To the Editor:

—We would like to thank Drs. Thrush and Downs for their interesting case report, “Vagotonia and Cardiac Arrest during Spinal Anesthesia.”1These authors discuss the contribution of sympathetic and parasympathetic nervous system imbalance during spinal anesthesia as a mechanism of asystole. They state that in a patient with vasovagal syncope, the combination of cardiac sympathetic blockade and vagal stimulation disturbed this autonomic balance even further. It is certainly intuitive to think that because the spinal anesthetic blocks cardiac sympathetic efferent nerves and not vagal efferent nerves, a relative parasympathetic dominance or vagotonic state would result. However, if this was the case, why would severe bradycardia and asystole not occur more often with high-spinal and epidural anesthesia?

As discussed in previous work, another neural pathway is probably involved. 2–3Instead of a relative vagal dominance, there was evidence of a decrease in both sympathetic and vagal outflows (efferents) in patients with cardiac sympathectomy after spinal anesthesia. The vagal outflow, which was not directly blocked by the anesthetic, was somehow concomitantly reduced or inhibited in parallel with the anesthetic blockade of the sympathetic efferent outflow. 3Therefore, a state of reduced sympathetic and vagal outflow resulted, which fortunately maintained sympathetic and vagal balance and maintained the baseline heart rate.

It has been proposed that complete blockade of sympathetic afferent pathways, which have an anatomical distribution similar to the sympathetic efferent pathways, will interrupt necessary visceral communication lines to central neural centers and will result in a self-protective reduction of parasympathetic activity. 3The activity of sympathetic and parasympathetic (vagal) efferents are normally under the continuous influence of and modulation by sympathetic and parasympathetic afferent input to central control centers. 4,5Therefore, blockade of both sympathetic efferent and afferent activity has significance in the overall mechanism of cardiac arrest during spinal anesthesia. We think that sympathectomy of the heart after spinal anesthesia should be thought of as a condition with the potential to develop clinically significant vagal dominance or vagotonia. Bradycardia, asystole, and cardiac arrest from autonomic imbalance during spinal anesthesia are more likely to result if precipitating events resulting in vagal stimulation occur while cardiac sympathetic blockade exists, as reported by Thrush and Downs. 1We agree with these authors that during spinal anesthesia the clinician should have a high index of suspicion for at-risk scenarios that could result in cardiac arrest and a low threshold for the initiation of prophylactic or resuscitative treatment throughout the perioperative period.

Thrush DN, Downs JB: Vagotonia and cardiac arrest during spinal anesthesia. A nesthesiology 1999; 91:1171–3
Pruett JK, Yodlowski EH, Introna RPS, Buggay DS, Crumrine RS: The influence of spinal anesthetics on heart rate variations. Pharmacology 1991; 10:51–5
Introna R, Yodlowski E, Pruett J, Montano N, Porta A, Crumrine R: Sympathovagal effects of spinal anesthesia assessed by heart rate variability analysis. Anesth Analg 1995; 80:315–21
Malliani A, Pagani M, Lombardi F, Cerutti S: Cardiovascular neural regulation in the frequency domain. Circulation 1991; 84:482–92
Malliani A: Cardiovascular sympathetic afferent fibers. Rev Physiol Biochem Pharmacol 1982; 94:11–74