Hepatic venous pressure gradient in cirrhosis: correlation with the size of varices, bleeding, ascites, and child's status.

The hepatic venous pressure gradient (HVPG) clearly reflects portal pressure in cirrhotic portal hypertension. Its relation with variceal bleeding has been well studied. We undertook to study the relation of HVPG to variceal size, Child's status, and etiology of cirrhosis. Patients with cirrhotic portal hypertension with esophageal varices underwent HVPG measurement as part of a prospective evaluation. One hundred seventy-six cirrhotics with varices (M:F, 140:36; mean age, 42.6 +/- 13.4 years), 104 with CLD related to viral etiology, 40 with alcoholic liver disease, 26 cryptogenic with cirrhosis, and 6 with miscellaneous causes of CLD underwent HVPG measurement. The mean HVPG was lower in patients with small varices (n = 77; 14.6 +/- 5.9 mm Hg) than in patients with large varices (n = 99; 19.2 +/- 6.6 mm Hg; P < 0.01). In patients with large varices, the mean HVPG in bleeders (n = 37) was higher than in nonbleeders (n = 62) (21.7 +/- 7.2 vs 17.9 +/- 6.2 mm Hg; P < 0.01). The mean HVPG was significantly higher in Child's B (n = 97; 17.4 +/- 6.9 mm Hg) and C (n = 56; 19.0 +/- 5.7 mm Hg) compared to Child's A cirrhotics (n = 23; 12.2 +/- 5.9 mm Hg; P < 0.01), and Child's C compared to Child's B cirrhotics (P = 0.05). HVPG was higher in alcoholic compared to nonalcoholic cirrhotics (20.8 +/- 7.3 vs 16.4 +/- 6.3 mm Hg; P < 0.05), but this was not significant in multivariate analysis. The HVPG was comparable between hepatitis B- and hepatitis C virus-related cirrhotics (P = 0.8). Cirrhotics with ascites had a higher HVPG than those without ascites (18.5 +/- 5.6 vs 16.6 +/- 7.6 mm Hg; P = 0.02). In multivariate analysis, only Child's status, size of varices, and variceal bleed predicted higher HVPG. HVPG is higher in cirrhotics with large varices and a history of bleed. There is a good correlation between HVPG and large varices, bleeder status, and ascites. A higher HVPG reflects more severe liver disease. The etiology of liver disease did not influence the portal pressure.

Influence of increased anatomical dead space no functional residual capacity of lungs and the lung clearance index.

A study of the influence of added anatomical dead space on the functional residual capacity of the lung was carried out on a total number of 40 healthy subjects of ages ranging between 21 and 50 years. The functional residual capacity was found to decrease as additional dead space was introduced in the breathing circuit. This decrease was associated with an increase in tidal volume, lung functions, as given by the lung clearance index, were found to deteriorate with each addition of dead space. There was also an increase in pulse rate in all age groups.