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Management of the Patient With Hemorrhaging Esophageal Varices
John P. Cello, MD;
Richard A. Crass, MD;
James H. Grendell, MD;
Donald D. Trunkey, MD
JAMA. 1986;256(11):1480-1484.
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| Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings. |
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AT REST, in the fasting state, total hepatic blood flow in the adult is approximately 1.5 L/min. This represents about 25% of the total cardiac output. Portal venous blood supplies nearly two thirds of the total hepatic blood flow and nearly 50% of the liver's oxygen demands. Portal venous perfusion of the liver occurs at low resistance, low pressure, and high flow. Relatively modest changes in resistance to portal venous flow will therefore result in increasing portal venous pressures. Increased portal venous resistance may occur at a presinusoidal, sinusoidal, or postsinusoidal level.
Presinusoidal portal hypertension is caused by occlusion of the main portal vein or its intrahepatic divisions. Sinusoidal portal hypertension has been proposed to occur with infiltration of collagen around the sinusoids or hepatocyte enlargement,1 producing increasing resistance to the sinusoidal flow of portal venous blood. Postsinusoidal portal hypertension occurs in two ways, either within the liver when
. . . [Full Text PDF of this Article]
Author Affiliations
From the Departments of Medicine (Drs Cello and Grendell) and Surgery (Drs Crass and Trunkey), University of California, San Francisco at San Francisco General Hospital.
Footnotes
Reprint requests to 3C-21, Gastrointestinal Unit, San Francisco General Hospital, 1001 Potrero Ave, San Francisco, CA 94110 (Dr Cello).
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