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The mechanism of orthodeoxia (OD), or decreased partial pressure of arterial o xygen (PaO2) from supine to upright, a characteristic feature of hepatopulmonary syndrome (HPS), has never been comprehensively elucidated. We therefore investi gated the intrapulmonary (shunt and ventilation-perfusion <> mismatching) a nd 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 orde r. We set out a cutoff value for OD, namely a PaO2 decrease ≥5%or ≥4mmHg (are a under the receiver operating characteristic curve, 0.96 each). Compared to sup ine, 5 patients stowed OD (PaO2 change, -11%±2%, -7 ±1 mm Hg, P < .05) wit h further VA/Q worsening (shunt +low VA/Q mode increased from 19%±7%to 21% ±7%of cardiac output <>, P < .05), as opposed to 15 patients who did not (+ 2%±2%, +1 ±1 mm Hg) with VA/Q improvement (from 20%±4%to 16%±4%of QT, P < .01). Cardiac output was significantly lower in OD patients in both positio ns. Changes in extrapulmonary factors at upright, such as increased minute venti lation and decreased QT, were of similar magnitude in both subsets of patients. In conclusion, our data suggest that gas exchange response to OD in HPS points t o a more altered pulmonary vascular tone inducing heterogeneous blood flow redis tribution to lung zones with prominent intrapulmonary vascular dilatations.
The mechanism of orthodeoxia (OD), or decreased partial pressure of arterial xygen (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 -Flow << VA / Q >> mismatching) a nd 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 orde r. We Set out a cutoff value for OD, ie a PaO2 decrease ≥5% or ≥4 mmHg (are a under the receiver operating characteristic curve, 0.96 each). Compared to 5 patients stowed OD (PaO2 change, -11% ± 2 %, -7 ± 1 mm Hg, P <.05) wit h further VA / Q worsening (shunt + low VA / Q mode increased from 19% ± 7% to 21% ± 7% of cardiac output << QT >> , P <.05), as opposed to 15 patients who did not (+ 2% ± 2%, +1 ± 1 mm Hg) with VA / Q improvement (from 20% ± 4% to 16% ± 4% of QT , P <.01). Cardiac output was significantly low er in OD patients in both positio ns. Changes in extrapulmonary factors at upright, such as increased minute venti lation and decreased QT, were similar magnitude in both subsets of patients. In conclusion, our data suggest that gas exchange response to OD in HPS points toa more altered pulmonary vascular tone inducing heterogeneous blood flow redis tribution to lung zones with prominent intrapulmonary vascular dilatations.