Abstract
Cirrhosis is the consequence of chronic liver disease. When the cause of liver damage is not removed, a chronic inflammatory reaction develops, which is typically accompanied by the accumulation of fibrillar extracellular matrix, nodular regeneration [1], neoangiogenesis, and the establishment of portal hypertension (PH), i.e., high blood pressure in the portal vein, its branches, and tributaries. While PH increases, the hemodynamic derangement extends beyond the splanchnic circulation due to a net increase in circulating vasodilating molecules. This increase is secondary to a systemic and sustained inflammatory reaction and leads to hyperdynamic circulation. The latter is characterized by an increased heart rate and cardiac output as well as a decreased systemic vascular resistance with low arterial blood pressure. Inflammation, altered hemodynamics, and tissue perfusion, together with parenchymal extinction, are also accompanied by a profound metabolic derangement that characterizes cirrhosis in its more advanced stages.
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Rosselli, M., Pinzani, M. (2014). Cirrhosis. In: Lammert, E., Zeeb, M. (eds) Metabolism of Human Diseases. Springer, Vienna. https://doi.org/10.1007/978-3-7091-0715-7_28
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DOI: https://doi.org/10.1007/978-3-7091-0715-7_28
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