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Ann Thorac Surg 2001;72:849
© 2001 The Society of Thoracic Surgeons

Invited commentary

^a Cardiothoracic Centre, Guy’s and St. Thomas’ Hospital, London, England SE1 7EH, United Kingdom

e-mail: ciblauth{at}aol.com

Cerebral injury after cardiac surgery spans a broad clinical spectrum from major stroke to subtle neuropsychological change of uncertain significance. A number of causes have been implicated one of which is embolism. Plochl and colleagues have postulated that transient reduction of cerebral blood flow during periods of high risk for embolism during surgery should reduce the embolic fraction reaching the brain, and have verified this by therapeutic hypocapnia in an experimental model using microspheres. They now report the application of this technique in a randomized clinical study where a more modest reduction in PaCO₂ (9 mm Hg) during one of three high risk periods for embolism (removal of the aortic clamp) appeared to reduce the number of unilateral transcranial Doppler embolic signals, although there remains a 31.5% probability that the difference was due to chance. Despite the unproven efficacy of this intervention in a clinical setting the authors conclude that it is clinically justifiable and should be considered.

Given the potential morbidity of cerebral embolism, the relative simplicity of manipulating PaCO₂ on bypass seems appealing, but may not be entirely safe. The relationship between PaCO₂, cerebral perfusion pressure and neuropsychological deficit was studied by Nevin and colleagues [1] who found that intraoperative fluctuations in PaCO₂ were associated with postoperative deficits and advocated avoidance of hypocapnia immediately before and after the onset of bypass which are also periods of high risk for embolism.

Doctor Plöchl and colleagues quite rightly emphasize the limitations of transcranial Doppler signals which lack specificity in the detection of mixed populations of gaseous, atheromatous, platelet-fibrin, and calcific emboli and do not provide a reliable clinical index of neurological risk. Ultimately we need to know whether brief periods of hypocapnia can influence neurological outcome in patients, what the effects are on cerebral blood flow and cerebral autoregulation, what the target PaCO₂ should be, and also the optimum timing. Therapeutic hypocapnia during cardiac surgery is a more complex intervention than it seems, and a more comprehensive evaluation of its effects is needed before it can be recommended in clinical practice.

References

1. Nevin M., Colchester A.F.C., Adams S., Pepper J.R. Evidence for involvement of hypocapnia and hypoperfusion in aetiology of neurological deficit after cardiopulmonary bypass. Lancet 1987;ii:1493-1495.

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This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Christopher I. Blauth Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Blauth, C. I. Search for Related Content PubMed Articles by Blauth, C. I. Related Collections Extracorporeal circulation Related Article