HEMODYNAMIC ADAPTATION 2 MONTHS AFTER TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT (TIPS) IN CIRRHOTIC-PATIENTS

Background and Aims-In portal hypertensive patients, transjugular intr ahepatic portosystemic shunt (TIPS) acutely increases cardiac output a nd exaggerates peripheral vasodilatation. It has been suggested that t he worsened hyperdynamic state may progress to high output heart failu re. The aim was to evaluate the acute and short-term haemodynamic adap tation to this procedure. Methods-Systemic, splanchnic, and pulmonary haemodynamics were studied in 15 cirrhotic patients under stable haemo dynamic conditions before placement of TIPS, then 15-30 minutes after and two months later. For inclusion in the final analysis, an uneventf ul post-TIPS at two months follow up and a stable portacaval gradient were required. The following variables were measured or calculated: po rtacaval gradient; cardiac index (thermodilution); systolic and diasto lic mean arterial, atrial, pulmonary arterial, and wedged pulmonary ca pillary pressures; heart rate; and total peripheral and pulmonary vasc ular resistances. Blood flow in the shunt was measured using duplex Do ppler ultrasound. Results-The portacaval gradient decreased by 56% and remained stable thereafter. Shunt blood flow was unchanged when measu red immediately after TIPS and two months later. Immediately after TIP S there was a pronounced increase in cardiac index (+32%; p<0.05) in a ssociation with a decrease in peripheral and pulmonary vascular resist ance (-21%; p<0.05 and -14%; NS). Two months later, whereas the initia l rise in cardiac index was attenuated, peripheral vascular resistance s remained similar and pulmonary vascular resistances decreased furthe r (-33%; p<0.05) compared with immediate post-TIPS values. Conclusions -Hyperdynamic circulation worsened immediately after TIPS, with a prog ressive adaptation during follow up. The mechanisms of post-TIPS induc ed haemodynamic changes include an abrupt volume load resulting from s planchnic decompression and an increased delivery of gut derived vasod ilators to the systemic circulation. The persistence of decreased peri pheral and pulmonary vascular resistances despite the reduction in hig h cardiac output two months after TIPS suggests that vasodilatation is not solely a compensatory response to a TIPS induced increased preloa d. Vasodilatory substances shunted away from the liver probably play a n important part in this phenomenon.