CENTRAL BLOOD-VOLUME IN CIRRHOSIS - MEASUREMENT WITH RADIONUCLIDE ANGIOGRAPHY

In patients with cirrhosis a diminished effective central arterial blo od volume associated with systemic arterial vasodilatation has been pr oposed as the mechanism that initiates renal sodium retention. Fur Fur thermore, total central blood volume has recently been reported as red uced in cirrhosis, and the controversy over the stimulus for sodium re tention in cirrhosis remains. The aim of this study was to assess the central blood volume with radionuclide angiography to determine whethe r there is effective arterial underfilling in cirrhosis. Twenty-nine p atients (13 with and 16 without ascites) and 10 age- and sex-matched c ontrol subjects were studied under metabolic conditions. Radionuclide ventricular volume and total central blood volume were determined from gated images, taking into account the Tc-99 count activity per millil iter of blood volume and attenuation. The pulmonary volumes were simil arly derived. The cirrhotic patients as a group had significantly high er total central blood volume (1,287 +/- 105 ml/m(2) in control subjec ts vs. 1,874 +/- 106 ml/m(2) in cirrhotic patients, p < 0.01), right a nd left pulmonary blood volumes (217 +/- 20 ml/m(2) in control subject s vs. 309 +/- 20 ml/m(2) in cirrhotic patients, p = 0.03 and 185 +/- 1 8 ml/m(2) in control subjects vs 288 +/- 22 ml/m(2) in cirrhotic patie nts, p = 0.02, respectively), cardiac and central vascular blood volum e (885 +/- 79 ml/m(2) in control subjects vs. 1,276 +/- 75 ml/m(2) in cirrhotic patients, p = 0.01), cardiac output (5.36 +/- 0.56 L/min in control subjects vs. 7.19 +/- 0.50 L/min in cirrhotic patients, p = 0. 05), heart rate (65 +/- 3 beats/min in control subjects vs. 75 +/- 2 b eats/min in cirrhotic patients, p = 0.04) and significantly lower syst emic vascular resistance (1,443 +/- 121 dyne sec cm(-5) in control sub jects vs. 1084 +/- 68 dyne sec cm(-5) in cirrhotic patients, p = 0.02) . All volumes were significantly higher in both the nonascitic and the ascitic patients when compared with the control subjects. Significant ly increased cardiac output and reduced systemic vascular resistance, however, were only observed in the ascitic patients. Neurohumoral mark ers were increased in the ascitic patients compared with both the cont rol subjects and nonascitic patients, but the difference was not stati stically significant. There was no correlation between any of the volu me measurements with neurohumoral markers of an effective arterial blo od volume. In conclusion, the ascitic patients with cirrhosis have evi dence of central hypervolemia and hyperdynamic circulation, as indicat ed by peripheral vasodilatation, an increased cardiac output and heart rate. In contrast, the nonascitic patients with cirrhosis who have pr eviously been shown to have a compensated sodium handling abnormality demonstrate an increased total central blood volume without significan t peripheral vasodilatation and evidence of arterial underfilling. Thi s suggests that peripheral vasodilatation is not solely responsible fo r the sodium retention and central blood volume expansion in cirrhosis .