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

Citation
O. Stenqvist et al., Luxury lung perfusion in end-stage liver disease during liver transplantation, ACT ANAE SC, 43(4), 1999, pp. 447-451
Citations number
20
Categorie Soggetti
Aneshtesia & Intensive Care","Medical Research Diagnosis & Treatment
Journal title
ACTA ANAESTHESIOLOGICA SCANDINAVICA
ISSN journal
00015172 → ACNP
Volume
43
Issue
4
Year of publication
1999
Pages
447 - 451
Database
ISI
SICI code
0001-5172(199904)43:4<447:LLPIEL>2.0.ZU;2-Z
Abstract
Background: End-stage liver disease is accompanied by a hyperkinetic circul ation sometimes combined with hypoxaemia. Nitric oxide overproduction has b een described as a possible cause by dilating the vasculature and decreasin g cardiac afterload. The aim of this study was to evaluate haemodynamics, v entilation/perfusion matching, alveolar and alveolar dead space ventilation and resistance of systemic and pulmonary vasculature during liver transpla ntation. Methods: Ten liver transplantation patients were studied. Cardiac output, C O, was measured with thermodilution technique. Pulmonary shuntflow was calc ulated from standard formulas. Effective cardiac output, COeff, was defined as the CO in contact with alveolar ventilation, (V) over dot A. Effective alveolar ventilation, (V) over dot A(eff), was defined as (V) over dot A in contact with pulmonary circulation. Measurements were performed during dis section, anhepatic and reperfusion phases. Results: During the dissection phase the shunt was 23+/-3%, COeff was 7.9+/ -0.6 l/min, SVR was 620+/-67 dyn . s/cm(5), (V) over dot A(eff) was 3.4+/-0 .5 l/min, SaO(2) was 98+/-1% and S (v) over bar O-2 was 86+/-2%. Correspond ing 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 reperfus ion phase the values returned to levels close to that of the dissection pha se. The reduction of COeff between the dissection and the anhepatic phase w as significant (P<0.01): Conclusions: The low vascular resistance is accompanied by a high cardiac o utput. In spite of the high shunt fraction, these patients were not hypoxae mic. This is explained by the fact that the increased cardiac output leads to a decrease in arterio-mixed venous oxygen content difference and an incr ease in mixed venous oxygenation level, S (v) over bar O-2 86-88%, normal v alue approximate to 70%. The (V) over dot A(eff)/COeff in this study was ap proximate to 0.5, i.e. the effective cardiac output, COeff/COeff in this st udy was approximate to 0.5, i.e. the effective cardiac output, COeff is 235 , 180 and 197% of the effective alveolar ventilation, (V) over dot A(eff) d uring 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.