Quantitative modeling of the physiology of ascites in portal hypertension.
Bottom Line: This communication presents an explanation of ascites based solely on pathophysiological alterations within the peritoneal cavity.A quantitative model is described based on experimental vascular and intraperitoneal pressures, lymph flow, and peritoneal space compliance.The model's predictions accurately mimic clinical observations in ascites, including the magnitude and time course of changes observed following paracentesis or diuretic therapy.
Although the factors involved in cirrhotic ascites have been studied for a century, a number of observations are not understood, including the action of diuretics in the treatment of ascites and the ability of the plasma-ascitic albumin gradient to diagnose portal hypertension. This communication presents an explanation of ascites based solely on pathophysiological alterations within the peritoneal cavity. A quantitative model is described based on experimental vascular and intraperitoneal pressures, lymph flow, and peritoneal space compliance. The model's predictions accurately mimic clinical observations in ascites, including the magnitude and time course of changes observed following paracentesis or diuretic therapy.
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Mentions: It is of interest to see how the ascites volume is altered by the hemodynamic changes produced by diuretics. As indicated in Table 1, diuretics reduce both the hepatic venous pressure gradient (PHVPG) and the right atrial pressure (PRA). Figure 3 shows how the steady state ascites volume in the original untreated condition (black line) is altered by either a) a 20% decrease in gradient (green line); b) a reduction in PRA from 5 to 2 mm Hg (blue line), or c) a combination of both (a) and (b) (red line) as a function of the initial PHVPG. For an initial gradient of 20 mm Hg, the ascites volume is reduced from about 6.5 to 1.0 liter if diuretics induced both of the above noted changes in PHVPG and PRA. If the initial gradient is 16 mm Hg or less, diuretics should produce complete reabsorption of the ascites. The reductions in PHVPG and PRA both contribute to the ascites reabsorption, but in different ways. At high initial PHVPG (> 18 mm Hg), when the hepatic vein pressure becomes decoupled from PRA (eq. (13)), lowering PRA (Figure 3, blue line) has a relatively small effect, while lowering PHVPG (green line) has a larger effect. In contrast, in the low pressure regime when the hepatic vein pressure is equal to (PRA + 2) (eq. (12)) lowering PRA (blue line) has a dramatic effect. For example, if the initial PHVPG is less than 13 mm Hg, lowering PRA from 5 to 2 mm Hg is enough by itself to completely resolve the ascites. These predicted results indicate that the small changes in PHVPG and PRA clinically achievable with diuretics (see Table 1) can link the systemic changes induced by diuretics to fluid accumulation in the abdomen.