Hyperdynamic circulation

Abstract: Two dissimilar hemodynamic hypotheses, the “backward flow” theory and the “forward flow” theory, have been advanced to define splanchnic hemodynamics in portal hypertension. An animal model with portal hypertension and high-grade portal-systemic shunting, the portal vein-stenotic rat, was studied to determine whether a hemodynamic picture compatible with either theory would develop. Splanchnic and systemic hemodynamics and portal-systemic shunting were measured by radioactive microsphere techniques. The portal-hypertensive rats (portal pressure, 12.8 +/- 0.5 vs. 8.3 +/- 0.4 mmHg) with greater than 95% portal-systemic shunting had a 60% increase in portal venous inflow (23.46 +/- 2.54 vs. 14.97 +/- 1.61 ml/min; P less than 0.01) with a concomitant 50% decrease in splanchnic arteriolar resistance (3.86 +/- 0.43 vs. 7.60 +/- 0.80 dyn . s . cm-5 . 10(5); P less than 0.001) compared with control rats. Cardiac index (391 +/- 17 vs. 250 +/- 20 ml . min-1 . kg-1) was elevated 50% (P less than 0.001), and total peripheral resistance (7.1 +/- 0.4 vs. 11.7 +/- 0.8 dyn . s . cm-5 . 10(4)) was decreased 60% (P less than 0.001). The resistance to portal blood flow in portal vein-stenotic rats (4.77 +/- 0.57 dyn . s . cm-5 . 10(4)) was similar to the resistance to portal blood flow in control rats (4.82 +/- 0.43 dyn . s . cm-5 . 10(4)), indicating that the hyperdynamic portal venous inflow, not resistance, provided the main impetus for maintaining the elevated portal venous pressure. The splanchnic hemodynamic observations directly support the forward flow theory of portal hypertension. The relation between splanchnic arteriolar resistance and total peripheral resistance (r = 0.67; P less than 0.01) indicated that the systemic hemodynamic parameters were secondarily altered by the splanchnic hemodynamic changes. This animal model of chronic portal hypertension gave evidence for a generalized splanchnic arteriolar vasodilation occurring in the presence of high-grade portal-systemic shunting.

Abstract: A decade ago, it was proposed that peripheral arterial vasodilation was an important event in the pathophysiology of ascites formation in patients with cirrhosis.1 At the same time, nitric oxide was demonstrated to be a potent vasodilator with a major role in the regulation of vascular tone,2 and it was hypothesized that nitric oxide could be the cause of the hyperdynamic circulation of patients with cirrhosis.3 Since then, studies in animals and humans with portal hypertension have provided evidence suggesting that nitric oxide has an important role in the hemodynamic abnormalities that characterize cirrhosis and the associated sodium and water . . .

Abstract: Background Hereditary hemorrhagic telangiectasia, or Rendu–Osler–Weber disease, is an autosomal dominant disorder characterized by angiodysplastic lesions (telangiectases and arteriovenous malformations) that affect many organs. Liver involvement in patients with this disease has not been fully characterized. Methods We studied the clinical findings and results of hemodynamic, angiographic, and imaging studies in 19 patients with hereditary hemorrhagic telangiectasia and symptomatic liver involvement. Results We evaluated 14 women and 5 men who ranged in age from 34 to 74 years. All but one of the patients had a hyperdynamic circulation (cardiac index, 4.2 to 7.3 liters per minute per square meter of body-surface area). In eight patients, the clinical findings were consistent with the presence of high-output heart failure. The cardiac index and pulmonary-capillary wedge pressure were elevated in the six patients in whom these measurements were performed. After a median period of 24 months, the condition o...