Publication: Hyperdynamic circulation in portal hypertension: A comparative model of arterio-venous fistula
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Issued Date
2000
Resource Type
File Type
application/pdf
ISSN
3069877
Other identifier(s)
2-s2.0-0033868262
Rights Holder(s)
Scopus
Bibliographic Citation
Medical Hypotheses. Vol 55, No.1 (2000), p.77-87
Suggested Citation
Wattanasirichaigoon S., Gordon F.D., Resnick R.H. Hyperdynamic circulation in portal hypertension: A comparative model of arterio-venous fistula. Medical Hypotheses. Vol 55, No.1 (2000), p.77-87. doi:10.1054/mehy.1999.1034 Retrieved from: https://hdl.handle.net/20.500.14740/7068
Author(s)
Abstract
Complications of portal hypertension remain perplexing physiologic phenomena in the understanding of shunt hemodynamics with multiple theories. Hyperdynamic circulation was also found in sepsis, chronic anemia and arterio-venous (A-V) fistula which relate to an increase in nitric oxide. We hypothesize that portosystemic collaterals may mimic an A-V fistula in which the high-pressure portal blood connects with the lower pressure systemic venous circulation. Although these collaterals decompress the portal circulation, a number of secondary hemodynamic phenomena occur which increase portal blood flow and tend to counteract the portal hypotensive effect of the portosystemic shunt. The consequent increases in cardiac output and portal blood flow perfuse the compromised liver. As portal blood flow increases, collateral flow increases and is nearly totally shunted in the systemic circulation. This shunt may eventually introduce a vicious cycle of hyperdynamic circulation into a compromised host. Ultimately, high-output cardiac failure occurs, leading to cirrhotic cardiomyopathy. (C) 2000 Harcourt Publishers Ltd.