THE IMMEDIATE CARDIAC DEPRESSION BY ANAESTHETICS IN CONSCIOUS DOGS BY

The time course of circulatory changes during induction with halothane and/or nitrous oxide was studied in six healthy awake dogs. Beat-to-beat changes in cardiac perfor-mance were measured with chronically implanted aortic electromagnetic flowmeters, and pressures were recorded from atria, pulmonary artery, and descending aorta. The dogs were trained to wear masks designed for delivering gases, and to acclimatize to the odour of halothane. Both 3 per cent halothane and 60 per cent nitrous oxide reduced peak aortic flow and maximum acceleration within 4-8 seconds after the first breath. This depression was more pronounced with halothane than nitrous oxide, and was even more severe with the combination of halothane and nitrous oxide. Cardiac accelera-tion fell before any decline in cardiac output, aortic or central pressures, thus indicating a direct myocardial effect. This was confirmed in dogs studied after surgical cardiac denervation when halothane and nitrous oxide alone and in combination produced the same immediate cardiac depression. Studies on the cardiac effects of inhalation anaes-thetics are handicapped by the necessity of using previously anaesthetized animals or subjects, and by methods requiring the steady state condition. This study examines the time course and the nature of circulatory alterations during the initial breaths of nitrous oxide and/or halothane. Beat-to-beat changes in cardiac performance were measured with an ascending aortic flowmeter in the trained dog while awake and unsedated. This method permits a close look at an important phase of the haemodynamic response to anaesthesia; that is, the changing state about which there is little information. In order to exclude neural in-fluences on the heart during the transient exposure to anaesthetics, half the dogs were studied several weeks after surgical denervation of the heart. METHOD