Arterial oxygen desaturation in patients with cirrho-L sis of the liver was first described by Snell in 1935; however, in spite of numerous studies, the mechanism of the alterations in gas exchange in these patients remains obscure. The diffusing capacity does not appear to be altered, and the shift to the right of the oxyhemoglobin dissociation curve is too small to account for the degree of desaturation; however, the increase in alveolar-arterial oxygen partial pressure difference and the moderate increase in blood saturation during oxygen breathing are in favor of venous admixture as the cause of arterial hypoxemia. Postmortem findings indicate the existence of intrapul-monary arteriovenous shunts or a portopulmonary venous bypass in some patients. More recently, it has been suggested that this abnormality in gas exchange is due to an inappropriate pulmonary blood flow relative to ventilation distribution,10 to an altered distribution of ventilation caused by an increase in closing volume,11 or to an impairment of HPY. In short, hypoxemia in patients with hepatic disease is common and is probably of multifactorial origin, but severe hypoxemia is unusual. This study was designed to investigate the mechanism of the alteration in gas exchange in severely hypoxemic cirrhotic patients using the multiple inert gas elimination technique to estimate Va/Q inequalities. read
Materials and Methods
Six patients (three men and three women) with clinical and laboratory evidence of cirrhosis of the liver (Table 1) were studied. A previous liver biopsy confirmed the diagnosis in five of them. In the sixth case the diagnosis was indicated by the presence of hepatomegaly, splenomegaly, esophageal varices, history of acute hepatic failure with edema, ascites, and biochemical evidence of hepatic deficiency. None of the patients had a history of intrinsic pulmonary or cardiac disease. There was no clinical or roentgeno-graphic evidence of pulmonary disease. Five patients had stopped smoking for at least two years, and one had never smoked; however, they all suffered from severe breathlessness with serious hypoxemia and hypocapnia (Table 2). The spirometric data, obtained using a constant-volume body plethysmograph, were close to normal (Table 2). All of the patients had normal or subnormal coagulation parameters (Table 1). Relationships of Va/Q were determined in a respiratory steady state, using the multiple inert gas method after right catheterization. All patients currently had no acute hepatic disease and gave their informed consent to the procedure.
Table 1—Physical Characteristics and Type of Cirrhosis
|Case, Sex, Age (yr)||Weight,kg||Height,cm||Biopsy||Type of Cirrhosis*||Platelet Count x 103||Prothrombin times percent of Control||Albumin,S’L||Globuling’L|
|1,M,31||80||187||+||BC; PH; SPCS||280||80||26.0||39.1|
Table 2—Blood Gas Levels and Spirometric Data
|Case||Pa02, mm Hg||PaC02, mm Hg||pH||FEV,||FVC, percent of predicted||FEV/FVC||FEF25-75, percent of predicted*||TLC, percent of predicted*|
|IVsec||Percent of Predicted*||Percent||Percent of Predicted*|
|Mean ± SD||56±6||28±4||7.47 ±0.04||2.82 ± 1.08 88 ±8||116± 16||67 ±4||89 ±7||84 ± 11||112 ± 16|
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