Circulatory and cardiac compromise in cirrhosis has been well studied. The primary pathophysiology stems from portal hypertension, which is induced from an increased resistance to flow secondary to distorted sinusoidal architecture and is further sustained from an increase in portal venous flow.1 Portal hypertension induces both progressive splanchnic and systemic vasodilation mediated via nitric oxide and other vasoactive molecules secondary to endothelial stretching and sheer stress.2 A hyperdynamic state then ensues with an increase in cardiac output, increase in heart rate, and a low systemic vascular resistance secondary to systemic vasodilatation. The decreased effective arterial blood volume activates neurohormonal systems such as the renin‐angiotensin‐aldosterone system (RAAS), leading to further volume expansion via sodium and water retention. However, because of portosystemic shunting and splanchnic vasodilatation, effective central blood volume remains low and the hyperdynamic state continues, eventually leading to high‐output heart failure (Fig. ​(Fig.1).1). A lower mean arterial pressure (MAP) of 60 to 65 mm Hg is often tolerated in compensated and stable patients through these compensatory mechanisms, which allow end‐organ perfusion to be maintained.1, 2 Any degree of insult to this system can result in significant hypotension and decompensation. Open in a separate window Figure 1 Pathophysiology of hypotension in cirrhosis.