A patient with a previous history of myocardial infarction and ventricular arrhythmia is on treatment for a few months. He developed fatigue, dyspnea, and weight gain. He had also developed pulmonary fibrosis. Which of the following drugs is responsible for the side effects mentioned above?

Correct Answer: B. Amiodarone

Amiodarone is a Class III antiarrhythmic with iodine-rich structure that causes multiple organ toxicities with chronic use. The clinical triad presented—fatigue, dyspnea, weight gain, and pulmonary fibrosis—is pathognomonic for amiodarone toxicity. Pulmonary fibrosis occurs in 1–17% of patients on long-term amiodarone and is one of the most serious dose-dependent and cumulative adverse effects. The mechanism involves direct cytotoxic injury to pneumocytes and alveolar macrophages, leading to inflammation and fibrosis. Fatigue and dyspnea are early manifestations of amiodarone-induced pulmonary toxicity. Weight gain results from amiodarone's effect on thyroid metabolism—it causes both hypothyroidism (due to iodine content blocking thyroid hormone synthesis) and hyperthyroidism (due to iodine-induced thyroiditis). Other well-documented amiodarone toxicities include hepatotoxicity, corneal deposits (reversible), photosensitivity, blue-gray skin discoloration, and QT prolongation. In Indian practice, amiodarone remains a first-line agent for ventricular arrhythmias post-MI despite these risks, requiring regular monitoring of pulmonary function, liver enzymes, and thyroid function (TSH, free T4) every 6 months. The cumulative dose and duration of therapy are critical risk factors.

Why the other options are wrong

A. Atenolol — Atenolol is a selective β1-blocker used safely in post-MI patients and arrhythmia management. It does not cause pulmonary fibrosis, weight gain, or fatigue as primary adverse effects. While fatigue can occur with beta-blockers, it is mild and reversible; pulmonary fibrosis is not an established toxicity. This is a distractor leveraging the patient's cardiac history. C. Spironolactone — Spironolactone is a potassium-sparing diuretic used in heart failure and post-MI settings. Its main adverse effects are hyperkalemia, gynecomastia, and sexual dysfunction—not pulmonary fibrosis or the constellation of systemic toxicities described. NBE may include this to test whether students confuse diuretic side effects with antiarrhythmic toxicities. D. Aspirin — Aspirin is an antiplatelet agent used universally in post-MI patients for secondary prevention. It causes GI bleeding, dyspepsia, and rarely Reye syndrome—not pulmonary fibrosis, weight gain, or systemic fatigue. This is a standard post-MI drug with a well-defined, benign adverse effect profile unrelated to the presented symptoms.

High-Yield Facts

Mnemonics

AMIODARONE TOXICITY (A-TOXIN) Arrhythmia (QT prolongation, torsades), Thyroid (hypo/hyperthyroidism), Ophthalmic (corneal deposits), Xanthomas (blue-gray skin), Interstitial fibrosis (pulmonary), Neurotoxicity (tremor, ataxia), Elevated LFTs (hepatotoxicity). Use when reviewing amiodarone's multi-organ toxicity profile. PFT Monitoring in Amiodarone (DLCO-FVC) Diffusing capacity (DLCO) drops first in amiodarone-induced pulmonary fibrosis; Forced vital capacity (FVC) follows. A >20% drop in DLCO or FVC warrants amiodarone discontinuation. Bedside memory: 'DLCO dips before FVC falls.'

NBE Trap

NBE pairs amiodarone with post-MI/arrhythmia history to lure students into thinking beta-blockers (atenolol) or diuretics (spironolactone) are the culprits. The specific mention of pulmonary fibrosis is the discriminator—only amiodarone causes this in the given drug list.

Clinical Pearl

In Indian practice, amiodarone remains the gold standard for life-threatening ventricular arrhythmias post-MI despite toxicity risks. A patient on amiodarone >6 months presenting with dyspnea and fatigue should trigger immediate PFT and TSH testing—early detection of pulmonary fibrosis (DLCO decline) can prevent irreversible lung damage by prompt drug discontinuation.

_Reference: KD Tripathi Ch. 31 (Antiarrhythmic Drugs); Harrison Ch. 226 (Arrhythmias); Robbins Ch. 15 (Lung Pathology—Drug-Induced Fibrosis)_