Tachycardia-Induced Bradycardia: A Rare Side Effect of Vagus Nerve Stimulator

Document Type

Conference Proceeding

Publication Date

10-2024

Publication Title

Chest

Abstract

INTRODUCTION: Vagus nerve stimulation (VNS) is a distinct epilepsy treatment for medically intractable seizures. We present the case of a male with Lennox-Gastaut syndrome who presented with septic shock and refractory bradycardia, in whom temporary inactivation of VNS resulted in improvement of heart rate and clinical status. CASE PRESENTATION: A young male with a history of Lennox-Gastaut requiring VNS placement 3 years ago, intellectual disability, and nephrolithiasis, presented with septic shock post-cystoscopy and ureteral stent placement. Laboratory tests revealed leukocytosis and urinalysis was suggestive of a urinary tract infection. Imaging showed a left-sided nephroureteral stent without obstruction. Norepinephrine was started for presumed septic shock. Subsequent echo evaluation yielded normal findings. Notably, bradycardia emerged after initiating the patient on norepinephrine and persisted upon transition to dopamine. These medications inherently have positive chronotropic effects causing tachycardia. Given the uncommon occurrence of bradycardia in this patient, further investigation suggested that tachycardia caused by vasopressors further triggered the VNS auto-stimulation system causing bradycardia. This was exacerbated by the effect of recent ureteral stent placement. Therefore, with the help of the VNS technician, deactivating the VNS and auto-stimulation improved his bradycardia. After improvement of septic shock and discontinuation of vasopressors, VNS was reactivated and the patient was discharged in stable condition. DISCUSSION: The vagus nerve forms part of the main peripheral nerve structure of the parasympathetic autonomic nervous system (ANS), containing afferent and efferent nerve fibers that innervate smooth muscle, internal organs, and vasculature of most major organ systems. Studies have shown that patients who benefit the most from VNS are those with post-traumatic epilepsy (79% seizure reduction), tuberous sclerosis (68%), and Lennox-Gastaut syndrome (48%) (3). In the heart, the postganglionic efferent vagal fibers can cause negative chronotropic and inotropic effects (4). The most common side effects of VNS include hoarseness, pharyngitis, cough, and laryngeal muscle spasms. Bradyarrhythmias, syncope, AV block, and asystole are rare but most serious adverse effects of VNS. The VNS has an auto-stimulation system that is designed to detect tachycardia as a warning sign of seizure and deliver extra stimulation accordingly. In our case, bradycardia was precipitated by activation of the VNS auto-stimulation secondary to vasopressor and inotrope-induced tachycardia. Ureteral stents can also cause vagal nerve stimulation leading to bradycardia, which was also explored in this case. Collaborative input from the VNS technician, electrophysiologist, and neurologist was pivotal in understanding the pathophysiology of VNS causing bradycardia in our patient. With increasing indications and use of VNS, it is important to be vigilant of the cardiovascular side effects of VNS. VNS deactivation may be both diagnostic and therapeutic in patients experiencing such adverse effects. CONCLUSIONS: Although uncommon, bradyarrhythmias have been documented as potential side effects during the operative and perioperative periods of VNS placement. However, these side effects could precipitate in patients who have remained asymptomatic for many years, as seen in our patient. Understanding the pathophysiology and functionality of the VNS auto-stimulation system was instrumental in our case. Timely recognition and intervention with a multidisciplinary approach can be lifesaving.

Volume

166

Issue

4 Suppl

First Page

A2830

Last Page

A2831

Comments

Chest 2024 Annual Meeting, October 6-9, 2024, Boston, MA

DOI

10.1016/j.chest.2024.06.1713

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