Treatment of refractory ascites: Current strategies and new landscape of non-selective beta-blockers

This is a review in American English I worked on:

The structural changes associated with cirrhosis lead to an elevation in intrahepatic vascular resistance and, thus, causing the production of endogenous vasoactive substances such as nitric oxide (NO). The lessening in the degradation of these factors due to liver dysfunction generates splanchnic arterial vasodilation and so reduces the effective circulating volume.⁶ Some of these vasodilators are transferred to the systemic circulation through portosystemic shunts, produced by the reperfusion and dilatation of pre-existing vessels,⁷ but also through new vessels generated by angiogenic factors, like the vascular endothelial growth factor.8, 9

Systemic vasodilation leads to a lower mean arterial pressure on account of a reduction in the systemic vascular resistance that, while in the early stages of cirrhosis, gets compensated with an increase in the cardiac output in order to keep mean arterial pressure within normal ranges.¹⁰ However, as cirrhosis progresses, the systemic vascular resistance lowers markedly, and the rise of cardiac output is no longer able to compensate for it. This conducts to the worsening of the effective circulating volume, relative hypovolemia, and systemic hypotension, thus explaining the hyperdynamic circulation in these patients.¹¹