The Effect of Advancing Age on the Sympathetic Response to Laryngoscopy and Tracheal Intubation

The effect of aging on the hemodynamic and sympathetic response to tracheal intubation was evaluated in 27 patients aged 18 to 80 years, ASA Class I and II, given atropine 0.4 mg and diazepam 10 mg as premedication and thiopental, 4.0 mg/kg, and succinylcholine 100 mg for anesthesia induction. Layngoscopy and tracheal intubation was performed 60 seconds after induction. The elderly had significantly less chronotropic response to intubation 2, 3, 4, and 5 minutes after induction so that the maximum increase in heart rate above awake values was negatively correlated with age (R = −0.66, P < 0.001). Baseline systolic blood pressure (SBP) and mean BP increased significantly with age (R = 0.81, P < 0.001 and R = 0.76, P < 0.001, respectively) but age was not significantly related to increases in SBP and mean BP following intubation. Baseline plasma norepinephrine (NE) levels increased with age (R = 0.51, P < 0.01). Following intubation, mean plasma NE concentrations were significantly higher in elderly patients than young patients, despite the diminished heart rate response. Heart rate (HR) per pg/ml of NE, a measure of cardiac sensitivity to beta stimulation, was therefore significantly less 2, 3, and 4 mins after induction in elderly patients than in younger patients. To determine if this alteration in cardiac sensitivity to endogenous catecholamines was reflected by changes in beta receptor function on lymphocytes, beta receptor density and the proportion of receptor binding agonist with high affinity (%RH) were measured. No significant correlation between beta-receptor afinity for agonist, %RH, or receptor density was found with age, HR, or HR per pg/ml NE. Our results indicate that the elderly have a significantly lower chronotropic response to intubation than do the young. As plasma catecholamines were higher in the elderly, while the blood pressure rise was not different, we conclude that this loss of response is probably not due to diminished sympathetic response or baroreceptor function. However, we were not able to correlate the heart response to norepinephrine with direct measures of beta2 receptor function on circulating lymphocytes.