Interrelationship between cardiac output and vascular resistance as determinants of effective arterial blood volume in cirrhotic patients

Interrelationship between cardiac output and vascular resistance as determinants of effective arterial blood volume in cirrhotic patients. The effect of head-out water immersion (HWI) in decompensated cirrhotic patients to correct sodium and water excretion has been found to be incomplete and variable. The explanation may be that the efficacy of HWI in correcting a decreased effective arterial blood volume (EABV) in decompensated cirrhotic patients is limited by an accompanying decrease in systemic vascular resistance (SVR) and thus a relative increase in arterial vascular holding capacity. The present studies were undertaken to examine this possibility by maintaining SVR (dynes · sec · cm−5) nearly constant during HWI with an exogenous infusion of norepinephrine (HWI + NE). In six decompensated cirrhotic patients, neither HWI nor NE infusion alone significantly increased sodium excretion (UNaV, 13 vs. 19 and 13 µEq/min, respectively), but each maneuver increased the excretion of a 20 ml/kg water load (28 to 60 and 61%, respectively, both P < 0.05). The combination of HWI + NE, however, significantly increased UNaV to 70 µEq/min (P < 0.05) and percentage of water excretion to 95 (P < 0.001), values significantly greater than those achieved with either maneuver alone. These differences were not explained by any changes in inulin clearance. With HWI alone, cardiac index (CI) increased (4.2 to 5.3 liter/min/m2, P < 0.01), but SVR decreased (872 to 613 dynes · sec · cm−5, P < 0.001) and mean arterial pressure (MAP) remained constant (83 vs. 78mm Hg). However, with HWI + NE, CI increased identically (4.2 to 5.3 liter/min/m2, P < 0.001), whereas SVR fell less (872 to 750 dynes · sec · cm−5, P < 0.05) and therefore MAP increased (83 to 98mm Hg, P < 0.01). Thus, decompensated, hyponatremic cirrhotic patients with ascites demonstrate normal renal sodium and water excretion in response to increased central blood volume with concomitant maintenance of SVR. These results are supportive of a decrease in EABV mediating the sodium and water retention in decompensated cirrhotic patients.