Gas exchange mechanism of orthodeoxia in hepatopulmonary syndrome

The mechanism of orthodeoxia (OD), or decreased partial pressure of arterial oxygen (PaO2) from supine to upright, a characteristic feature of hepatopulmonary syndrome (HPS), has never been comprehensively elucidated. We therefore investigated the intrapulmonary (shunt and ventilation‐perfusion [V̇A/Q̇] mismatching) and extrapulmonary factors governing PaO2 in 20 patients with mild to severe HPS (14 males, 6 females; 50 ± 3 years old SE) at upright and supine, in random order. We set out a cutoff value for OD, namely a PaO2 decrease ≥5% or ≥4 mm Hg (area under the receiver operating characteristic curve, 0.96 each). Compared to supine, 5 patients showed OD (PaO2 change, −11% ± 2%, −7 ± 1 mm Hg, P < .05) with further V̇A/Q̇ worsening (shunt + low V̇A/Q̇ mode increased from 19% ± 7% to 21% ± 7% of cardiac output [Q̇T], P < .05), as opposed to 15 patients who did not (+2% ± 2%, +1± 1 mm Hg) with V̇A/Q̇ improvement (from 20% ± 4% to 16% ± 4% of Q̇T, P < .01). Cardiac output was significantly lower in OD patients in both positions. Changes in extrapulmonary factors at upright, such as increased minute ventilation and decreased Q̇T, were of similar magnitude in both subsets of patients. In conclusion, our data suggest that gas exchange response to OD in HPS points to a more altered pulmonary vascular tone inducing heterogeneous blood flow redistribution to lung zones with prominent intrapulmonary vascular dilatations. (HEPATOLOGY 2004;40:660–666.)