Abolished ventilation and perfusion of lung caused by blood clot in the left main bronchus: auto-downregulation of pulmonary arterial blood supply.

It is generally assumed that the lungs possess arterial autoregulation associated with bronchial obstruction. A patient with pneumonia and congestive heart failure unexpectedly developed frequent haemoptysis. High-resolution CT and diagnostic CT were performed as well as ventilation/perfusion (V/Q) scintigraphy with single-photon emission CT (SPECT)/CT. V/Q SPECT/CT demonstrated abolished ventilation due to obstruction of the left main bronchus and markedly reduced perfusion of the entire left lung, a condition that was completely reversed after removal of a blood clot. We present the first pictorially documented case of hypoxia-induced pulmonary vasoconstriction and flow shift in a main pulmonary artery due to a complete intrinsic obstruction of the ipsilateral main bronchus. The condition is reversible, contingent on being relieved within a few days.

Does comprilan bandage have any influence on peripheral perfusion in patients with oedema?

AIM: Comprilan bandage may be an attractive treatment of leg oedema, but theoretically bandage could compromise peripheral circulation. The present study was undertaken to investigate circulation in the first toe before, during, and after treatment with comprilan bandage. METHODS AND STUDY POPULATION: Blood flow rate was measured by the heat-washout method in the pulp of the first toe of 10 patients (eight women, two men, aged 75-94) with leg oedemas, and systolic toe blood pressure was determined by the strain gauge method. Oedema was scored according to a visual scale, and the patients were treated with comprilan (short stretch) bandage for 1 week. Toe blood flow rate was measured before, during and after the use of the bandages, and toe blood pressure was measured before and after the use of bandages. RESULTS: According to the visual scale, all subject benefited from the treatment by reduction of oedema, and they reported increased well-being after. Blood flow rate was not significantly altered during and after the treatment. Systolic toe pressure was normal in all patients (R/L = 94/83 mmHg), and no significant change took place during and after the use of the bandages (92/90 mmHg). CONCLUSION: Comprilan bandage has a positive effect on legs oedemas, visually as well as according to the patients well-being. The treatment does not have any significant influence on toe blood pressure. It cannot, however, be excluded that the use of comprilan bandage may compromise toe blood flow rate slightly (<5%). A larger study with more subjects has to be made to come this closer, and additional capillary blood flow rate should be measured in an area without arteriovenous anastomoses.

Low cardiac output predicts development of hepatorenal syndrome and survival in patients with cirrhosis and ascites.

OBJECTIVES: Recent studies suggest that cardiac dysfunction precedes development of the hepatorenal syndrome. In this follow-up study, we aimed to investigate the relation between cardiac and renal function in patients with cirrhosis and ascites and the impact of cardiac systolic function on survival. PATIENTS AND DESIGN: Twenty-four patients with cirrhosis and ascites were included. Cardiac function was investigated by gated myocardial perfusion imaging (MPI) for assessment of cardiac index (CI) and cardiac volumes. The renal function was assessed by determination of glomerular filtration rate (GFR) and renal blood flow (RBF) and the patients were followed up for 12 months. RESULTS: In patients with a CI below 1.5 l/min/m(2) on MPI, GFR was lower (39 (SD 24) vs 63 (SD 23) ml/min, p = 0.03), RBF was lower (352 (SD 232) vs 561 (SD 229) ml/min, p = 0.06), and serum creatinine was higher (130 (SD 46) vs 78 (SD 29) mumol/l, p<0.01). The number of patients who developed hepatorenal syndrome type 1 within 3 months was higher in the group with low CI than in the high CI group (43% vs 5%, p = 0.04). Patients with the lowest CI (N = 8) had significantly poorer survival at 3, 9, and 12 months compared to those with a higher CI (N = 16), p<0.05. In contrast, the Model for End-stage Liver Disease (MELD) score failed to predict mortality in these patients. CONCLUSIONS: The development of renal failure and poor outcome in patients with advanced cirrhosis and ascites seem to be related to a cardiac systolic dysfunction. Other parameters may be more important than MELD score to predict prognosis.

Cardiovascular complications of cirrhosis.

Cardiovascular complications of cirrhosis include cardiac dysfunction and abnormalities in the central, splanchnic and peripheral circulation, and haemodynamic changes caused by humoral and nervous dysregulation. Cirrhotic cardiomyopathy implies systolic and diastolic dysfunction and electrophysiological abnormalities, an entity that is different from alcoholic heart muscle disease. Being clinically latent, cirrhotic cardiomyopathy can be unmasked by physical or pharmacological strain. Consequently, caution should be exercised in the case of stressful procedures, such as large volume paracentesis without adequate plasma volume expansion, transjugular intrahepatic portosystemic shunt (TIPS) insertion, peritoneovenous shunting and surgery. Cardiac failure is an important cause of mortality after liver transplantation, but improved liver function has also been shown to reverse the cardiac abnormalities. No specific treatment can be recommended, and cardiac failure should be treated as in non-cirrhotic patients with sodium restriction, diuretics, and oxygen therapy when necessary. Special care should be taken with the use of ACE inhibitors and angiotensin antagonists in these patients. The clinical significance of cardiovascular complications and cirrhotic cardiomyopathy is an important topic for future research, and the initiation of new randomised studies of potential treatments for these complications is needed.

Cardiovascular complications of cirrhosis.

Cardiovascular complications of cirrhosis include cardiac dysfunction and abnormalities in the central, splanchnic and peripheral circulation, and haemodynamic changes caused by humoral and nervous dysregulation. Cirrhotic cardiomyopathy implies systolic and diastolic dysfunction and electrophysiological abnormalities, an entity that is different from alcoholic heart muscle disease. Being clinically latent, cirrhotic cardiomyopathy can be unmasked by physical or pharmacological strain. Consequently, caution should be exercised in the case of stressful procedures, such as large volume paracentesis without adequate plasma volume expansion, transjugular intrahepatic portosystemic shunt (TIPS) insertion, peritoneovenous shunting and surgery. Cardiac failure is an important cause of mortality after liver transplantation, but improved liver function has also been shown to reverse the cardiac abnormalities. No specific treatment can be recommended, and cardiac failure should be treated as in non-cirrhotic patients with sodium restriction, diuretics, and oxygen therapy when necessary. Special care should be taken with the use of ACE inhibitors and angiotensin antagonists in these patients. The clinical significance of cardiovascular complications and cirrhotic cardiomyopathy is an important topic for future research, and the initiation of new randomised studies of potential treatments for these complications is needed.

Q-T interval (QT(C)) in patients with cirrhosis: relation to vasoactive peptides and heart rate.

OBJECTIVE: Prolonged Q-T interval (QT) has been reported in patients with cirrhosis who also exhibit profound abnormalities in vasoactive peptides and often present with elevated heart rate (HR). The aim of this study was to relate QT to the circulating level of endothelins (ET-1 and ET-3) and calcitonin gene-related peptide (CGRP) in patients with cirrhosis. In addition, we studied problems with HR correction of QT. MATERIAL AND METHODS: Forty-eight patients with cirrhosis and portal hypertension were studied during a haemodynamic investigation. Circulating levels of ETs and CGRP were determined by radioimmunoassays. Correction of QT for HR above 60 beats per min was performed using the methods described by Bazett (QT(C)) and Fridericia (QT(F)). RESULTS: Prolonged QT(C) (above 440 ms), found in 56% of the patients, was related to the presence of significant portal hypertension and liver dysfunction (p < 0.05 to 0.001), but not to elevated ET-1, ET-3 or CGRP. When corrected according to Bazett, QT(C) showed no significant relation to differences in HR between patients (r = 0.07, ns). QTF showed some undercorrection of HR (r = -0.36; p < 0.02). During HR variation in the individual patient, QT(C) revealed a small but significant overcorrection (2.6 ms per heartbeat per min; p < 0.001). This value was significantly (p < 0.02) smaller with QTF (1.2 ms per heartbeat per min). CONCLUSIONS: The prolonged QT(C) in cirrhosis is related to liver dysfunction and the presence of portal hypertension, but not to the elevated powerful vasoconstrictor (ET-1) or vasodilator (CGRP, ET-3) peptides. The problems with correction of the QT for elevated HR in cirrhosis are complex, and the lowest HR should be applied for determination of the QT.

Arterial hypertension in cirrhosis: arterial compliance, volume distribution, and central haemodynamics.

BACKGROUND AND AIMS: Arterial hypertension is a common disorder. Hyperkinetic circulation and reduced effective volaemia are central elements in the haemodynamic dysfunction in cirrhosis. The aim of the present study was to investigate whether cirrhotic patients with arterial hypertension are normokinetic and normovolaemic or whether they reveal the same circulatory dysfunction as their normotensive counterparts. MATERIAL AND METHODS: Thirty three patients with arterial hypertension were identified among 648 patients with cirrhosis: 14 in Child class A, 12 in class B, and seven in class C. Controls were 130 normotensive cirrhotic patients, 19 controls with normal arterial blood pressure and without liver disease, and 16 patients with essential arterial hypertension. All groups underwent haemodynamic investigation with determination of cardiac output (CO), plasma volume (PV), central blood volume (CBV), hepatic venous pressure gradient (HVPG), hepatic blood flow (HBF), arterial compliance (AC), and systemic vascular resistance (SVR) in the supine position. RESULTS: Liver function, as evaluated by galactose elimination capacity, indocyanine green clearance, HBF, and Child score, was significantly better in hypertensive cirrhotics than in their normotensive counterparts (p<0.05-0.01) but portal pressure was similar (HVPG 13 v 15 mm Hg; NS). AC was significantly lower and normal in the arterial hypertensive cirrhotic group (1.07 v 1.39 mm Hg/ml; p<0.02) and SVR was significantly higher and normal (1475 v 1020 dynxs/cm5; p<0.01). Arterial hypertensive cirrhotic patients were hyperdynamic (CO 6.80 v 7.14 l/min; NS) and central hypovolaemic (CBV 19.8 v 20.6 ml/kg; NS), as were normotensive patients, but differences were found in relation to arterial blood pressure. Whereas arterial pressure was inversely correlated with CO, PV, and Child score in the normotensive group (p< 0.01), the same correlations were either direct or insignificant in arterial hypertensive cirrhotics. CONCLUSION: Arterial hypertensive cirrhotic patients are hyperkinetic and central hypovolaemic, in common with their normotensive counterparts, but vasodilatation is reduced and regulation of arterial blood pressure may be less deranged.

BNP and N-terminal proBNP are both extracted in the normal kidney.

BACKGROUND: Increased plasma concentrations of cardiac-derived B-type natriuretic peptide (BNP) and N-terminal pro-B-type natriuretic peptide (proBNP) are both associated with left ventricular dysfunction. Information on the regional elimination of the peptides is, however, still scarce. We therefore examined the renal and peripheral extraction of N-terminal proBNP and BNP. MATERIALS AND METHODS: The study comprised 18 patients with essential arterial hypertension, 51 with cirrhosis, and 18 control patients without kidney or liver disease. All patients underwent a haemodynamic investigation with catheterization of the femoral artery and femoral and renal veins. Blood sampling from the catheters allowed determination of the arteriovenous extraction ratio of N-terminal proBNP and BNP. RESULTS: Neither the peripheral N-terminal proBNP (13, 11, 19 pmol L(-1), NS) nor the BNP plasma concentrations (4, 12, 9 pmol L(-1), NS) differed between the patient groups. In addition, similar renal extractions were observed in the groups. The renal extraction of N-terminal proBNP (0.16) was not different from that of BNP (0.16). In contrast, the N-terminal proBNP extraction in the lower extremity was markedly lower compared with BNP (0.00 vs. 0.125, P = 0.007). CONCLUSIONS: A comparable renal elimination of N-terminal proBNP and BNP is contrasted by a selective extraction of BNP in the lower extremity. Our results suggest a different elimination mechanism in the renal and peripheral circulation, which partly may explain the higher N-terminal proBNP compared with BNP concentrations in normal plasma.

Validation of a self-administered modified CAGE test (CAGE-C) in a somatic hospital ward: comparison with biochemical markers.

OBJECTIVE: The time frame for the original CAGE questionnaire is lifetime and it does not quantify drinking frequency and may be less suitable in a population with very few teetotalers. The purpose of this study was to validate a variant of the CAGE questionnaire and compare it with the outcome of a thorough interview according to DSM-III and ICD-10 criteria and to the outcome of biochemical markers in inpatients in a somatic hospital setting. MATERIAL AND METHODS: The questionnaire and biochemical markers were tested on a random sample of 130 patients admitted to a department of orthopedic surgery. The result of a diagnostic interview with a trained staff member from the local alcohol treatment unit was used as the gold standard. Data were analyzed by means of receiver operating characteristic (ROC) curves. RESULTS: In this population 25 % had an alcohol problem and the questionnaire proved to be valid, with a sensitivity and specificity of 0.94 and 0.88, respectively, while the positive predictive value (PVpos) was 0.73 and the negative predictive value (PVneg) was 0.98. Carbohydrate-deficient transferrin (CDT) had a sensitivity and a specificity of 0.47 and 0.96, and PVpos and PVneg of 0.80 and 0.85, respectively. CONCLUSIONS: This new diagnostic questionnaire is simple, easy to administer and suitable for screening purposes in populations with a high prevalence of at-risk drinkers.

Arterial hypertension and chronic liver disease.

This review looks at the alterations in the systemic haemodynamics of patients with chronic liver disease (cirrhosis) in relation to essential hypertension and arterial hypertension of renal origin. Characteristic findings in patients with cirrhosis are vasodilatation with low overall systemic vascular resistance, high arterial compliance, increased cardiac output, secondary activation of counterregulatory systems (renin-angiotensin-aldosterone system, sympathetic nervous system, release of vasopressin), and resistance to vasopressors. The vasodilatory state is mediated through adrenomedullin, calcitonin gene-related peptide, nitric oxide, and other vasodilators, and is most pronounced in the splanchnic area. This provides an effective (although relative) counterbalance to raised arterial blood pressure. Subjects with arterial hypertension (essential, secondary) may become normotensive during the development of chronic liver disease, and arterial hypertension is rarely manifested in patients with cirrhosis, even in those with renovascular disease and high circulating renin activity. There is much dispute as to the understanding of homoeostatic regulation in cirrhotic patients with manifest arterial hypertension. This probably includes the combination of vasodilatation and vasoconstriction in parallel.

Volume adaptation in chronic liver disease: on the static and dynamic location of water, salt, protein and red cells in cirrhosis.

Adequate size and distribution of the circulating medium are important for cardiovascular function, tissue oxygenation and fluid homoeostasis. Patients with cirrhosis have an abnormal distribution of increased blood volume, increased total vascular compliance and increased arterial compliance. The pattern and temporal relations of plasma and blood volume expansion are important for pathophysiological, diagnostic and therapeutic purposes and depend highly on the type of load (water, saline, oncotic material, red blood cells). In some aspects patients with cirrhosis respond differently from healthy subjects. Thus the reaction during volume expansion may be somewhat blunted, and in advanced cirrhosis, the non-central parts of the circulation in particular, including the splanchnic blood volume, are expanded by a volume load. The use of vasoactive drugs has provided important information on the changes in haemodynamic and homoeostatic mechanisms in patients with cirrhosis. Infusion of oncotic material (preferably albumin) may prevent circulatory dysfunction during certain types of stress. Volume expansion in advanced cirrhosis is qualitatively and quantitively different from that of healthy subjects and those with early cirrhosis. Timely volume handling is essential, but difficult as it is a balance between hypovolaemia and excess extravascular volume loading with further circulatory dysfunction in these patients with a hyperdynamic, but hyporeactive circulation.

Review article: pathogenesis and pathophysiology of hepatorenal syndrome--is there scope for prevention?

The hepatorenal syndrome (HRS) is a functional impairment of the kidneys in chronic liver disease caused by a circulatory failure. The prognosis is poor, particularly with type 1 HRS, but also type 2, and only liver transplantation is of lasting benefit. However, recent research into the pathophysiology of ascites and HRS has stimulated new enthusiasm in their prevention and treatment. Patients with HRS have hyperdynamic circulatory dysfunction with reduced arterial blood pressure and reduced central blood volume, owing to preferential splanchnic arterial vasodilatation. Activation of potent vasoconstricting systems, including the sympathetic nervous and renin-angiotensin-aldosterone systems, counteracts the arterial vasodilatation and leads to a pronounced renal vasoconstriction with renal hypoperfusion, a reduced glomerular filtration rate, and intense sodium-water retention. Thus prevention of HRS should seek to improve liver function, limit arterial hypotension and central hypovolaemia, and reduce renal vasoconstriction and the renal and interstitial pressures. Portal pressure can be reduced with beta-adrenergic blockers and transjugular intrahepatic portosystemic shunt (TIPS). Precipitating events, like infections, bleeding, and postparacentesis circulatory syndrome, should be treated to avoid further circulatory failure. Improvement in arterial blood pressure and central hypovolaemia can be achieved with vasoconstrictors, such as terlipressin (Glypressin), and plasma expanders such as human albumin. In the future endothelins, adenosine antagonists, long-acting vasoconstrictors, and antileukotriene drugs may play a role in preventing and treating HRS.

Effect of terlipressin on blood volume distribution in patients with cirrhosis.

BACKGROUND: Patients with cirrhosis and portal hypertension have an altered blood volume distribution and a hyperdynamic systemic circulation. Terlipressin is known to reduce portal pressure by decreasing splanchnic inflow, but its effect on the blood volume distribution is unknown. The aim of the study was to investigate changes in regional blood volume distribution and systemic haemodynamics after administration of terlipressin to patients with cirrhosis. METHODS: Blood volume distribution was determined in 13 patients with cirrhosis and portal hypertension by a dual-head gamma-camera technique and systemic haemodynamics was measured before and after intravenous administration of terlipressin (2 mg). RESULTS: Terlipressin increased the blood volume in the thorax region (+6.0%, P < 0.002) and the liver region (+12.2%, P < 0.002), whereas blood volume in the splanchnic region remained unchanged. Systemic vascular resistance (SVR) and mean arterial blood pressure increased after terlipressin (+34 and +21%, P < 0.001). The increase in liver blood volume correlated directly with the increase in SVR (r = 0.88. P < 0.001). CONCLUSIONS: Terlipressin ameliorates the hyperdynamic circulation, increases thorax and liver blood volumes, but produces no effect on the splanchnic blood volume. Besides decreasing the splanchnic inflow, terlipressin may affect portal pressure by causing vasodilatation of intrahepatic vessels.

Increased circulating pro-brain natriuretic peptide (proBNP) and brain natriuretic peptide (BNP) in patients with cirrhosis: relation to cardiovascular dysfunction and severity of disease.

BACKGROUND AND AIMS: Cardiac dysfunction may be present in patients with cirrhosis. This study was undertaken to relate plasma concentrations of cardiac peptides reflecting early ventricular dysfunction (pro-brain natriuretic peptide (proBNP) and brain natriuretic peptide (BNP)) to markers of severity of liver disease, cardiac dysfunction, and hyperdynamic circulation in patients with cirrhosis. PATIENTS AND METHODS: Circulating levels of proBNP and BNP were determined in 51 cirrhotic patients during a haemodynamic investigation. RESULTS: Plasma proBNP and BNP were significantly increased in cirrhotic patients (19 and 12 pmol/l, respectively) compared with age matched controls (14 and 6 pmol/l; p<0.02) and healthy subjects (<15 and <5.3 pmol/l; p<0.002). Circulating proBNP and BNP were closely correlated (r = 0.89, p<0.001), and the concentration ratio proBNP/BNP was similar to that of control subjects (1.8 v 2.3; NS). Circulating proBNP and BNP were related to severity of liver disease (Child score, serum albumin, coagulation factors 2, 7, and 10, and hepatic venous pressure gradient) and to markers of cardiac dysfunction (QT interval, heart rate, plasma volume) but not to indicators of the hyperdynamic circulation. Moreover, in multiple regression analysis, proBNP and BNP were also related to arterial carbon dioxide and oxygen tensions. The rate of hepatic disposal of proBNP and BNP was not significantly different in cirrhotic patients and controls. CONCLUSION: Elevated circulating levels of proBNP and BNP in patients with cirrhosis most likely reflects increased cardiac ventricular generation of these peptides and thus indicates the presence of cardiac dysfunction, rather than being caused by the hyperdynamic circulatory changes found in these patients.

Increased arterial compliance in cirrhosis is related to decreased arterial C-type natriuretic peptide, but not to atrial natriuretic peptide.

BACKGROUND: Increased arterial compliance (COMPart) has recently been described in patients with cirrhosis, particularly in advanced disease. The aim of the present study was to relate COMPart with arterial levels of the circulating natriuretic peptides: atrial natriuretic peptide (ANP) and C-type natriuretic peptide (CNP), both of which are vasodilators. METHODS: Thirty-one patients with cirrhosis, 14 non-cirrhotic patients with circulatory disturbances of the ischaemic and hypertensive type, and 10 healthy controls were investigated during a haemodynamic examination. RESULTS: The patients with cirrhosis showed the well-known hyperdynamic circulation with elevated cardiac output, low arterial blood pressure, and reduced systemic vascular resistance. COMPart in the patients with cirrhosis (1.30 mL/mmHg) was significantly (P < 0.01) increased compared to that of non-cirrhotic patients (0.99 mL/mmHg) and controls (1.01 mL/mmHg). In the patients with cirrhosis, a significant inverse correlation was found between CNP and COMPart (r = -0.42, P < 0.01), but not between CNP and systemic vascular resistance (r = 0.31, P = 0.08). In the non-cirrhotic patients, CNP had a significant inverse correlation to COMPart (r = -0.68, P < 0.01) and a direct correlation to systemic vascular resistance (r = 0.62, P < 0.02). ANP was not significantly related to COMPart nor to systemic vascular resistance in any of the groups. CONCLUSION: The finding of an inverse relation between CNP and COMPart may suggest that a compensatory down-regulation of CNP occurs in patients with cirrhosis and other types of circulatory disorders when vasodilation persists. Regulation of large and small arteries by CNP may be different in cirrhosis. Arterial ANP is not related to properties of the large or small arteries.

Review article: volume expansion in patients with cirrhosis.

Adequate size and distribution of the circulating medium are important for cardiovascular function, tissue oxygenation, and fluid homoeostasis. Patients with cirrhosis have cardiovascular dysfunction with a hyperkinetic systemic circulation, abnormal distribution of the blood volume, vasodilation with low systemic vascular resistance, increased whole-body vascular compliance, and increased arterial compliance. The effectiveness and temporal relations of plasma/blood volume expansion depend highly on the type of load (water, saline, oncotic material, red blood cells). Patients with cirrhosis respond in some aspects differently from healthy subjects, owing to their disturbed circulatory function and neurohormonal activation. Thus the increase in cardiac output and suppression of the renin-angiotensin-aldosterone system and sympathetic nervous system during volume expansion may be somewhat blunted, and in advanced cirrhosis, especially the non-central parts of the circulation, including the splanchnic blood volume, are expanded by a volume load. Infusion of oncotic material (preferably albumin) is important in the prevention of post-paracentesis circulatory dysfunction. In conclusion, volume expansion in advanced cirrhosis is qualitatively and quantitatively different from that of healthy subjects, and in those with early cirrhosis. Timely handling is essential, but difficult as it is a balance between the risks of excess extravascular volume loading and further circulatory dysfunction in these patients with a hyperdynamic, but hyporeactive, circulation.

Elevated arterial compliance in patients with cirrhosis is not related to arterial endothelin-1.

BACKGROUND: Patients with cirrhosis and portal hypertension have a hyperkinetic systemic circulation. A number of circulating vasoactive peptides, including endothelin-1 (ET-1), are elevated and, recently, increased arterial compliance has been described in these patients. The aim of the present study was to investigate a potential relation between altered arterial compliance and arterial ET-1 in patients with cirrhosis. As ET-1 may be manipulated by somastostatin, the study includes infusion of octreotide in a subset of patients. METHODS: A total of 67 patients with cirrhosis and 27 controls were studied during a haemodynamic investigation. Arterial ET-1 was determined by two different radioimmunoassays and arterial compliance was determined as the stroke volume/pulse pressure index. RESULTS: Arterial compliance was elevated by 32%-40% in the cirrhotic patients as compared to the controls (P < 0.005). Arterial ET-1 was elevated by 26%-170% in the cirrhotic patients (P<0.001). No significant relationships could be established between arterial compliance and arterial ET-1 (r = -0.15 to 0.23, ns). Intravenous bolus injection and infusion of octreotide (100 pg + 100 microg/h, n = 9) did not significantly change either arterial compliance or arterial ET-1. CONCLUSION: Both arterial compliance and arterial ET- I are substantially elevated in patients with cirrhosis, but there is no significant relation between arterial compliance and arterial ET- I in these patients.

Cirrhotic cardiomyopathy: a pathophysiological review of circulatory dysfunction in liver disease.

The systemic circulation in patients with cirrhosis is hyperdynamic with an increased cardiac output and heart rate and a reduced systemic vascular resistance as the most pronounced alterations. The concomitant cardiac dysfunction has recently been termed "cirrhotic cardiomyopathy", which is an entity different from that seen in alcoholic heart muscle disease. Clinically, these patients present with sodium fluid retention and strain often unmasks the presence of latent heart failure. No specific treatment can yet be recommended but caution should be used with respect to procedures that may stress the heart such as shunt implantation and liver transplantation.