TY - JOUR
T1 - Hemodynamic changes in patients developing effective hypovolemia after total paracentesis
AU - Vila, Maria Carme
AU - Solà, Ricard
AU - Molina, Lluis
AU - Andreu, Montserrat
AU - Coll, Susanna
AU - Gana, Jordi
AU - Marquez, Judith
AU - Palá, Joaquin
AU - Bory, Felipe
AU - Pons, Silvia
AU - Szescielinski, Luis
AU - Jimenez, Wladimiro
PY - 1998/1/1
Y1 - 1998/1/1
N2 - Background/Aims: In many centers paracentesis is considered the treatment of choice for tense ascites. However, the mechanism of effective hypovolemia after paracentesis, the main complication associated with this procedure, remains unknown. In the current study, systemic hemodynamics was sequentially studied before and after total paracentesis in 46 patients with cirrhosis and tense ascites. The aim of the study was to assess the mechanism of effective hypovolemia after paracentesis. Methods: Plasma renin activity and aldosterone, mean arterial pressure, cardiac output (ECO-Doppler) and systemic vascular resistance were measured before, and 3 h, 6 h and 6 days after total paracentesis associated with plasma volume expansion. Results: Effective hypovolemia after paracentesis (defined as 50% increase in plasma renin activity up to a level over 4 ng · m-1 · h-1 at the 6th day after paracentesis) occurred in 20 cases (plasma renin activity increased from 8 ± 17 to 19 ± 2.7 ng · m-1 · h-1). In the remaining 26 cases no changes in plasma renin activity (8.5 ± 2.4 vs. 8.7 ± 2.2 ng · m-1 · h-1) were observed. The amounts of ascitic fluid volume removed were similar. Effective hypovolemia after paracentesis was associated with a significant decrease in mean arterial pressure (89 ± 2 vs. 81 ± 3 mmHg) and systemic vascular resistance (1263 ± 67 vs. 1014 ± 80 dyn · s-1 · cm-5) 6 days after treatment. In contrast, no significant changes in these parameters were observed in patients not developing this complication. In the whole group of patients a significant inverse relation was observed between changes in plasma renin activity and in systemic vascular resistance (r=0.74;p<0.001). Conclusions: These results indicate that effective hypovolemia after paracentesis in cirrhosis is predominantly due to an accentuation of the arteriolar vasodilation already present in these patients.
AB - Background/Aims: In many centers paracentesis is considered the treatment of choice for tense ascites. However, the mechanism of effective hypovolemia after paracentesis, the main complication associated with this procedure, remains unknown. In the current study, systemic hemodynamics was sequentially studied before and after total paracentesis in 46 patients with cirrhosis and tense ascites. The aim of the study was to assess the mechanism of effective hypovolemia after paracentesis. Methods: Plasma renin activity and aldosterone, mean arterial pressure, cardiac output (ECO-Doppler) and systemic vascular resistance were measured before, and 3 h, 6 h and 6 days after total paracentesis associated with plasma volume expansion. Results: Effective hypovolemia after paracentesis (defined as 50% increase in plasma renin activity up to a level over 4 ng · m-1 · h-1 at the 6th day after paracentesis) occurred in 20 cases (plasma renin activity increased from 8 ± 17 to 19 ± 2.7 ng · m-1 · h-1). In the remaining 26 cases no changes in plasma renin activity (8.5 ± 2.4 vs. 8.7 ± 2.2 ng · m-1 · h-1) were observed. The amounts of ascitic fluid volume removed were similar. Effective hypovolemia after paracentesis was associated with a significant decrease in mean arterial pressure (89 ± 2 vs. 81 ± 3 mmHg) and systemic vascular resistance (1263 ± 67 vs. 1014 ± 80 dyn · s-1 · cm-5) 6 days after treatment. In contrast, no significant changes in these parameters were observed in patients not developing this complication. In the whole group of patients a significant inverse relation was observed between changes in plasma renin activity and in systemic vascular resistance (r=0.74;p<0.001). Conclusions: These results indicate that effective hypovolemia after paracentesis in cirrhosis is predominantly due to an accentuation of the arteriolar vasodilation already present in these patients.
KW - Ascites
KW - Circulatory dysfunction
KW - Cirrhosis
KW - Therapeutic paracentesis
UR - https://www.scopus.com/pages/publications/0031961441
U2 - 10.1016/S0168-8278(98)80288-2
DO - 10.1016/S0168-8278(98)80288-2
M3 - Article
SN - 0168-8278
VL - 28
SP - 639
EP - 645
JO - Journal of Hepatology
JF - Journal of Hepatology
IS - 4
ER -