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Luxury lung perfusion in end‐stage liver disease during liver transplantation
Author(s) -
Stenqvist O.,
Olausson M.,
Karlsen K. L.
Publication year - 1999
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1034/j.1399-6576.1999.430413.x
Subject(s) - medicine , cardiac output , liver transplantation , vascular resistance , transplantation , cardiology , pulmonary artery , perfusion , lung , ventilation (architecture) , anesthesia , hemodynamics , mechanical engineering , engineering
Background: End‐stage liver disease is accompanied by a hyperkinetic circulation sometimes combined with hypoxaemia. Nitric oxide overproduction has been described as a possible cause by dilating the vasculature and decreasing cardiac afterload. The aim of this study was to evaluate haemodynamics, ventilation/perfusion matching, alveolar and alveolar dead space ventilation and resistance of systemic and pulmonary vasculature during liver transplantation. Methods: Ten liver transplantation patients were studied. Cardiac output, CO, was measured with thermodilution technique. Pulmonary shuntflow was calculated from standard formulas. Effective cardiac output, CO eff , was defined as the CO in contact with alveolar ventilation, V˙ A . Effective alveolar ventilation, V˙ A eff , was defined as V˙ A in contact with pulmonary circulation. Measurements were performed during dissection, anhepatic and reperfusion phases. Results: During the dissection phase the shunt was 23±3%, CO eff was 7.9±0.6 l/min, SVR was 620±67 dyn · s/cm 5 , V˙ A eff was 3.4±0.5 l/min, SaO 2 was 98±1% and Sv¯O 2 was 86±2%. Corresponding values during the anhepatic phase were 16±2%, 5.6±0.4 l/min, 931±78 dyn · s/cm 5 , 3.1±0.2 l/min, 99±1% and 88±1%. During the reperfusion phase the values returned to levels close to that of the dissection phase. The reduction of CO eff between the dissection and the anhepatic phase was significant ( P <0.01). Conclusions: The low vascular resistance is accompanied by a high cardiac output. In spite of the high shunt fraction, these patients were not hypoxaemic. This is explained by the fact that the increased cardiac output leads to a decrease in arterio‐mixed venous oxygen content difference and an increase in mixed venous oxygenation level, Sv¯O 2 86–88%, normal value ≈70%. The V˙ A eff /CO eff in this study was ≈0.5, i.e. the effective cardiac output, CO eff is 235, 180 and 197% of the effective alveolar ventilation, V˙ A eff during the three phases. Thus, about twice the amount blood is oxygenated as compared to a normodynamic situation, which compensates for the effect of the shunt flow on oxygenation.