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Ann Thorac Surg 2002;74:1172
© 2002 The Society of Thoracic Surgeons
a John Radcliffe Hospital, Oxford Heart Centre, Headley Way, Headington, OX3190U Oxford, United Kingdom
e-mail: david.taggart{at}orh.nhs.uk
A decade ago we reported in The Annals that lung injury is detectable in all patients undergoing coronary artery bypass grafting (CABG) using cardiopulmonary bypass (CPB), and is more severe than that observed after general surgical operations [1]. We noted that the severity of lung injury, as defined by impairment of gas exchange, was maximal on the second postoperative day and that one-quarter of patients still had an arterial oxygen tension of less than 8 kPa (60 mm Hg) while breathing room air (the conventional definition of respiratory failure) on the 6th postoperative day.
The aetiology of impaired gas exchange after CPB is complex and multifactorial. General anesthesia itself impairs respiratory mechanics and causes ventilation perfusion mismatching. A myriad of inflammatory mediators activated during CPB adversely affect lung function, and the lungs are subjected to a degree of ischaemia-reperfusion injury as a consequence of low or no flow in the pulmonary arteries during CPB.
Sievers and colleagues explored this latter aspect in an elegant study in which they allocated 24 patients undergoing various cardiac operations to conventional CPB (group I, n = 7) to additional lung perfusion (group II: n = 9) or to additional lung perfusion and filtration (group III, n = 8). Briefly, there was no difference in elevation of alpha-2 macroglobulin or elastase-alpha-1-proteinase inhibitor complex in plasma but a reduction in the latter in broncho-alveolar lavage fluid (BALF) in group III. There was a larger increase in the alveolar-arterial oxygen gradient in the conventional group at the end of CPB but no differences in pulmonary artery pressures, time to extubation, or duration of stay in the intensive care unit.
There are two possible explanations for these essentially negative findings. First, this was a small nonrandomized study of heterogeneous cardiac surgical procedures and may, simply, have been underpowered to detect clinically significant differences amongst the groups. More importantly, contemporary CPB may not be the major cause of respiratory dysfunction in patients undergoing cardiac surgery [2]. We recently reported a similar severity of impairment in several indices of gas exchange in on-pump and off-pump CABG patients, in spite of a greater inflammatory response in the CPB group [2].
Whether the interventions described by Sievers and colleagues may have a role in patients with pre-existing respiratory dysfunction and/or exposed to prolonged periods of CPB merits further exploration. However, in an era when a less interventional philosophy increasingly prevails, this would require demonstration of significant clinical benefits and, as a minimum, reduction in postoperative respiratory dysfunction.
References
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