[Hepatopulmonary syndrome: relationship with liver dysfunction and systemic hemodynamic disorder]

The hepatopulmonary syndrome (HPS) causes an increased alveolar to arterial gradient of oxygen and in advanced phases hypoxemia, as the result of pulmonary vasodilation. In liver cirrhosis, it has been demonstrated the existence of splachnic vasodilation and also in other vascular beds. Our main objectives were to know the hemodynamic status, the renal function and the condition of some humoral systems in patient diagnosed of HPS.

We studied consecutively 32 cirrhotic patients Divided in two groups, a group of 18 cirrhotic patients with normal gaseous exchange (NGE), and another group of 14 cirrhotic patients diagnosed of HPS by contrast-enhanced transthoracic echocardiography and/or lung and brain scintigraphy with 99Tc albumin macroaggregates. They were all in rest in bed, upon alcohol and tobacco abstinence and on a diet of 50 mEq of sodium. Cardiovascular drugs were all withheld during 4 days in order to reach steady state.

Patients of the HPS group were characterized by a more advanced index of Child-Pugh and presence of clubbing and vascular spiders. They presented a greater degree of hypoxemia in a sitting position, greater hypocapnia and smaller transference factor values (TLCO). They also showed a hyperkinetic circulatory condition characterized by smaller arterial blood pressure, greater cardiac index, smaller vascular resistances and greater femoral flows, with smaller clearance of creatinine, elimination of urinary sodium, urinary volume/24 h and an increased plasmatic volume, accompanied with a greater activation of the renin-angiotensin-aldosterone axis and a greater urinary elimination of nitrites and nitrates.

The pulmonary vasodilation that explains the HPS is a constitutive part of the systemic vasodilation occurring in liver cirrhosis, and it is related to the degree of liver dysfunction as measured by the classification of Child-Pugh. The greater activation of the renin-aldosterone system and the rise of the plasmatic volume express a highest grade of arterial underfilling caused by an increment in the nitric oxide production.