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

Application of high-silica zeolites in a special adsorber allows complete selective adsorption of the inhalation anaesthetic desflurane from the outlet port of the scavenging system of the anaesthesia machine. In comparison with charcoal filters, zeolites allow almost complete desorption at moderate temperatures followed by condensation of the desflurane to the liquid phase. The adsorption of scavenged desflurane by zeolites was measured in 13 patients. The duration of the anaesthesia was between 70 and 130 min. A minimal-flow regime (0.5 L min-1 fresh gas inflow) was used for maintenance in seven patients and a higher-flow regime (3 L min-1 fresh gas flow) was used for maintenance in six patients. In minimal-flow anaesthesia, 62% of the delivered desflurane was adsorbed by the zeolite while 86% of the delivered desflurane was adsorbed in higher-flow anaesthesia. Preliminary results show that about 85% of the adsorbed desflurane could be recovered as liquid with high purity via desorption.

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Both desflurane and sevoflurane possess a similar profile with regard to their hypnotic effects and a similar outline in depressing propagation within the sensory nervous system. Cortical nervous effects are mirrored closely in heart rate and systolic blood pressure.

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The effect of metabolic and hypercapnic acidosis on myocardial blood flow was studied during intravenous infusions of hydrochloric acid solutions (n = 12) and during passive ventilation with 5% CO2 (n = 5) in anaesthetized, closed chest dogs. Below a pH of 7.2 metabolic acidosis at normal arterial CO2-tensions caused an increase of coronary blood flow and a decrease of coronary vascular resistance associated with a narrowed myocardial arteriovenous O2-difference, indicating vasodilation at unchanged myocardial oxygen consumption. In propranolol-pretreated dogs myocardial blood flow and coronary oxygen AV difference remained unaffected, suggesting that the coronary dilatory effect of metabolic acidemia involves beta adrenergic stimulation. Coronary vasodilation induced by increasing arterial pCO2 was found to the significantly greater as compared with the dilatory effect of metabolic acidosis at the same blood pH level. Blocking of beta receptors did not reduce the coronary response to increased arterial CO2-tensions. It is concluded that the coronary vasodilation observed during hypercapnic acidosis is neither mediated by a beta adrenergic stimulation nor dependent of the concomitant change in blood pH. The possible sites of the coronary dilatory actions of increased arterial CO2-tensions are discussed.