Cardiac patients and cardiac rehabilitation staff are often concerned about travel to moderate altitude (3,000 to 10,000 ft) after a cardiac event. With increasing altitude, the barometric pressure decreases, resulting in a reduction in arterial oxygen partial pressure and content. Conceivably, this relative hypoxia could disrupt the balance between myocardial oxygen demand and supply, precipitating cardiac symptoms or a clinical event. Physiologic responses to moderate altitude exposure include increased pulmonary ventilation and heart rate (transient increase at rest and a more prolonged increase with submaximal exercise), hemoconcentration, a possible rightward shift in the oxyhemoglobin dissociation curve, and a modest reduction in physical work capacity. Medical concerns include such altitude disorders as acute mountain sickness (AMS) and high-altitude pulmonary edema (HAPE) as well as potential cardiac problems such as angina pectoris, arrhythmia, sudden death, congestive failure, and myocardial infarction. Acute mountain sickness is commonly experienced but is of little significance; on the other hand, HAPE, a noncardiac form of pulmonary edema, is potentially fatal but is extremely rare. Review of the physiologic responses and clinical experience at moderate altitude indicates that, for most cardiac patients, mountain travel constitutes a negligible risk. Subgroups of patients with preexisting pulmonary hypertension, uncompensated congestive heart failure, unstable angina pectoris, recent myocardial infarction, and patients with severe anemia or a decreased arterial oxygen saturation may be at higher risk than other cardiac patients.