Presentation Details
| Unmasked: Severe Perioperative Bradycardia Following GLP-1 Receptor Agonist Withdrawal in Undiagnosed Sinus Node Dysfunction Geoffrey Carl G.Rodriguez, MBA, MLS, Olivia Valentine, BS, Lara R.India, MD, FASA, , Harvey J.Woehlck, MD. Department of Anesthesiology - Medical College of Wisconsin, Milwaukee, WI, USA |
Abstract
CASE PRESENTATION: A 72-year-old male was evaluated before elective cranioplasty. His history included atrial fibrillation, Mobitz I AV block, HTN, OSA, TIIDM, and bradycardia. Two weeks prior, his cardiologist discontinued his β-blocker due to resting HR in the low 50s. Five days before surgery, he presented to the preoperative clinic, where he remained asymptomatic with HR 54 bpm. He was advised to hold his GLP-1-RA, dulaglutide, for at least seven days before surgery per hospital policy; this resulted in a twelve-day hold due to a previous missed dose. On the day of surgery, he presented with sinus bradycardia (30 bpm) with preserved perfusion and alertness. After receiving 1mg glycopyrrolate cumulatively without chronotropic response, surgery was cancelled. Emergency Department evaluation revealed normal electrolytes and thyroid function and ruled out acute ischemia or other major adverse cardiac events (MACE). Telemetry monitoring showed persistent sinus bradycardia with intermittent sinoatrial exit block. A permanent pacemaker was later implanted.
DISCUSSION: GLP-1-RA's exert direct chronotropic effects on the SA node through sympathetic activation and calcium-handling pathways. Thus, tachycardia is a side effect of GLP-1-RA therapy. Discontinuation removes this compensatory effect and may precipitate bradycardia in patients with conduction disease. This case highlights a perioperative vulnerability: GLP-1-RA withdrawal can uncover sinus node dysfunction despite absence of metabolic triggers or MACE. Failure of anticholinergic therapy underscores that GLP-1-RA withdrawal affects intrinsic SA node physiology rather than vagally-mediated mechanisms. This suggests GLP-1-RA therapy may have masked progressive conduction disease in this patient.
CONCLUSIONS: GLP-1-RA discontinuation can unmask underlying sinus dysfunction, producing acute-on-chronic bradycardia refractory to anticholinergic therapy. Current guidelines focus on aspiration risk associated with GLP-1-RA therapy but don't address withdrawal as a potential hemodynamic stressor in patients with conduction abnormalities. This case underscores the need for evidence-based perioperative guidelines addressing withdrawal timing and cardiac monitoring in high-risk patients.
No part of this publication may be reproduced, distributed, or transmitted in any form or by any means, including photocopying, recording, or other electronic or mechanical methods, without the prior written permission of the author.
DISCUSSION: GLP-1-RA's exert direct chronotropic effects on the SA node through sympathetic activation and calcium-handling pathways. Thus, tachycardia is a side effect of GLP-1-RA therapy. Discontinuation removes this compensatory effect and may precipitate bradycardia in patients with conduction disease. This case highlights a perioperative vulnerability: GLP-1-RA withdrawal can uncover sinus node dysfunction despite absence of metabolic triggers or MACE. Failure of anticholinergic therapy underscores that GLP-1-RA withdrawal affects intrinsic SA node physiology rather than vagally-mediated mechanisms. This suggests GLP-1-RA therapy may have masked progressive conduction disease in this patient.
CONCLUSIONS: GLP-1-RA discontinuation can unmask underlying sinus dysfunction, producing acute-on-chronic bradycardia refractory to anticholinergic therapy. Current guidelines focus on aspiration risk associated with GLP-1-RA therapy but don't address withdrawal as a potential hemodynamic stressor in patients with conduction abnormalities. This case underscores the need for evidence-based perioperative guidelines addressing withdrawal timing and cardiac monitoring in high-risk patients.
No part of this publication may be reproduced, distributed, or transmitted in any form or by any means, including photocopying, recording, or other electronic or mechanical methods, without the prior written permission of the author.
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