ACUTE HEMODYNAMIC-CHANGES AFTER ORAL CARVEDILOL, A VASODILATING BETA-BLOCKER, IN PATIENTS WITH CIRRHOSIS

Citation
Eh. Forrest et al., ACUTE HEMODYNAMIC-CHANGES AFTER ORAL CARVEDILOL, A VASODILATING BETA-BLOCKER, IN PATIENTS WITH CIRRHOSIS, Journal of hepatology, 25(6), 1996, pp. 909-915
Citations number
26
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
ISSN journal
01688278
Volume
25
Issue
6
Year of publication
1996
Pages
909 - 915
Database
ISI
SICI code
0168-8278(1996)25:6<909:AHAOCA>2.0.ZU;2-Z
Abstract
Background/Aims: Combinations of beta-blockers and vasodilators have b een assessed for their ability to lower portal pressure and so prevent variceal haemorrhage. However, reservations have been raised particul arly with respect to renal function and perfusion after the use of the se medicines in patients with chronic liver disease. We studied the ac ute effects of carvedilol, a new vasodilating betablocker which combin es non-selective beta-blockade with alpha-1 receptor antagonism, upon the haemodynamics of patients with cirrhosis. Methods: Sixteen patient s completed the study which measured the changes approximately 1h afte r the administration of 25 mg oral carvedilol. Results: The hepatic ve nous pressure gradient fell from 16.7 +/- 0.9 to 13.6 +/- 1.0 mmHg (p < 0.00001), accounted for largely by reductions in the wedged hepatic venous pressure. Despite this, the azygos blood flow did not change. T here was a significant fall in mean arterial pressure (94.8 +/- 4.4 cf . 84.6 +/- 4.3 mmHg; p = 0.0001), which was particularly apparent in t he diastolic blood pressure of those patients with ascites. The heart rate only fell significantly in the ascitic subjects. No significant c hanges occurred in the cardiac output or systemic vascular resistance. Unilateral renal vein flow as measured by the reverse thermodilution technique remained constant. Conclusions: Carvedilol is therefore a po tent acute portal hypotensive agent which does not appear to compromis e renal perfusion. However, patients with ascites are at greater risk of its systemic hypotensive action.