SAT-591 Heart Failure Increases Likelihood of Asystolic Cardiac Arrest in Acute Hyperthyroidism

Introduction: Thyrotoxicosis produces multiple catabolic effects including arrhythmias and heart failure. Rapid treatment of overt hyperthyroidism is important to prevent permanent end-organ damage. Clinical Case: A 55yo M with no prior past medical history presents to the ED with 2 weeks of progressive dyspnea on exertion and bilateral lower extremity and scrotal edema, with unintentional 40lb weight gain in 6 months. N-terminal pro-BNP was elevated to 3965pg/mL (normal 5-125pg/mL), with cardiomegaly and right-sided pleural effusion on chest x-ray, concerning for new-onset heart failure. While in the ED, the patient went into rapid atrial fibrillation. He was given 30mg IV Diltiazem bolus, and started on a Diltiazem infusion @ 15cc/h. His new onset heart failure was treated with 60mg IV Lasix. One day later, heart rates remained elevated to 120s, so he was started on metoprolol succinate 25mg in order to optimize rate control. TSH was noted to be less than 0.01mIU/L (normal 0.27 -4.20 mIU/L), with free T4 greater than 7.77ng/dL (normal 0.80 - 1.90 ng/dL). Endocrine was consulted for hyperthyroidism. On Day 2 of hospitalization, metoprolol was switched to propranolol 80mg TID. Methimazole 30mg daily was also started. The patient received a dose of Metoprolol at approximately 830AM. His first dose of propranolol was given at approximately 4PM. Diltiazem infusion and Lasix infusions were continuing at this time as well. After receiving first dose of propranolol, the patient became bradycardiac, hypotensive to 80s/50s within 30 minutes. Poison control was contacted. Diltiazem infusion and Lasix were discontinued. Propranolol was decreased to 40mg TID, although beta blocker toxicity less likely given rapid onset of symptoms. One hour later, the patient went into asystolic cardiac arrest. Conclusion: In the absence of heart failure, symptoms of thyrotoxicosis improve with use of beta-blockers. However, patients with heart failure and thyroid crisis depend on the inotropic effects of excess T3 to maintain their cardiac output and support hemodynamics. Rate controlling medications in these scenarios further reduces inotropic function and predisposes to cardiac arrest. There are prior case reports demonstrating circulatory collapse after administration of non-selective beta blockers, in patients with thyroid storm. However, although prompt treatment of thyrotoxicosis is important, increased caution should be taken when treating hyperthyroidism with associated heart failure to avoid increased risk of circulatory collapse and cardiac arrest. References: Abubakar H, Singh V, Arora A, Alsunaid S. Propranolol-Induced Circulatory Collapse in a Patient With Thyroid Crisis and Underlying Thyrocardiac Disease: A Word of Caution. Journal of Investigative Medicine High Impact Case Reports. 2017;5(4):2324709617747903. doi:10.1177/2324709617747903.