Amiodarone pulmonary toxicity is a major clinical problem limiting the utility of this powerful therapeutic agent. The clinical manifestations of amiodarone lung toxicity are protean, but the most common presentation is that of an indolent illness characterized by dyspnea and often associated with cough and/or fever. Diffuse radiographic abnormalities are common, but localized infiltrates can be seen as well. The typical physiologic changes are the development of diffusing impairment and a restrictive ventilatory defect. In the absence of a 15% decline in DLCO from the pretreatment value, significant amiodarone toxicity appears to be unlikely. The diagnosis is made by the careful exclusion of other causes for the observed illness and the finding of clinical, radiographic, physiologic, and pathologic abnormalities compatible with amiodarone toxicity. Although the pathologic findings of amiodarone lung can be distinctive, the histologic demonstration of foam cells and ultrastructural lamellar inclusions alone does not distinguish toxic from nontoxic patients receiving amiodarone. If reasonable alternative antiarrhythmic therapy is available, amiodarone should be withdrawn. If the severity of illness warrants, a trial of corticosteroid therapy is reasonable. Some patients can be maintained on continued therapy despite toxicity, if the drug is deemed to be absolutely essential and clinical deterioration does not continue. The prognosis of patients who develop amiodarone pulmonary toxicity seems to be poor, but may be largely determined by the underlying cardiac disease.