High cardiac output of advanced liver disease persists after orthotopic liver transplantation

Henderson, J. Michael; Mackay, Gregory J.; Hooks, Michael A.; Chezmar, J L; Galloway, John R.; Dodson, Thomas F.; Kutner, Michael

doi:10.1002/hep.1840150214

Cited by 87 publications

(61 citation statements)

References 21 publications

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“…This is caused by persistence of the splanchnic hyperemia associated with portal hypertension, the hepatic arterial vasodilatation caused by hepatic artery denervation of the graft, or both mechanisms. 9,[12][13][14] In most cases, the graft could accommodate this increased blood flow. In other cases, however, the increase in hepatic blood flow would increase the sinusoidal pressure if a difficulty in hepatic venous outflow was present and thereby contribute to the ascites formation.…”

Section: Discussionmentioning

confidence: 99%

Ascites after liver transplantation

et al. 2000

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Massive ascites after liver transplantation, although uncommon, usually represents a serious adverse event. The pathogenesis of this complication has not been adequately investigated. To determine the incidence, characteristics, and pathogenic factors of massive ascites after liver transplantation (ascitic fluid G 500 mL/d for G10 days), the charts of 378 liver transplant recipients were reviewed. Massive ascites occurred in 25 patients (7%). Mean ascitic fluid production was 960 mL/d (range, 625 to 2,350 mL/d), and the duration of ascites was 77 days (range, 15 to 223 days). The ascitic fluid had a high protein content (36 ؎ 7 g/L; range, 25 to 50 g/L). When patients who did and did not develop massive ascites were compared, significant differences were found in receptor sex (men, 88% v 60%, respectively; P F .01) and surgical technique (inferior vena cava preservation with piggyback technique, 72% v 41%; P F .01). Significantly increased wedged and free hepatic venous pressures and gradients between hepatic vein and right atrial pressures were found in patients who developed ascites, suggesting a difficulty in graft blood outflow. Massive ascites was associated with renal impairment, increased incidence of abdominal infection, prolonged hospitalization, and a tendency toward reduced survival. In conclusion, massive ascites after liver transplantation is relatively uncommon but associated with increased morbidity and mortality and is predominantly related to difficulties of hepatic venous drainage. Measurement of hepatic vein and atrial pressures to detect a significant gradient and correct possible alterations in hepatic vein outflow should be the first approach in the management of these patients.

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Section: Discussionmentioning

confidence: 99%

Ascites after liver transplantation

et al. 2000

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“…9 Although both groups have low peripheral resistance, it seems that the peripheral resistance vessels in ALF still have an ability to change tone, and this ability is lost in severe chronic liver disease. 48 This is illustrated by the observation that the hyperkinetic syndrome can persist for up to 2 years after liver transplantation in patients with advanced cirrhosis 49 as opposed to patients with ALF where the hemodynamics normalize within a few days. 50 One interesting finding in the present study is that the splanchnic resistance did not change during HVP in any of the two groups.…”

Section: Discussionmentioning

confidence: 99%

Hepatic Blood Flow and Splanchnic Oxygen Consumption in Patients With Liver Failure. Effect of High–Volume Plasmapheresis

Clemmesen

Gerbes²,

Gülberg³

et al. 1999

Hepatology

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Liver failure represents a major therapeutic challenge, and yet basic pathophysiological questions about hepatic perfusion and oxygenation in this condition have been poorly investigated. In this study, hepatic blood flow (HBF) and splanchnic oxygen delivery (DO 2,sp ) and oxygen consumption (VO 2,sp ) were assessed in patients with liver failure defined as hepatic encephalopathy grade II or more. Measurements were repeated after high-volume plasmapheresis (HVP) with exchange of 8 to 10 L of plasma. HBF was estimated by use of constant infusion of D-sorbitol and calculated according to Fick's principle from peripheral artery and hepatic vein concentrations. In 14 patients with acute liver failure (ALF), HBF (1.78 ؎ 0.78 L/min) and VO 2,sp (3.9 ؎ 0.9 mmol/min) were higher than in 11 patients without liver disease (1.07 ؎ 0.19 L/min, P F .01) and (2.3 ؎ 0.7 mmol/min, P F .001). In 9 patients with acute on chronic liver disease (AOCLD), HBF (1.96 ؎ 1.19 L/min) and VO 2,sp (3.9 ؎ 2.3 mmol/min) were higher than in 18 patients with stable cirrhosis (1.00 ؎ 0.36 L/min, P F .005; and 2.0 ؎ 0.6 mmol/min, P F .005). During HVP, HBF increased from 1.67 ؎ 0.72 to 2.07 ؎ 1.11 L/min (n‫)11؍‬ in ALF, and from 1.89 ؎ 1.32 to 2.34 ؎ 1.54 L/min (n‫)7؍‬ in AOCLD, P F .05 in both cases. In patients with ALF, cardiac output (thermodilution) was unchanged (6.7 ؎ 2.5 vs. 6.6 ؎ 2.2 L/min, NS) during HVP. Blood flow was redirected to the liver as the systemic vascular resistance index increased (1,587 ؎ 650 vs. 2,020 ؎ 806 Dyne · s · cm ؊5 · m 2 , P F .01) whereas splanchnic vascular resistance was unchanged. In AOCLD, neither systemic nor splanchnic vascular resistance was affected by HVP, but as cardiac output increased from 9.1 ؎ 2.8 to 10.1 ؎ 2.9 L/min (P F .01) more blood was directed to the splanchnic region. In all liver failure patients treated with HVP (n‫,)81؍‬ DO 2,sp increased by 15% (P F .05) whereas VO 2,sp was unchanged. Endothelin-1 (ET-1) and ET-3 were determined before and after HVP. Changes of ET-1 were positively correlated with changes in HBF (P F .005) and VO 2,sp (P F .05), indicating a role for ET-1 in splanchnic circulation and oxygenation. ET-3 was negatively correlated with systemic vascular resistance index before HVP (P F .05) but changes during HVP did not correlate. Our data suggest that liver failure is associated with increased HBF and VO 2,sp . HVP further increased HBF and DO 2,sp but VO 2,sp was unchanged, indicating that splanchnic hypoxia was not present.(HEPATOLOGY 1999;29: 347-355.)A basic requirement for organ function is adequate blood flow and oxygen delivery. Hepatic blood flow (HBF) and splanchnic oxygenation in patients with liver failure (in the present study, defined as having developed hepatic encephalopathy [HE] grade II or more) have not been assessed because a method to estimate HBF in such patients has not been available until recently. 1,2 Knowledge in this field, therefore, rests on indirect evidence and animal experiments. The observation that whole-body (systemic) oxygen consumpti...

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“…14 It has been shown that the peripheral vasodilatation associated with liver disease normalizes in the post-liver transplantation period. 4,5 Increase in circulating endothelin in the early postoperative period has been proposed as one of the mechanisms by which this occurs. 15 The resultant increase in afterload could be responsible for the heart failure seen in our patients.…”

Section: Discussionmentioning

confidence: 99%

“…2 This hyperdynamic circulatory state usually resolves in the weeks after transplantation, 3,4 although it can sometimes persist even after successful liver transplantation. 5 We describe a small subset of post-OLT patients who showed an initial hyperdynamic circulatory state, followed by a period of markedly reduced cardiac function associated with cardiac dilatation and associated clinical heart failure. This document is the first to characterize this syndrome of reversible, dilated cardiomyopathy after OLT.…”

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confidence: 99%

Post-liver transplantation myocardial dysfunction

et al. 1998

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Patients with end-stage liver disease usually show a hyperdynamic circulatory state. It has previously been reported that patients who develop myocardial depression in the early post-liver transplantation period are more prone to organ failure and death. We reviewed the records of 754 adult patients undergoing liver transplantation at our institution and identified 7 patients who initially showed hyperdynamic circulation, but then developed reversible dilated cardiomyopathy in the early posttransplantation period. All identifiable causes of cardiac dysfunction, such as myocardial ischemia, thyroid dysfunction, and electrolyte imbalances, were excluded. Left ventricular ejection fraction decreased from a preoperative median baseline of 60% to 20% (P ‫؍‬ .02), with four-chamber dilatation on echocardiogram. All these patients required supportive care, including mechanical ventilation, afterload reduction, inotropic support, and monitoring in the intensive care unit. Cardiac function subsequently improved in all patients, with ejection fraction increasing to a median of 50%. All patients were discharged from the hospital. At a median follow-up of 15 months, there was no recurrence of heart failure. The increased peripheral resistance seen after successful liver transplantation may be an important causative factor. Copyright 1998 by the American Association for the Study of Liver Diseases H yperdynamic circulation has been repeatedly documented in patients with liver disease since the first description of the hyperdynamic circulatory state by Kowalski and Abelman in 1953. 1 Even those patients who were not previously hyperdynamic can respond to recirculation at the time of orthotopic liver transplantation (OLT) by developing a hyperdynamic circulatory state. 2 This hyperdynamic circulatory state usually resolves in the weeks after transplantation, 3,4 although it can sometimes persist even after successful liver transplantation. 5 We describe a small subset of post-OLT patients who showed an initial hyperdynamic circulatory state, followed by a period of markedly reduced cardiac function associated with cardiac dilatation and associated clinical heart failure. This document is the first to characterize this syndrome of reversible, dilated cardiomyopathy after OLT. Materials and MethodsWe reviewed a summary of the medical records of 754 adults (Ͼ18 years of age) undergoing OLT at the Mayo Clinic (Rochester, MN) from March 1985 through December 1996. The medical records of patients with chest radiograph evidence of pulmonary edema were carefully reviewed to identify a subset of patients with myocardial dysfunction, all of whom had echocardiographic evidence of a dilated cardiomyopathy post-OLT. We excluded patients with myocardial infarction at the time of congestive heart failure. Myocardial infarction was defined as elevation of cardiac enzyme levels with or without electrocardiographic changes. We also excluded patients who had intraoperative cardiac complications such as myocardial infarction, severe persistent hy...

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High cardiac output of advanced liver disease persists after orthotopic liver transplantation

Cited by 87 publications

References 21 publications

Ascites after liver transplantation

Ascites after liver transplantation

Hepatic Blood Flow and Splanchnic Oxygen Consumption in Patients With Liver Failure. Effect of High–Volume Plasmapheresis

Post-liver transplantation myocardial dysfunction

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