Effects of therapeutic paracentesis on systemic and hepatic hemodynamics and on renal and hormonal function

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Abstract
Thirteen patients with cirrhosis and tense ascites (six with and seven without peripheral edema) underwent 4- to 15-liter paracentesis without intravenous “colloid” replacement. Cardiac output increased from 6.6 ± 0.7 liters per min at baseline to 8.2 ± 0.7 liters per min (p < 0.003) 1 hr after large-volume paracentesis completion and fell to 7.5 ± 0.69 liters per min (p < 0.05 vs. baseline, p < 0.02 vs. 1 hr) 24 hr after large-volume paracentesis completion. There was no change in mean arterial pressure or mean pulmonary artery pressure. Central venous pressure fell from 9.1 ± 0.8 mm Hg at baseline to 8.6 ± 1.4 mm Hg 1 hr post-large-volume paracentesis to 6.8 ± 1.0 mm Hg (p < 0.005 vs. baseline, p < 0.02 vs. 1 hr value) at 24 hr, and pulmonary capillary wedge pressure fell from 13.1 ± 0.9 to 11.1 ± 1.3 mm Hg 1 hr after large-volume paracentesis and to 9.89 ± 1.2 (p < 0.01 vs. baseline, p < 0.03 vs. 1 hr after large-volume paracentesis) at 24 hr. Heart rate fell from 90 ± 3.0 to 85 ± 2.9 beats per min (p < 0.01) 1 hr after large-volume paracentesis completion, but increased to 89 ± 2.5 beats per min (p < 0.02 vs. 1 hr after large-volume paracentesis) at 24 hr. Blood urea nitrogen fell from 13.3 ± 1.8 to 11.7 ± 1.6 mg per dl (p < 0.004) 1 hr after large-volume paracentesis, but was unchanged at 24 and 48 hr after large-volume paracentesis. Serum creatinine did not change during the study, but creatinine clearance fell from 77 ± 12.0 ml per min at baseline to 67 ± 7.0 ml per min (p < 0.05 vs. baseline) 24 hr after large-volume paracentesis and to 60 ± 7.5 ml per min (p < 0.05 vs. baseline) 48 hr after large-volume paracentesis. Serum sodium concentration at baseline was 135 ± 1.2 mEq per liter; 1 hr after large-volume paracentesis decreased to 133 ± 1.5 mEq per liter (p < 0.03); and at 48 hr was 132 ± 2.1 mEq per liter (p < 0.03). Serum aldosterone fell from 59.3 ± 17.0 to 41 ± 12 ng per dl 1 hr after large-volume paracentesis (p < 0.05), but increased to 59 ± 17.0 mg per dl (p < 0.05 vs. 1 hr after large-volume paracentesis) at 24 hr. Plasma renin activity did not change at 1 hr, but increased from baseline 21.8 ± 5.9 to 35.9 ± 12.0 ng per ml per hr 24 hr after large-volume paracentesis (p < 0.07 vs. 1 hr and baseline value). There was no change in plasma atrial natriuretic factor levels from baseline to 1 hr post-large-volume paracentesis, but it did fall from baseline (176 ± 22 pg per ml) to 24 hr after large-volume paracentesis (156 ± 20 pg per ml, p < 0.05). Estimated hepatic blood flow (assessed by galactose clearance) did not change during the study. Nonedematous patients had greater drop in central venous pressure at 24 hr after large-volume paracentesis (5 ± 1.7 vs. 8 ± 1.3 mm Hg, p < 0.05) than those with edema and also had an increase in heart rate (82 ± 3.1 to 84 ± 3.4 beats per min) compared to a fall (97 ± 2.7 to 93 ± 2.0 beats per min) at 24 hr in those with edema (p < 0.03). We conclude that large-volume paracentesis has no immediate adverse cardiovascular effect, but does produce a progressive decline of renal function without restoring the decreased plasma volume.