GASTROENTEROLOGY 1995;109:1917-1925 Effect of Volume Expansion on Systemic Hemodynamics and Central and Arterial Blood Volume in Cirrhosis SOREN MOLLER,* FLEMMING BENDTSEN,* and JENS H. HENRIKSEN* Departments of *Clinical Physiologyand *Gastroenterology, HvidovreHospital, Universityof Copenhagen, Copenhagen, Denmark Background & Aims: Systemic vasodilatation in cirrho- sis may lead to hemodynamic alterations with reduced effective blood volume and decreased arterial blood pressure. This study investigates the response of acute volume expansion on hemodynamics and regional blood volumes in patients with cirrhosis and in controls. Methods: Thirty-nine patients with cirrhosis (12 pa- tients with Child-Turcotte class A, 14 with class B, and 13 with class C) and 6 controls were studied. Dur- ing hepatic vein catheterization, cardiac output, sys- temic vascular resistance, central and arterial blood volume, noncentral blood volume, and arterial pressure were determined before and during a volume expansion induced by infusion of a hyperosmotic galactose solu- tion. Results: During volume expansion, the central and arterial blood volume increased significantly in patients with class A and controls, whereas no significant change was found in patients with either class B or class C. Conversely, the noncentral blood volume in- creased in patients with class B and C. In both patients and controls, the cardiac output increased and the sys- temic vascular resistance decreased, whereas the mean arterial blood pressure did not change signifi- cantly. Conclusions: Only in mild cirrhosis is the effec- tive blood volume able to increase in response to vol- ume expansion. Our results are consistent with the peripheral vasodilatation hypothesis and the circula- tory hyporeactivity occurring in advanced cirrhosis. B esides portal hypertension, patients with cirrhosis present a spectrum of circulatory disturbances. 1-3 These include increased cardiac output and heart rate and decreased systemic vascular resistance and arterial blood pressure. 4-6 According to the "peripheral arterial vasodilatation hypothesis, ''2'7-9 systemic vasodilatation leads to arterial underfilling. Arterial underfilling, to- gether with sequestration of fluid into the peritoneal cavity, activates Saltwater-retaining mechanisms and va- sopressor systems to counteract the otherwise very low arterial blood pressure. 1°-.4 Plasma and blood volumes are increased in the presence of cirrhosis, ~'<s'9'~1but there are signs of abnormal distributionT'S; it is now generally accepted that patients with decompensated cirrhosis and ascites have a decreased "effective blood volume. ''6-s'12'~'15 However, in early cirrhosis, the size of the central vascular compartment where volume receptors and baroreceptors are located remains controversial. We and others have recently produced evidence for a central and arterial blood volume contraction, <1<~7 whereas others question this) However, the effects of an acute volume expansion on the size of the different regions of the vascular compart- ment have not hitherto been investigated. The present study was undertaken to determine the response of an acute volume expansion on systemic hemo- dynamics and central and noncentral blood volumes in patients with cirrhosis and different degrees of liver dys- function and in a control group. Patients and Methods Study Population The study population comprised 39 patients with a biopsy-verified cirrhosis; their mean age was 53 years (range, 34-73 years). All the patients had a history of alcohol abuse, i.e., a consumption exceeding 50 g/day for more than 5 years. They had abstained from alcohol for at least 1 week before the study and had shown no signs of withdrawal symptoms at the time of the study. According to the modified Child-Turcotte classification, 18 12 patients were in class A, 14 in class B, and 13 in class C. Twenty-two patients had ascites; they were receiving diuretics and had been put on a sodium restricted diet of 40 mmol/day. Eight patients received a diuretic dose of 100 mg of spironolactone, 7 patients received 40 mg of furosemide, and 7 patients received 80 mg of furosemide. Ad- ditional cardiovascular medication was not prescribed for any of the patients. The presence of slight or moderate ascites was confirmed by ultrasonography or paracentesis. The diet of patients without fluid retention was not restricted. None of the patients had hepatic encephalopathy above grade I or had experienced recent gastrointestinal bleeding. The serum con- centrations of albumin; bilirubin; aspartate aminotransferase; alkaline phosphatase; coagulation factors II, VII, and X; creati- nine; sodium; and potassium were determined by routine methods in an autoanalyzer (SMAC, Technicon Instruments © 1995 by the AmericanGastroenterological Association 0016-5085/95/S3.00