CABDIOVASCLrLAlq DEPRESSION on induction of anaesthesia is a common complication, especially in patients with impaired myocardial function. This disturbance of circulation is the result of one or more of reduced venous return following peripheral vasodilatation, negative inotropie effects, and an unbalanced ratio between myocardial oxygen demand and oxygen supply. The simultaneous effect of various intravenous induction agents upon haemodynamies, the inotropic state of the heart, coronary blood flow, and myocardial oxygen consumption in healthy individuals were studied by Sonntag and coworkers. 21,~zaS,a6 For their measurements, anaesthetic and haemodynamic steady state conditions were required. Such conditions were established by continuous infusion of the anaesthetics studied, or were taken for granted after the sharp exponential decline of the anaesthetic blood level following intravenous administration of the drug. However, since a steady state does not occur at induction, the purpose of this study was to explore the acute effects of some induction agents upon the cardiovascular system in man. Clinical dosages of the following drugs were scheduled for investigation.The short-acting, non-barbiturate hypnotic etomidate, lo,2z the new steroid anaesthetic agent althesin, 6-s,st and the short-acting narcotic fentanyl, which is frequently utilized as a sole anaesthetic in patients requiring open-heart surgery. METHODSThe investigations were performed in 15 patients undergoing genera] anaesthesia for urological surgery. Pre-operatively all patients were informed of the nature of the anaesthetic procedure and the haemodynamie measurements during anaesthesia. The age of the patients studied ranged from 38 to 74 years (average 61 years). All were ASA physical status I and II. None had a history or objective evidence of any cardiopulmonary or metabolic disease.Premeditation, consisting of meperidine 50-100 mg, promethazine 50 mg, and atropine 0.5 mg, was given intramuscularly one hour before induction.Anaesthesia was induced with thiopentone 3.0 mg/kg (etomidate-and althesin group) and etomidate 0.5 mg/kg (fentanyl group) respectively. Tracheal intubation was facilitated with succinylcholine 1.0 mg/kg. Anaesthesia was maintained with 0.3 volumes per cent of halothane (etomidate-and althesin group) and 0.3 volumes per cent of isoflurane (fentanyl group) respectively in nitrous oxide and

The cardiovascular effects of naloxone 15 microgram/kg following morphine 2.0 mg/kg were studied in closed-chest dogs during light nitrous oxide-halothane anaesthesia. The bolus injection of naloxone caused an increase in heart rate (73%), cardiac output (20%) and mean arterial pressure (20%). Total peripheral resistance was unaffected. LV dP/dt max and LV dP/dt max/IP increased by 25% and 14% respectively, but positive inotropic effects could not be shown when load data, heart rate and the decrease in left ventricular ejection fraction (22%) were taken into consideration. The cardiovascular stimulation resulted in an increase in myocardial oxygen demand (66%) which was met by an increase in coronary blood flow (59%). The data suggest that the antagonism of narcotics with high doses of naloxone may impair the myocardial oxygen supply in patients suffering from coronary insufficiency. It is concluded that naloxone should be titrated for each patient to ensure adequate reversal of respiratory depression and to avoid circulatory stress.

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