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Can J Anaesth. 1998 Jun;45(6):533-40.

Dissociation between haemodynamics and sympathetic activation during anaesthetic induction with desfluranes.

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Mount Zion Medical Center, Department of Anaesthesia, University of California, San Francisco 94115, USA.



To compare the simultaneous haemodynamic effects, sympathetic activation and cardiac risks associated with desflurane used in a balanced technique, with those of isoflurane anaesthesia.


A prospective, randomized, open label study was conducted at a University medical centre. Forty patients undergoing major non-cardiac surgery were randomized to receive either desflurane or isoflurane as the primary anaesthetic agent. After premedication, fentanyl and thiopentone were administered i.v.. Anaesthesia was increased up to 1.0 MACET in O2 via controlled mask ventilation and maintained at 1.0 MAC before tracheal intubation. Maintenance consisted of N2O, O2 and desflurane or isoflurane for 10 min. During the study, HR and arterial BP were continuously measured, as were ECG ST-segments and ventricular dysrhythmias using a 3-channel Holter ECG recorder. Left ventricular global and regional function were measured using precordial echocardiography. Serial plasma catecholamine concentrations were measured.


For both groups, HR was maintained without increases over baseline values while systolic BP showed a progressive decrease during induction. Use of beta blockade during induction was higher in the desflurane (7/20 = 35%) than in the isoflurane group (1/20 = 5%), P = 0.04. The plasma norepinephrine concentrations progressively increased in the desflurane group but not in the isoflurane group. Four patients in the desflurane and three in the isoflurane group developed transient worsening of regional function but no change in mean left ventricular ejection fraction area and no ECG ischaemia occurred during anaesthetic induction.


Desflurane differs from isoflurane in that sympathetic stimulation persisted despite blunting of potential hyperdynamic haemodynamic responses by narcotic and beta blockade. However, this sympathetic activation did not appear to increase cardiac risks.

[Indexed for MEDLINE]

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