Comparison of age-differentiated incidence of sympathetic stimulation effect from rapid increases in desflurane concentration during induction of anesthesia with propofol and remifentanil; prospective

Abstract

Desflurane, since its introduction in clinical anesthetic practice in the 1990’s, had been known to have sympathetic stimulation effects, including tachycardia and/or hypertension, when administered rapidly in > 1 minimal alveolar concentration (MAC) during induction of anesthesia. The present study is to compare hemodynamic responses to inhalation anesthetics of 1 MAC desflurane with those to 1 MAC sevoflurane, which were calculated with age-based formula in adult patients undergoing elective spine surgery. A total of 400 patients were enrolled in this prospective, randomized, single-blinded investigation. They were divided into two groups: the Desflurane (D) group and the Sevoflurane (S) group. Each group was subdivided by age: 20-29, 30-39, 40-49 and 50-59 years (D20, D30, D40, D50, and S20, S30, S40, S50, respectively). 1 MAC of desflurane or sevoflurane was calculated with an age-based formula, suggested by Mapleson WW. Measured parameters were compared between the D and S groups, and between age subgroups in each group. When a patient arrived in the operating room, electrocardiogram lead Ⅱ, pulse oximetry, non-invasive blood pressure, oxygen saturation (SPO2) and Bispectral index (BIS) were applied. Intravenous (IV) remifentanil infusion of 0.1㎍/㎏/min was initiated, and for 5-10 minutes, the heart rate, systolic, diastolic and mean arterial pressure, and peripheral oxygen saturation were measured, and used as baseline values. Anesthesia was induced with IV propofol of 1-1.5㎎/㎏, and 10㎎ was additionally given until the patient was unconscious. 1 MAC of desflurane of sevoflurane in oxygen (O2)/air > 5L/min was given via the face mask with manual ventilation. IV rocuronium of 0.4㎎/㎏ was given to induce muscle relaxation. Heart rate(HR), systolic, diastolic and mean arterial pressure (SAP, DAP and MAP) were measured and recorded every minute for five minutes. After endotracheal intubation, hemodynamic parameters were measured and recorded every minute for five minutes with mechanical ventilation. Inter-group comparison: After induction of anesthesia, the HR was elevated in the D group, in contrast to reductions in the S group (p<0.01 every minute, except for 2 min.). After endotracheal intubation, the HR was elevated in both groups, but significantly more elevated in the D group (p<0.01, except for 1 min.). In both groups, the arterial blood pressures were generally reduced after induction and after intubation, but the decreases were significantly greater in the S group after induction (p<0.05, except for 2min.). Intra-group comparison: In the D group, the HR in patients older than 30 years was reduced from the baseline values, in contrast to continuous elevations in D20. After endotracheal intubation, the elevated HR was maintained in all groups, but significantly less elevated in D40 and D50 at 3,4, and 5 min. compared to that in D20 (p<0.05, except for D40 at 2 min.). In the S group, the changes in HR after induction of anesthesia were diverse in direction without significant differences among age subgroups. Compared to sevoflurane, 1 MAC of desflurane given for induction of anesthesia caused more elevations in HR, especially in younger patients. And, this might be related to baroreceptor reflex to desflurane-induced vasodilation because inhalation of 1 MAC desflurane did not induce hypertensive responses in all age subgroups. Further investigations are necessary to find methods to mitigate adverse hemodynamic effects of inhalation anesthetics.