Cardiovascular control mechanisms during anaesthesia and surgery : with special reference to muscle nerve sympathetic activity

Abstract

Knowledge of effects of anaesthetics on cardiovascular control is based mainly on studies during undisturbed anaesthesia. However, in the clinical situation the cardiovascular characteristics of different anaesthetics are related to the balance between the dose of the anaesthetic and the intensity of surgical stimulation. Therefore, a general aim of the present studies was to investigate the effects of anaesthetics on cardiovascular control mechanisms both during undisturbed anaesthesia and during surgery. Since the trend in general anaesthesia is to use anaesthetics with short duration, the studies were focused on propofol in particular but also on methohexitone and isoflurane. Microlaryngoscopy was used as a surgical stress model since microlaryngoscopy evokes an intense and relatively stable afferent stimulation associated with a reproducible pressor response. Methods: A main method in the human studies was microneurography of s ympathetic vasoconstrictor nerve traffic to skeletal muscle blood vessels. It was thereby possible to differentiate between neurogenic effects and direct effects on the blood vessels from circulating factors including the anaesthetics themselves. Cardiac output (impedance cardiography) and regional blood flows (leg plethysmography, skin laser Doppler flowmetry, photoelectric pulse plethysmography) were recorded. Arterial catechol amine concentrations were measured. In addition, an experimental open loop baroreflex model (isolated carotid sinuses) was studied in the cat. Results: Sympathetic activity to skeletal muscle (MSA) w as depressed by propofol, methohexitone and isoflurane, whereas nitrous oxide was associated with an increase in MSA. The depression of MSA during undisturbed propofol infusion was to a large extent restored during microlaryngoscopy in spite of a more than three times increased propofol infusion rate. Vasodilation during propofol anaesthesia was caused by an inhibition of central sympathetic outflow and probably also by a direct vascular effect. In a comparative study during microlaryngoscopy, propofol was a better alternative than equianaesthetic doses of m ethohexitone, which in a low infusion dose was insufficient to control the microlaryngoscopy- induced pressor response and in a high infusion dose was associated with prolonged recovery. A large difference in leg blood flow was noted between the low and high-dose methohexitone groups whereas no difference was observed between the low and high-dose propofol groups. In the cat, the baroreflex sensitivity was better maintained during anaesthesia with propofol than with methohexitone or isoflurane. In humans, both cardiac and muscle sympathetic baroreflex sensitivities were depressed by propofol. The further depression of the cardiac baroreflex that was observed during surgery may have been due to a central vagal inhibition similar to that found in a nimals during defence area stimulation. The muscle nerve sympathetic baroreflex sensitivity was determined by a balance between an augmented central sympathetic outflow due to surgical stress and inhibition due to the anaesthetic. Conclusions: Sympathetic activity to skeletal muscle is profoundly influenced by the choice of anaesthetic agent. A suppression of activity is more common than an increase. A decrease in MSA is counteracted by surgical stress. During propofol, methohexitone and isoflurane anaesthesia, the muscle nerve sympathetic baroreflex is qualitatively operative but the baroreflex sensitivity is depressed to a variable extent depending on the anaesthetic agent and depth of an aesthesia