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Ann Thorac Surg 2001;72:187-192
© 2001 The Society of Thoracic Surgeons

Original article: cardiovascular

Cerebral oxygen saturation before congenital heart surgery

C. Dean Kurth, MDa,c,d,f, James L. Steven, MDa,c,d,f, Lisa M. Montenegro, MDa,d, H. Marc Watzman, MDa,d, J. William Gaynor, MDb,e, Thomas L. Spray, MDb,e, Susan C. Nicolson, MDa,d a Department of Anesthesiology and Critical Care Medicine, The Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania, USA
b Department of Surgery, The Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania, USA
c Department of Pediatrics, The Children’s Hospital of Philadelphia, Philadephia, Pennsylvania, USA
d Department of Anesthesia, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
e Department of Surgery, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
f Department of Pediatrics, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA

Accepted for publication March 2, 2001.

Address reprint requests to Dr Kurth, Department of Anesthesiology, The Children’s Hospital of Philadelphia, 34th St and Civic Center Blvd, Philadelphia, PA 19104
e-mail: kurth{at}email.chop.edu

Background. In congenital heart disease (CHD), neurologic abnormalities suggestive of hypoxia-ischemia are often apparent before cardiac surgery. To evaluate preoperative cerebral oxygenation, this study determined cerebral O2 saturation (ScO2) in CHD and healthy children.

Methods. Ninety-one CHD and 19 healthy children aged less than 7 years were studied before surgical or radiologic procedures. Arterial saturation (SaO2) and ScO2 were measured by pulse-oximetry and near infrared cerebral oximetry. Cerebral O2 extraction (CEO2) was calculated (SaO2-ScO2). SaO2, ScO2, and CEO2 were compared among diagnoses. Multivariable regression was performed between ScO2 and clinical variables.

Results. In healthy subjects, ScO2 (68% ± 10%) and CEO2 (30% ± 11%) were similar to patients with ventricular septal defect, aortic coarctation, and single ventricle after Fontan operation. ScO2 was significantly decreased in patients with patent ductus arteriosus (53% ± 8%), tetralogy of Fallot (57% ± 12%), hypoplastic left heart syndrome (46% ± 8%), pulmonary atresia (38% ± 6%), and single ventricle after aortopulmonary shunt (50% ± 7%), or bidirectional Glenn operation (43% ± 6%). CEO2 was significantly different only in patent ductus arteriosus (46% ± 8%) and hypoplastic left heart syndrome (38% ± 12%). In multivariable regression, only SaO2 was related to ScO2 (R = 0.63, p < 0.001).

Conclusions. Cerebral oxygenation in CHD varies with anatomy and arterial saturation, and in some patients, it is very low compared with healthy subjects.




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