Effects of anaesthesia on the sympathetic system

Cardiovascular homoeostasis is largely regulated by the autonomic nervous system, which controls heart rate, myocardial contractility, vascular resistance, and the tone of the venous capacitance vessels. Anaesthesia alters basic sympathetic tone as well as the sympathetic response to painful (surgical) stimuli. It is essential for the anaesthetist to be familiar with the interaction of anaesthesia with the autonomous nervous system in order to evaluate and treat haemodynamic disorders that may occur during anaesthesia. Current knowledge about the interaction of anaesthetic agents with the sympathetic nervous system is based mainly on studies of plasma catecholamine levels, assessment of baroreceptor

reflex response, and direct recordings of sympathetic nerve activity.2-12 Sympathetic nerve activity

Muscle sympathetic nerve activity can be recorded from the peroneal nerve. A very thin epoxy coated needle (0-2 mm) with a small tip (5p,m) is placed within the peroneal nerve below the bony prominence at the head of the fibula. Using a reference electrode and a special set-up with a differential preamplifier and a bandpass filter, identification of characteristic muscle sympathetic nerve activity is possible (Fig 10.1). Sympathetic nerve activity is quantified by the number of bursts per minute or number of bursts per 100 cardiac cycles, or as total activity calculated from the

Fig 10.1 Respiratory movements, muscle sympathetic nerve activity, and blood pressure in a patient undergoing induction of anaesthesia with propofol. The upper panel shows condensed recordings, the lower panel depicts selected periods in an enlarged time scale. Induction of anaesthesia with propofol decreases muscle sympathetic nerve activity and blood pressure (upper panel). Tracheal intubation causes a dramatic increase in muscle sympathetic nerve activity. (Modified from Sellgren et al.11)

Fig 10.1 Respiratory movements, muscle sympathetic nerve activity, and blood pressure in a patient undergoing induction of anaesthesia with propofol. The upper panel shows condensed recordings, the lower panel depicts selected periods in an enlarged time scale. Induction of anaesthesia with propofol decreases muscle sympathetic nerve activity and blood pressure (upper panel). Tracheal intubation causes a dramatic increase in muscle sympathetic nerve activity. (Modified from Sellgren et al.11)

product of bursts per minute and mean burst amplitude. Efferent bursts frequently occur in pulse synchronous groupings and are often phase locked to late expiration and early inspiration efforts.7 This pattern is thought to be caused by baroreceptor modulation.10Effects of induction of anaesthesia on sympathetic nerve activity

Effects of induction of anaesthesia on sympathetic nerve activity

There are a number of investigations on the effects of induction of anaesthesia, tracheal intubation, and surgical stimulation on muscle sympathetic nerve activity. Most of the work has been performed by the groups of Ebert et al. and Sellgren et al.7 9-15 Induction of anaesthesia decreased sympathetic outflow (Fig 10.2). Propofol and thiopentone (thiopentone) had the most pronounced effects,7 10-11 whereas etomidate preserved muscle sympathetic nerve activity7(Fig 10.2). Moreover, the decrease of muscle sympathetic nerve activity after propofol is more pronounced in unpremedicated patients than in those who received benzodiazepine premedication7 11. Obviously, baseline sympathetic drive seems to be an important determinant of the impact of anaesthesia on sympathetic outflow and the resulting haemodynamic effects. These findings are in accordance with the clinical observation that propofol occasionally causes severe hypotension, particularly in patients who presumably are under an increased sympathetic drive in the conscious state, for example, patients with borderline hypovolaemia or compensated myocardial failure. Induction of anaesthesia with methohexital (methohexitone) has also been reported to decrease muscle sympathetic nervous activity.10 These experimental data would support the clinical impression that etomidate is the induction anaesthetic agent of choice for patients with compromised cardiovascular performance and compensatory increased sympathetic drive. Laryngoscopy as well as surgical stimulation are associated with an immediate and often dramatic increase of sympathetic activity (Fig 10.1). Under such conditions, the pulse synchronous

Fig 10.2 Effect of various anaesthetics on muscle sympathetic nerve activity. Muscle sympathetic nerve activity is given as bursts per minute and percent change of baseline values. Induction of anaesthesia with thiopentone (TH, 4 mg/kg), propofol (P, 2 5 mg/kg), and propofol after premedication with diazepam (P & pm, 2-2 5 mg/kg and 0 25 mg/kg, respectively), is associated with a significant decrease in muscle sympathetic nerve activity, whereas etomidate (ETO, 0 3 mg/kg) exerts only minor effects. Isoflurane alone (ISO 1 2 vol% and ISO 0 6 vol%) also inhibits muscle sympathetic nerve activity. In contrast, nitrous oxide (N2O, 70%) causes sympathetic hyperactivity, which is counterbalanced by combination with isoflurane (ISO

Fig 10.2 Effect of various anaesthetics on muscle sympathetic nerve activity. Muscle sympathetic nerve activity is given as bursts per minute and percent change of baseline values. Induction of anaesthesia with thiopentone (TH, 4 mg/kg), propofol (P, 2 5 mg/kg), and propofol after premedication with diazepam (P & pm, 2-2 5 mg/kg and 0 25 mg/kg, respectively), is associated with a significant decrease in muscle sympathetic nerve activity, whereas etomidate (ETO, 0 3 mg/kg) exerts only minor effects. Isoflurane alone (ISO 1 2 vol% and ISO 0 6 vol%) also inhibits muscle sympathetic nerve activity. In contrast, nitrous oxide (N2O, 70%) causes sympathetic hyperactivity, which is counterbalanced by combination with isoflurane (ISO

0 6 vol% & N2O 70%, ISO 0 3 vol% and N2O 70%). (Data from Ebert et al.7 12 and Sellgren et al.10)

rhythmicity is lost and a more continuous activity pattern is observed in some patients.11

Effects of maintenance of anaesthesia on sympathetic nerve activity

As maintenance of anaesthesia is inevitably associated with suppression of cerebral activity, it is to be expected that all maintenance anaesthetic agents, that non-specifically inhibit neuronal activity, will also decrease sympathetic outflow. This has been demonstrated for propofol and halothane.10 11 In contrast to other volatile anaesthetic agents, larger concentrations of desflurane are associated with increasing sympathetic outflow, and sympathetic activation is amplified during rapid increase in the inspired desflurane concentration.14 There is evidence that this effect is caused by effector sites within the lungs.15 Desflurane caused marked increases in heart rate and blood pressure. These haemodynamic responses may pose a risk for myocardial ischaemia to patients with ischaemic heart disease (Fig 10.3).15 Isoflurane and sevoflurane were not associated with increases in muscle sympathetic nerve activity, even when the concentration was rapidly increased.16 17 Nitrous oxide (N2O) is also known to enhance sympathetic drive under certain circumstances. In healthy volunteers, a progressive increase in muscle sympathetic nerve activity was observed when low doses of N2O (25% and 40%) are inhaled via a facemask.9 These changes are associated with a significant increase in blood pressure. Sellgren et al11 also observed that sympathetic nerve activity is enhanced by N2O in comparison to the conscious state and that the combination of isoflurane and N2O increases sympathetic nervous activity compared with isoflurane alone11 (see Fig 10.2). Fentanyl 3 p,g/kg given before induction of anaesthesia to a spontaneously breathing patient induces a temporary slight increase in muscle sympathetic nerve activity,10 possibly because of associated hypercapnia. Data for sufentanil or alfentanil are currently not available.

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