Key result
Portal hypertension and vasodilators drive hyperdynamic circulation in cirrhosis, increasing CO and lowering SVR.
Why the study?
Hyperdynamic circulation in liver cirrhosis with portal hypertension involves complex hemodynamic alterations whose pathogenesis requires further understanding to develop novel treatments.
Hyperdynamic circulation in liver cirrhosis is driven by portal hypertension, portosystemic shunting, and overproduction of vasodilators like NO, leading to secondary activation of vasoconstrictive systems.
Supports mechanistic model in cirrhosis; leaves open targeted trials of vasodilator modulation before practice change.
Hyperdynamic circulation in patients with liver cirrhosis is characterized by increased cardiac output and heart rate, and decreased systemic vascular resistance with low arterial blood pressure and currently focused on understanding the pathogenesis because of possibility of developing novel treatment modality. Basically, these hemodynamic alternations arise from portal hypertension. Portosystemic collaterals develop to counterbalance the increased intrahepatic vascular resistance to portal blood flow and induce an increase in venous return to heart. Increased shear stress in vascular endothelial cell related high blood flow by portosystemic shunting contributes to this upregulation of eNOS resulting in NO overproduction. Additionally, bypassing through portosystemic collaterals and escaping degradation of over-produced circulating vasodilators in the diseased liver can promote the peripheral arterial vasodilation. Vasodilation of the systemic and splanchnic circulations lead to a reduced systemic vascular resistance, and increased cardiac output and splanchnic blood flow. Furthermore, neurohumoral vasoconstrictive systems including systemic nervous system, rennin angiotensin aldosterone system, and vasopressin are intensively activated secondary to vasodilation. However, hyperdynamic circulation would be more aggravated by the activated vasoconstrictive systems. With the progression of the cirrhotic process, hyperdynamic alternations can be more profound due to hyporesponsiveness to vasoconstrictors and increased shunt formation in conjunction with autonomic neuropathy. Eventually, splanchnic arterial vasodilation results in an increase portal venous inflow, maintaining the elevated portal venous pressure. Hyperdynamic circulation is intimately involved in portal hypertension with liver cirrhosis, therefore it is reasonable to have an interest in complete understanding of the pathogenesis of hyperdynamic circulation to develop novel treatment modality.
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Kim et al. (2009) conducted a review in Liver cirrhosis and portal hypertension. Hyperdynamic circulation in liver cirrhosis is driven by portal hypertension and vasodilators like nitric oxide, leading to increased cardiac output and decreased systemic vascular resistance.
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