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Yusuff H, Chawla S, Sato R, Dugar S, Bangash MN, Antonini MV, Shelley B, Valchanov K, Roscoe A, Scott J, Akhtar W, Rosenberg A, Dimarakis I, Khorsandi M, Zochios V. Mechanisms of Acute Right Ventricular Injury in Cardiothoracic Surgical and Critical Care Settings: Part 2. J Cardiothorac Vasc Anesth 2023; 37:2318-2326. [PMID: 37625918 DOI: 10.1053/j.jvca.2023.07.018] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/25/2023] [Revised: 07/05/2023] [Accepted: 07/17/2023] [Indexed: 08/27/2023]
Abstract
The right ventricle (RV) is intricately linked in the clinical presentation of critical illness; however, the basis of this is not well-understood and has not been studied as extensively as the left ventricle. There has been an increased awareness of the need to understand how the RV is affected in different critical illness states. In addition, the increased use of point-of-care echocardiography in the critical care setting has allowed for earlier identification and monitoring of the RV in a patient who is critically ill. The first part of this review describes and characterizes the RV in different perioperative states. This second part of the review discusses and analyzes the complex pathophysiologic relationships between the RV and different critical care states. There is a lack of a universal RV injury definition because it represents a range of abnormal RV biomechanics and phenotypes. The term "RV injury" (RVI) has been used to describe a spectrum of presentations, which includes diastolic dysfunction (early injury), when the RV retains the ability to compensate, to RV failure (late or advanced injury). Understanding the mechanisms leading to functional 'uncoupling' between the RV and the pulmonary circulation may enable perioperative physicians, intensivists, and researchers to identify clinical phenotypes of RVI. This, consequently, may provide the opportunity to test RV-centric hypotheses and potentially individualize therapies.
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Affiliation(s)
- Hakeem Yusuff
- Department of Cardiothoracic Critical Care Medicine and ECMO Unit, Glenfield Hospital, University Hospitals of Leicester NHS Trust, Leicester, United Kingdom; Department of Respiratory Sciences, University of Leicester, Leicester, United Kingdom.
| | - Sanchit Chawla
- Department of Critical Care Medicine, Respiratory Institute, Cleveland Clinic, Cleveland, OH
| | - Ryota Sato
- Division of Critical Care Medicine, Department of Medicine, The Queen's Medical Center, Honolulu, HI
| | - Siddharth Dugar
- Department of Critical Care Medicine, Respiratory Institute, Cleveland Clinic, Cleveland, OH; Cleveland Clinic Lerner College of Medicine, Case Western University Reserve University, Cleveland, OH
| | - Mansoor N Bangash
- Liver Intensive Care Unit, Queen Elizabeth Hospital Birmingham, Mindelsohn Way, Birmingham, United Kingdom; Birmingham Liver Failure Research Group, Institute of Inflammation and Ageing, College of Medical and Dental sciences, University of Birmingham, Birmingham, United Kingdom; Birmingham Acute Care Research Group, Institute of Inflammation and Ageing, College of Medical and Dental sciences, University of Birmingham, Birmingham, United Kingdom
| | - Marta Velia Antonini
- Anesthesia and Intensive Care Unit, Bufalini Hospital, AUSL della Romagna, Cesena, Italy; Department of Biomedical, Metabolic and Neural Sciences, University of Modena & Reggio Emilia, Modena, Italy
| | - Benjamin Shelley
- Department of Cardiothoracic Anesthesia and Intensive Care, Golden Jubilee National Hospital, Clydebank, United Kingdom; Anesthesia, Perioperative Medicine and Critical Care research group, University of Glasgow, Glasgow, United Kingdom
| | - Kamen Valchanov
- Department of Anesthesia and Perioperative Medicine, Singapore General Hospital, Outram Road, Singapore
| | - Andrew Roscoe
- Department of Anesthesia and Perioperative Medicine, Singapore General Hospital, Outram Road, Singapore; Department of Anesthesiology, Singapore General Hospital, National Heart Centre Singapore, Singapore
| | - Jeffrey Scott
- Jackson Health System / Miami Transplant Institute, Miami, FL
| | - Waqas Akhtar
- Royal Brompton and Harefield Hospitals, Part of Guys and St. Thomas's National Health System Foundation Trust, London, United Kingdom
| | - Alex Rosenberg
- Royal Brompton and Harefield Hospitals, Part of Guys and St. Thomas's National Health System Foundation Trust, London, United Kingdom
| | - Ioannis Dimarakis
- Division of Cardiothoracic Surgery, University of Washington Medical Center, Seattle, WA
| | - Maziar Khorsandi
- Division of Cardiothoracic Surgery, University of Washington Medical Center, Seattle, WA
| | - Vasileios Zochios
- Department of Cardiothoracic Critical Care Medicine and ECMO Unit, Glenfield Hospital, University Hospitals of Leicester NHS Trust, Leicester, United Kingdom; Department of Cardiovascular Sciences, University of Leicester, Leicester, United Kingdom
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Allegretti AS, Subramanian RM, Francoz C, Olson JC, Cárdenas A. Respiratory events with terlipressin and albumin in hepatorenal syndrome: A review and clinical guidance. Liver Int 2022; 42:2124-2130. [PMID: 35838488 PMCID: PMC9762017 DOI: 10.1111/liv.15367] [Citation(s) in RCA: 25] [Impact Index Per Article: 8.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/18/2022] [Revised: 07/06/2022] [Accepted: 07/12/2022] [Indexed: 12/13/2022]
Abstract
Hepatorenal syndrome-acute kidney injury (HRS-AKI) is a serious complication of severe liver disease with a clinically poor prognosis. Supportive care using vasoconstrictors and intravenous albumin are the current mainstays of therapy. Terlipressin is an efficacious vasoconstrictor that has been used for 2 decades as the first-line treatment for HRS-AKI in Europe and has demonstrated greater efficacy in improving renal function compared to placebo and other vasoconstrictors. One of the challenges associated with terlipressin use is monitoring and mitigating serious adverse events, specifically adverse respiratory events, which were noted in a subset of patients in the recently published CONFIRM trial, the largest randomized trial examining terlipressin use for HRS-AKI. In this article, we review terlipressin's pharmacology, hypothesize how its mechanism contributes to the risk of respiratory compromise and propose strategies that will decrease the frequency of these events by rationally selecting patients at lower risk for these events.
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Affiliation(s)
- Andrew S. Allegretti
- Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA
| | - Ram M. Subramanian
- Divisions of Gastroenterology and Hepatology and Pulmonary and Critical Care Medicine, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia, USA
| | - Claire Francoz
- Hepatology and Liver intensive Care Unit, Hospital Beaujon, Clichy, France
| | - Jody C. Olson
- Divisions of Gastroenterology, Hepatology, Pulmonary and Critical Care Medicine, University of Kansas Medical Center, Kansas City, Kansas, USA
| | - Andrés Cárdenas
- GI and Liver Unit, Institut de Malalties Digestives, Hospital Clinic, Barcelona, Spain. Institut d'Investigacions Biomèdiques August Pi-Sunyer (IDIBAPS), Barcelona and Ciber de Enfermedades Hepáticas y Digestivas (CIBEREHD), Barcelona, Spain
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Morkane CM, Sapisochin G, Mukhtar AM, Reyntjens KMEM, Wagener G, Spiro M, Raptis DA, Klinck JR. Perioperative fluid management and outcomes in adult deceased donor liver transplantation - A systematic review of the literature and expert panel recommendations. Clin Transplant 2022; 36:e14651. [PMID: 35304919 DOI: 10.1111/ctr.14651] [Citation(s) in RCA: 15] [Impact Index Per Article: 5.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/12/2022] [Revised: 02/28/2022] [Accepted: 02/28/2022] [Indexed: 02/04/2023]
Abstract
BACKGROUND Fluid management practices during and after liver transplantation vary widely among centers despite better understanding of the pathophysiology of end-stage liver disease and of the effects of commonly used fluids. This reflects a lack of high quality trials in this setting, but also provides a rationale for both systematic review of all relevant studies in liver recipients and evaluation of new evidence from closely related domains, including hepatology, non-transplant abdominal surgery, and critical care. OBJECTIVES To develop evidence-based recommendations for perioperative fluid management to optimize immediate and short-term outcomes following liver transplantation. DATA SOURCES Ovid MEDLINE, Embase, Scopus, Google Scholar, and Cochrane Central. METHODS Systematic review following PRISMA guidelines and recommendations using the GRADE approach derived from an international expert panel. Studies included those evaluating the following postoperative outcomes: acute kidney injury, respiratory complications, operative blood loss/red cell units required, and intensive care length of stay. PROSPERO protocol ID: CRD42021241392 RESULTS: Following expert panel review, 18 of 1624 screened studies met eligibility criteria for inclusion in the final quantitative synthesis. These included six single center RCTs, 11 single center observational studies, and one observational study comparing centers with different fluid management techniques. Definitions of interventions and outcomes varied between studies. Recommendations are therefore based substantially on expert opinion and evidence from other clinical settings. CONCLUSIONS A moderately restrictive or "replacement only" fluid regime is recommended, especially during the dissection phase of the transplant procedure. Sustained hypervolemia, based on absence of fluid responsiveness, elevated filling pressures and/or echocardiographic findings, should be avoided (Quality of Evidence: Moderate | Grade of Recommendation: Weak for restrictive fluid regime. Strong for avoidance of hypervolemia). Mean Arterial Pressure (MAP) should be maintained at >60-65 mmHg in all cases (Quality of Evidence: Low | Grade of Recommendation: Strong). There is insufficient evidence in this population to support preferential use of any specific colloid or crystalloid for routine volume replacement. However, we recommend against the use of 130/.4 HES given the high incidence of AKI in this population.
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Affiliation(s)
- Clare M Morkane
- Department of Intensive Care Medicine, Kings College Hospital, London, UK
| | - Gonzalo Sapisochin
- Multio-Organ Transplant & HPB Surgical Oncology, Division of General Surgery, University Health Network, University of Toronto, Toronto, Canada
| | | | - Koen M E M Reyntjens
- Department of Anesthesiology, Rijksuniversiteit, University Medical Center Groningen, Groningen, The Netherlands
| | - Gebhard Wagener
- Department of Anesthesiology, Columbia University Medical Center, New York, USA
| | - Michael Spiro
- Department of Anesthesia and Intensive Care Medicine, Royal Free Hospital, London, UK.,Division of Surgery & Interventional Science, University College London, London, UK
| | - Dimitri A Raptis
- Clinical Service of HPB Surgery and Liver Transplantation, Royal Free Hospital, London, UK.,Division of Surgery & Interventional Science, University College London, London, UK
| | - John R Klinck
- Division of Perioperative Care, Addenbrooke's Hospital, Cambridge, UK
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- Department of Intensive Care Medicine, Kings College Hospital, London, UK
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Mukhtar A, Lotfy A, Hussein A, Fouad E. Splanchnic and systemic circulation cross talks: Implications for hemodynamic management of liver transplant recipients. Best Pract Res Clin Anaesthesiol 2020; 34:109-118. [PMID: 32334781 DOI: 10.1016/j.bpa.2019.12.003] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/01/2019] [Accepted: 12/11/2019] [Indexed: 12/21/2022]
Abstract
The interaction between splanchnic and systemic circulation has many hemodynamic and renal consequences during liver transplant. In a patient with liver cirrhosis, splanchnic vasodilatation causes arterial steal from the systemic circulation into the splanchnic bed, which decreases the effective blood volume. Moreover, rapid volume loading in these patients has less impact on the cardiac output because a higher proportion of infused fluid is shifted to the splanchnic area. Thus, in dissection phase, the traditional approach of volume loading to maintain intraoperative hemodynamic stability not only seems ineffective, but it may also aggravate surgical bleeding. Two approaches of volume therapy have been mentioned to maintain hemodynamic stability during liver transplantation: splanchnic volume reduction by volume restriction with or without phlebotomy to maintain low central venous pressure (CVP), and splanchnic decongestion using splanchnic vasoconstrictors. After reperfusion, an increase in the central blood volume was thought to have a deleterious effect on the new graft function; however, the precise central venous pressure value that causes hepatic congestion after reperfusion is unknown.
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Affiliation(s)
- Ahmed Mukhtar
- Department of Anesthesia, Surgical Intensive Care and Pain Management, Faculty of Medicine, Cairo University, 1 Alsaray st, Almanial, Cairo, Egypt.
| | - Ahmed Lotfy
- Department of Anesthesia, Surgical Intensive Care and Pain Management, Faculty of Medicine, Cairo University, 1 Alsaray st, Almanial, Cairo, Egypt.
| | - Amr Hussein
- Department of Anesthesia, Surgical Intensive Care and Pain Management, Faculty of Medicine, Cairo University, 1 Alsaray st, Almanial, Cairo, Egypt.
| | - Eman Fouad
- Department of Anesthesia, Surgical Intensive Care and Pain Management, Faculty of Medicine, Cairo University, 1 Alsaray st, Almanial, Cairo, Egypt.
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Mukhtar A, Awad M, Elayashy M, Hussein A, Obayah G, El Adawy A, Ahmed M, Dahab HA, Hasanin A, Elfouly A, Abdo M, Abdelaal A, Teboul JL. Validity of mini-fluid challenge for predicting fluid responsiveness following liver transplantation. BMC Anesthesiol 2019; 19:56. [PMID: 30987597 PMCID: PMC6463636 DOI: 10.1186/s12871-019-0728-4] [Citation(s) in RCA: 7] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/05/2019] [Accepted: 04/03/2019] [Indexed: 01/17/2023] Open
Abstract
BACKGROUND Mini-fluid challenge is a well tested and effective tool to predict fluid responsiveness under various clinical conditions. However, mini-fluid challenge has never been tested in patients with end-stage liver disease. This study investigated whether infusion of 150 ml albumin 5% can predict fluid responsiveness in cirrhotic patients following liver transplant. METHODS Fifty patients receiving living donor liver transplant were included in the analysis. Mini-fluid challenge composed of 150 ml of albumin 5% administered over 1 min in three consecutive 50-ml fluid boluses. An additional 350 ml was then infused at a constant rate over 15 min (for a total of 500 ml). Stroke volume (SV) was measured as the product of the subaortic velocity time integral (VTI) and left ventricular outflow tract (LVOT) area. Fluid responsiveness was defined as an increase in SV by ≥15% after the infusion. RESULTS Fifty patients were enrolled in the study. Fourteen patients were classified with Child A, 15 patients with Child B, and 21 patients with Child C cirrhosis. Thirty four patients were fluid responders and 16 patients were fluid non-responders. After 150 ml of albumin 5%, the SV increased significantly in our cohort. The area under receiver operating curve (AUROC) was 0.7 (95% confidence interval [CI] 0.5-0.8, P = 0.005). In subgroup analysis, the SV increased significantly after mini fluid challenge in the Child A group (P = 0.017) but not Child B or C groups (P = 0.3 and 0.29, respectively). The AUROC for mini-fluid challenge in the Child A group was 0.86 (95% confidence interval [CI] 0.6-0.9, P = 0.0004), while mini-fluid challenge failed to discriminate between responders and non-responders in Child B and C groups. CONCLUSION A mini-fluid challenge of 150 ml albumin 5% can predict fluid responsiveness in liver transplant patients with fair sensitivity and specifiicty. Subgroup analyis revealed that minifluid challenge can predict fluid responsiveness in patients with Child A cirrhosis but not patients with Child B or C cirrhosis. TRIAL REGISTRATION NCT03396159 . (Prospective registered). Initial registration date was 10/01/2018.
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Affiliation(s)
- Ahmed Mukhtar
- Department of Anesthesia, Surgical Intensive Care and Pain Management, Faculty of Medicine, Cairo University, Cairo, Egypt. .,, Cairo, Egypt.
| | - Maha Awad
- Department of Critical Care, Faculty of Medicine, Cairo University, Cairo, Egypt
| | - Mohamed Elayashy
- Department of Anesthesia, Surgical Intensive Care and Pain Management, Faculty of Medicine, Cairo University, Cairo, Egypt
| | - Amr Hussein
- Department of Anesthesia, Surgical Intensive Care and Pain Management, Faculty of Medicine, Cairo University, Cairo, Egypt
| | - Gihan Obayah
- Department of Anesthesia, Surgical Intensive Care and Pain Management, Faculty of Medicine, Cairo University, Cairo, Egypt
| | - Akram El Adawy
- Department of Anesthesia, Surgical Intensive Care and Pain Management, Faculty of Medicine, Cairo University, Cairo, Egypt
| | - Mai Ahmed
- Department of Anesthesia, Surgical Intensive Care and Pain Management, Faculty of Medicine, Cairo University, Cairo, Egypt
| | - Hisham Abul Dahab
- Department of Anesthesia, Surgical Intensive Care and Pain Management, Faculty of Medicine, Cairo University, Cairo, Egypt
| | - Ahmed Hasanin
- Department of Anesthesia, Surgical Intensive Care and Pain Management, Faculty of Medicine, Cairo University, Cairo, Egypt
| | - Amr Elfouly
- Department of Internal Medicine, Faculty of Medicine, Helwan University, Cairo, Egypt
| | - Mostafa Abdo
- Department of Surgery, Ainshams University, Cairo, Egypt
| | - Amr Abdelaal
- Department of Surgery, Ainshams University, Cairo, Egypt
| | - Jean Louis Teboul
- Medical ICU, Bicêtre Hospital, Paris-South University, Paris, France
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Shasthry SM, Kumar M, Khumuckham JS, Sarin SK. Changes in cardiac output and incidence of volume overload in cirrhotics receiving 20% albumin infusion. Liver Int 2017; 37:1167-1176. [PMID: 28135785 DOI: 10.1111/liv.13375] [Citation(s) in RCA: 17] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/04/2016] [Accepted: 01/17/2017] [Indexed: 12/16/2022]
Abstract
BACKGROUND & AIMS Patients with cirrhosis are prone to develop volume over load, have increased capillary permeability and latent or overt cardiomyopathy. Whether albumin infusion causes volume overload in cirrhotics has not been adequately studied. METHODS Ninety nine consecutive cirrhotic patients receiving 1gm per kg albumin infusion were evaluated for development of volume overload. Clinical, echocardiographic and haemodynamic changes were closely monitored during and after albumin infusion. RESULTS Thirty (30.30%) patients developed volume overload. Patients with higher BMI (P=.003), lower CTP (P=.01) and MELD (P=.034) were more often associated with the development of volume overload. Though baseline diastolic dysfunction was present in 82.8% of the patients, it did not influence the development of volume overload or changes in the cardiac output. The cardiac output increased significantly after albumin infusion (4.9±1.554 L/min to 5.86±1.85 L/min, P<.001) irrespective of the development of volume overload, or the presence of diastolic dysfunction or the Child's status. CONCLUSION Nearly, one-third of cirrhotics receiving standard albumin infusion develop volume overload, specially, those with higher BMI and lower severity of liver disease. Cardiac output increases after albumin infusion, and, baseline diastolic dysfunction has little effect on the development of volume overload or changes in cardiac output.
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Affiliation(s)
- Saggere M Shasthry
- Department of Hepatology, Institute of Liver and Biliary Sciences, New Delhi, India
| | - Manoj Kumar
- Department of Hepatology, Institute of Liver and Biliary Sciences, New Delhi, India
| | - Jelen S Khumuckham
- Department of Cardiology, Institute of Liver and Biliary Sciences, New Delhi, India
| | - Shiv Kumar Sarin
- Department of Hepatology, Institute of Liver and Biliary Sciences, New Delhi, India
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Villanueva C, Albillos A, Genescà J, Abraldes JG, Calleja JL, Aracil C, Bañares R, Morillas R, Poca M, Peñas B, Augustin S, Garcia-Pagan JC, Pavel O, Bosch J. Development of hyperdynamic circulation and response to β-blockers in compensated cirrhosis with portal hypertension. Hepatology 2016; 63:197-206. [PMID: 26422126 DOI: 10.1002/hep.28264] [Citation(s) in RCA: 113] [Impact Index Per Article: 12.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/06/2015] [Accepted: 09/28/2015] [Indexed: 12/25/2022]
Abstract
UNLABELLED Nonselective β-blockers are useful to prevent bleeding in patients with cirrhosis and large varices but not to prevent the development of varices in those with compensated cirrhosis and portal hypertension (PHT). This suggests that the evolutionary stage of PHT may influence the response to β-blockers. To characterize the hemodynamic profile of each stage of PHT in compensated cirrhosis and the response to β-blockers according to stage, we performed a prospective, multicenter (tertiary care setting), cross-sectional study. Hepatic venous pressure gradient (HVPG) and systemic hemodynamic were measured in 273 patients with compensated cirrhosis before and after intravenous propranolol (0.15 mg/kg): 194 patients had an HVPG ≥10 mm Hg (clinically significant PHT [CSPH]), with either no varices (n = 80) or small varices (n = 114), and 79 had an HVPG >5 and <10 mm Hg (subclinical PHT). Patients with CSPH had higher liver stiffness (P < 0.001), worse Model for End-Stage Liver Disease score (P < 0.001), more portosystemic collaterals (P = 0.01) and splenomegaly (P = 0.01) on ultrasound, and lower platelet count (P < 0.001) than those with subclinical PHT. Patients with CSPH had lower systemic vascular resistance (1336 ± 423 versus 1469 ± 335 dyne · s · cm(-5) , P < 0.05) and higher cardiac index (3.3 ± 0.9 versus 2.8 ± 0.4 L/min/m(2) , P < 0.01). After propranolol, the HVPG decreased significantly in both groups, although the reduction was greater in those with CSPH (-16 ± 12% versus -8 ± 9%, P < 0.01). The HVPG decreased ≥10% from baseline in 69% of patients with CSPH versus 35% with subclinical PHT (P < 0.001) and decreased ≥20% in 40% versus 13%, respectively (P = 0.001). CONCLUSION Patients with subclinical PHT have less hyperdynamic circulation and significantly lower portal pressure reduction after acute β-blockade than those with CSPH, suggesting that β-blockers are more suitable to prevent decompensation of cirrhosis in patients with CSPH than in earlier stages.
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Affiliation(s)
- Càndid Villanueva
- Hospital de la Santa Creu i Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain.,Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain
| | - Agustín Albillos
- Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain.,Hospital Universitario Ramón y Cajal (IRYCIS), Universidad de Alcalá, Madrid, Spain
| | - Joan Genescà
- Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain.,Hospital Universitari Vall d'Hebron, Institut de Recerca (VHIR), Universitat Autònoma de Barcelona, Barcelona, Spain
| | - Juan G Abraldes
- Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain.,Barcelona Hepatic Hemodynamic Laboratory, Liver Unit, Institut Malalties Digestives i Metaboliques, IDIBAPS, Hospital Clínic, Barcelona, Spain
| | | | | | - Rafael Bañares
- Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain.,Hospital General Universitario Gregorio Marañón (IISGM), Facultad de Medicina, Universidad Complutense, Madrid, Spain
| | - Rosa Morillas
- Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain.,Hospital Germans Trias, Badalona, Spain
| | - María Poca
- Hospital de la Santa Creu i Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain.,Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain
| | - Beatriz Peñas
- Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain.,Hospital Universitario Ramón y Cajal (IRYCIS), Universidad de Alcalá, Madrid, Spain
| | - Salvador Augustin
- Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain.,Hospital Universitari Vall d'Hebron, Institut de Recerca (VHIR), Universitat Autònoma de Barcelona, Barcelona, Spain
| | - Joan Carles Garcia-Pagan
- Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain.,Barcelona Hepatic Hemodynamic Laboratory, Liver Unit, Institut Malalties Digestives i Metaboliques, IDIBAPS, Hospital Clínic, Barcelona, Spain
| | - Oana Pavel
- Hospital de la Santa Creu i Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain.,Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain
| | - Jaume Bosch
- Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain.,Barcelona Hepatic Hemodynamic Laboratory, Liver Unit, Institut Malalties Digestives i Metaboliques, IDIBAPS, Hospital Clínic, Barcelona, Spain
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Ozier Y, Cadic A, Dovergne A. Prise en charge des troubles de l’hémostase chez l’insuffisant hépatique. Transfus Clin Biol 2013; 20:249-54. [DOI: 10.1016/j.tracli.2013.02.007] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/29/2022]
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Caraceni P, Santi L, Mirici F, Montanari G, Bevilacqua V, Pinna AD, Bernardi M. Long-term treatment of hepatorenal syndrome as a bridge to liver transplantation. Dig Liver Dis 2011; 43:242-5. [PMID: 20833118 DOI: 10.1016/j.dld.2010.08.001] [Citation(s) in RCA: 19] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/22/2010] [Revised: 07/09/2010] [Accepted: 08/05/2010] [Indexed: 12/11/2022]
Abstract
BACKGROUND/AIMS Terlipressin plus albumin is first-line treatment for hepatorenal syndrome (HRS). Therapy lasts from a few days to two weeks, whereas the efficacy and safety of long-term administration remain unsettled. METHODS We describe our experience of prolonged terlipressin and albumin treatment as a bridge to liver transplantation in three patients with cirrhosis and recurrent HRS. RESULTS The length of treatment ranged from 62 days to eight months. Attempts to suspend terlipressin or to switch treatment to midodrine plus octreotide were consistently associated with a deterioration of serum creatinine and oliguria. No major side-effects were observed. All patients were transplanted, but two died from peri-operative complications. CONCLUSIONS These clinical cases suggest that long-term terlipressin administration in selected patients with recurrent HRS awaiting liver transplantation may represent an option to prevent irreversible renal failure and the need for dialysis until an organ becomes available.
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Affiliation(s)
- Paolo Caraceni
- Department of Clinical Medicine, Alma Mater Studiorum University of Bologna, Italy.
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10
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Abstract
PURPOSE OF REVIEW Patients with cirrhosis have total extracellular fluid overload but central effective circulating hypovolaemia. The resulting neurohumoral compensatory response favours the accumulation of fluids into the peritoneal cavity (ascites) and may hinder renal perfusion (hepatorenal syndrome). Their deranged systemic haemodynamics (hyperdynamic circulatory syndrome) is characterized by elevated cardiac output with decreased systemic vascular resistance and low blood pressure. RECENT FINDINGS Molecular and biological mechanisms determining cirrhosis-induced haemodynamic alterations are progressively being elucidated. The need for a goal-directed assessment of volume resuscitation (especially with volumetric techniques) in patients with cirrhosis is becoming more and more evident. The role of fluid expansion with albumin and the use of splanchnic vasopressors in a variety of cirrhosis-related conditions has recently been investigated. SUMMARY The response to fluid loading in patients with advanced cirrhosis is abnormal, primarily resulting in expansion of their noncentral blood volume compartment. Colloid solutions, in particular albumin, are best used in these patients. Albumin may be effective in preventing the haemodynamic derangements associated with large-volume paracentesis (paracentesis-induced circulatory dysfunction), in preventing renal failure during spontaneous bacterial peritonitis and, in association with splanchnic vasopressors, in caring for patients with the hepatorenal syndrome.
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11
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Effects of phlebotomy and phenylephrine infusion on portal venous pressure and systemic hemodynamics during liver transplantation. Transplantation 2010; 89:920-7. [PMID: 20216483 DOI: 10.1097/tp.0b013e3181d7c40c] [Citation(s) in RCA: 50] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/14/2022]
Abstract
BACKGROUND A regimen of fluid restriction, phlebotomy, vasopressors, and strict, protocol-guided product replacement has been associated with low blood product use during orthotopic liver transplantation. However, the physiologic basis of this strategy remains unclear. We hypothesized that a reduction of intravascular volume by phlebotomy would cause a decrease in portal venous pressure (PVP), which would be sustained during subsequent phenylephrine infusion, possibly explaining reduced bleeding. Because phenylephrine may increase central venous pressure (CVP), we questioned the validity of CVP as a correlate of cardiac filling in this context and compared it with other pulmonary artery catheter and transesophageal echocardiography-derived parameters. In particular, because optimal views for echocardiographic estimation of preload and stroke volume are not always applicable during liver transplantation, we evaluated the use of transmitral flow (TMF) early peak (E) velocity as a surrogate. METHODS In study 1, the changes in directly measured PVP and CVP were recorded before and after phlebotomy and phenylephrine infusion in 10 patients near the end of the dissection phase of liver transplantation. In study 2, transesophageal echocardiography-derived TMF velocity in early diastole was measured in 20 patients, and the changes were compared with changes in CVP, pulmonary artery pressure (PAP), pulmonary capillary wedge pressure (PCWP), cardiac output (CO), and calculated systemic vascular resistance (SVR) at the following times: postinduction, postphlebotomy, preclamping of the inferior vena cava, during clamping, and postunclamping. RESULTS Phlebotomy decreased PVP along with CO, PAP, PCWP, CVP, and TMF E velocity. Phenylephrine given after phlebotomy increased CVP, SVR, and arterial blood pressure but had no significant effect on CO, PAP, PCWP, or PVP. The change in TMF E velocity correlated well with the change in CO (Pearson correlation coefficient 95% confidence interval 0.738-0.917, P< or =0.015) but less well with the change in PAP (0.554-0.762, P< or =0.012) and PCWP (0.576-0.692, P< or =0.008). TMF E velocity did not correlate significantly with CVP or calculated SVR. CONCLUSION Phlebotomy during the dissection phase of liver transplantation decreased PVP, which was unaffected when phenylephrine infusion was used to restore systemic arterial pressure. This may contribute to a decrease in operative blood loss. CVP often increased in response to phenylephrine infusion and did not seem to reflect cardiac filling. The changes in TMF E velocity correlated well with the changes in CO, PAP, and PCWP during liver transplantation but not with the changes in CVP.
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12
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S. Møller, J. H. Henriksen. Cardiovascular Dysfunction in Cirrhosis: Pathophysiological Evidence of a Cirrhotic Cardiomyopathy. Scand J Gastroenterol 2009. [DOI: 10.1080/00365520120972] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 04/01/2023]
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13
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Argo CK, Balogun RA. Blood products, volume control, and renal support in the coagulopathy of liver disease. Clin Liver Dis 2009; 13:73-85. [PMID: 19150312 DOI: 10.1016/j.cld.2008.09.007] [Citation(s) in RCA: 14] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/31/2023]
Abstract
Plasma-based products are commonly used in patients who have chronic liver disease to treat perceived coagulopathy despite unproven efficacy and potentially severe risks, such as transfusion-related acute lung injury, which carries a high mortality rate. Moreover, volume expansion may acutely worsen portal hypertension and increase bleeding from the collateral portal vascular bed. Although factor replacement therapy may be warranted in selected situations, its use should be restricted because of the limitations of target tests, such as international normalized ratio, which poorly reflects presence of bleeding diatheses in patients who have cirrhosis. Renal replacement therapies are frequent adjuncts in patients who have cirrhosis and are acutely decompensated, and may correct uremia-related bleeding diathesis and assist in controlling vascular volume, although they are generally limited to use as a bridge to liver transplantation. Novel extracorporeal therapies are emerging and may also have significant interaction with the hemostatic system. Volume contraction and blood conservation therapies are relatively new and promising approaches to reduce use of blood products in liver transplantation.
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Affiliation(s)
- Curtis K Argo
- University of Virginia, Department of Medicine, Division of Gastroenterology and Hepatology, Box 800708, Charlottesville, VA, USA.
| | - Rasheed A Balogun
- University of Virginia, Department of Medicine, Division of Nephrology, Charlottesville, VA, USA
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14
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Abstract
PURPOSE OF REVIEW Prevention of excessive blood loss is an important issue in the perioperative management of liver transplantation. This review describes changing trends in blood products use, risk predicting of blood transfusion, variability in use and practices, as well as transfusion safety during liver transplantation. RECENT FINDINGS Over the last 20 years, the average use of blood products per case has considerably decreased. There are marked interinstitutional differences in blood use. Differences in patient population characteristics and surgical techniques are a partial explanation, but differences in transfusion practices probably account for a substantial part of the variability. Recent data have sparked off ongoing controversy relating to volume replacement therapy and its impact on blood loss. New studies emphasize the risks associated with transfusion in liver transplantation. SUMMARY Recent studies call for continuing every reasonable effort to minimize the use of blood components and can guide us in new approaches to this vital problem.
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Li Y, Liu H, Gaskari SA, Tyberg JV, Lee SS. Altered mesenteric venous capacitance and volume pooling in cirrhotic rats are mediated by nitric oxide. Am J Physiol Gastrointest Liver Physiol 2008; 295:G252-9. [PMID: 18556420 DOI: 10.1152/ajpgi.00436.2007] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/31/2023]
Abstract
In cirrhosis, despite augmented blood volume, effective circulating volume is decreased. This implies abnormal regulation of blood volume, i.e., venous pooling. Because gut veins are the main blood reservoir, we studied mesenteric venous capacitance and compliance in a rat model of cirrhosis. Cirrhosis was induced by bile duct ligation (4 wk). Controls were sham operated. Changes in first-order mesenteric vein diameters induced by drugs, hemorrhage, and stepwise increases in portal pressure (inflatable cuff) were directly observed by intravital microscopy. Effects of nitric oxide on responses to acute graded hemorrhage were studied by use of selective NO synthase (NOS) isoform inhibitors. Pressures were related to diameters to assess capacitance and compliance. Compared with controls, cirrhotic rats demonstrated increased mesenteric venous capacitance and decreased compliance. Norepinephrine induced venoconstriction but did not affect compliance. Prazosin markedly diminished compliance in controls but not cirrhotics. Conversely, the nonspecific NOS inhibitor N-nitro-l-arginine methyl ester (l-NAME) decreased compliance in cirrhotics, but not controls. Tetrodotoxin venodilated controls, venoconstricted cirrhotics, and markedly decreased compliance in both groups. When hemorrhaged, controls rapidly venoconstricted to compensate for initial hypotension, whereas cirrhotic rats remained hypotensive because venoconstriction was severely blunted. Pretreatment with l-NAME or the selective neuronal NOS inhibitors S-methyl-l-thiocitrulline and 7-nitroindazole normalized the homeostatic responses of cirrhotic rats, whereas the selective endothelial-constitutive NOS inhibitor N-iminoethyl-l-ornithine did not affect the response. In conclusion, mesenteric veins of cirrhotic rats showed enhanced capacitance, attenuated compensatory constrictive response to hemorrhage, and decreased compliance. The first two abnormalities were caused by neuronal NOS-derived nitric oxide.
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Affiliation(s)
- Yang Li
- Liver Unit, Gastrointestinal Research Group, Calgary, Alberta, Canada
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16
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Andreu V, Garcia-Pagan JC, Lionetti R, Piera C, Abraldes JG, Bosch J. Effects of propranolol on venous compliance in conscious rats with pre-hepatic portal hypertension. J Hepatol 2006; 44:1040-5. [PMID: 16581151 DOI: 10.1016/j.jhep.2005.10.024] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/26/2005] [Revised: 10/03/2005] [Accepted: 10/24/2005] [Indexed: 12/29/2022]
Abstract
BACKGROUND/AIMS The venous system is the primary capacitance region in the body. However, the influence of active changes in the venous system on the hemodynamic alterations of portal hypertension is poorly understood. To investigate venous compliance (VC) in conscious partial portal vein ligated rats (PPVL) and the effect of propranolol on VC. METHODS Venous compliance was derived from the relationship between changes in mean circulatory filling pressure (MCFP) and changes in blood volume (BV). Measurements were performed before and after i.v. propranolol (7.5 mg/Kg) or placebo in rats with portal hypertension due to PPVL and sham operated controls. RESULTS PPVL rats had an increased VC when compared to Sham (4.9+/-1.4 vs. 3.7+/-0.9 ml kg-1 mm Hg-1; P<0.02). VC did not change after placebo but was significantly reduced by Propranolol in PPVL (-32.9+/-15.7%; P<0,007). Propranolol did not modify venous compliance in sham operated rats (+10.9+/-13.4%; P=ns). CONCLUSIONS Venous compliance is increased in portal hypertensive rats, suggesting that the venous system contributes to the profound circulatory changes encountered in portal hypertension. The increased venous compliance is markedly attenuated by propranolol, suggesting that this abnormality is related to increased adrenergic activity.
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Affiliation(s)
- Victoria Andreu
- Hepatic Hemodynamic Lab., Liver Unit, Institut Clínic de Malalties Digestives i Metabolisme, Hospital Clínic de Barcelona, Institut de Investigacions Biomédiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain
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17
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Abstract
Characteristic findings in patients with cirrhosis are vasodilatation with low overall systemic vascular resistance, high arterial compliance, increased cardiac output, secondary activation of counter-regulatory 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 constitutes an effective (although relative) counterbalance to increased arterial blood pressure. This review considers the alterations in systemic hemodynamics in patients with cirrhosis in relation to essential hypertension and arterial hypertension of the renal origin. Subjects with arterial hypertension (essential, secondary) may become normotensive during the development of cirrhosis, and arterial hypertension is rarely manifested in patients with cirrhosis, even in cases 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 most likely includes the combination of vasodilatation and vasoconstriction in parallel.
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Affiliation(s)
- Jens H Henriksen
- Department of Clinical Physiology, 239 Hvidovre University Hospital, DK-2650 Hvidovre, Denmark.
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18
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Abstract
Patients with cirrhosis and portal hypertension exhibit characteristic cardiovascular and pulmonary hemodynamic changes. A vasodilatatory state and a hyperdynamic circulation affecting the cardiac and pulmonary functions dominate the circulation. The recently defined cirrhotic cardiomyopathy may affect systolic and diastolic functions, and imply electromechanical abnormalities. In addition, the baroreceptor function and regulation of the circulatory homoeostasis is impaired. Pulmonary dysfunction involves diffusing abnormalities with the development of the hepatopulmonary syndrome and portopulmonary hypertension in some patients. Recent research has focused on the assertion that the hemodynamic and neurohumoral dysregulation are of major importance for the development of the cardiovascular and pulmonary complications in cirrhosis. This aspect is important to take into account in the management of these patients.
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19
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Hernández-Guerra M, López E, Bellot P, Piera C, Turnes J, Abraldes JG, Bosch J, García-Pagán JC. Systemic hemodynamics, vasoactive systems, and plasma volume in patients with severe Budd-Chiari syndrome. Hepatology 2006; 43:27-33. [PMID: 16374846 DOI: 10.1002/hep.20990] [Citation(s) in RCA: 30] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]
Abstract
Budd-Chiari syndrome (BCS) causes postsinusoidal portal hypertension, which leads to complications similar to those observed in cirrhosis. However, no studies have investigated whether patients with BCS develop the hyperdynamic circulatory syndrome present in patients with cirrhosis who have portal hypertension. We evaluated systemic and cardiopulmonary hemodynamics, plasma renin activity, aldosterone and norepinephrine levels, and plasma volume in patients with BCS admitted for complications of portal hypertension. BCS patients had mean systemic and cardiopulmonary pressures and cardiac indices that were within the normal range but were significantly different from those of a group of patients with cirrhosis matched by sex, body surface, and liver function (cardiac index 3.1 +/- 0.7 vs. 4.9 +/- 1.2 L.min(-1).m(-2); P < .001; systemic vascular resistance [SVR] index, 2,189 +/- 736 vs. 1,377 +/- 422 dyne.s.cm(-5).m(-2), P < .001). Despite normal systemic vascular resistance, BCS patients had activation of the neurohumoral vasoactive systems, as evidenced by increased plasma renin activity, aldosterone and norepinephrine levels (15.0 +/- 21.5 ng/mL . h, 76.7 +/- 106.8 ng/dL, 586 +/- 868 pg/mL; respectively) and plasma volume expansion. The analysis of individual BCS patients identified that 7 of the 21 patients actually had reduced SVR index. These patients had the greatest plasma volume expansion. A significant inverse correlation between plasma volume and SVR index was observed. In conclusion, patients with BCS had activation of vasoactive neurohumoral systems and expanded plasma volume. This outcome was observed even though most of these patients did not exhibit systemic vasodilation and cardiac output was not increased, in marked contrast with what is observed in patients with cirrhosis.
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Affiliation(s)
- Manuel Hernández-Guerra
- Hepatic Hemodynamic Laboratory, Institut de Malalties Digestives, Hospital Clinic, Institut d'Investigaciones Biomédiques August Pi i Sunyer, Barcelona, Spain
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20
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Abstract
Arterial hypertension is a common disorder with a frequency of 10% to 15% in subjects in the 40- to 60-year age group. Yet most reports find the prevalence of arterial hypertension in patients with chronic liver disease (cirrhosis) much lower. In this review, we consider the alterations in systemic hemodynamics in cirrhosis. The most characteristic findings in cirrhotic patients are vasodilatation with low systemic vascular resistance, increased cardiac output, high arterial compliance, secondary activation of counterregulatory systems (sympathetic nervous system, renin-angiotensin-aldosterone system, neuropituitary release of vasopressin), and resistance to vasopressors. The vasodilatory state is mediated through nitric oxide, calcitonin gene-related peptide, adrenomedullin, and other vasodilators, and is most pronounced in the splanchnic area. This constitutes an effective (although relative) counterbalance to increased arterial blood pressure. Subjects with established arterial hypertension (essential, secondary) may become normotensive during the development of cirrhosis, and arterial hypertension is rarely manifested in patients with cirrhosis, even in cases with renovascular disease and high circulating renin activity. There is much dispute as to the understanding of homeostatic regulation in cirrhotic patients with manifest arterial hypertension. This is a topic for future research.
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Affiliation(s)
- Jens H Henriksen
- Department of Clinical Physiology, 239, Hvidovre University Hospital, DK-2650 Hvidovre, Denmark.
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21
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Affiliation(s)
- Yves Ozier
- Departement d'Anesthesie-Reanimation Chirurgicale, Hôpital Cochin, Paris, France
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22
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Salerno F, Cazzaniga M, Pagnozzi G, Cirello I, Nicolini A, Meregaglia D, Burdick L. Humoral and cardiac effects of TIPS in cirrhotic patients with different "effective" blood volume. Hepatology 2003; 38:1370-7. [PMID: 14647047 DOI: 10.1016/j.hep.2003.09.030] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/27/2022]
Abstract
The aim of this study was to evaluate the cardiac effects of transjugular intrahepatic portosystemic shunts (TIPS) in cirrhotic patients with different effective blood volume. Two-dimensional echocardiography was performed before and 7 and 28 days after TIPS insertion in 7 cirrhotic patients with PRA <4 ng/mL/h (group A, normal effective blood volume) and 15 with PRA >4 ng/mL/h (group B, reduced effective blood volume). Before TIPS, most cirrhotic patients showed diastolic dysfunction as indicated by reduced early maximal ventricular filling velocity (E)/late filling velocity (A) ratio. Patients of group B differed from patients of group A because of smaller left ventricular volumes and stroke volume, indicating central underfilling. After TIPS insertion, portal decompression was associated with a significant increase of cardiac output (CO) and a decrease of peripheral resistances. The most important changes were recorded in patients of group B, who showed a significant increase of both the end-diastolic left ventricular volumes and the E/A ratio and a significant decrease of PRA. In conclusion, these results show that the hemodynamic effects of TIPS differ according to the pre-TIPS effective blood volume. Furthermore, TIPS improves the diastolic cardiac function of cirrhotic patients with effective hypovolemia. This result is likely due to a TIPS-related improvement of the fullness of central blood volume.
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23
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Henriksen JH, Kiszka-Kanowitz M, Bendtsen F. Review article: volume expansion in patients with cirrhosis. Aliment Pharmacol Ther 2002; 16 Suppl 5:12-23. [PMID: 12423449 DOI: 10.1046/j.1365-2036.16.s5.3.x] [Citation(s) in RCA: 35] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/31/2023]
Abstract
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.
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Affiliation(s)
- J H Henriksen
- Department of linical Physiology 239, Hvidovre Hospital, University of Copenhagen, Denmark.
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24
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Niemann CU, Yost CS, Mandell S, Henthorn TK. Evaluation of the splanchnic circulation with indocyanine green pharmacokinetics in liver transplant patients. Liver Transpl 2002; 8:476-81. [PMID: 12004348 DOI: 10.1053/jlts.2002.33218] [Citation(s) in RCA: 16] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Abstract
Although indocyanine green (ICG) can be used to estimate cardiac output (CO) and blood volume independently, a recirculatory multicompartmental ICG model enables description of these and additional intravascular factors. This model was used to describe the effect of end-stage liver disease (ESLD) on systemic and splanchnic hemodynamics in patients undergoing orthotopic liver transplantation. ICG disposition was determined during the dissection phase in six patients with ESLD undergoing orthotopic liver transplantation and six healthy adult living liver donors. After injecting ICG, plasma concentrations were obtained for approximately 10 to 12 minutes by noninvasive pulse dye densitometry. The recirculatory model characterizes three distinct intravascular circuits: lumped parallel fast (presumably nonsplanchnic circulation) and slow peripheral (splanchnic) circuits and a central circuit (central blood volume). Mean transit time (MTT) in the fast peripheral circuit was not different in patients with ESLD and controls. However, ESLD resulted in a significant decrease in MTT in the central (0.11 +/- 0.028 [SD] v 0.24 +/- 0.094 minutes in controls; P <.001) and slow peripheral circuit (0.67 +/- 0.41 v 1.37 +/- 0.37 minutes in controls; P <.001) because of increased flows to the central and slow peripheral circuits. These findings are consistent with the described hyperdynamic systemic and splanchnic circulations in patients with ESLD. In conclusion, the ICG model is able to derive estimates of not only blood volume and CO, but also splanchnic hemodynamics under different physiological conditions. This model can be a useful tool to evaluate the effect of pharmacological manipulation of splanchnic hemodynamics.
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Affiliation(s)
- Claus U Niemann
- Department of Anesthesia and Perioperative Care, University of California, San Francisco 94143-0648, USA.
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25
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Andreu V, Perello A, Moitinho E, Escorsell A, García-Pagán JC, Bosch J, Rodés J. Total effective vascular compliance in patients with cirrhosis. Effects of propranolol. J Hepatol 2002; 36:356-61. [PMID: 11867179 DOI: 10.1016/s0168-8278(01)00300-2] [Citation(s) in RCA: 35] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/18/2022]
Abstract
BACKGROUND Total effective vascular compliance (TEVC), may be increased in cirrhosis. However, its significance is unclear. AIMS To investigate TEVC in patients with cirrhosis, and the effects of propranolol. METHODS Seven patients without liver disease and 44 cirrhotic patients were studied before and after double-blind administration of propranolol (n=33) or placebo (n=11). MEASUREMENTS TEVC (right atrial pressure response to rapid central volume expansion), hepatic venous pressure gradient (HVPG) and systemic hemodynamics. RESULTS TEVC (ml x mmHg(-1) x kg(-1)) was increased in cirrhotics (1.67 +/- 0.66 versus 1.33 +/- 0.32 in controls; P<0.05). TEVC was not modified by placebo, but was markedly reduced by propranolol (from 1.74 +/- 0.75 to 1.33 +/- 0.56; P<0.01). Propranolol decreased HVPG >10% in 20 patients ('responders': -20 +/- 9%) but <10% in 13 'non-responders'. TEVC was normalized by propranolol in HVPG 'responders' (from 1.76 +/- 0.88 to 1.21 +/- 0.51; P<0.01), but not in 'non-responders' (1.69 +/- 0.48 to 1.52 +/- 0.59; NS). Reduction of TEVC in responders was accompanied by increased free hepatic vein pressure (+21 +/- 20%, P=0.05; approximately 60% of the fall in HVPG), which was not observed in non-responders (+3 +/- 11%, NS). CONCLUSIONS TEVC is increased in cirrhosis. This abnormality is corrected by propranolol in patients exhibiting a >10% fall in HVPG, suggesting that changes in vascular compliance may influence the portal pressure response to propranolol.
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Affiliation(s)
- Victoria Andreu
- Liver Unit, Hospital Clínic, Villarroel 170, 08036, Barcelona, Spain
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Abstract
Since the description of HRS more than 100 years ago, significant advances have been made in understanding the pathophysiology of HRS and in the management of these patients. There is now a therapeutic armamentarium: medical (ornipressin plus plasma volume expansion), radiographic (TIPS shunt), and surgical (liver transplantation). The diagnosis of HRS is no longer synonymous with a death sentence; instead, it is a therapeutic challenge, and a coordinated approach by intensivists, hepatologists, nephrologists, interventional radiologists, and transplant surgeons is needed to continue to improve the prognosis of cirrhotic patients presenting with HRS. Increased understanding of HRS will allow preventative rather than therapeutic measures to be used. As in all fields of medicine, these advances will come only with innovative clinical investigation.
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Affiliation(s)
- F Wong
- Division of Gastroenterology, Department of Medicine, University of Toronto, Toronto, Ontario, Canada
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27
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Møller S, Christensen E, Henriksen JH. Continuous blood pressure monitoring in cirrhosis. Relations to splanchnic and systemic haemodynamics. J Hepatol 1997; 27:284-94. [PMID: 9288602 DOI: 10.1016/s0168-8278(97)80173-0] [Citation(s) in RCA: 15] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/05/2023]
Abstract
BACKGROUND/AIMS Low arterial blood pressure is recognised as a distinctive factor in the hyperdynamic circulation in cirrhosis. 24-hour monitoring of the blood pressure and heart rate has recently revealed a reduced circadian variation with relation to liver function. However, associations with other clinical and haemodynamic characteristics have not been investigated and the aim of the present study was to identify splanchnic and systemic determinants of the 24-h blood pressure and heart rate in cirrhosis. METHODS The variables were measured by an automatic ambulant device for monitoring blood pressure and related to the results of an invasive haemodynamic investigation, including measurements of intra-arterial blood pressure (9.00-11.00 h) in 37 patients with cirrhosis. RESULTS The 24-h blood pressures were significantly lower and the heart rate was significantly higher in patients with cirrhosis than in matched controls (p < 0.05-0.001). To identify determinants of 24-h or intra-arterial blood pressures and heart rate, pertinent variables were included in a multivariate regression model. This model revealed that independent determinants of a low 24-h arterial blood pressure were a high post-sinusoidal resistance, a low plasma volume, a short central circulation time, and the presence of ascites. In contrast, a low intra-arterial blood pressure was determined by a low serum sodium, a low haemoglobin, and a high cardiac output. Diuretic treatment did not influence this model. CONCLUSIONS Although the 24-h blood pressure and the intra-arterial blood pressure were determined by different variables, the overall results indicate that abnormalities in both splanchnic and central haemodynamics and sodium-water retention are important in the pathophysiology of arterial hypotension in patients with portal hypertension.
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Affiliation(s)
- S Møller
- Department of Clinical Physiology, Hvidovre Hospital, Copenhagen, Denmark
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Hartleb M, Rudzki K, Karpel E, Becker A, Waluga M, Boldys H, Nowak A, Nowak S. Cardiovascular status after postural change in compensated cirrhosis: an argument for vasodilatory concept. LIVER 1997; 17:1-6. [PMID: 9062872 DOI: 10.1111/j.1600-0676.1997.tb00770.x] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 02/03/2023]
Abstract
It seems that hypervolemia and vasodilatation coincide in compensated cirrhosis, but neither rank nor importance of these factors has been fully clarified in adaptive response to postural change. We studied, with gated equilibrium radionuclide angiography and thoracic electrical bioimpedance the hemodynamic status of 19 patients with compensated cirrhosis and 18 healthy subjects in upright and supine positions. In the upright position, the cirrhotic patients were hypotensive and had decreased peripheral vascular resistance despite increased cardiac output. The transition to the supine position was accompanied by a significant fall in the heart rate and an increase in the stroke volume in both controls (92 +/- 22 to 63 +/- 10 beats/min, and 38 +/- 9 to 62 +/- 19 ml/m2, respectively) and cirrhotic patients (101 +/- 20 to 79 +/- 13 beats/min, and 44 +/- 15 to 63 +/- 19 ml/m2, respectively). Besides, the diastolic arterial pressure fell in controls from 89 +/- 9 mmHg to 81 +/- 11 mmHg; p < 0.01, while it remained unchanged in cirrhotic patients (77 +/- 17 vs 82 +/- 13 mmHg). In the supine position, the cirrhotic patients presented tachycardia and left ventricular hyperkinesy (increased velocity of left ventricular filling and emptying). In conclusion, these results show that in compensated cirrhosis the decreased arterial tone and peripheral blood pooling are important factors of adaptive hemodynamic reaction to postural change.
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Affiliation(s)
- M Hartleb
- Department of Gastroenterology, Silesian Medical School, Katowice, Poland
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Huang YT, Chang SP, Lin HC, Yang MC, Hong CY. Inositol phosphate responses in portal veins from portal hypertensive rats: receptor- and nonreceptor-mediated responses. J Hepatol 1997; 26:376-81. [PMID: 9059960 DOI: 10.1016/s0168-8278(97)80055-4] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/03/2023]
Abstract
BACKGROUND/AIMS Venous hyporesponsiveness in portal hypertension has been reported previously by us. The present study was undertaken to investigate possible changes of phosphoinositide signal transduction pathway in the portal veins from portal hypertensive rats METHODS Portal hypertension was induced by partial portal vein ligation. Fourteen days after surgery, portal veins were removed for measurement of [3H]inositol phosphate responses to both receptor- and nonreceptor-mediated stimuli. RESULTS Basal [3H]inositol phosphate formation was similar between the two groups. Both phenylephrine and angiotensin II stimulated [3H]inositol phosphate formation in portal veins, but the responses were attenuated in the portal hypertensive group. In contrast, the [3H]inositol phosphate formation by nonreceptor-mediated stimuli (GTP gamma S, NaF/AlCl3, and phospholipase C) was similar between the two groups. CONCLUSION Our results showed that the receptor-mediated [3H]inositol phosphate formation was attenuated, while the non-receptor-mediated formation was unaltered, in the portal vein from portal hypertensive rats.
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Affiliation(s)
- Y T Huang
- Institute of Traditional Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan
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Huang YT, Lin HC, Yu PC, Lee FY, Tsai YT, Lee SD, Yang MC. Decreased vascular reactivity of portal vein in rats with portal hypertension. J Hepatol 1996; 24:194-9. [PMID: 8907573 DOI: 10.1016/s0168-8278(96)80029-8] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/03/2023]
Abstract
BACKGROUND/AIMS Vascular hyporesponsiveness in portal hypertension is well documented in the arterial tissue. The present study aimed to investigate the possible changes in the portal vein from portal hypertensive rats. METHODS Portal hypertension was induced by partial portal vein ligation. Fourteen days after surgery, portal veins were removed for contractile study and measurement of cAMP, cGMP and [Ca2+]i. RESULTS In vitro tension preparation showed a decreased maximum response to norepinephrine in portal vein of portal vein ligated rats (38.3 +/- 4.1 vs. 23.4 +/- 1.5 mN/mm2). The pA2 values of WB4101 and yohimbine (alpha1- and alpha2-adrenoceptor antagonist, respectively) were not different between the two groups. Tissue cAMP (14.4 +/- 0.9 vs. 12.2 +/- 0.7 pmol/mg protein), but not cGMP, content was increased and intracellular calcium [Ca2+]i levels (247 +/- 9 vs. 281 +/- 13 nM) were decreased in portal vein ligated rats. CONCLUSIONS These results showed that in portal vein from portal vein ligated rats, vascular hyporesponsiveness and an increase in basal cAMP content and a decrease in basal [Ca2+]i were observed.
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Affiliation(s)
- Y T Huang
- Institute of Traditional Medicine, School of Medicine, National Yang-Ming University, Taiwan
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Moreau R, Valla D. [Indications and role of albumin, plasma volume expansion excluded, in the preoperative or postoperative management of portal hypertension]. ANNALES FRANCAISES D'ANESTHESIE ET DE REANIMATION 1996; 15:514-24. [PMID: 8881492 DOI: 10.1016/0750-7658(96)83214-x] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 02/02/2023]
Abstract
Low serum albumin levels are common in patients with cirrhosis and liver failure. Decreased synthesis is the main but not the only mechanism leading to decreased serum levels. The consequences of low albumin concentrations are a decreased plasma colloid osmotic pressure and a decreased binding of liposoluble xenobiotics and endogenous substances. Besides the fluid accumulation in pleura and peritoneum, the complications directly related to low serum albumin levels have been only poorly assessed. An increase in serum albumin levels (by a few g.L-1) for a few days can be achieved by the infusion of large amounts of human albumin (approximately 120 g over 3 days). The efficacy of this treatment has been only tested in association with large paracentesis: albumin infusion, which induces volume expansion, reduced the incidence of hyponatremia and functional renal failure. No significant effect on ascites production rate or survival has been observed. Similar results were achieved through polygelin or dextran-70 infusions. No well-conducted controlled study on the value of albumin infusion in other circumstances apart from cirrhotic patients is available. In conclusion, albumin infusion should be reserved to the treatment of hyponatraemia or functional renal failure complicating cirrhosis with severe liver failure and marked hypoalbuminaemia, when the infusion of colloids failed to correct these anomalies.
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Affiliation(s)
- R Moreau
- Service d'hépatologie, Inserm U24, hôpital Beaujon, Clichy, France
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Lin HC, Tsai YT, Yang MC, Lee FY, Hou MC, Chen LS, Lee SD. Effect of octreotide on total effective vascular compliance in patients with posthepatitic cirrhosis. J Hepatol 1996; 24:81-7. [PMID: 8834029 DOI: 10.1016/s0168-8278(96)80190-5] [Citation(s) in RCA: 10] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/02/2023]
Abstract
BACKGROUND/AIMS This study aimed to evaluate the effect of octreotide on total effective vascular compliance, measured during rapid volume expansion, in patients with posthepatitic cirrhosis. METHODS Twenty-nine patients with posthepatitic cirrhosis were randomly assigned to receive a 100-micrograms/h infusion of octreotide after a 100-micrograms bolus (n = 15), or a placebo (n = 14). Hemodynamic measurements were recorded before and 30 min after drug administration. Thereafter, rapid volume expansion was performed in each patient and hemodynamic measurements were repeated immediately after volume expansion. RESULTS Before volume expansion, placebo administration did not affect any of the hemodynamic values, while the hepatic blood flow was significantly decreased following octreotide administration. After volume expansion, the hemodynamic changes were similar between patients receiving octreotide and the placebo. However, the increase in right atrial pressure from the beginning to the end of volume expansion was higher and the total effective vascular compliance was lower in patients receiving octreotide (+3.5 +/- 0.3 mmHg, p = 0.05 and 1.69 +/- 0.16 ml.mmHg-1.kg-1, p < 0.05) compared to patients receiving placebo (+2.5 +/- 0.3 mmHg, 2.60 +/- 0.34 ml.mmHg-1.kg-1). CONCLUSIONS The present study suggests that octreotide decreased total effective vascular compliance in patients with posthepatitic cirrhosis. It is possible that, in patients with posthepatitic cirrhosis, venoconstriction was induced following octreotide administration.
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Affiliation(s)
- H C Lin
- Department of Medicine, National Yang-Ming University, Taipei, Taiwan, Republic of China
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Møller S, Bendtsen F, Henriksen JH. Effect of volume expansion on systemic hemodynamics and central and arterial blood volume in cirrhosis. Gastroenterology 1995; 109:1917-25. [PMID: 7498657 DOI: 10.1016/0016-5085(95)90759-9] [Citation(s) in RCA: 99] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/25/2023]
Abstract
BACKGROUND & AIMS Systemic vasodilatation in cirrhosis may lead to hemodynamic alterations with reduced effective blood volume and decreased arterial blood pressure. This study investigates the response of acute volume expansion on hemodynamics and regional blood volumes in patients with cirrhosis and in controls. METHODS Thirty-nine patients with cirrhosis (12 patients with Child-Turcotte class A, 14 with class B, and 13 with class C) and 6 controls were studied. During hepatic vein catheterization, cardiac output, systemic vascular resistance, central and arterial blood volume, noncentral blood volume, and arterial pressure were determined before and during a volume expansion induced by infusion of a hyperosmotic galactose solution. RESULTS During volume expansion, the central and arterial blood volume increased significantly in patients with class A and controls, whereas no significant change was found in patients with either class B or class C. Conversely, the noncentral blood volume increased in patients with class B and C. In both patients and controls, the cardiac output increased and the systemic vascular resistance decreased, whereas the mean arterial blood pressure did not change significantly. CONCLUSIONS Only in mild cirrhosis is the effective blood volume able to increase in response to volume expansion. Our results are consistent with the peripheral vasodilatation hypothesis and the circulatory hyporeactivity occurring in advanced cirrhosis.
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Affiliation(s)
- S Møller
- Department of Clinical Physiology, Hvidovre Hospital, University of Copenhagen, Denmark
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Fernández-Rodriguez C, Prieto J, Quiroga J, Zozaya JM, Andrade A, Rodriguez-Martinez D. Atrial natriuretic factor in cirrhosis: relationship to renal function and hemodynamic changes. J Hepatol 1994; 21:211-6. [PMID: 7989711 DOI: 10.1016/s0168-8278(05)80397-6] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/28/2023]
Abstract
Plasma atrial natriuretic factor concentrations and different hemodynamic parameters, including the evaluation of femoral arteriovenous shunting by measuring the arteriovenous difference of oxygen content (Ca-vO2), were determined in eight healthy subjects and 24 patients with cirrhosis without renal failure (group I: seven patients without ascites, group II: nine patients with ascites and UNaV > 10 mEq/24 h and group III: eight patients with ascites and UNaV < or = 10 mEq/24 h). Atrial natriuretic factor was 34 +/- 4.7 pg/ml in the control group and 44.28 +/- 5.4, 67.89 +/- 8.8 and 84 +/- 10.8 pg/ml in groups I, II and III respectively (p < 0.001. group III vs. I and control and II vs. control). Atrial natriuretic factor directly correlated with cardiac index (p < 0.01), blood volume (p: 0.01), femoral blood flow (p < 0.01) and inversely with systemic and femoral vascular resistances (p < 0.02), Ca-vO2 (p < 0.01), serum albumin (r: -0.61; p < 0.01) and prothrombin index (r: -0.63; p < 0.02). These results indicate that plasma atrial natriuretic factor is increased in patients with cirrhosis, especially in those with advanced disease and marked renal sodium retention. This suggests that in cirrhosis, arteriolar vasodilation and peripheral arteriovenous shunting influence renal function while inducing a state of overflow at the central venous compartment leading to increased atrial natriuretic factor secretion. Increased production of this vasodilatory hormone may thus contribute to the hyperkinetic circulation of cirrhosis.
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