In patients with decompensated cirrhosis, there are multiple intrahepatic and extrahepatic factors contributing to hemodynamic alterations at baseline, including endothelial cell dysfunction, hepatic stellate cell activation promoting increase in vasoconstrictors, decrease in vasodilators, and angiogenesis leading to worsening of portal hypertension. Increased resistance to hepatic blood flow leads to increased production of nitric oxide and other vasodilators leading to splanchnic vasodilation, decreased effective blood volume, activation of the renin angiotensin system, sodium, and water retention. In addition to portal hypertension and splanchnic vasodilation, there is a decrease in systemic vascular resistance and hyperdynamic circulation with increased cardiac output. As cirrhosis progresses to the decompensated stage, patients may develop cirrhotic cardiomyopathy, characterized by impaired cardiac response to stress, manifesting as systolic and diastolic dysfunction, and electrophysiological abnormalities such as QT prolongation leading to hypotension and dysregulated response to fluid resuscitation.

Early recognition of septic shock in these patients can be challenging when using traditional criteria due to their baseline hypotension, tachycardia, systemic vasodilation, and propensity for volume overload with fluid resuscitation. Elevated lactate levels in acutely ill patients are an independent risk factor for mortality in patients with cirrhosis. However, lactate levels >2mmol/L need not necessarily define sepsis in these patients, as these patients have decreased lactate clearance. Understanding the intricate interplay between the cardiac pump, vascular tone, and afterload is essential in managing shock in these individuals. Aggressive volume resuscitation may not be well tolerated, emphasizing the need for frequent hemodynamic assessments and prompt initiation of vasopressors when indicated.