Abstract: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.
“…Multivariate analysis also showed a significant correlation between these two variables. Previous studies showed that insufficient bronchial artery blood flow during CPB could result in lung tissue ischemia and pulmonary lactate release, which correlated with prolonged mechanical ventilation [29], [30]. Also, CPB causes activation of the complement system and the release of various pro-inflammatory cytokines, which results in post-CPB lung dysfunction and systemic inflammation.…”
PurposePostoperative respiratory failure is a major problem which can prolong the stay in the intensive care unit in patients undergoing cardiac surgery. We measured the serum levels of the soluble isoform of the receptor for advanced glycation end products (sRAGE), and we studied its association with postoperative respiratory failure.MethodsEighty-seven patients undergoing elective cardiac surgery were enrolled in this multicenter observational study in three university hospitals. Serum biomarker levels were measured perioperatively, and clinical data were collected for 7 days postoperatively. The duration of mechanical ventilation was studied for 28 days.ResultsSerum levels of sRAGE elevated immediately after surgery (median, 1751 pg/mL; interquartile range (IQR) 1080–3034 pg/mL) compared with the level after anesthetic induction (median, 884 pg/mL; IQR, 568–1462 pg/mL). Postoperative sRAGE levels in patients undergoing off-pump coronary artery bypass grafting (median, 1193 pg/mL; IQR 737–1869 pg/mL) were significantly lower than in patients undergoing aortic surgery (median, 1883 pg/mL; IQR, 1406–4456 pg/mL; p = 0.0024) and valve surgery (median, 2302 pg/mL; IQR, 1447–3585 pg/mL; p = 0.0005), and postoperative sRAGE correlated moderately with duration of cardiopulmonary bypass (rs = 0.44, p<0.0001). Receiver operating characteristic curve analysis demonstrated that postoperative sRAGE had a predictive performance with area under the curve of 0.81 (95% confidence interval 0.71–0.88) for postoperative respiratory failure, defined as prolonged mechanical ventilation >3 days. The optimum cutoff value for prediction of respiratory failure was 3656 pg/mL, with sensitivity and specificity of 62% and 91%, respectively.ConclusionsSerum sRAGE levels elevated immediately after cardiac surgery, and the range of elevation was associated with the morbidity of postoperative respiratory failure. Early postoperative sRAGE levels appear to be linked to cardiopulmonary bypass, and may have predictive performance for postoperative respiratory failure; however, large-scale validation studies are needed.
“…Multivariate analysis also showed a significant correlation between these two variables. Previous studies showed that insufficient bronchial artery blood flow during CPB could result in lung tissue ischemia and pulmonary lactate release, which correlated with prolonged mechanical ventilation [29], [30]. Also, CPB causes activation of the complement system and the release of various pro-inflammatory cytokines, which results in post-CPB lung dysfunction and systemic inflammation.…”
PurposePostoperative respiratory failure is a major problem which can prolong the stay in the intensive care unit in patients undergoing cardiac surgery. We measured the serum levels of the soluble isoform of the receptor for advanced glycation end products (sRAGE), and we studied its association with postoperative respiratory failure.MethodsEighty-seven patients undergoing elective cardiac surgery were enrolled in this multicenter observational study in three university hospitals. Serum biomarker levels were measured perioperatively, and clinical data were collected for 7 days postoperatively. The duration of mechanical ventilation was studied for 28 days.ResultsSerum levels of sRAGE elevated immediately after surgery (median, 1751 pg/mL; interquartile range (IQR) 1080–3034 pg/mL) compared with the level after anesthetic induction (median, 884 pg/mL; IQR, 568–1462 pg/mL). Postoperative sRAGE levels in patients undergoing off-pump coronary artery bypass grafting (median, 1193 pg/mL; IQR 737–1869 pg/mL) were significantly lower than in patients undergoing aortic surgery (median, 1883 pg/mL; IQR, 1406–4456 pg/mL; p = 0.0024) and valve surgery (median, 2302 pg/mL; IQR, 1447–3585 pg/mL; p = 0.0005), and postoperative sRAGE correlated moderately with duration of cardiopulmonary bypass (rs = 0.44, p<0.0001). Receiver operating characteristic curve analysis demonstrated that postoperative sRAGE had a predictive performance with area under the curve of 0.81 (95% confidence interval 0.71–0.88) for postoperative respiratory failure, defined as prolonged mechanical ventilation >3 days. The optimum cutoff value for prediction of respiratory failure was 3656 pg/mL, with sensitivity and specificity of 62% and 91%, respectively.ConclusionsSerum sRAGE levels elevated immediately after cardiac surgery, and the range of elevation was associated with the morbidity of postoperative respiratory failure. Early postoperative sRAGE levels appear to be linked to cardiopulmonary bypass, and may have predictive performance for postoperative respiratory failure; however, large-scale validation studies are needed.
“…The levels of pulmonary lactate release correlate well with systemic lactate levels. This lactate release is increased in procedures employing CPB and correlates with prolonged respiratory support 6. Furthermore, deflated/unventilated lungs during CPB induce atelectasis,12 which may further induce pro-inflammatory cytokine production 17.…”
Section: Discussionmentioning
confidence: 99%
“…Gasparovic et al 6 studied pulmonary lactate release and changes in ΔA–aO 2 during CPB. They reported that the lungs were a significant source of lactate release and there was a correlation between pulmonary lactate release and peripheral lactate concentrations.…”
IntroductionCardiopulmonary bypass causes a series of inflammatory events that have adverse effects on the outcome. The release of cytokines, including interleukins, plays a key role in the pathophysiology of the process. Simultaneously, cessation of ventilation and pulmonary blood flow contribute to ischaemia–reperfusion injury in the lungs when reperfusion is maintained. Collapse of the lungs during cardiopulmonary bypass leads to postoperative atelectasis, which correlates with the amount of intrapulmonary shunt. Atelectasis also causes post-perfusion lung injury. In this study, we aimed to document the effects of continued low-frequency ventilation on the inflammatory response following cardiopulmonary bypass and on outcomes, particularly pulmonary function.MethodsFifty-nine patients subjected to elective coronary bypass surgery were prospectively randomised to two groups, continuous ventilation (5 ml/kg tidal volume, 5/min frequency, zero end-expiratory pressure) and no ventilation, during cardiopulmonary bypass. Serum interleukins 6, 8 and 10 (as inflammatory markers), and serum lactate (as a marker for pulmonary injury) levels were studied, and alveolar–arterial oxygen gradient measurements were made after the induction of anaesthesia, and immediately, one and six hours after the discontinuation of cardiopulmonary bypass.ResultsThere were 29 patients in the non-ventilated and 30 in the continuously ventilated groups. The pre-operative demographics and intra-operative characteristics of the patients were comparable. The serum levels of interleukin 6 (IL-6) increased with time, and levels were higher in the non-ventilated group only immediately after discontinuation of cardiopulmonary bypass. IL-8 levels significantly increased only in the non-ventilated group, but the levels did not differ between the groups. Serum levels of IL-10 and lactate also increased with time, and levels of both were higher in the non-ventilated group only immediately after the discontinuation of cardiopulmonary bypass. Alveolar–arterial oxygen gradient measurements were higher in the non-ventilated group, except for six hours after the discontinuation of cardiopulmonary bypass. The intubation time, length of stay in intensive care unit and hospital, postoperative adverse events and mortality rates were not different between the groups.ConclusionDespite higher cytokine and lactate levels and alveolar–arterial oxygen gradients in specific time periods, an attenuation in the inflammatory response following cardiopulmonary bypass due to low-frequency, low-tidal volume ventilation could not be documented. Clinical parameters concerning pulmonary and other major system functions and occurrence of postoperative adverse events were not affected by continuous ventilation.
“…Dixon et al [11] found that marked prothrombotic response after CPB is associated with elevated lactate levels. Gasparovic et al [12] maintain that the lungs are an additional possible source of lactate during CPB. Besides anaerobic glycolysis, increased aerobic glycolysis by catecholamine-stimulated Na ?…”
Hyperlactatemia is common after cardiac surgery. Maximal lactate threshold ≥4.4 mmol/l in the first 10 h after operation accurately predicts postoperative mortality.
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