common sense

hyperdynamic changes are related to the severity of the liver disease, therefore ... 

http://www.ncbi.nlm.nih.gov/pubmed/3781335

http://www.ncbi.nlm.nih.gov/pubmed/8289984

http://www.ncbi.nlm.nih.gov/pubmed/2680727

Actually this exactly is the point. I agree with the patophysiology of process, but this is the basically same thing that we learned for several decades now. However, in modern age medicine we are obliged to constantly improve clinical practice with high ranked level of medical evidence (EBM). At the time being we do not have evidence based informations/guidelines with rank of evidence 1a. There were no studies (controlled) on clinical endpoints i.e. prognosis difference (mortality, quality of life, incidence of heart failure, NYHA class, rate of complications, hospitalizations/rehospitalizations per year, costs of treatment, or other) (if any) in patients with defined type of cirrhosis and hyperdynamic circulation vs controls without hyperdynamic circulation. At the time being there are no large enough controlled observational / interventional studies in this manner .

Concerning other side, and (treatment options) there also exist relative scarcity of studies. In particular, the propranolol was invented in 1960s, this was 50 years ago. There are at least dozen b-blockers that could have better efficiency/safety/tolerability than technology of 50 years ago, and there are no head-to head trials, is it not so?  Although several clinical recomendations are on suggesting utilization of propranolol, those are the best ranked 2b, whats more important, some of studies reported on its deleterious effects (PMID: 20583214). There is scarcity in prospective controlled studies of sufficient power in any terms (non-inferiority, equality, superiority, safety profile, tolerance, quality of life, mortality or others). In concern to other pharmaceutical agents, I do not feel that we made any significant improvement in conceptualizaiton of pharmacotherapy or efficiency in terms of EBM of treatment of cirrhosis for decades. Approach is in deed conservative over the years. On the other hand, studies of major importance (guidelines level) were introduced in treatment of HCV in 2014, and 2011 as significant and imporant novelty due to introduce of DAAs (most of recomendations are 1a, or 1b type, whilst other 1a ranked studies prior to 2011 (IFN-PG+RBV) were outdated  and substituted with more efficient ones. those reported on significant improvements in treament efficiency with add-on or switch to DAAs. Study population (quantity, quality, reproducibility) is also important- most of the studies on HCV enrolled 300-500 patients per arm , and were connected with clinical endpoints, which is quite some difference to all above mentioned studies, which were focused mostly on patophysiology. 

Systemic and splanchnic vasodilatation are the main hemodynamic disorders of cirrhosis. Even more, there is a correlation of hemodynamic changes with complications and survival of these patients, particularly with : refractory ascites, hepatorenal syndrome, portal hypertension-related esophageal variceal bleeding. More systemic and splachnic vasodilatation, higher portal hypertension, renal vasoconstriction, hyperdinamic circulation and lower systemic vascular resistance, mean arterial pressure. Those changes lead to organ dysfunction and death and are also related to liver function deterioration.

The main focus in prevention of cirrhosis complication related with hemodynamic changes is the use of vasoconstrictors and plasma expanders such as albumin. They have been used since long time ago for the treatment of some of these complications: a) Acute variceal bleeding, primary and secondary prophylaxis of variceal bleeding; b) prevention of paracentesis induced circulatory dysfunction after large volume paracentesis; c) treatment and prevention of type 1 hepatorenal syndrome.

Long term prospective administration of these agents (particularly beta blockers drugs) has been tested in prospective studies. Results show that they are effective for reducing first and recurrent bleeding episode in cirrhotic portal hypertension. It shows that modifying hemodynamic parameters in cirrhotic patients, appearance of complications may also be modified. Survival is not improved since it depends on liver function. Vasoconstrictors and plasma expanders do not improve liver function.

Pro b-blockers: Lebrec et al 1981 (n=74; 96 vs 50% free of recurrent GI bleeding, mortality not studied), Pascal 1987(230), Lebrec1988 (n=53; free of first vaiceal bleeding 97 vs 77%, p 0.02. no significant effect on mortality), Ideo 1998 (n=79) , Italian study (n=174) J Hepatol. 1989 Jul;9(1):75-83.

Contra b-blockers: Groszmann 2005 (213 pts; no statistically sig.difference in development of varices), Krag 2010 (meta analysis) , Sereste 2010 (n=151pts; 1 year survival 19% b-blocker vs 64% no-b-blocker).

Bottom line: grade of evidence for b-blockers (in most studied endpoints is lesser 2b, in generally most commonly 3)

This outlines  my primer consideration; I in deed had not find any studies that in pRCT manner analyzed clinical endpoints in sufficient number of population in concern to hyperdynamic syst. cir + cirrhosis  vs controls norm syst circ + cirrhosis (prognosis/mortality, head to head compare of drugs, non inferiority, different type of drugs).