Absence of Reflex Tachycardia After Spinal Anesthesia in the Elderly

To the Editor: We have read with interest the recent dose-response study of IV atropine after spinal anesthesia in elderly patients (1). The authors hypothesized that depressed reflex tachycardia might contribute to the pathogenesis of hypotension and demonstrated that a small dose of IV atropine effectively reduced the need of ephedrine to treat predefined, spinal anesthesia-induced hypotension in patients >60 yr of age. Their finding was clinically useful; however, their explanation for the depressed reflex tachycardia raises some questions. First, the authors stated that the absence of reflex tachycardia might result from the blockade of cardioaccelerator sympathetic fibers with a reference (2), although higher level of sensory analgesia had not been determined in this article. In fact, we frequently observe in elderly patients after subarachnoid blockade that no clinically significant increase in heart rate (HR) occurs even with the higher level of analgesia below T10 and with clinically significant hypotension, which would otherwise produce HR increases in younger patients. Second, the authors also speculated “reverse” Bainbridge reflex as another etiology. However, physiological importance or even the existence of Bainbridge reflex is questionable in humans (3–5). Rather, depressed arterial baroreflex control of HR (6,7) and age-dependent reduction of β1-receptor-mediated responsiveness (8) are more likely explanations for the attenuated HR response to spinal anesthesia-induced hypotension in the elderly.