Abstract

In Response: We would like to thank Dr. Azzam for his interest in our study [1]. We do not think that temporary atrial right-left (R-L) shunt was the cause of transient desaturation in our patients. Of the 12 patients who presented with brief desaturation, 6 did not have lesions associated with increased pulmonary blood flow (one case each: collateral vein division, pacemaker wire insertion, diagnostic thoracoscopy, pericardial effusion drainage, vascular ring division, and thoracic duct interruption). Of the remaining six, five had a patent ductus arteriosus (PDA), and one had an aortopulmonary collateral, which might be considered to have a pathophysiology similar to PDA. In all of these the patients, desaturation occurred before interruption of the PDA or collateral. It is conceivable that, regardless of the underlying lesion, retraction of the lung and consequent hypoventilation, hypocarbia, and increased pulmonary vascular resistance induced R-L atrial shunting in the presence of a patent foramen ovale. Any attempt to compare the patients of Marshall et al. [2] with those of our study must be done with caution. The patients reported by Marshall et al. were uniformly small premature infants with PDA. Second, the cause of desaturation in these patients was never defined. Although the fall in transcutaneous PO2 (tCO2) occurred after ligation of the PDA in these patients, it also required left lung inflation to resolve. Finally, these premature infants did not receive any anesthetic or analgesic drug beyond local infiltration of the skin. Therefore, it is likely that their stress response to the procedure was significant. The use of fentanyl in preterm infants undergoing PDA ligation has been shown to attenuate the perioperative stress response, reduce ventilatory requirements, and decrease metabolic and circulatory complications [3]. It is also possible that the desaturation in Marshall et al.'s patients was at least in part caused by increased right-sided cardiac filling pressures (and, hence, R-L atrial shunting) due to elevated PVR and shifting of circulating blood volume from the systemic to the pulmonary circulation caused by elevated blood catecholamine concentrations [4]. Josee Lavoie, MD, FRCP Department of Anaesthesia; Montreal Children's Hospital; Montreal, Quebec, H3H 1P3, Canada Frederick A. Burrows, MD Department of Anesthesia; Arkansas Children's Hospital; Little Rock, AR 72202 Dolly D. Hansen, MD Department of Anesthesia; Children's Hospital; Boston, MA 02115

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