High altitude pulmonary edema is characterized hemodynamically by a markedly restricted pulmonary vascular bed. Pulmonary vascular resistance is six to eight times higher than control values at altitude, and mean pulmonary pressure is generally elevated two to four-fold over control values. We wished to compare the effect of various vasodilators on the hemodynamics of HAPE, both to gauge their potential effectiveness in treatment of HAPE, and also to gain clues as to the mechanism of the altered pulmonary circulation. In a series of field experiments using a total of 16 subjects with HAPE and 10 well controls, we measured pulmonary hemodynamics by non-invasive Doppler echocardiography. The per cent reduction in pulmonary vascular resistance and mean pulmonary artery pressure, respectively, were 46 and 33 for oxygen, 30 and 29 for nifedipine, 29 and 25 with hydralazine, 57 and 42 with phentolamine, and 72 and 52 when oxygen and phentolamine were combined. All the vasodilators improved gas exchange, suggesting a link between edema formation and pulmonary vasoconstriction. A number of vasodilators may be useful in the treatment of HAPE; the superiority of an alpha adrenergic blocker may implicate the sympathetic nervous system in the pathophysiology of high altitude pulmonary edema.

To examine the role of barometric pressure in high-altitude pulmonary edema, we randomly exposed five unanesthetized chronically instrumented sheep with lung lymph fistulas in a decompression chamber to each of three separate conditions: hypobaric hypoxia, normobaric hypoxia, and normoxic hypobaria. A combination of slow decompression and/or simultaneous adjustment of inspired PO2 provided three successive stages of simulated altitudes of 2,600, 4,600, and 6,600 m during which hemodynamics and lymph flow were monitored. Under both hypoxic conditions we noted significant and equivalent elevations in pulmonary arterial pressure (Ppa), cardiac output, and heart rate, with left atrial and systemic pressures remaining fairly constant. Normoxic hypobaria was also accompanied by a smaller but significant rise in Ppa. Lymph flow increased to a highly significant maximum of 73% above base line, accompanied by a slight but significant decrease in lung lymph-to-plasma protein ratio, only under conditions of combined hypobaric hypoxia but not under equivalent degrees of alveolar hypoxia or hypobaria alone. Arterial hypoxemia was noted under all three conditions, with arterial PO2 being uniformly lower under hypobaric conditions than when identical amounts of inspired PO2 were delivered at normal atmospheric pressure. We therefore hypothesize that alveolar pressure significantly alters the Starling forces governing transcapillary fluid flux in the lung and may affect the alveolar-arterial gradient for O2 as well.

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