Relationship between systemic hemodynamics, renal dysfunction, and fluid retention in cirrhosis.

Abstract

(Fig. 1).Phase 1: Hyperdynamic Circulation Keeps Patients Freeof Ascites Despite the Progression of Splanchnic ArterialVasodilation. Splanchnic arterial vasodilation is an impor-tant feature associated with portal hypertension. It increasesportal venous inflow and maintains the progression of portalhypertension despite the collateral circulation, and it impairssystemic circulatory function. In compensated cirrhosis,splanchnic arterial vasodilation is not followed by an impair-ment of the effective arterial blood volume because patientsdevelop parallel increases in plasma volume and cardiac out-put (hyperdynamic circulation). During this phase, the arte-rial pressure, renal function, plasma renin activity (PRA),plasma norepinephrine (NE) level, and antidiuretic hormone(ADH) concentration are normal.Phase 2: The Onset of Sodium Retention and AscitesDevelop in the Absence of Activation of the Renin-Angiotensin-Aldosterone System (RAAS) and the Sympa-thetic Nervous System (SNS). With the progression ofcirrhosis, patients become unable to excrete their regular so-dium intake. Sodium is then retained with water and accu-mulates as ascites. During this phase, in comparison withphase 1, patients display higher portal pressures, probablyhigher peripheral vascular resistance, increased cardiac out-put, and moderately reduced sodium excretion. In contrast,renal perfusion, GFR, free water excretion, PRA, NE, andADH are normal.