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LETTER TO THE EDITOR
Children's Hospital of Philadelphia has been at the forefront in the study and use of various gas mixtures to manipulate pulmonary vascular resistance in the preoperative single ventricle setting. The remarks of Dr. Jobes (2) from the Department of Anesthesia pertaining to the superiority of inhaled carbon dioxide to achieve hemodynamic stability in the immediate perioperative setting complement the published study of Dr. Tabutt and her colleagues (5) from the same institution, as reviewed in detail in our original Counterpoint (4).
Dr. Prakesh (2) raises some interesting points. We agree that buffering hypercapnic acidosis with sodium bicarbonate will worsen the intracellular pH in any situation when ventilation is inadequate, and by no means advocate its use. Indeed, the pulmonary protective effects of hypercapnic acidosis are lost when sodium bicarbonate is used to buffer the acidosis associated with hypercarbia (3). Likewise sodium bicarbonate would be counterproductive with regard to the goal of therapy, which is maintenance of an elevated pulmonary vascular resistance. It is notable that alveolar hypoxia has not been shown to confer the same pulmonary- or neuro-protective effects as have been demonstrated with hypercapnic acidosis. Dr. Prakesh (2) also notes from the Tabbutt study that hypercapnic acidosis narrows the arteriovenous oxygen difference and infers this is a result of diminished oxygen extraction. Given that the oxygen consumption was not directly measured, the Fick equation can not be manipulated to form that conclusion (5). Additionally, the observed increase in blood pressure with hypercapnia would suggest that the narrowed arteriovenous oxygen difference was in fact secondary to an improved cardiac output with resultant increased oxygen delivery rather than diminished oxygen utilization.
Dr. Day's (2) published experience with subambient oxygen for patients with single ventricle hearts awaiting transplantation is invaluable and demonstrates that there is certainly a role for its use, namely in the situation where the neonate is spontaneously breathing and is not in decompensated shock. We believe his concern about Tabbutt's study regarding the unmeasured antegrade flow across the aortic valve is negated by her randomized cross-over design (6). Finally, his entreaty to be clear about the use of the term "hypoxia" must, of course, be heeded.
Dr. Yildiz's (7) vote with Dr. Ebenroth is noted. We also like Dr. Ebenroth very much.
Finally, to Dr. Ebenroth, we concede that our statement that surgery, not hypoxia, is the optimal means of reducing pulmonary blood flow was an unfair statement in the context of this debate. The point is to be emphasized, nonetheless, that until pulmonary blood flow is controlled by the restrictive shunt, it can be quite difficult to manipulate and measure by whatever means is chosen. We ask that he forgive us this indiscretion, as he has been a worthy opponent, and remains a good friend.
FOOTNOTES
Address for reprint requests and other correspondence: J. L. Aschner, Neonatology, The Monroe Carell Jr. Children's Hospital at Vanderbilt, 11111 Doctor's Office Tower, 2200 Children's Way, Nashville, TN 37232-9544 (e-mail: judy.aschner{at}vanderbilt.edu)
REFERENCES
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