Patients with heart failure may be susceptible to increased physiologic cardiorespiratory changes with altitude exposure. The main acute perturbation is related to increased sympathetic activity resulting in hemodynamic changes (vasoconstriction, tachycardia) as well as release of vasoactive factors (inflammatory mediators).
Regarding the systemic circulation, increases in sympathetic activity elevate the systemic vascular resistance, blood pressure, and heart rate resulting in a reduced exercise capacity. Systemic vasoconstriction may also occur as a reflex response to the high pulmonary arterial pressures. In practice, however, it has been shown that altitude-induced changes in systemic blood pressure do not appear to be clinically relevant.
On the pulmonary circulation side, pulmonary vasoconstriction at altitude leads to pulmonary hypertension (particularly during exercise), increasing sympathetic activity even more, and further impairing right ventricle filling and output. This increase in pulmonary circulatory pressure appears to be most significant factor in reducing cardiopulmonary performance in patients with heart failure.
Several studies deserve mention. One study involving ischemic cardiomyopathy patients noted a slightly reduced exercise capacity during a maximal symptom-limited bicycle stress test at moderate altitude, 2,500 m (8,200 ft), when compared with low altitude, 155 versus 162 watts, respectively ( P < .05). In the ischemic cardiomyopathy patients, the test was stopped more frequently because of dyspnea than at sea level (36% vs 9%). Because of the paucity of data, we discuss one study of simulated altitude-induced hypoxia on exercise capacity in patients with chronic heart failure. They performed cardiopulmonary exercise tests with inspired oxygen fractions equal to those at sea level and simulating low, moderate, and high altitude on 38 patients with clinically stable heart failure and on 14 healthy subjects. Of the patients with heart failure, about one third had maximal oxygen consumption > 20 mL/kg per minute; one third, 15 to 20 mL/kg per minute, and one third, < 15 mL/kg per minute at baseline. All subjects were able to complete the tests with no complications such as arrhythmia, angina, or ischemia. In the patients with heart failure, maximum work rate decreased in parallel with increasing simulated altitude, with a greater reduction in maximum physical activity in proportion to their exercise capacity at sea level.
In summary, patients with heart failure are likely to notice reduced functional capacity at moderate to high altitude when compared with at sea level. The main physiologic effect appears to be increased right ventricular afterload.
John P. Higgins, MD, MPhil, Troy Tuttle, MS, Johanna A. Higgins, MD