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Rodríguez-Roisin R. Hepatopulmonary Syndrome: A Forgotten Liver-induced Lung Vascular Disorder. Arch Bronconeumol 2023; 59:137-138. [PMID: 36609108 DOI: 10.1016/j.arbres.2022.12.007] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/19/2022] [Accepted: 12/19/2022] [Indexed: 12/24/2022]
Affiliation(s)
- Robert Rodríguez-Roisin
- Universitat de Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Hospital Clínic, Barcelona, Spain.
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Rodríguez-Roisin R, Krowka MJ, Agustí A. Hepatopulmonary Disorders: Gas Exchange and Vascular Manifestations in Chronic Liver Disease. Compr Physiol 2018; 8:711-729. [PMID: 29687908 DOI: 10.1002/cphy.c170020] [Citation(s) in RCA: 14] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/20/2022]
Abstract
This review concentrates on the determinants of gas exchange abnormalities in liver-induced pulmonary vascular disorders, more specifically in the hepatopulmonary syndrome. Increased alveolar-arterial O2 difference, with or without different levels of arterial hypoxemia, and reduced diffusing capacity represent the most characteristic gas exchange disturbances in the absence of cardiac and pulmonary comorbidities. Pulmonary gas exchange abnormalities in the hepatopulmonary syndrome are unique encompassing all three pulmonary factors determining arterial PO2 , that is, ventilation-perfusion imbalance, increased intrapulmonary shunt and oxygen diffusion limitation that, combined, interplay with two relevant nonpulmonary determinants, that is, increased total ventilation and high cardiac output. Behind the complexity of this lung-liver association there is an abnormal pulmonary vascular tone that combines inhibition of hypoxic pulmonary vasoconstriction with a reduced (or blunted) hypoxic vascular response. The pathology and pathobiology include the presence of intrapulmonary vascular dilatations with or without pulmonary vascular remodeling, i.e. angiogenesis. Liver transplantation, the only effective therapeutic approach to successfully improve and resolve the vast majority of complications induced by the hepatopulmonary syndrome, along with a large list of frustrating pharmacologic interventions, are also reviewed. Another liver-induced pulmonary vascular disorder with less gas exchange involvement, such as portopulmonary hypertension, is also considered. © 2018 American Physiological Society. Compr Physiol 8:711-729, 2018.
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Affiliation(s)
- Robert Rodríguez-Roisin
- Department of Medicine, Universitat de Barcelona (UB), Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona
| | - Michael J Krowka
- Division of Pulmonary and Critical Care, Transplant Research Center, Mayo Clinic, Rochester, MN, US
| | - Alvar Agustí
- Service of Pneumology, Respiratory Institute, Hospital Clínic, UB, Centro de Investigaciones Biomédicas en Red sobre Enfermedades Respiratorias (CIBERES), Barcelona
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3
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Study of pulmonary dysfunctions in liver cirrhosis. EGYPTIAN JOURNAL OF CHEST DISEASES AND TUBERCULOSIS 2014. [DOI: 10.1016/j.ejcdt.2014.05.008] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/22/2022] Open
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Polverino F, Santoriello C, Andò F, Girbino G, Cappetta D, D'Agostino B, Vatrella A, Polverino M, Milic-Emili J. Recumbent deoxygenation in mild/moderate liver cirrhosis: the "clinodeoxia". The ortho-clino paradigm. Respir Med 2014; 108:1040-8. [PMID: 24785153 DOI: 10.1016/j.rmed.2014.04.003] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/13/2013] [Revised: 04/01/2014] [Accepted: 04/05/2014] [Indexed: 11/27/2022]
Abstract
BACKGROUND While the effects of postural change on arterial oxygenation have been well documented in normal subjects, and attributed to the relationship of closing volume (CV) to the tidal volume, in liver cirrhosis such postural changes have been evaluated mainly in a rare, peculiar clinical end-stage condition which is characterized by increased dyspnea shifting from supine to upright position ("platypnea"). The latter is associated with worsening of PaO2 ("orthodeoxia"). We evaluated the effects of postural changes on arterial oxygenation in patients affected by mild/moderate liver cirrhosis. METHODS We performed pulmonary function tests and arterial blood gas evaluation in sitting and supine positions in 22 patients with mild/moderate liver cirrhosis, biopsy-proved, and 22 matched non-smokers control subjects. RESULTS Recumbency elicited a decrease of PaO2 (Δ(sup-sit)PaO2) in 19 out of 22 controls and in all but one cirrhotics. The magnitude of this postural change was significantly (p = 0.04) greater in cirrhotics (9.6 ± 5.3%) compared to controls (6.7 ± 3.7%). In the subset of cirrhotics younger than 60 yrs and with PaO2 greater than 80 mmHg in sitting position, the Δ(sup-sit)PaO2 in recumbency further increased to 12 ± 5.8%, significantly (p = 0.014) greater than in same subgroup of controls (7.1 ± 3.8%). CONCLUSIONS In mild/moderate liver cirrhosis the postural variations in PaO2 follow the normal trends, but are of greater magnitude probably as a consequence of hypoventilated units of lung for postural and disease-linked tidal airway closure, resulting in more pronounced recumbent hypoxemia ("clinodeoxia").
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Affiliation(s)
- Francesca Polverino
- Department of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA; The Lovelace Respiratory Research Institute, Albuquerque, NM, USA; Pulmonary Department, University of Parma, Parma, Italy.
| | - Carlo Santoriello
- Department of Pulmonary Medicine, Cava de' Tirreni Hospital, Cava de' Tirreni, Italy
| | - Filippo Andò
- Lung Diseases Institute, University of Messina Medical School, Messina, Italy
| | - Giuseppe Girbino
- Lung Diseases Institute, University of Messina Medical School, Messina, Italy
| | - Donato Cappetta
- Department of Experimental Medicine, Second University of Naples, Naples, Italy
| | - Bruno D'Agostino
- Department of Experimental Medicine, Second University of Naples, Naples, Italy
| | | | - Mario Polverino
- Department of Pulmonary Medicine, Cava de' Tirreni Hospital, Cava de' Tirreni, Italy; Lung Diseases Institute, University of Messina Medical School, Messina, Italy
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Abstract
Diseases of the pulmonary vasculature are a cause of increased pulmonary vascular resistance (PVR) in pulmonary embolism, chronic thromboembolic pulmonary hypertension (CTEPH), and pulmonary arterial hypertension or decreased PVR in pulmonary arteriovenous malformations on hereditary hemorrhagic telangiectasia, portal hypertension, or cavopulmonary anastomosis. All these conditions are associated with a decrease in both arterial PO2 and PCO2. Gas exchange in pulmonary vascular diseases with increased PVR is characterized by a shift of ventilation and perfusion to high ventilation-perfusion ratios, a mild to moderate increase in perfusion to low ventilation-perfusion ratios, and an increased physiologic dead space. Hypoxemia in these patients is essentially explained by altered ventilation-perfusion matching amplified by a decreased mixed venous PO2 caused by a low cardiac output. Hypocapnia is accounted for by hyperventilation, which is essentially related to an increased chemosensitivity. A cardiac shunt on a patent foramen ovale may be a cause of severe hypoxemia in a proportion of patients with pulmonary hypertension and an increase in right atrial pressure. Gas exchange in pulmonary arteriovenous malformations is characterized by variable degree of pulmonary shunting and/or diffusion-perfusion imbalance. Hypocapnia is caused by an increased ventilation in relation to an increased pulmonary blood flow with direct peripheral chemoreceptor stimulation by shunted mixed venous blood flow.
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Affiliation(s)
- C Mélot
- Department of Emergency Medicine, Erasme University Hospital, Brussels, Belgium.
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Lemyze M, Dharancy S, Nevière R, Wallaert B. Cardiopulmonary response to exercise in patients with liver cirrhosis and impaired pulmonary gas exchange. Respir Med 2011; 105:1550-6. [PMID: 21764574 DOI: 10.1016/j.rmed.2011.06.011] [Citation(s) in RCA: 25] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/04/2011] [Revised: 06/21/2011] [Accepted: 06/22/2011] [Indexed: 12/12/2022]
Abstract
Maximal exercise capacity and pulmonary gas exchange are both commonly impaired in liver cirrhosis. Apart from rare cases of hepatopulmonary syndrome, it is still unknown whether these moderate pulmonary gas exchange abnormalities can alter aerobic capacity of cirrhotic patients. Resting pulmonary function tests and symptom-limited cardiopulmonary exercise testing were prospectively investigated in 30 patients with liver cirrhosis exhibiting a widened alveolar-arterial oxygen gradient (P(A-a)O(2) > 30 mm Hg at peak exercise) without pulmonary vascular dilatations at contrast-enhanced echocardiography. Data were compared with those of 30 normoxemic cirrhotic controls (matched for age, gender, body mass index, etiology and severity of liver disease, smoking habits, hemoglobin level, and beta-blocker therapy). Resting cardiopulmonary parameters were within normal range in both groups except carbon monoxide lung transfer (TLCO, 60.4 ± 2.9 vs 74.3 ± 2.8% in controls, p = 0.0004) and P(A-a)O(2) (28.8 ± 2 vs 15.3 ± 2 mm Hg in controls, p < 0.0001). Cirrhotics with impaired gas exchange during exercise exhibited a significant reduction in maximal oxygen uptake (VO(2)max, 1.18 ± 0.07 (53% predicted) vs 1.41 ± 0.07 L/min (62% predicted), p = 0.004), a higher ventilation level at ventilatory threshold (V(E)/VO(2), 39.2 ± 1.5 vs 35.3 ± 1.5, p = 0.01) without ventilatory limitation, and a greater dead space to tidal volume ratio (V(D)/V(T)max, 0.32 ± 0.01 vs 0.25 ± 0.01, p = 0.01). VO(2)max correlates negatively with V(D)/V(T)max (r(2) = 0.36; p < 0.0001). There were no differences in cardiac or metabolic response to exercise between groups. Taken together these findings suggest that clinically undetectable pulmonary vascular disorders can slightly contribute to further reduce exercise capacity of cirrhotic patients.
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Affiliation(s)
- Malcolm Lemyze
- Department of Respiratory and Critical Care Medicine, Schaffner Hospital, 99 route de la Bassée, Lens, France.
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Sulieman BM, Hunsicker LG, Katz DA, Voigt MD. OPTN policy regarding prioritization of patients with hepatopulmonary syndrome: does it provide equitable organ allocation? Am J Transplant 2008; 8:954-64. [PMID: 18416736 DOI: 10.1111/j.1600-6143.2007.02124.x] [Citation(s) in RCA: 33] [Impact Index Per Article: 1.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/25/2023]
Abstract
United Network for Organ Transplantation (UNOS) policy 3.6.4.5.1 provides exception points to patients diagnosed with hepatopulmonary syndrome (HPS) to compensate for their reported increased mortality risk. We compared pre- and posttransplant and overall outcomes in 255 patients receiving exception points under this policy (HPS policy patients) with 32 358 nonexception control patients listed in the model for end-stage liver disease (MELD) era to determine whether the intent of the policy is being met. Overall, 92.5% of HPS policy patients versus 45.5% of controls had been transplanted, 5.1% versus 31.2% remained on waiting list and 1.5% versus 14.1% had died while awaiting transplant (p < 0.0001 for each comparison). Relative risk (RR) of death for HPS policy patients compared to controls was 0.158 (confidence interval [CI]: 0.059-0.420, p = 0.0002) pretransplant, and 0.827 (CI: 0.587-1.170, p = 0.28) posttransplant. Overall (combined waitlist and posttransplant) RR of death was 0.514 (CI: 0.374-0.707, p = 0.00004) compared with controls. After adjustment for laboratory MELD, overall RR was 0.807 (CI: 0.587-1.110, p = 0.19), indicating that HPS policy patients' mortality risk would be similar to that of controls had they been listed with their laboratory MELD score. HPS policy patients have a significant pretransplant survival advantage over standard liver transplant candidates because of the exception points awarded, and have similar posttransplant survival. Better criteria for diagnosing and grading of HPS are required.
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Affiliation(s)
- B M Sulieman
- Department of Internal Medicine, Divisions of Gastroenterology and Hepatology, Carver College of Medicine, University of Iowa, Iowa City, IA, USA
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Zhang HY, Han DW, Su AR, Zhang LT, Zhao ZF, Ji JQ, Li BH, Ji C. Intestinal endotoxemia plays a central role in development of hepatopulmonary syndrome in a cirrhotic rat model induced by multiple pathogenic factors. World J Gastroenterol 2007; 13:6385-95. [PMID: 18081228 PMCID: PMC4205458 DOI: 10.3748/wjg.v13.i47.6385] [Citation(s) in RCA: 22] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open
Abstract
AIM: To characterize the correlation between severity of hepatopulmonary syndrome (HPS) and degree of hepatic dysfunction, and to explore how intestinal endotoxemia (IETM) affects the development of HPS in cirrhotic rats.
METHODS: Male Wister rats were fed with a diet containing maize flour, lard, cholesterol, and alcohol and injected subcutaneously with CCl4 oil solution every two days for 8 wk to induce typical cirrhosis and development of HPS. The animals were also given a nitric oxide (NO) production inhibitor, Nω-nitro-L-arginine methyl ester (L-NAME) intraperitoneally, and an iNOS inhibitor, aminoguanidine hydrochloride (AG) via gavage daily from the end of the 4th wk to the end of the 6th or 8th wk, or a HO-1 inhibitor, zinc protoporphyrin (ZnPP) intraperitoneally 12 h prior to killing. Blood, liver and lung tissues were sampled.
RESULTS: Histological deterioration of the lung paralleled to that of the liver in the cirrhotic rats. The number of pulmonary capillaries was progressively increased from 6.1 ± 1.1 (count/filed) at the 4th wk to 14.5 ± 2.4 (count/filed) at the 8th wk in the cirrhotic rats. Increased pulmonary capillaries were associated with increased blood levels of lipopolysaccharide (LPS) (0.31 ± 0.08 EU/mL vs control 0.09 ± 0.03 EU/mL), alanine transferase (ALT, 219.1 ± 17.4 U/L vs control 5.9 ± 2.2 U/L) and portal vein pressure. Compared with normal control animals, the number of total cells in bronchoalveolar lavage fluid (BALF) of the cirrhotic rats at the 8th wk was not changed, but the number of macrophages and the ratio of macrophages to total cells were increased by nearly 2-fold, protein expression of inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) started to increase significantly at the 4th wk, and reached its peak at the 8th wk in the lung of cirrhotic rats. The increase of iNOS expression appeared to be quicker than that of eNOS. NO2-/NO3- was also increased, which was correlated to the increase of iNOS (r = 0.7699, P < 0.0001) and eNOS (r = 0.5829, P < 0.002). mRNA expression of eNOS and iNOS was highly consistent with their protein expression.
CONCLUSION: Progression and severity of HPS as indicated by both increased pulmonary capillaries and histological changes are closely associated with LPS levels and progression of hepatic dysfunction as indicated by increased levels of ALT and portal vein pressure. Intestinal endotoxemia plays a central role in the development of HPS in the cirrhotic rat model by inducing NO and/or CO.
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Lee J, Park CS, Chang HW, Kwon HJ, Choi JH. The Erythrocyte 2,3-diphosphoglycerate Concentration and Its Related Factors in Patients with End-stage Liver Disease. Korean J Anesthesiol 2007. [DOI: 10.4097/kjae.2007.52.4.430] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/10/2022] Open
Affiliation(s)
- Jaemin Lee
- Department of Anesthesiology and Pain Medicine, Kangnam St. Mary's Hospital, The Catholic University of Korea College of Medicine, Seoul, Korea
| | - Chul Soo Park
- Department of Anesthesiology and Pain Medicine, Kangnam St. Mary's Hospital, The Catholic University of Korea College of Medicine, Seoul, Korea
| | - Hae Wone Chang
- Department of Anesthesiology and Pain Medicine, Kangnam St. Mary's Hospital, The Catholic University of Korea College of Medicine, Seoul, Korea
| | - Hyun Joo Kwon
- Department of Anesthesiology and Pain Medicine, Kangnam St. Mary's Hospital, The Catholic University of Korea College of Medicine, Seoul, Korea
| | - Jong Ho Choi
- Department of Anesthesiology and Pain Medicine, Kangnam St. Mary's Hospital, The Catholic University of Korea College of Medicine, Seoul, Korea
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Maruyama S, Hirayama C, Maeda K, Yamamoto S, Koda M, Udagawa A, Inoue M, Umeki K. Development of hypoxemia in alcoholic liver disease. Dig Dis Sci 2005; 50:290-6. [PMID: 15745087 DOI: 10.1007/s10620-005-1597-x] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/09/2022]
Abstract
The aim of this study was to investigate the arterial hypoxemia in Japanese patients with alcoholic liver disease (ALD) with regard to alcohol consumption and/or disease severity. Hypoxemia was observed in 78% patients with ALD and in all 46 patients with alcoholic liver cirrhosis (ALC) and 33 (56%) of 59 patients with noncirrhotic alcoholic liver disease (NCALD) (P < 0.0001). The partial pressure of oxygen (PaO2) was 71.1 +/- 5.2 mm Hg in ALC and 78.7 +/- 6.3 mm Hg in NCALD (P < 0.0001). The oxygen consumption in ALD was significantly higher than that in control subjects (P < 0.0001), and a high oxygen consumption was seen in 88% of the patients with ALD, in all 46 ALC patients, and in 46 (78%) of 59 NCALD patients (P < 0.01). Following abstinence from alcohol, the PaO2 and oxygen consumption significantly recovered after day 2 (P < 0.0001), whereas the prothrombin index did not change in either NCALD or ALC patients. Multivariate analysis showed that alcohol consumption and oxygen consumption were significant independent predictors of PaO2. In conclusion, the present findings suggest that increased oxygen consumption due to alcohol ingestion is principally responsible for the hypoxemia in ALD patients.
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Affiliation(s)
- Shigeo Maruyama
- Department of Gastroenterology, Saiseikai Gotsu General Hospital, Gotsu, 695, Shimane, Japan
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Nitrini AMS, Stirbulov R, Rolim EG. Influência da ascite na avaliação da função pulmonar em portadores de hipertensão portal. J Bras Pneumol 2004. [DOI: 10.1590/s1806-37132004000100005] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/22/2022] Open
Abstract
INTRODUÇÃO: A oxigenação inadequada nos pacientes com hipertensão portal pode ser secundária a alterações na mecânica respiratória, determinadas pela presença da ascite. OBJETIVO: Avaliar a função pulmonar de doentes com hipertensão portal antes e após redução do volumeda ascite. Método: Quinze doentes com hipertensão portal e ascite foram submetidos a provas de função pulmonar, constituindo-se de espirometria e gasometria arterial, antes e após redução do volume da ascite. Os parâmetros analisados foram: capacidade vital forçada (CVF); volume expiratório no primeiro segundo (VEF1); fluxo expiratório entre 25 e 75% da CVF (FEF 25-75% ); volume de reserva expiratória (VRE); relação VEF1 / CVF; pressão arterial de oxigênio (PaO2), pressão arterial de dióxido de carbono (PaCO2) e saturação arterial de oxigênio (SaO2). RESULTADOS: Houve melhora significativa dos volumes pulmonares analisados após a diminuição da ascite com o tratamento diurético associado ou não à paracentese. CONCLUSÃO: Concluímos que nos doentes com hipertensão portal e ascite, há diminuição dos volumes pulmonares emrelação aos valores preditos, com melhora significativa após diminuição da ascite. Do mesmo modo, observamos aumento na PaO2 e na SaO2.
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Mazzeo AT, Lucanto T, Santamaria LB. Hepatopulmonary syndrome: a concern for the anesthetist? Pre-operative evaluation of hypoxemic patients with liver disease. Acta Anaesthesiol Scand 2004; 48:178-86. [PMID: 14995940 DOI: 10.1111/j.0001-5172.2004.00282.x] [Citation(s) in RCA: 27] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/23/2022]
Abstract
Liver cirrhosis and other chronic hepatic diseases are followed in a subset of affected patients by gas exchange abnormalities resulting from a syndrome called hepatopulmonary syndrome (HPS). The structural basis of this clinical entity is an alteration of pulmonary vasculature resulting in abnormal vasodilatation and mismatching of ventilation and perfusion of the lung. Dilatation of the capillary bed near the gas exchange area is the most important factor implicated; it precludes O2 molecules diffusing to the centrum of the dilated vessels to oxygenate venous blood. Contrast (microbubbles) echocardiography and lung perfusion scan are, respectively, the screening tests with the highest sensitivity and specificity for HPS diagnosis. Because of the high morbidity and mortality of HPS, clinicians have been trying to understand the pathophysiology of pulmonary vasodilatation in the hope that the process can be reversed pharmacologically or surgically. An imbalance between production and clearance of vasoactive circulating substances has been implicated in the pathogenesis of HPS with glucagon and nitric oxide among the principal responsible factors. To date various molecules have been implicated for therapy but without definitive positive results. Liver transplantation remains the only real therapy for HPS, and resolution of gas exchange defects outlines the possible functional reversible nature of vascular abnormalities of this syndrome. The need to perform surgery under general anesthesia for hepatic and extrahepatic procedures in patients with HPS is followed by an increased peri-operative risk. The authors emphasize the role of pre-operative clinical evaluation for proper patient management during the peri-operative period.
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Affiliation(s)
- A T Mazzeo
- Department of Neuroscience, Psychiatric and Anesthesiological Sciences, Section of Anesthesiology and Intensive Care, University Hospital Policlinico G. Martino, Via Consolare Valeria, 98121 Messina, Italy.
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Martínez GP, Barberà JA, Visa J, Rimola A, Paré JC, Roca J, Navasa M, Rodés J, Rodriguez-Roisin R. Hepatopulmonary syndrome in candidates for liver transplantation. J Hepatol 2001; 34:651-7. [PMID: 11434610 DOI: 10.1016/s0168-8278(00)00108-2] [Citation(s) in RCA: 162] [Impact Index Per Article: 6.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Abstract
BACKGROUND Hepatopulmonary syndrome (HPS) has been defined as a clinical triad, including chronic liver disease, gas exchange defects (increased alveolar-arterial PO2 difference irrespective of the presence of arterial hypoxemia), and widespread intrapulmonary vascular dilatations. We determined the incidence and the clinical and pulmonary functional characteristics of HPS in candidates for orthotopic liver transplantation (OLT) and tested their predicted accuracy. METHODS We studied 80 patients with cirrhosis prospectively, and carried out contrast-enhanced (CE) echocardiography and lung function tests, including ventilation-perfusion (V(A)/Q) distributions. RESULTS Fourteen patients had HPS (incidence, 17.5%). Patients with HPS (49 +/- 12 (+/-SD) years) had more cutaneous spiders, finger clubbing and dyspnea (P < 0.05 each) and a lower diffusing capacity (DLCO, 56 +/- 18% predicted; P < 0.001) than non-HPS patients (n = 66). Mild to moderate V(A)/Q inequalities and increased intrapulmonary shunt were predominant in HPS patients, but oxygen diffusion impairment was observed in those with hypoxemia (n = 8) only. The DLCO showed a considerable area under the receiver operating characteristic curve (0.89). CONCLUSIONS HPS in cirrhotic patient candidates for OLT shows a high incidence and these patients present with distinctive clinical and functional features compared with non-HPS individuals. The presence of a low DLCO may be of help for the diagnosis of HPS.
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Affiliation(s)
- G P Martínez
- Servei de Anestesiologia i Reanimació, Institut d'Investigacions Biomèdiques August Pi i Sunyer, Hospital Clinic, Universitat de Barcelona, Spain
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14
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Abstract
The hepatopulmonary syndrome is a triad of liver disease, increased alveolar-arterial oxygen gradient and intrapulmonary vascular dilatations. Manifestations include orthodeoxia, platypnoea and hyperdynamic circulation. Intrapulmonary vascular abnormalities, perhaps mediated by nitric oxide, cause hypoxaemia by shunting, a perfusion-diffusion defect, and ventilation-perfusion mismatching. Contrast-enhanced echocardiography is the method of choice for demonstrating pulmonary vascular abnormalities, although perfusion lung scanning is a more specific and sensitive test. Angiography is best reserved for patients with poor response to 100% oxygen and defines whether vascular dilatations are of the diffuse 'spongy' type or, less commonly, discrete arteriovenous communications amenable to embolization. About 80% of patients with the hepatopulmonary syndrome eventually have improved oxygenation after liver transplantation, thereby making worsening hypoxaemia the primary indication for transplantation in many instances. Nevertheless, severe hypoxaemia carries a peri-operative mortality of 30% and reliable predictors of successful outcome after transplantation remain to be determined.
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Affiliation(s)
- L S Aboussouan
- Division of Pulmonary and Critical Care Medicine, Wayne State University School of Medicine, Harper Hospital, 3-Hudson, 3990 John R, Detroit, MI 48201, USA
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Krenn CG, Plöchl W, Nikolic A, Metnitz PG, Scheuba C, Spiss CK, Steltzer H. Intrathoracic fluid volumes and pulmonary function during orthotopic liver transplantation. Transplantation 2000; 69:2394-400. [PMID: 10868647 DOI: 10.1097/00007890-200006150-00031] [Citation(s) in RCA: 18] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/27/2022]
Abstract
BACKGROUND Impaired pulmonary function is a frequent finding in patients undergoing orthotopic liver transplantation (OLT). Experimental data suggest an essential contribution of splanchnic ischemia and reperfusion as a result of intraoperative volume shifts, i.e., the accumulation of extravascular lung water (EVLW). Increases of intrathoracic blood volume (ITBV) and pulmonary blood volume (PBV) might additionally influence pulmonary capillary fluid filtration. The main objective of this study was to determine the intrathoracic volume changes during OLT and to test whether there were any relationships between intra- and extravascular volume shifts and pulmonary function, as determined by the calculation of venous admixture (QS/QT) and alveolar-arterial oxygen gradient (AaDO2). METHODS Twenty-five patients undergoing OLT were studied. Using the transpulmonary double indicator dilution method, ITBV, PBV, and EVLW were determined from the mean transit times and exponential decay times of the indocyanine green and the thermal indicator curves recorded simultaneously with a fiberoptic catheter in the descending aorta. Recordings were made after induction of anesthesia, at the end of the anhepatic stage, immediately after reperfusion, and 1 and 4 h postoperatively. RESULTS Significant increases in QS/QT related to changes of ITBV were observed after reperfusion. Only a minor impact on AaDO2 was perceived. EVLW remained constant during the study period. CONCLUSIONS Postreperfusion increases of ITBV influence pulmonary function, as demonstrated by the increase in QS/QT. However, they need not be associated with greater EVLW levels, and impact on oxygenation is less severe than assumed. Hence, sufficient mechanisms protecting oxygenation and stalling increased EVLW seem to be present during uncomplicated human OLT.
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Affiliation(s)
- C G Krenn
- Department of Anesthesiology and General Intensive Care, University of Vienna, Austria
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Maruyama S, Hirayama C, Oyake N, Kadowaki Y, Umeki K, Sagayama A, Kato K, Fukuda K, Kuzuo H, Ohuchi Y. Prevalence of hypoxemia in 102 Japanese patients with alcoholic and nonalcoholic cirrhosis. Am J Gastroenterol 1999; 94:2994-9. [PMID: 10520858 DOI: 10.1111/j.1572-0241.1999.01449.x] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/11/2022]
Abstract
OBJECTIVE Liver cirrhosis is often accompanied by arterial hypoxemia in the absence of cardiopulmonary disease. The aim of this study was to investigate the relationship between various clinicopathological conditions and the hypoxemia seen in Japanese patients with liver cirrhosis. METHODS In 102 consecutive patients with alcoholic (N = 45) and nonalcoholic (N = 57) cirrhosis not associated with cardiopulmonary disease, we performed lung perfusion scintigraphy, contrast echocardiography, and arterial blood gas analysis and measured oxygen consumption. RESULTS No abnormality was seen in pulmonary blood flow in cirrhotic patients, but 38 (38%) of them had a decreased partial pressure of oxygen (PaO2). The hypoxemic patients did not show any pulmonary signs or symptoms. The hypoxemia was not associated with the Child-Pugh grade, and was observed in 32 (71%) of the 45 alcoholic patients but in only six (11%) of the 57 nonalcoholic patients (p < 0.001). Oxygen consumption was significantly higher in the alcoholic group than in the nonalcoholic group (p < 0.0001), and a high incidence of oxygen consumption was seen in all 45 (100%) of the alcoholic patients and in 34 (60%) of the nonalcoholic subjects, the difference being significant (p < 0.01). The relationship between oxygen consumption and PaO2 in the 102 cirrhotic patients showed an inverse correlation (r = -0.85, p < 0.0001). Among the alcoholic patients, the incidence of hypoxemia did not differ between the 33 smokers and the 12 nonsmokers. After 1 wk of abstinence from alcohol a significant increase (p < 0.0001) in the PaO2 was seen in 14 of 19 patients with alcoholic cirrhosis. CONCLUSIONS We conclude that the hypoxemia in Japanese patients with liver cirrhosis occurs mainly in drinking alcoholic patients, presumably due to an increased oxygen consumption by alcohol.
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Affiliation(s)
- S Maruyama
- Department of Internal Medicine, Saiseikai Gotsu General Hospital, Gotsu-city, Shimane, Japan
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17
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Epstein SK, Zilberberg MD, Jacoby C, Ciubotaru RL, Kaplan LM. Response to symptom-limited exercise in patients with the hepatopulmonary syndrome. Chest 1998; 114:736-41. [PMID: 9743159 DOI: 10.1378/chest.114.3.736] [Citation(s) in RCA: 21] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/01/2022] Open
Abstract
OBJECTIVE To study the response to symptom-limited exercise in patients with the hepatopulmonary syndrome (HPS). DESIGN The response to maximal cardiopulmonary exercise (CPX) was studied in 5 patients with HPS and compared with 10 case control (normoxemic, NC) cirrhotics (matched for age, gender, etiology and severity of liver disease, tobacco use, and beta-blocker therapy) and 9 hypoxemic control cirrhotics (HC) without clinical evidence of HPS. SETTING Cardiopulmonary exercise physiology laboratory in a tertiary care referral center. PATIENTS Cirrhotics referred for CPX as part of their preliver transplantation evaluation. MEASUREMENTS Standard pulmonary function tests and echocardiography were performed to assess resting pulmonary and cardiac function. Peak oxygen consumption (VO2), minute ventilation, arterial blood gases, and dead space (VD/VT) were determined during symptom-limited maximal CPX. RESULTS Resting spirometry and lung volumes were similar between HPS and NC subjects, while HC subjects had restrictive physiology. Differences existed in diffusing capacity corrected for hemoglobin and alveolar volume percent predicted (HPS, 45+/-2 vs NC, 68+/-3, p<0.05; vs HC, 70+/-4, p<0.05), PaO2 (HPS, 70+/-5 mm Hg; HC, 79+/-3 mm Hg, vs NC, 102+/-3 mm Hg, p<0.05) and alveolar-arterial (A-a) O2 gradient (HPS, 42+/-8 mm Hg vs HC, 27+/-2 mm Hg, p<0.05; vs NC, 6+/-2 mm Hg, p<0.05). During CPX, HPS patients achieved a lower peak VO2 percent predicted (HPS, 55+/-6 vs NC, 73+/-3, p<0.05; vs HC, 71+/-5, p<0.05) and VO2 at the ventilatory threshold as percent predicted peak VO2 (HPS, 36+/-2 vs NC, 55+/-4, p<0.05; vs HC 55+/-5, p<0.05). While no differences existed in heart rate and breathing reserve, HPS patients had significantly lower PaO2 (HPS, 50+/-5 mm Hg vs NC, 97+/-4 mm Hg, p<0.05; vs HC, 87+/-6 mm Hg, p<0.05), wider A-a O2 gradient (HPS, 73+/-5 mm Hg vs NC, 13+/-3 mm Hg, p<0.05; vs HC, 31+/-5 mm Hg, p<0.05) and higher VD/VT (HPS, 0.36+/-.03 vs NC, 0.18+/-.02, p<0.05; vs HC, 0.28+/-.02, p<0.05) at peak exercise. For HPS patients, VO2 was negatively correlated with VD/VT (r2=0.9) and positively correlated with PaO2 (r2=0.41) at peak exercise. CONCLUSIONS Patients with HPS demonstrate a severe reduction in aerobic capacity, beyond that found in cirrhotics without syndrome. The significant hypoxemia and elevated VD/VT at peak exercise suggest that an abnormal pulmonary circulation contributes to further exercise limitation in patients with HPS.
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Affiliation(s)
- S K Epstein
- Department of Medicine, Tupper Research Institute, New England Medical Center, Tufts University School of Medicine, Boston, MA 02166, USA
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18
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Abstract
Chronic liver disease is often accompanied by hypoxaemia. We investigated the clinical factors that were related to the arterial oxygen tension (PaO2) in 40 women, all non-smokers with chronic liver disease. They were positive for hepatitis C virus (HCV) antibody and had no evidence of cardiopulmonary disease. Arterial blood was collected from patients at rest (> 15 min) for analysis of blood gases. We determined the correlation between blood gas tension and the clinical variables, i.e. the presence or absence of skin manifestations such as cutaneous spider nevi and palmar erythema, the presence or absence of splenomegaly, vital capacity, forced expiratory volume in one second, V25/body height, serum alanine aminotransferase (AST), serum asparate aminotransferase (ALT), serum cholinesterase, serum gamma-globulin/total protein, excretion of indocyanine green at 15 min (15-min retention rate, ICG level), blood level of ammonia, blood level of endotoxin, plasma level of glucagon and the serum level of type IV collagen-7S. The mean level of PaO2 was 78 +/- 11 (range: 43-95) torr. The mean alveolar-arterial oxygen tension gradient (A-aDO2) was 19 +/- 13 (range: 2-60) torr. Multiple regression analysis used PaO2 and A-aDO2 as objective variables, and the clinical findings as explanatory variables. The explanatory variables that were significantly correlated with blood gas values were ICG level, blood level of endotoxin and presence of skin manifestations. The ICG level showed a high correlation with blood gas values; the ICG level increased, the PaO2 decreased (r = -0.69), while the A-aDO2 showed a high positive correlation (r = +0.78, P < 0.001). Findings suggest that a reduction in hepatic blood flow and hepatocellular function interfere with the inactivation of vasoactive substances such as endotoxin by the liver, leading to the development of skin manifestations, the dilatation of intrapulmonary capillaries and the induction of hypoxaemia.
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Affiliation(s)
- K Fujimori
- Department of Medicine (II), Niigata University School of Medicine, Japan
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19
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Vachiéry F, Moreau R, Hadengue A, Gadano A, Soupison T, Valla D, Lebrec D. Hypoxemia in patients with cirrhosis: relationship with liver failure and hemodynamic alterations. J Hepatol 1997; 27:492-5. [PMID: 9314126 DOI: 10.1016/s0168-8278(97)80353-4] [Citation(s) in RCA: 57] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/05/2023]
Abstract
BACKGROUND/AIMS The relationship between hypoxemia, liver failure and the hemodynamic alterations in cirrhosis are unknown. This study examined the relationship between arterial hypoxemia, the severity of liver disease and hyperkinetic circulation in patients with cirrhosis. METHODS Arterial blood gases, the severity of cirrhosis (Child-Pugh score), and splanchnic and systemic hemodynamics were measured in 120 patients with cirrhosis and without cardiopulmonary disease. Hypoxemia was considered to be present when PaO2 was < or = 70 mmHg. RESULTS Seventeen patients had hypoxemia (14%). Hypoxemic patients had significantly lower pulmonary vascular resistance and a significantly higher alveolar-arterial oxygen gradient, Child-Pugh score and hepatic venous pressure gradient than non-hypoxemic patients. Cardiac index and right atrial and pulmonary pressures did not significantly differ between the two groups. CONCLUSIONS Hypoxemia occurs mainly in patients with severe liver disease and is associated with pulmonary vasodilation.
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Affiliation(s)
- F Vachiéry
- Laboratoire d'Hémodynamique Splanchnique et de Biologie Vasculaire, Unité de Recherches de Physiopathologie Hépatique (INSERM U-24), Hôpital Beaujon, Clichy, France
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20
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Rodriguez-Roisin R, Roca J. Hepatopulmonary syndrome: the paradigm of liver-induced hypoxaemia. BAILLIERE'S CLINICAL GASTROENTEROLOGY 1997; 11:387-406. [PMID: 9395754 DOI: 10.1016/s0950-3528(97)90046-4] [Citation(s) in RCA: 19] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Abstract
The current chapter deals with the concept, clinical manifestations and diagnostic tools of the hepatopulmonary syndrome (HPS) and highlights its most salient pathophysiological, mechanistic and therapeutic aspects. Defined as a clinical triad, including a chronic liver disorder, pulmonary gas exchange abnormalities and generalized pulmonary vascular dilatations, in the absence of intrinsic cardiopulmonary disease, this entity is currently growing in interest with both clinicians and surgeons. The combination of arterial hypoxaemia, high cardiac output with normal or low pulmonary artery pressure, and finger clubbing in a patient with advanced liver disease should strongly suggest the diagnosis of HPS. Its potential high prevalence together with failure of numerous therapeutic approaches depicts a life-threatening unique clinical condition that may dramatically benefit with an elective indication of liver transplantation (LT). A better orchestration of the concepts of the pathophysiology of this lung-liver interplay may foster our knowledge and improve the clinical management and indications of LT.
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Affiliation(s)
- R Rodriguez-Roisin
- Departament de Medicina, Hospital Clínic, Universitat de Barcelona, Spain
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21
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Chang SC, Chang HI, Chen FJ, Shiao GM, Wang SS, Lee SD. Therapeutic effects of diuretics and paracentesis on lung function in patients with non-alcoholic cirrhosis and tense ascites. J Hepatol 1997; 26:833-8. [PMID: 9126796 DOI: 10.1016/s0168-8278(97)80249-8] [Citation(s) in RCA: 13] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/04/2023]
Abstract
BACKGROUND/AIMS Ascites may cause or aggravate pulmonary dysfunction in patients with liver cirrhosis. Diuretics and paracentesis are the main therapies for ascites. The aim of the present study was to evaluate and compare the therapeutic effects of diuretics and large-volume paracentesis on lung function in 26 male patients with non-alcoholic cirrhosis and tense ascites. METHODS The patients were divided into two groups. Group A was composed of 13 subjects who were treated with diuretics including spironolactone (100-400 mg/day) and furosemide (80-320 mg/day). In group B, 13 subjects received large-volume paracentesis plus intravenous albumin (6-8 g/l ascites removed). Pulmonary function tests including spirometry, plethysmography, single-breath carbon-monoxide diffusing capacity (DLco) and arterial blood gases, were done 1 day before diuretic treatment and 1 day after termination of the study in group A patients, and 1 day before and after large-volume paracentesis in group B subjects. RESULTS Before treatment, the clinical and laboratory data were comparable between the two groups. After treatment, ventilatory function as evidenced by forced expiratory volume in 1 s, forced vital capacity, total lung capacity, functional residual capacity and expiratory reserve volume, and DLco increased significantly in both groups. Arterial PO2 and PCO2 increased significantly and AaPO2 (alveolar-arterial PO2 difference) decreased significantly in the subjects treated with diuretics. Nevertheless, paracentesis did not improve arterial blood gases. The changes in lung volumes, DLco and PaO2 after treatment (the data after minus those before treatment) were comparable, except that a significant decrease in AaPO2 was observed in the diuretic group. CONCLUSIONS Both diuretic therapy and large-volume paracentesis significantly improved the ventilatory function in patients with tense cirrhotic ascites. In terms of oxygenation improvement as evaluated by AaPO2, diuretic treatment may be superior to large-volume paracentesis.
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Affiliation(s)
- S C Chang
- Chest Department, Veterans General Hospital-Taipei, Taiwan, ROC
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22
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Paradoxical air embolism detected by transesophageal echocardiography during hepatic resection. J Anesth 1996; 10:147-150. [DOI: 10.1007/bf02483353] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/21/1995] [Accepted: 01/29/1996] [Indexed: 10/24/2022]
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23
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Abstract
Hepatopulmonary syndrome is part of the spectrum of pulmonary vascular disorders seen in advanced liver disease. The pathophysiology of these entities likely is dependent on the degree of pulmonary vasoconstriction or vasodilation that occurs. Our understanding of hepatopulmonary syndrome has helped further our knowledge of the interaction of the liver and the lung. Advances in the management of this disorder, especially liver transplantation, finally have allowed us to offer some hope to patients with this disease.
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Affiliation(s)
- M Castro
- Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA
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24
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Abstract
The preoperative pulmonary evaluation of organ transplant candidates involves the diagnosis of unexplained pulmonary infiltrates or symptoms, interpretation of pulmonary function abnormalities, and an assessment of surgical risk. Pretransplant pulmonary considerations in patients with end-stage hepatic diseases relate primarily to hypoxemia from poorly understood intrapulmonary vascular dilatations, mechanical dysfunction, and states of increased extravascular lung water. Except in severe cases, however, these generally do not prohibit liver transplantation, and even are likely to improve after transplant surgery. Early postoperative complications may be categorized as those expected from extensive intra-abdominal surgery that requires significant volume resuscitation, which typically are managed in the usual manner for those clinical situations. As immunosuppression begins to have an effect, the LTx recipient becomes susceptible to the same opportunistic infectious organisms (with their frequent pulmonary involvement) that cause significant morbidity and mortality in recipients of other solid organ transplants. Because many of the immunosuppressive agents also are the same, noninfectious side effects such as pulmonary edema and malignancy also are similar. As with all immunocompromised patients, prophylaxis, when possible, persistent infection surveillance, and an aggressive diagnostic and therapeutic approach help decrease the impact of pulmonary dysfunction in LTx recipients.
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Affiliation(s)
- J D O'Brien
- Department of Internal Medicine, Barnes Hospital, St. Louis, Missouri, USA
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25
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Agusti AG, Roca J, Rodriguez-Roisin R. Mechanisms of gas exchange impairment in patients with liver cirrhosis. Clin Chest Med 1996; 17:49-66. [PMID: 8665790 DOI: 10.1016/s0272-5231(05)70298-7] [Citation(s) in RCA: 59] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/01/2023]
Abstract
This article reviews the basic pathophysiologic mechanisms underlying the abnormal pulmonary gas exchange often seen in patients with cirrhosis. To summarize, the following keypoints seem appropriate: (1) Patients with cirrhosis have a low pulmonary vascular tone characterized by a poor or absent hypoxic pressor response. This results in a marked dilation of the pulmonary vasculature. (2) This abnormal pulmonary vascular tone, independently of airway disease, causes VA/Q mismatch and mild to moderate hypoxemia. Yet, as liver disease progresses and hepatocellular function deteriorates, more severe degrees of intrapulmonary shunt emerge and, probably, O2 diffusion limitation ensues, causing severe respiratory failure (see Table 1). (3) At rest, the high cardiac output and minute ventilation of cirrhosis minimize the degree of arterial hypoxemia that otherwise would be expected from the observed degree of both VA/Q inequality and intrapulmonary shunt. During exercise, the relative "normalization' (with respect to metabolic demands) of the hemodynamic and ventilatory status of the patient explains the fall in PaO2. (4) A clear pathogenic mechanism of these pathophysiologic abnormalities is still lacking, although available evidence suggests that both the liver and the endothelial cells may play a pivotal role in the regulation of the pulmonary vascular tone in these patients. (5) To date, no pharmacologic intervention has been effective in treating hypoxemia in these patients. Yet liver transplantation helps in most of them. This observation reinforces the functional nature of the gas exchange abnormalities of cirrhosis.
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Affiliation(s)
- A G Agusti
- Pulmonary Service, Hospital Universitari Son Dureta, Mallorca (AGNA), Spain
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26
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Manier G, Castaing Y. Contribution of multiple inert gas elimination technique to pulmonary medicine--4. Gas exchange abnormalities in pulmonary vascular and cardiac disease. Thorax 1994; 49:1169-74. [PMID: 7831638 PMCID: PMC475285 DOI: 10.1136/thx.49.11.1169] [Citation(s) in RCA: 16] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/27/2023]
Affiliation(s)
- G Manier
- Laboratoire d'Exploration Fonctionnelle Respiratoire, Hôpital Pellegrin, Bordeaux, France
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27
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Angueira CE, Kadakia SC. Effects of large-volume paracentesis on pulmonary function in patients with tense cirrhotic ascites. Hepatology 1994; 20:825-8. [PMID: 7927222 DOI: 10.1002/hep.1840200409] [Citation(s) in RCA: 30] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/27/2023]
Abstract
Large-volume paracentesis is an accepted therapeutic modality for the treatment of tense ascites in patients with cirrhosis. Whereas the effects of large-volume paracentesis on the cardiovascular system have been studied in great detail, the effects of tense ascites and large-volume paracentesis on the respiratory system have undergone only limited evaluation. Most patients report symptomatic improvement in breathing after large-volume paracentesis. The aim of our study was to prospectively evaluate the effects of large-volume paracentesis on the pulmonary function of patients with tense ascites. Nine patients with alcoholic cirrhosis and tense ascites underwent large-volume paracentesis (mean, 3,500 ml of ascites removed) followed by intravenous albumin infusion (10 gm/L ascites removed). Pulmonary function tests were performed just before and 2 hr after large-volume paracentesis. The functional residual capacity increased from 2.46 +/- 0.92 to 2.99 +/- 0.97 L (p = 0.01) and total lung capacity from 5.08 +/- 1.18 to 5.72 +/- 1.32 L (p = 0.03). The forced vital capacity, expiratory reserve volume and residual volume also increased but were not statistically significant (p = 0.07 for all). We noted no significant improvement in forced expiratory volume in 1 sec, forced expiratory effort 25% to 75%, vital capacity or diffusion capacity. There was marked symptomatic improvement in all patients. We conclude that large-volume paracentesis improves measured lung volumes within hours in patients with tense ascites.
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Affiliation(s)
- C E Angueira
- Department of Medicine, Brooke Army Medical Center, San Antonio, Texas
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28
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Söderman C, Juhlin-Dannfelt A, Lagerstrand L, Eriksson LS. Ventilation-perfusion relationships and central haemodynamics in patients with cirrhosis. Effects of a somatostatin analogue. J Hepatol 1994; 21:52-7. [PMID: 7963422 DOI: 10.1016/s0168-8278(94)80136-3] [Citation(s) in RCA: 29] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/28/2023]
Abstract
The ventilation-perfusion relationships of the lung (VA/Q) and central haemodynamics were studied in seven patients with cirrhosis before and 30 min after a bolus injection of a somatostatin analogue, octreotide (Sandostatin, 50 micrograms i.v.), to elucidate the role of this substance in the hepatopulmonary syndrome. In the basal state all patients had normal spirometry but reduced diffusing capacity. Three patients had various degrees of hypoxaemia (6.9-8.3 kPa) and three had clubbing of the fingers. In the basal state VA/Q distributions, determined by inert gas elimination technique, showed an intrapulmonary shunt of 7.9 +/- 2.2% of cardiac output (range 1.5 to 17.1) and perfusion of lung regions with "low VA/Q" of 4.4 +/- 2.2% of cardiac output (range 0 to 15.4). After octreotide, the amount of shunting increased (10.9 +/- 4.4% of cardiac output; non-significant), while "low VAQ" was unchanged (3.7 +/- 1.3% of cardiac output). Arterial oxygen tension decreased from 10.2 +/- 1.1 to 9.7 +/- 1.1 kPa (non-significant). The mean pulmonary arterial pressure increased from 14.5 +/- 1.9 to 16.3 +/- 1.8 mmHg (p < 0.01). No alterations were seen in heart rate, stroke volume, cardiac output, central pressures or vascular resistances. The results of the present study do not support the hypothesis that octreotide improves hypoxaemia and ventilation-perfusion relationships in patients with hepatopulmonary syndrome.
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Affiliation(s)
- C Söderman
- Department of Internal Medicine, Huddinge Hospital, Sweden
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29
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Chao Y, Wang SS, Lee SD, Shiao GM, Chang HI, Chang SC. Effect of large-volume paracentesis on pulmonary function in patients with cirrhosis and tense ascites. J Hepatol 1994; 20:101-5. [PMID: 8201208 DOI: 10.1016/s0168-8278(05)80474-x] [Citation(s) in RCA: 18] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/29/2023]
Abstract
The effect of large-volume paracentesis on lung function was evaluated in 12 male patients with cirrhosis. All underwent pulmonary function tests including spirometry, plethysmography and single-breath carbon-monoxide diffusing capacity 1 day before and after paracentesis. The amount of ascitic fluid removed ranged from 3.6 to 131 (mean +/- SD, 7.4 +/- 3.01). After paracentesis, forced vital capacity, forced expiratory volume at 1 s, total lung capacity, functional residual capacity, inspiratory capacity, expiratory reserve volume, diffusing capacity and alveolar volume increased significantly. In contrast, Kco (diffusing capacity corrected by alveolar volume) decreased significantly. After paracentesis, the increase in diffusing capacity was highly correlated with lung volumes and the amount of removed ascitic fluid. Nevertheless, a significantly negative correlation was found between the change of Kco before and after paracentesis and that of lung volumes. The increase in lung volumes and ventilation to the lower lungs with unfavorable ventilation-perfusion matching might explain the discrepancy between changes in diffusing capacity and Kco after large-volume paracentesis. In conclusion, these results suggest that pulmonary function in patients with cirrhosis and tense ascites is partly improved by large-volume paracentesis. Large-volume paracentesis might be useful for symptomatic relief in selected patients with tense ascites.
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Affiliation(s)
- Y Chao
- Department of Medicine, Veterans General Hospital-Taipei, Taiwan, Republic of China
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30
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Kobayashi S, Aida A, Aoi K, Nishimura M, Kawakami Y. Liver cirrhosis with severe hypoxemia and paradoxic pulmonary vascular response to graded inspiratory oxygen tension. Chest 1993; 103:958-60. [PMID: 8449105 DOI: 10.1378/chest.103.3.958] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/30/2023] Open
Abstract
We present the findings in a patient with liver cirrhosis who showed oppositional pulmonary vascular responses to various alveolar oxygen tensions. In this case the pulmonary artery constricted on exposure to hyperoxia and then gradually dilated during progressive hypoxic inhalation. Such a paradoxic response must result in severe arterial hypoxemia because of severe V/Q mismatching.
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Affiliation(s)
- S Kobayashi
- First Department of Medicine, Hokkaido University School of Medicine, Sapporo, Japan
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31
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Andrivet P, Cadranel J, Housset B, Herigault R, Harf A, Adnot S. Mechanisms of impaired arterial oxygenation in patients with liver cirrhosis and severe respiratory insufficiency. Effects of indomethacin. Chest 1993; 103:500-7. [PMID: 8432144 DOI: 10.1378/chest.103.2.500] [Citation(s) in RCA: 51] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/30/2023] Open
Abstract
The mechanisms of impaired arterial oxygenation that occur in certain patients with chronic liver cirrhosis are still debated. In the present study, we investigated nine cirrhotic patients with severe respiratory disability (mean PaO2, 64 +/- 5 mm Hg), using the inert gas elimination technique to assess the distribution of ventilation-perfusion (VA/Q) ratios. We also determined shunt fraction during pure oxygen breathing, both in supine and sitting positions. To test the hypothesis that vasodilating prostaglandins could contribute to alter gas exchange in such patients with cirrhosis, we examined the hemodynamic and gasometric responses to indomethacin, 50 mg IV, in six of them. During baseline conditions, patients had high cardiac index (CI, 4.9 +/- 0.2 L/min/m2), and low pulmonary (PVR, 1.78 +/- 0.37 mm Hg/L/min/m2) or systemic (SVR, 17.7 +/- 1.15 mm Hg/L/min/m2) vascular resistances. Large intrapulmonary shunt fraction was documented in each patient with a mean value of 19.6 +/- 2.7 percent. Small perfusion in low VA/Q areas was associated with shunt in only three patients (2.5 to 5.3 percent of blood flow). Arterial PO2 was negatively related to shunt (p < 0.01) and to the dispersion of blood flow distribution (p < 0.02). There was no difference between measured and predicted PaO2. Shunt estimates from the inert gas and the 100 percent O2 breathing techniques were, respectively, 19.6 +/- 2.7 percent and 21.7 +/- 3.0 percent. During 100 percent oxygen breathing, changing from supine to sitting position decreased PaO2 from 401 +/- 50 to 333 +/- 64 mm Hg (p < 0.02), while O2 shunt remained unchanged, arteriovenous difference widened, and mixed venous PO2 decreased, from 61 +/- 3 to 47 +/- 4 mm Hg (p < 0.001). Indomethacin did not improve gas exchange or VA/Q distribution and did not affect systemic or pulmonary hemodynamics. The results show that in cirrhotic patients with severe respiratory disability, intrapulmonary shunting is the main determinant of impaired gas exchange, with no evidence of a defect in oxygen diffusion or an extrapulmonary shunt. Vasodilating prostaglandins do not appear to contribute to these alterations.
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Affiliation(s)
- P Andrivet
- Service d'explorations Fonctionnelles Respiratoires, Hôpital Universitaire Henri Mondor, Creteil, France
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Shijo H, Sasaki H, Sakata H, Kusuhara H, Ueki T, Okumura M. Reversibility of hepatopulmonary syndrome evidenced by serial pulmonary perfusion scan. GASTROENTEROLOGIA JAPONICA 1993; 28:126-31. [PMID: 8440418 DOI: 10.1007/bf02775013] [Citation(s) in RCA: 12] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/30/2023]
Abstract
A patient with liver cirrhosis who exhibited marked hypoxemia is presented. An abnormal dilatation of intrapulmonary capillaries was evidenced by perfusion lung scan, contrast-enhanced echocardiography, and histological examinations of lungs. Serial perfusion lung scan disclosed that the radioisotope uptake by extrapulmonary organs was significantly increased and uptake by both lungs was significantly decreased during the state of severer hypoxemia. Shunt quantification method revealed that intrapulmonary right-to-left shunt ratio also paralleled the extent of hypoxemia. The pathophysiology of hepatopulmonary syndrome appeared to involve a reversible intrapulmonary vascular dilatation. The perfusion lung scan could semiquantitate the severity of intrapulmonary vascular dilatation and could offer the efficient method to follow their progress.
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Affiliation(s)
- H Shijo
- First Department of Internal Medicine, School of Medicine, Fukuoka University, Japan
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Abstract
On the basis of previous work, our own experience and findings, and the considerations discussed above, we propose a set of four diagnostic criteria for the hepatopulmonary syndrome: 1. presence of chronic hepatic disease (alcoholic, postnecrotic, or primary biliary cirrhosis or active chronic hepatitis)--severe liver dysfunction may not be mandatory; 2. absence of intrinsic cardiopulmonary disease, with normal chest radiograph or with nodular basal shadowing; 3. pulmonary gas exchange abnormalities--an increased alveolar-arterial oxygen gradient (> or = 2.0 kPa) with or without hypoxaemia; 4. the extrapulmonary appearance of intravenous radiolabelled microspheres or a positive contrast enhanced echocardiogram, suggesting intrapulmonary vascular abnormalities. Although these four criteria appear straightforward, there may be other features that are not always present--namely: 1. low transfer factor (diffusing capacity); 2. shortness of breath, with or without platypnoea and orthodeoxia; 3. increased cardiac output and reduced pulmonary vascular pressures; 4. small (or no) increase in pulmonary vascular resistance when the patient is breathing low oxygen mixtures. From the physiological viewpoint, the hepatopulmonary syndrome provides an excellent model for clinical research in the pathophysiology of pulmonary gas exchange. So far it has been possible to show that arterial hypoxaemia in this condition is (1) partitioned into components resulting from VA/Q mismatching, intrapulmonary shunt, and limitations of oxygen diffusion; (2) modulated by the interplay between the intrapulmonary and the extrapulmonary determinants of PaO2, such as cardiac output and minute ventilation; (3) vulnerable to the influence of inadequate pulmonary vascular tone; and (4) resolved when the injured liver is replaced and hepatic function is restored to within normal limits.
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McAlister V, Leasa D, Grant DR. Ventilation/perfusion after liver transplantation in decompensated cirrhosis. J Gastroenterol Hepatol 1991; 6:626-7. [PMID: 1782379 DOI: 10.1111/j.1440-1746.1991.tb00923.x] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/28/2022]
Affiliation(s)
- V McAlister
- Multiorgan Transplant Unit, University Hospital, London, UK
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Eriksson LS. Is intrapulmonary arteriovenous shunting and hypoxemia a contraindication for liver transplantation? Hepatology 1991; 14:575-6. [PMID: 1874503 DOI: 10.1002/hep.1840140328] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/29/2022]
Affiliation(s)
- L S Eriksson
- Department of Medicine, Huddinge Hospital Karolinska Institute, Sweden
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Ettinger NA, Trulock EP. Pulmonary considerations of organ transplantation. Part I. THE AMERICAN REVIEW OF RESPIRATORY DISEASE 1991; 143:1386-405. [PMID: 2048827 DOI: 10.1164/ajrccm/143.6.1386] [Citation(s) in RCA: 61] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 12/30/2022]
Affiliation(s)
- N A Ettinger
- Respiratory and Critical Care Division, Washington University School of Medicine, St. Louis, Missouri
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Eriksson LS, Söderman C, Ericzon BG, Eleborg L, Wahren J, Hedenstierna G. Normalization of ventilation/perfusion relationships after liver transplantation in patients with decompensated cirrhosis: evidence for a hepatopulmonary syndrome. Hepatology 1990; 12:1350-7. [PMID: 2258151 DOI: 10.1002/hep.1840120616] [Citation(s) in RCA: 98] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/31/2022]
Abstract
To examine the effect of liver transplantation on the respiratory and cardiovascular functions, ventilation/perfusion relationships were determined by multiple inert gas elimination technique in six patients with end-stage liver disease 1 to 19 mo before and 2 to 6 mo after liver transplantation. Cardiac output and pulmonary vascular pressures were measured after catheterization of the pulmonary artery. All patients had normal spirometry and chest x-ray films before transplantation. PaO2 before transplantation was 78.8 +/- 7.4 mm Hg (range = 51.8 to 102.8 mm Hg). All patients had perfusion of poorly ventilated lung regions (low ventilation/perfusion relationships) varying from 3% to 19% of cardiac output (mean = 8.5% +/- 2.4% of cardiac output) and two patients had intrapulmonary shunting (3% and 20% of cardiac output). Measured and calculated PaO2 agreed closely, indicating absence of pulmonary diffusion abnormality, as well as of extrapulmonary shunting. After transplantation, PaO2 normalized in all patients, and both shunting and low ventilation/perfusion relationships disappeared. Cardiac output decreased from 9.1 +/- 1.4 to 6.6 +/- 0.5 L/min (p less than 0.05), and the pulmonary vascular resistance increased from 0.69 +/- 0.14 to 1.64 +/- 0.43 mm Hg/L/min (p less than 0.05). The systemic vascular resistance also increased (before = 8.7 +/- 1.0; after = 15.3 +/- 1.1 mm Hg/L/min; p less than 0.001). Normalization of respiratory and cardiovascular alterations, after liver transplantation, in patients with end-stage liver disease indicates that these changes have a direct functional relationship to the diseased liver. It is hypothesized that this is part of a "hepatopulmonary syndrome,' which in similarity to the hepatorenal syndrome disappears with improved liver function.
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Affiliation(s)
- L S Eriksson
- Department of Internal Medicine, Huddinge University Hospital, Karolinska Institute, Sweden
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Agusti AG, Roca J, Bosch J, Garcia-Pagan JC, Wagner PD, Rodriguez-Roisin R. Effects of propranolol on arterial oxygenation and oxygen transport to tissues in patients with cirrhosis. THE AMERICAN REVIEW OF RESPIRATORY DISEASE 1990; 142:306-10. [PMID: 2382894 DOI: 10.1164/ajrccm/142.2.306] [Citation(s) in RCA: 32] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 12/31/2022]
Abstract
Patients with cirrhosis may show ventilation-perfusion (VA/Q) inequality in the absence of any intrinsic heart or lung disease. However, the high cardiac output of cirrhosis generally prevents or minimizes the appearance of a severe degree of arterial hypoxemia. Propranolol has been used to reduce cardiac output and portal pressure in these patients. We wondered whether it might alter arterial oxygenation and reduce O2 transport to tissues. We studied eight patients (three women) 54 +/- 3 (SEM) yr of age before and after intravenous propranolol (0.1 mg/kg followed by 2 mg/h). Cardiac output (QT) fell from 7.8 +/- 0.7 to 6.0 +/- 0.7 L/min (p less than 0.05), and portal pressure was reduced (22 +/- 2 to 19 +/- 2 mm Hg, p less than 0.01). Arterial PO2 did not change (88 +/- 4 to 89 +/- 5 mm Hg) because the fall in mixed venous PO2 (43 +/- 1 to 40 +/- 1 mm Hg, p less than 0.01) that followed the lower QT was counterbalanced by a lower intrapulmonary shunt (multiple inert gas technique) (4 +/- 2 to 2 +/- 1%, p less than 0.05) and a shift of the VA/Q distributions toward a higher VA/Q ratio. Paralleling the fall in QT, oxygen transport to tissues (QO2) was reduced (19 +/- 2 to 14 +/- 1 ml/min/kg, p less than 0.01). However, O2 uptake (VO2) remained constant (3.4 +/- 0.2 to 3.6 +/- 0.2 ml/min/kg) because O2 extraction by the tissues increased appropriately (22 +/- 2 to 28 +/- 1%, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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Affiliation(s)
- A G Agusti
- Servei de Pneumologia Hospital, Universitat de Barcelona, Spain
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Gunnarsson L, Eleborg L, Eriksson LS. Anesthesia for liver transplantation in patients with arterial hypoxemia. Transpl Int 1990; 3:103-7. [PMID: 2206214 DOI: 10.1007/bf00336213] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/30/2022]
Abstract
Arterial oxygenation during anesthesia and time of postoperative mechanical ventilation were investigated in 17 patients with chronic liver disease who underwent liver transplantation. Six patients had arterial hypoxemia (PaO2 64 +/- 3 mm Hg) and the other 11 patients had normal PaO2 (105 +/- 5 mm Hg) before transplantation. None of the patients were smokers and all had normal preoperative pulmonary X-ray and spirometry. During transplantation, PaO2 increased in both groups, but PaO2 was still approximately 20% lower and PA-aO2 was 40%-60% higher in the hypoxemic group than in the normoxemic patients (P less than 0.05). The median postoperative time on mechanical ventilation was three times longer in the hypoxemic group (56 h) than in the normoxemic patients (18 h; P = NS). Number or severity of postoperative complications and outcome did not differ between the two groups. It is therefore suggested that patients with arterial hypoxemia without overt lung disease should also be accepted for liver transplantation.
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Affiliation(s)
- L Gunnarsson
- Department of Anesthesia and Intensive Care, Karolinska Institute, Huddinge University Hospital, Sweden
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Cutaia M, Rounds S. Hypoxic pulmonary vasoconstriction. Physiologic significance, mechanism, and clinical relevance. Chest 1990; 97:706-18. [PMID: 2407454 DOI: 10.1378/chest.97.3.706] [Citation(s) in RCA: 75] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/31/2022] Open
Affiliation(s)
- M Cutaia
- Veterans Administration Medical Center, Brown University Program in Medicine, Providence, Rhode Island 02908
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Abstract
To summarize, nowadays it seems clear that in patients with cirrhosis: (a) the pulmonary circulation is usually markedly dilated. (b) This vasodilation is due to a loss of vascular tone and it is characterized by a poor (or even absent) vascular reactivity in front of the hypoxic stimulus. (c) This abnormal behaviour of the pulmonary circulation results in VA/Q mismatching (basically perfusion of low VA/Q units) independently of airway disease, and may lower arterial PO2. (d) In the most severe cases, shunt (and perhaps O2 diffusion limitation) is becoming progressively more important. (e) The high cardiac output and minute ventilation of these patients minimize or prevent the appearance of arterial hypoxemia at rest. (f) The fall in arterial PO2 during exercise is not due to a deterioration of the degree of VA/Q mismatching seen at rest nor to any limitation in the diffusion of oxygen. It is caused by the relative 'normalization' (with respect to the metabolic demands) of the haemodynamic and ventilatory status of the patient. This may not apply to patients with severe resting arterial hypoxemia in whom the mechanisms modulating pulmonary gas exchange during exercise have not yet been addressed. What remains to be elucidated at the present time? (a) Which is (are) the precise biochemical mediator(s) of this low pulmonary vascular tone and, presumably, failure of hypoxic pulmonary vasoconstriction? It might be either a substance(s) that the failing liver fails to produce or detoxify. Thus, the ultimate biochemical basis of these physiological abnormalities must still necessarily remain speculative while awaiting future studies.(ABSTRACT TRUNCATED AT 250 WORDS)
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Affiliation(s)
- A G Agustí
- Serveis de Pneumologia i Hepatologia, Hospital Clinic, Barcelona, Spain
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Gunnarsson L, Eleborg L, Eriksson LS. Anesthesia for liver transplantation in patients with arterial hypoxemia. Transpl Int 1990. [DOI: 10.1111/j.1432-2277.1990.tb01902.x] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/31/2022]
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Edell ES, Cortese DA, Krowka MJ, Rehder K. Severe hypoxemia and liver disease. THE AMERICAN REVIEW OF RESPIRATORY DISEASE 1989; 140:1631-5. [PMID: 2513764 DOI: 10.1164/ajrccm/140.6.1631] [Citation(s) in RCA: 77] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/01/2023]
Abstract
Severe hypoxemia and orthodeoxia in patients with chronic liver disease is uncommon, but, when present, it is incapacitating. The purpose of this study was to determine the distribution of alveolar ventilation-perfusion (VA/Q) in six patients with mild liver disease and severe hypoxemia (PaO2 at rest in sitting or standing position ranged from 35 to 67 mm Hg). Orthodeoxia was documented with improvement in PaO2 in the supine position in each patient (PaO2 at rest in supine position ranged from 46 to 75 mm Hg). VA/Q distribution was measured by the multiple inert gas elimination technique. The dispersion of VA/Q was increased with small portions of the cardiac output (0.5 to 14.8%) perfusing low VA/Q areas (O less than VA/Q less than 0.1). Another major finding was a large right-to-left shunt (VA/Q less than 0.005) that ranged from 4 to 28%. The VA/Q mismatching and the right-to-left shunt both contributed to the hypoxemia. The predicted PaO2 was 5.5 mm Hg (p less than 0.01) larger than the measured PaO2. In each patient, the mean pulmonary artery pressure was low and the cardiac output was elevated. These results show that the low PaO2 in these patients was due to both increased right-to-left shunt and VA/Q mismatching, but impaired diffusion could not be ruled out.
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Affiliation(s)
- E S Edell
- Division of Thoracic Diseases and Internal Medicine, Mayo Clinic, Rochester, MN 55905
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