Mechanisms of improvement of water and sodium excretion by immersion in decompensated cirrhotic patients

Abstract

Eight patients with alcoholic liver disease, ascites, and edema were found to have impaired water (36 ± 6% in 5 hr) and sodium (3.9 ± 1.1 mEq/5 hr) excretion during a 20 ml/kg water load. These patients were submitted to a 5-hr head-out water immersion (HWI) with hemodynamic monitoring (Swann-Ganz). HWI increased cardiac index (3.3 to 4.2 liters/min/m2), right atrial pressure (RAP, 3.9 to 9.0 mm Hg), and wedge capillary pulmonary pressure (9.8 to 15.4 mm Hg), (all P < 0.01). HWI decreased plasma renin activity (6.4 to 4.5 ng/ml/hr, P < 0.001), aldosterone (73 to 43 ng/dl, P < 0.001), arginine vasopressin (AVP, 1.03 ± 0.15 to 0.76 ± 0.08 pg/ml, P < 0.005), norepinephrine (NE, 584 to 435 pg/ml, P < 0.001) and increased the percentage of water load excreted (36 to 63%, P < 0.005) and urinary sodium excretion (3.9 to 9.7 mEq/5 hr, P < 0.05). The percentage of water load excreted was inversely correlated to AVP levels (r = 0.52, P < 0.05) and directly correlated to RAP (r = 0.74, P < 0.05). A significant positive correlation was also found between the increase in fractional excretion of sodium (ΔFE(Na)) and the increase in RAP (r = 0.77, P < 0.01). FE(Na) also correlated inversely with NE levels (r = 0.56, P < 0.05). Thus, central blood volume expansion increases renal water excretion in decompensated cirrhotic patients, at least in part by suppressing AVP, and the magnitude of the increase in water excretion and in FE(Na) correlate most closely with the changes in RAP.