Hemodynamic Studies in Acute-on-Chronic Liver Failure

Background Patients with decompensated cirrhosis and acute liver failure have circulatory dysfunctions leading to high portal pressure and cardiac output (CO) and low systemic vascular resistance (SVR). Circulatory changes in acute-on-chronic liver failure (ACLF) patients have not been studied. We studied the portal, systemic, and pulmonary hemodynamics in patients with ACLF and compared them with compensated and decompensated cirrhotics. Patients and Methods Clinical features and hemodynamic profile were studied in patients with ACLF and compared with age- and sex-matched compensated and decompensated cirrhotics with portal hypertension. Results The study cohort comprised 144 patients categorized into one of three groups (ACLF, compensated cirrhosis, and decompensated cirrhosis), with 48 (33%) patients in each group. All values are given as the mean +/- standard deviation, except for frequencies (%). The mean arterial pressure (MAP) and SVR were lower in the ACLF than the compensated group and were similar to those of the decompensated group (MAP 90 +/- 16 vs. 99 +/- 15 vs. 96 +/- 16 mmHg; SVR 912 +/- 435 vs. 1350 +/- 449 vs. 891 +/- 333 dyn s/cm(5)). The mean CO of the ACLF patients was higher than that of the compensated group and similar to that of the decompensated group (CO 8.9 +/- 3.5 vs. 6.1 +/- 1.7 vs. 9.0 +/- 3.0 l/min). The pulmonary vascular resistance (PVR) and pulmonary capillary wedge pressures (PCWP) were similar in all the three groups (PVR 78 +/- 48 vs. 109 +/- 70 vs. 61 +/- 47 dyn s/cm(5); PCWP 8 +/- 4 vs. 8 +/- 4 vs. 10 +/- 5 mmHg). The mean hepatic venous pressure gradient (HVPG) in the ACLF group was 15.1 +/- 6.3 mmHg, which was significantly higher than that of the compensated group (11.7 +/- 6.3 mmHg), but lower than that of the decompensated cirrhosis group (20.2 +/- 6.0 mmHg). When patients of ACLF were categorized on the basis of their variceal size, the mean HVPG in ACLF patients with small varices was similar to that of compensated cirrhotics (13.7 +/- 5.7 vs. 11.7 +/- 6.3 mmHg; P = 0.146), while in the ACLF patients with large varices, the HVPG was comparable to that of the decompensated cirrhotics (18.7 +/- 6.6 vs. 20.2 +/- 6.0 mmHg; P = 0.442). Conclusions The systemic hemodynamics in patients with ACLF is similar to that in decompensated cirrhotics. The portal pressure in these patients is higher than that in the compensated cirrhotics, and in the subgroup with large varices, it becomes similar to that of decompensated cirrhotics.