Atrial fibrillation is a common manifestation seen in patients with hyperthyroidism and thyroid storm. The presence of excess thyroid hormone (TH) alters adrenergic receptors in the heart and blood vessels, thereby causing an increase in sympathetic function and atrial fibrillation as a sequela of this excess circulating hormone. Excess thyroid hormone (T3) shortens the action potential of cardiomyocytes in the pulmonary vein, which facilitates the generation of reentrant circuits causing atrial fibrillation. Thyroid hormone can regulate cardiac beta-adrenergic receptor expression leading to enhanced catecholamine sensitivity of beta-adrenergic coupled cardiac response. We present a case of a 64-year-old female with a history of hypertension (HTN), nonobstructive coronary artery disease (CAD), congestive heart failure (CHF) [ejection fraction (EF) 35-40%], chronic obstructive pulmonary disease (COPD) on long-term oxygen therapy (LTO2), obstructive sleep apnea (OSA)/hypoventilation syndrome, atrial flutter/atrial fibrillation with a loop recorder on rivaroxaban, and obesity who presented to the emergency department (ED) with gastroenteritis symptoms precipitating difficulty breathing and atrial fibrillation with a rapid ventricular response (HR 140-150) requiring ICU admission for rate and rhythm control. During the course of hospitalization, she was treated with an amiodarone infusion, which induced thyrotoxicosis and increased the ectopic electrical activity in the atrium, worsening atrial fibrillation. On day 3, amiodarone was stopped, and IV esmolol and metoprolol tartrate PO were continued with no resolution of atrial fibrillation. The patient was transitioned to propranolol, which achieved adequate heart rate control prior to discharge. The aim of our review is to highlight that propranolol should be used over metoprolol in patients with hyperthyroidism-induced atrial fibrillation due to the effect of propranolol on blocking the activity of T4 conversion to active T3 and, as such, blocking its effect on cardiac myocytes, terminating reentrant atrial excitation.