SYMPATHETIC HYPERACTIVITY DURING DESFLURANE ANESTHESIA IN HEALTHY-VOLUNTEERS - A COMPARISON WITH ISOFLURANE

Background. Desflurane has been reported to produce more tachycardia a nd hypertension on induction than isoflurane. The present study employ ed microneurography to determine whether these cardiovascular effects were related to sympathetic outflow. Methods: In 14 healthy, young (ag e 20-31 yr) volunteers, arterial pressure was measured from the radial artery, forearm blood flow was derived by strain gauge plethysmograph y, and sympathetic nerve activity (SNA) directed to skeletal muscle bl ood vessels was recorded from a tungsten needle placed percutaneously into the peroneal nerve. Heart rate, blood pressure, muscle SNA, respi ration, tidal volume, end-tidal carbon dioxide, and desflurane or isof lurane concentrations (infrared spectroscopy) were continuously monito red before and during anesthesia. Two minutes after administering thio pental (5 mg/kg) and vecuronium (0.2 mg/kg), desflurane (n = 7) or iso flurane (n = 7) was titrated gradually to the inspired gas over severa l minutes to 1.5 MAC. Results: The initiation of desflurane anesthesia resulted in significant changes that included a 2.5-fold increase in SNA, hypertension (peak mean arterial pressure 114 +/- 3 mmHg), tachyc ardia (peak heart rate 102 +/- 6 beats/min), facial flushing, and tear ing. Moderate upper airway obstruction developed in three subjects app roximately 4 min after initiating desflurane, despite neuromuscular bl ockade. These responses were not observed in subjects receiving isoflu rane. After tracheal intubation, the anesthetic concentration was main tained at 0.5 MAC for 30 min. Steady-state measurements of hemodynamic s and SNA were obtained. Similar steady-state measurements were obtain ed 15 min after establishing 1.0 and 1.5 MAC. Both anesthetics produce d a progressive reduction in blood pressure and forearm vascular resis tance, and muscle SNA gradually increased. In subjects receiving desfl urane, heart rate remained unchanged until the 1.5-MAC level was reach ed, at which time tachycardia (a 10-beat/min increase) was noted. The transition from 1.0 to 1.5 MAC desflurane resulted in significant hear t rate increases (>30 beats/min), hypertension (> 30 mmHg), and a doub ling of SNA that persisted for several minutes. These responses did no t occur in the isoflurane group. Conclusions. Titration of desflurane following thiopental induction and increasing the concentration of des flurane from 1.0 to 1.5 MAC result in sympatho-excitation, hypertensio n and tachycardia in healthy, young volunteers. Until methods are dete rmined to attenuate these responses, desflurane should be administered with great caution to patients who may be placed at risk by these res ponses.