Literature DB >> 17904857

Pulmonary lactate release following cardiopulmonary bypass.

Hrvoje Gasparovic1, Stjepko Plestina, Zeljko Sutlic, Ino Husedzinovic, Vedran Coric, Visnja Ivancan, Ivan Jelic.   

Abstract

OBJECTIVE: The etiology of lung injury following cardiopulmonary bypass (CPB) is multifactorial. Our study focused on quantifying the lactate release from the lungs precipitated by extracorporeal circulation at different time points after the insult. This was complemented by an evaluation of the gas exchange at the level of the alveolar-capillary membrane.
METHODS: Forty consecutive patients (age 61+/-11 years, EuroScore 4.7+/-2.7) undergoing CABG were prospectively analyzed. The data are presented as medians and the interquartile range.
RESULTS: The pulmonary lactate release (PLR) increased from a baseline value of 0.033 (range -0.077 to 0.170) to 0.465 mmol/min/m2 (range 0.113-0.922), which was seen 6h postoperatively (P<0.001). The A-a O2 gradient increased from 12.7 (range 8.8-15) to 39.1 kPa (range 30.3-46.5) upon discontinuation of CPB (P<0.001). The systemic arterial lactate (LS) concentration increased from 1.22 (range 1-1.44) to 3.03 mmol/l (range 2.29-4.76) 6h after surgery (P<0.001). The veno-arterial pCO2 difference (V-A dpCO2) rose from 0.6 (range 0.5-0.9) to 0.9 kPa (range 0.7-1) (P=0.014). The mortality in the studied group was 5% (2/40).
CONCLUSIONS: The lungs were found to be a significant source of lactate, and this pulmonary lactate flux was accentuated by CPB. The PLR correlated with systemic hyperlactatemia as well as the A-a O2 gradient, and was found to be higher in patients requiring prolonged mechanical ventilatory support. The duration of CPB had a significant impact on the systemic lactate concentrations, V-A dpCO2 and the A-a O2 gradient, but not on the PLR.

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Year:  2007        PMID: 17904857     DOI: 10.1016/j.ejcts.2007.09.001

Source DB:  PubMed          Journal:  Eur J Cardiothorac Surg        ISSN: 1010-7940            Impact factor:   4.191


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