Systemic and Pulmonary Hemodynamics in Patients with Extra-Hepatic Portal Vein Obstruction (EHPVO)

Abstract

Purpose: Extra-hepatic portal vein obstruction (EHPVO) is a common cause of portal hypertension and variceal bleeding. Few studies have been done on hemodynamic alterations in patients with non-cirrhotic portal hypertension especially EHPVO in contrast to many reports on hemodynamics in cirrhotics. We evaluated alterations of systemic and pulmonary vascular system in patients with EHPVO and compared them with patients with compensated cirrhosis. The rationale for this investigation was to study the role of portal hypertension per se on systemic and pulmonary hemodynamics in EHPVO as compared to the hemodynamic changes produced by hepatic dysfunction plus portal hypertension in cirrhotics. Methods: Consecutive patients of EHPVO, ≥15 years of age were included, Controls were consecutive patients with compensated cirrhosis and history of variceal bleed, matched for variceal status (to ensure that they had same degree of portal hypertension) and body surface area, attending our department during the same period. The hemodynamic studies were HVPG, right atrial pressure (RAP), pulmonary arterial pressure (PAP), pulmonary capillary wedge pressure (PCWP) and mean arterial pressure (MAP). Cardiac output (CO), systemic vascular resistance and pulmonary vascular resistance were calculated. Results: The baseline parameters in the two groups were comparable. Both EHPVO patients and cirrhotics had similar values in all the measured hemodynamic parameters. The mean cardiac output in EHPVO was 6.5 (±2.6) L/min while it was 7.9 (±3.2) L/min in cirrhosis (P= 0.212). The systemic vascular resistance in EHPVO was 1242 (±494) dyn.s.cm−5, which was similar to that in cirrhotics (1018 [± 355], P= 0.167). Similarly the values of pulmonary vascular resistance were comparable in the two groups (68 [± 60] vs. 71 [± 70], P= 0.905). A subgroup analysis was done of 8 patients of EHPVO and 8 age matched compensated cirrhotics which also revealed similar cardiac index, cardiac output, systemic vascular resistance index, systemic vascular resistance, pulmonary vascular resistance index, and pulmonary vascular resistance in the two groups. Conclusion: EHPVO has features of hyperdynamic circulation, ie increased cardiac output, decreased systemic and pulmonary vascular resistance. These changes are similar to that seen in patients with cirrhosis. This suggests a predominant role of increased resistance and thus increased porto-systemic collateral circulation per se rather than hepatocellular injury in the genesis of these hemodynamic alterations.