Transpulmonary lactate gradient after hypothermic cardiopulmonary bypass
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Several studies demonstrated that the lungs could produce lactate in patients with acute lung injury (ALI). Because after cardiopulmonary bypass (CPB) some patients develop ALI, the effect of CPB on pulmonary lactate release was investigated.
Prospective observational clinical study.
Twenty-beds, surgical ICU at a university hospital.
Sixteen deeply sedated, ventilated and post-cardiac surgery patients, all equipped with a pulmonary artery catheter.
Measurements and results
Lactate concentration was measured using a lactate analyser in simultaneously drawn arterial (A) and mixed venous (V) blood samples. Three measurements per patients were taken at 30-min interval, after body temperature reached 37°C. Concomitantly, measurements of cardiac output were also obtained. Pulmonary lactate release was calculated as the product of transpulmonary A-V lactate and cardiac index. The mean cardiopulmonary bypass duration was 100±44 min (SD), and the aortic cross-clamping time was 71±33 min. After CPB, lactate release was 0.136±0.210 mmol/min m−2. These values were not correlated with cardiopulmonary bypass duration.
The present study shows that in patients receiving mechanical ventilation after CPB, the lung is a source of lactate production. This pulmonary release was not dependent on cardiopulmonary bypass duration.
KeywordsExtracorporeal circulation Respiratory failure Lactic acid Lung injury Artificial respiratory support
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