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Eur J Cardiothorac Surg 2007;32:882-887. doi:10.1016/j.ejcts.2007.09.001
Copyright © 2007, European Association for Cardio-thoracic Surgery. Published by Elsevier. All rights reserved.

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Hrvoje Gasparovic
Zeljko Sutlic
Vedran Coric
Ivan Jelic
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Right arrow Extracorporeal circulation

Pulmonary lactate release following cardiopulmonary bypass

Hrvoje Gasparovica,*, Stjepko Plestinab, Zeljko Sutlicc, Ino Husedzinovicc, Vedran Corica, Visnja Ivancana, Ivan Jelica

a Department of Cardiac Surgery, University Hospital Rebro Zagreb, Zagreb, Croatia
b Department of Internal Medicine, University Hospital Rebro Zagreb, Zagreb, Croatia
c Department of Cardiac Surgery, Clinical Hospital Dubrava, Zagreb, Croatia

Received 6 March 2007; received in revised form 23 July 2007; accepted 3 September 2007.

* Corresponding author. Address: University Hospital Rebro Zagreb, Department of Cardiac Surgery, Kispaticeva 12, 10 000 Zagreb, Croatia. Tel.: +385 1 242 1595; fax: +385 1 242 1595. (Email: hgasparovic{at}kbc-zagreb.hr).

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 6 h 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 (L S) concentration increased from 1.22 (range 1–1.44) to 3.03 mmol/l (range 2.29–4.76) 6 h 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.

Key Words: Pulmonary lactate release • Cardiopulmonary bypass • Alveolar–arterial oxygen gradient







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Copyright © 2007 European Association for Cardio-Thoracic Surgery. Published by Elsevier. All rights reserved.