[Lung problems in acute to subacute exposure to medium altitudes]

The hypobaric hypoxia of moderate altitude elicits various mechanisms of acute to subacute physiologic adaptations of the healthy lung: First of all it causes a hyperventilation, which increases the diminished arterial pO2. Because of hypoxemia-induced vasoconstriction, pulmonary arterial hypertension develops. The adrenergic stimulation of the cardiac output also increases the pulmonary perfusion. Most likely because of the diminished density of ambient air there is a measurable increase of exspiratory bronchial flow or, respectively, a diminution of the peripheral airway resistance. In higher altitudes, limitation of oxygen-diffusion under physical exertion is observed. The consequences of acute hypobaric hypoxia for diseased lungs depend on preexisting ventilation/perfusion mismatch or diffusion impairment. Arterial hypoxemia and hence also pulmonary arterial hypertension are increased. In the presence of normal chemoreceptor sensitivity (type pink puffer), a hyperventilation, which is often perceived as dyspnea by the patient, is induced. Mostly patients with chronic obstructive pulmonary disease adapt, however, surprisingly well to moderate altitude. Bronchial asthma improves frequently because allergen concentrations are low and air density is diminished. On the other hand, physical exertion in dry and cold ambient air may also elicit acute asthmatic exacerbations. The assessment of moderate altitude tolerance by patients with chronic lung diseases and prophylactic precautions before the ascent are discussed. The only altitude-specific disease of the healthy lung is the so-called high-altitude pulmonary edema. The major pathogenetic factor for its development is an inadequate or overshooting response to hypobaric hypoxia (nonuniform pulmonary arterial vasoconstriction, diminished hypoxic ventilatory drive, retention of fluid, centralization of blood volume and capillary leak). Prophylactic and therapeutic implications are discussed.