Effects of therapeutic paracentesis on systemic and hepatic hemodynamics and on renal and hormonal function
1987
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.
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