Progressive Alterations in Systemic and Cardiopulmonary Hemodynamics Occur in Patients with Cirrhosis and Predict Death in Decompensated Cirrhosis

Beta adrenergic blockade and decompensated cirrhosis

“…The longitudinal assessment of prognostic scores reflecting liver dysfunction (i.e., the model for endstage liver disease [MELD] and the Child-Pugh scores) is used to identify patients who have progressed to a more advanced stage. In the decompensated stage, these prognostic scores together with a relative decrease in cardiac index and the presence of left ventricular dysfunction represent important predictors of mortality [38]. Recent data presented at the International Liver Congress TM (ILC) in Barcelona showed that systolic ventricular dysfunction was more prevalent in patients with higher MELD scores, and NSBBs may impact on cardiac contractility only in very severe disease, i.e., MELD score >25 [39].…”

Reply to: “Relationship of hyperdynamic circulation and cardiodynamic states in cirrhosis”

“…1 Our initial goal was to describe hepatic and systemic hemodynamics at each of the recently described prognostic stages (PSs) of cirrhosis and to identify predictors of decompensation/death at each of the PSs. 1,2 We classified the patients at the time of their first measurement of hepatic venous pressure gradient (HVPG)/hemodynamic study and, as for any prognostic study, looked at their clinical course thereafter. We cannot make any assumptions or comments regarding their previous state (hemodynamic or other).…”

“…In fact, Dr. Alvarado et al have recently shown, in patients with decompensated cirrhosis, that an NSBB-induced decrease in cardiac output to levels below 5 L/min (or CI <3 L/min/m 2 ) was predictive of poor survival. 7 Laura Turco 1 Guadalupe Garcia-Tsao 1,2,3 Rosario Rossi 4 Erica Villa 1…”

Nonselective beta blockers in patients with ascites: implications of a nationwide study

“…Although there is no association between the reduction in heart rate and hepatic venous pressure gradient (HVPG) , in the absence of biomarkers and the restricted availability of HVPG‐guided therapy , NSBB doses are commonly titrated to a heart rate target of 50–55 bpm . Parallel to the progression of liver disease, the severity of systemic haemodynamic alterations (subsumed in the term hyperdynamic circulation) increases, which might lead to higher baseline heart rates in sicker patients . Vice versa, the most vulnerable patients might be treated with the highest NSBB doses if they are titrated to the same heart rate target.…”