ± 0,02 el que chez tons, l’oxygénation était adéquate. Le débit cardiaque passa de 4,8 ± 0,7 à 5,7 ± 0,8 L-min− 1 (P < 0,05) et la pression moyenne de l’artére pulmonaire de 11 ± 1 à 17 ± 2 mmHg (P < 0,01). La tension artérielle systémique, le pouls, la pression pulmonaire capillaire bloquée el la pression de l’oreillette droite resterént les mêmes. Nous avons mesuré les niveaia de cathécolamines plasmatiques chez trois patients et avons identifié une petite augmentation de la noradrenaline chez tous trois lors du test (NS) alors que l’adrénaline, elle, variait tiés pen. L’amplitude de la réponse hémodynamique à une hypercarbie aigué mesurée dans notre étude est beaucoup moindre que celle notée chez des volontaires conscients on chez des patients sous anesthésie générale. L’augmentation, limitée certes, de la noradrenaline plasmatique indique toutefois qu’il persistait une certaine réponse sympathoadrénergique, probablemenl d’origine spinale, pouvant contrecarrer l’effet dépresseur direct de l’hypercarbie aiguë sur la circulation. Bref, le test d’apnée n’entraîne pas de perturbations hemodynamiques lorsque l’acidose respiratoire se limite à un pH de 7,17 ± 0,02 et à une PaCO2 entre 60 et 80 mmHg.
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Ebata, T., Watanabe, Y., Amaha, K. et al. Haemodynamic changes during the apnoea test for diagnosis of brain death. Can J Anaesth 38, 436–440 (1991). https://doi.org/10.1007/BF03007579
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DOI: https://doi.org/10.1007/BF03007579