The acute effects of the peritoneovenous shunt (LeVeen) on hemodynamics and pulmonary gas exchange in 6 consecutive patients with intractable ascites and cirrhosis were evaluated. After opening the peritoneovenous shunt, there was a marked increase in cardiac index, (from 3.78 ± 0.4 to 5.86 ± 0.4 l/min. m2, p < 0.01), and mean pulmonary artery pressure (from 17.3 ± 1.9 to 23.3 ± 1.5 mmHg, p < 0.05), while a significant decrease in systemic vascular resistances (from 1086 ± 116 to 694 ± 52 dynes.sec. cm-5, p < 0.05) was observed. In all patients there was a drop in arterial oxygen tension (P(a)O2) (from 76 ± 3 to 67 ± 3 torr, p < 0.01) and an increase in venous admixture (QS(p)/Qt) from 13.1 ± 2 to 18.9 ± 2%, p < 0.01). The comparable increase in cardiac output and in venous admixture produced by opening the peritoneovenous shunt, might be related to the massive transfusion of ascitic fluid into the intravascular compartment. It is therefore concluded that this impairment of tas exchange further support discarding an appropriate amount of ascitic fluid at the time of shunt insertion.
Brandi, L.S., Grana, M., D'Elia, F., Ferrari, M., Oleggini, M., Carmellini, M., et al. (1988). Acute effects of peritoneousvenous shunt on the hemodynamics and gas exchange in patients with hepatic intractable ascites. THE ITALIAN JOURNAL OF SURGICAL SCIENCES, 18(2), 137-142.
Acute effects of peritoneousvenous shunt on the hemodynamics and gas exchange in patients with hepatic intractable ascites
Carmellini M.;
1988-01-01
Abstract
The acute effects of the peritoneovenous shunt (LeVeen) on hemodynamics and pulmonary gas exchange in 6 consecutive patients with intractable ascites and cirrhosis were evaluated. After opening the peritoneovenous shunt, there was a marked increase in cardiac index, (from 3.78 ± 0.4 to 5.86 ± 0.4 l/min. m2, p < 0.01), and mean pulmonary artery pressure (from 17.3 ± 1.9 to 23.3 ± 1.5 mmHg, p < 0.05), while a significant decrease in systemic vascular resistances (from 1086 ± 116 to 694 ± 52 dynes.sec. cm-5, p < 0.05) was observed. In all patients there was a drop in arterial oxygen tension (P(a)O2) (from 76 ± 3 to 67 ± 3 torr, p < 0.01) and an increase in venous admixture (QS(p)/Qt) from 13.1 ± 2 to 18.9 ± 2%, p < 0.01). The comparable increase in cardiac output and in venous admixture produced by opening the peritoneovenous shunt, might be related to the massive transfusion of ascitic fluid into the intravascular compartment. It is therefore concluded that this impairment of tas exchange further support discarding an appropriate amount of ascitic fluid at the time of shunt insertion.File | Dimensione | Formato | |
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https://hdl.handle.net/11365/8404
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