Thyrotoxic periodic paralysis (TPP) is a rare complication primarily associated with thyrotoxicosis, particularly in individuals with Graves’ disease. While more common in males aged 20 to 40, it can occur across all ethnic backgrounds. It is the most common type of acquired periodic paralysis. The condition is triggered by factors like exercise, stress, diet, and certain medications. The diagnosis is confirmed by severe hypokalemia and elevated thyroid hormones in the presence of acute flaccid paralysis. Immediate treatment involves correcting hypokalemia, while long-term management focuses on normalizing thyroid levels. In this article, we will report a case of a 30-year-old Middle Eastern man who presented to the emergency room with severe muscle weakness following extensive exertion and a high-carbohydrate diet. Physical examination revealed motor weakness in all limbs, particularly his lower limbs. Initial tests showed marked hypokalemia and biochemical thyrotoxicosis with suppressed thyroid-stimulating hormone (TSH) and elevated free triiodothyronine (T3) and free thyroxine (T4). An electrocardiogram (ECG) indicated signs of severe hypokalemia with an atrioventricular (AV) block. After he was diagnosed with TPP, the patient received oral and intravenous potassium infusions and was started on anti-thyroid medications, most importantly beta (β)-blockers. Following acute treatment, his potassium levels normalized, and he regained full muscle function. Ultimately, he was maintained on anti-thyroid medications at discharge to maintain an euthyroid state in order to prevent future recurrences of symptoms. Consequently, in patients presenting with acute flaccid paralysis, potassium level, and thyroid function should be investigated in order to promptly diagnose complications of thyrotoxicosis and to start an early appropriate combined therapy. The early and rapid management of TPP can prevent serious cardiopulmonary complications.