Another possibility for the reduced Pa02 in cirrhotic patients with portal hypertension is the presence of anastomoses between the portal venous system and the low pressure pulmonary veins.- Unfortunately, this portopulmonary bypass could not be evaluated by the multiple inert gas method used in the present study. In addition, a significant difference between the measured Pa02 and the Pa02 predicted from the values of Va/Q distribution, Ve, and Q may stem from an anatomic shunt (bronchial, thebesian veins . . .), which is not assessed by the inert gas elimination technique, or a defect in diffusion.
The significant difference between the predicted and measured PaOz (A=+9.27±5.9 mm Hg; p<0.01) was probably a result of both mechanisms: (1) the unmeasured post-pulmonary shunt between portal and pulmonary veins probably only accounting for a small fraction of the observed hypoxemia; and (2) a diffusion defect caused by a reduced transit time in overperfused areas of the lung related to the high Q, assuming that the pulmonary capillary blood volume is not significantly altered in our patients. To our knowledge, a change in pulmonary capillary volume has not been reported in cirrhosis of the liver. Further investigations, especially during pure oxygen breathing, could have separated these two mechanisms. In short, whatever the mechanism, these results demonstrated the presence of a large intrapulmonary shunt in cirrhotic patients with severe hypoxia. In addition, a contribution from an extrapulmonary shunt could not be ruled out.
The hemodynamic profile of our patients was rather unusual. Since the pulmonary arterial pressures were recorded downstream from the heart, the observed alterations in pulmonary pressures and vascular resistances must have been due to an anatomic abnormality in the ptilmonary vascular bed. These hemodynamic findings, which are consistent with the gas exchange results showing a marked true shunt, could be attributed to pulmonary arteriovenous anastomoses, the microcirculation assumed to be unaffected. This is supported by the fact that cardiac output markedly increases on opening an experimental arteriovenous fistula. The moderate increase in Vo2 and the requirement for oxygen transport in spite of the low arterial oxygen concentration probably contributed to the increase in cardiac output.
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