Luxury lung perfusion in end‐stage liver disease during liver transplantation

Stenqvist, O.; Olausson, Michael; Karlsen, K. L.

doi:10.1034/j.1399-6576.1999.430413.x

Cited by 10 publications

(9 citation statements)

References 13 publications

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“…Other authors have also reported the elevation of MPAP after reperfusion during OLT in humans with end-stage liver disease [17][18][19]. At reperfusion, the expansion in preload and cardiac output without a similar afterload decrease is responsible for the steady increase in pressure [19].…”

Section: Discussionmentioning

confidence: 90%

“…Mean pulmonary arterial pressure is frequently increased during the early postoperative period, in patients without previously observed pulmonary hypertension [18]. However, this preoperative increase of pulmonary pressure has not definitely been associated with later adverse outcomes.…”

Section: Discussionmentioning

confidence: 98%

“…Following median laparotomy the descending aorta, the abdominal aorta, and the portal vein were identified and dissected. Sequentially, 300 i.u.kg -1 of heparin were administered (due to extensive thrombosis that may frequently occur during liver transplantation), and the grafts were flushed with University of Wisconsin solution (4°C) by administering 1 L via the abdominal aorta and 1 L via the portal vein, through large bore William Harvey catheters (no [14][15][16][17][18]. The livers were stored in 500 mL of the same solution in sterile plastic bags and packed on ice.…”

Section: Pig Liver Transplantationmentioning

confidence: 99%

See 2 more Smart Citations

Liver Transplantation in Pigs: NO, Oxygen Free Radicals, Pulmonary Hemodynamics

Kostopanagiotou

Tierris

Arkadopoulos

et al. 2008

Journal of Surgical Research

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Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 98%

Section: Pig Liver Transplantationmentioning

confidence: 99%

See 1 more Smart Citation

Liver Transplantation in Pigs: NO, Oxygen Free Radicals, Pulmonary Hemodynamics

Kostopanagiotou

Tierris

Arkadopoulos

et al. 2008

Journal of Surgical Research

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“…The effective alveolar ventilation is defined as the ventilation in contact with the pulmonary circulation (26). Although the term "effective alveolar ventilation" is not currently used in respiratory physiology textbooks, Levy and Simmons (15), in 1974, introduced this term to characterize exclusively the ventilation of areas with maintained or increased perfusion.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms underlying gas exchange alterations in an experimental model of pulmonary embolism

Ferreira¹,

Terzi²,

Paschoal³

et al. 2006

Braz J Med Biol Res

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The aim of the present study was to determine the ventilation/perfusion ratio that contributes to hypoxemia in pulmonary embolism by analyzing blood gases and volumetric capnography in a model of experimental acute pulmonary embolism. Pulmonary embolization with autologous blood clots was induced in seven pigs weighing 24.00 ± 0.6 kg, anesthetized and mechanically ventilated. Significant changes occurred from baseline to 20 min after embolization, such as reduction in oxygen partial pressures in arterial blood (from 87.71 ± 8.64 to 39.14 ± 6.77 mmHg) and alveolar air (from 92.97 ± 2.14 to 63.91 ± 8.27 mmHg). The effective alveolar ventilation exhibited a significant reduction (from 199.62 ± 42.01 to 84.34 ± 44.13 mL) consistent with the fall in alveolar gas volume that effectively participated in gas exchange. The relation between the alveolar ventilation that effectively participated in gas exchange and cardiac output (V A eff/Q ratio) also presented a significant reduction after embolization (from 0.96 ± 0.34 to 0.33 ± 0.17 fraction). The carbon dioxide partial pressure increased significantly in arterial blood (from 37.51 ± 1.71 to 60.76 ± 6.62 mmHg), but decreased significantly in exhaled air at the end of the respiratory cycle (from 35.57 ± 1.22 to 23.15 ± 8.24 mmHg). Exhaled air at the end of the respiratory cycle returned to baseline values 40 min after embolism. The arterial to alveolar carbon dioxide gradient increased significantly (from 1.94 ± 1.36 to 37.61 ± 12.79 mmHg), as also did the calculated alveolar (from 56.38 ± 22.47 to 178.09 ± 37.46 mL) and physiological (from 0.37 ± 0.05 to 0.75 ± 0.10 fraction) dead spaces. Based on our data, we conclude that the severe arterial hypoxemia observed in this experimental model may be attributed to the reduction of the V A eff/Q ratio. We were also able to demonstrate that V A eff/Q progressively improves after embolization, a fact attributed to the alveolar ventilation redistribution induced by hypocapnic bronchoconstriction. Correspondence

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“…Nevertheless only in the last decade has the pathogenesis of hepatopulmonary syndrome (HPS) and its related clinical implications been discussed in depth (2)(3)(4)(5)(6)(7)(8). On the contrary, the paucity of publications in anesthesiological literature is evident and unexplainable (9)(10)(11)(12)(13). Yet, with the increasing prevalence of liver disease in the population and improved survival of these patients, a growing number of hepatopathic patients will undergo surgery (14,15) and consequently will require not only a surgeon's but also an anesthestist's attention.…”

mentioning

confidence: 99%

Hepatopulmonary syndrome: a concern for the anesthetist? Pre‐operative evaluation of hypoxemic patients with liver disease

Mazzeo

Lucanto

Santamaria

2004

Acta Anaesthesiol Scand

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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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Luxury lung perfusion in end‐stage liver disease during liver transplantation

Cited by 10 publications

References 13 publications

Liver Transplantation in Pigs: NO, Oxygen Free Radicals, Pulmonary Hemodynamics

Liver Transplantation in Pigs: NO, Oxygen Free Radicals, Pulmonary Hemodynamics

Mechanisms underlying gas exchange alterations in an experimental model of pulmonary embolism

Hepatopulmonary syndrome: a concern for the anesthetist? Pre‐operative evaluation of hypoxemic patients with liver disease

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