Background: Postoperative blood hyperlactaemia is an indicator of organ anaerobic metabolism and is associated with morbidity after cardiac surgery. This prospective study aims to explore the source, triggers and clin...Background: Postoperative blood hyperlactaemia is an indicator of organ anaerobic metabolism and is associated with morbidity after cardiac surgery. This prospective study aims to explore the source, triggers and clinical implications for hyperlactaemia in patients undergoing mitral valve surgery using Custodiol cardioplegia. Methods: Twenty consecutive elective patients undergoing open-heart surgery for mitral valve repair/replacement using Custodiol (based on Bretschneider’s HTK-solution) cardioplegia were recruited. A serial measurement of arterial blood lactate was performed. Pre-, intra-and post-operative clinical data were obtained and cardiac injury was determined by serial plasma measurement of postoperative release of CK-MB. Results: There were no in-hospital deaths. Most of the patients (n = 16) needed intraoperative direct current cardioversion to treat ventricular arrhythmias or post-operative vasopressors (n = 13) to treat vasoplegia. There was significant cardiac injury as determined by the marked increase of serum CK-MB (p 0.05). A significant (p 0.05) increase in blood lactate was found to follow a biphasic profile. The first peak (from 0.54 ± 0.03 to 1.3 ± 0.07 mM) was observed immediately following the release of the aortic cross-clamp and remained high for 1 hour. This was followed by a second peak at 12 hours post-operatively (1.9 ± 0.2 mM). The second rise in lactate was seen only in patients that required post-operative vasopressors (1.3 ± 0.2 vs 2.2 ±0.3 mM, p 0.05), in whom a significant late decrease in CVP was also observed (12.2 ± 1.0 to 7.7 ± 1.0 for 1 and 12 hours postoperative, respectively). Hyperlactaemia did not correlate with any other variables including CK-MB levels, cross-clamp or cardiopulmonary bypass time. Conclusions: In patients undergoing mitral valve surgery with Custodiol cardioplegia there is marked cardiac injury and a biphasic release of blood lactate. The initial peak in lactate occurs immediately following unclamping the aorta and is likely to be of organ (e.g. heart and lungs) origin. A second peak is only seen in patients requiring postoperative vasopressors to treat vasoplegia. Hyperlactaemia following mitral valve surgery with Custodiol cardioplegia does not seem to be related to myocardial injury as expressed by CK-MB release.展开更多
文摘Background: Postoperative blood hyperlactaemia is an indicator of organ anaerobic metabolism and is associated with morbidity after cardiac surgery. This prospective study aims to explore the source, triggers and clinical implications for hyperlactaemia in patients undergoing mitral valve surgery using Custodiol cardioplegia. Methods: Twenty consecutive elective patients undergoing open-heart surgery for mitral valve repair/replacement using Custodiol (based on Bretschneider’s HTK-solution) cardioplegia were recruited. A serial measurement of arterial blood lactate was performed. Pre-, intra-and post-operative clinical data were obtained and cardiac injury was determined by serial plasma measurement of postoperative release of CK-MB. Results: There were no in-hospital deaths. Most of the patients (n = 16) needed intraoperative direct current cardioversion to treat ventricular arrhythmias or post-operative vasopressors (n = 13) to treat vasoplegia. There was significant cardiac injury as determined by the marked increase of serum CK-MB (p 0.05). A significant (p 0.05) increase in blood lactate was found to follow a biphasic profile. The first peak (from 0.54 ± 0.03 to 1.3 ± 0.07 mM) was observed immediately following the release of the aortic cross-clamp and remained high for 1 hour. This was followed by a second peak at 12 hours post-operatively (1.9 ± 0.2 mM). The second rise in lactate was seen only in patients that required post-operative vasopressors (1.3 ± 0.2 vs 2.2 ±0.3 mM, p 0.05), in whom a significant late decrease in CVP was also observed (12.2 ± 1.0 to 7.7 ± 1.0 for 1 and 12 hours postoperative, respectively). Hyperlactaemia did not correlate with any other variables including CK-MB levels, cross-clamp or cardiopulmonary bypass time. Conclusions: In patients undergoing mitral valve surgery with Custodiol cardioplegia there is marked cardiac injury and a biphasic release of blood lactate. The initial peak in lactate occurs immediately following unclamping the aorta and is likely to be of organ (e.g. heart and lungs) origin. A second peak is only seen in patients requiring postoperative vasopressors to treat vasoplegia. Hyperlactaemia following mitral valve surgery with Custodiol cardioplegia does not seem to be related to myocardial injury as expressed by CK-MB release.
