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Ann Thorac Surg 2001;72:845-849
© 2001 The Society of Thoracic Surgeons
a Department of Cardiothoracic and Vascular Anesthesiology and Intensive Care, University of Vienna, Vienna, Austria
b Department of Anesthesiology, Mayo Clinic, Rochester, Minnesota, USA
c Department of Cardiothoracic Surgery and Ludwig-Boltzmann-Institut For Cardiosurgical Research, University of Vienna, Vienna, Austria
d Department of Pediatrics, University of Vienna, Vienna, Austria
Accepted for publication May 9, 2001.
Address reprint requests to Dr Plöchl, Department of Cardiothoracic and Vascular Anesthesiology and Intensive Care, General Hospital of Vienna, Währinger Gürtel 18-20, A-1090 Vienna, Austria
e-mail: walter.ploechl{at}univie.ac.at
Background. Cerebral embolization is a major cause of central nervous dysfunction after cardiopulmonary bypass. Experimental studies demonstrate that reductions in arterial carbon dioxide tension (PaCO2) can reduce cerebral embolization during cardiopulmonary bypass. This study examined the effects of brief PaCO2 manipulations on cerebral embolization in patients undergoing cardiac valve procedures.
Methods. Patients were prospectively randomized to either hypocapnia (PaCO2 = 30 to 32 mm Hg, n = 30) or normocapnia (PaCO2 = 40 to 42 mm Hg, n = 31) before aortic cross-clamp removal. With removal of the aortic cross-clamp embolic signals were recorded by transcranial Doppler ultrasonography for the next 15 minutes.
Results. Despite significant differences in PaCO2, groups did not differ statistically in total cerebral emboli counts. The mean number of embolic events was 107 ± 100 (median, 80) in the hypocapnic group and 135 ± 115 (median, 96) in the normocapnic group, respectively (p = 0.315).
Conclusions. Due to the high between-patient variability in embolization, reductions in PaCO2 did not result in a statistically significant decrease in cerebral emboli. In contrast to experimental studies, the beneficial effect of hypocapnia on cerebral embolization could not be demonstrated in humans.
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