Rakhshinda Zafar.
Amiodarone Toxicity.
Biomedica Jan ;14:56-8.

M I A. a 61 year old male patient with past medical history of mild congestive heart failure secondary to cardiomyopathy for 15 years, left ventricular ejection fraction reported on serial echocardiograms of 40-50%, atrial fibrillation for 5 years treated with Amiodrone and Non-Insulin dependent Diabetes mellitus. He was first seen on January 10, 1998 at Akram Medical Complex. He presented with symptoms of Class-IV dyspnea for the last 4 months and gross swelling of feet and for 2-3 month duration. 4 months ago on development of these symptoms he was admitted to a local hospital, where he ruled out acute myocardial infarction by electrocardiograms and cardiac isoenzymes. He was diagnosed to have hypothyroidism on blood work and amiodrone was discontinued. On examination, he was an average built man, with mild to moderate respiratory distress. Pulse was 54/min regular, BP was 140/90 mmHg, respiratory rate 20-24/min. There was jugular venous distention. Pulmonary examination was positive for bilateral lower zone rales. Cardiovascular examination revealed PMI (Point of Maximal Impulse) in 5th intercostal space in midclavicular line. On auscultation normal first and second heart sounds were heard, no extra heart sound or murmur was audible. Abdominal examination was positive for ascites and lower extremities revealed 2-3+ pitting edema of feet and legs upto knees. Lab results were T3 = 0.8, T4 = 28, TSH 53.4 units. ECG showed Type I atrial flutter with atrial rate of 200/min, and ventricular rate of 58/min with 3:1 block, left ventricular hypertrophy with secondary ST segment and T-wave changes and incomplete right bundle branch block. Pulmonary Function tests showed: PaO2 79.7, PCO2 35.1, pH 7.42, O2 Saturation 96.1%, FEV 1.27L/min, FVC 1.27L/min.

Diagnosis of Amiodrone toxicity was made. It was manifested as hypothyroidism, pulmonary involvement resulting in hypoxemia at rest on room air and restrictive pattern on peak flow metry, cardiovascular involvement resulting in slow rates of atrial flutter and slow A-V condution, also worsening of congestive heart failure.

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