Separating the direct effect of hypoxia from the indirect effect of changes in cardiac output on the maximum pressure difference across the tricuspid valve in healthy humans

In healthy humans, changes in cardiac output are commonly accommodated with minimal change in pulmonary artery pressure. Conversely, exposure to hypoxia is associated with substantial increases in pulmonary artery pressure. In this study we used non-invasive measurement of an index of pulmonary artery pressure, the maximum systolic pressure difference across the tricuspid valve (ΔPmax), to examine the pulmonary vascular response to changes in blood flow during both air breathing and hypoxia. We used Doppler echocardiography in 33 resting healthy humans breathing air over 6-24 h to measure spontaneous diurnal variations in ΔPmax and cardiac output. Cardiac output varied by up to ∼2.5 l/min; ΔPmax varied little with cardiac output [0.61±0.74 (SD) mmHg min l -1]. Eight of the volunteers were also exposed to eucapnic hypoxia (end-tidal PO2 = 50 mmHg) for 8 h. In this group ΔP max rose progressively from 21 mmHg to 37 mmHg over 8 h. By comparing diurnal variations in ΔPmax during air breathing with changes in ΔPmax during hypoxia in the same eight individuals, we concluded that only approximately 5% of the changes in ΔPmax during hypoxia could be attributed to concurrent changes in cardiac output. The low sensitivity of ΔPmax to changes in cardiac output makes it a useful index of hypoxic pulmonary vasoconstriction in healthy humans. © Springer-Verlag 2005.