To the Editor:-In reviewing the recent report by Hogan et al. [1]regarding hypoxic apnea in rabbits receiving epidural anesthesia, I was struck by the similarity of their report to a phenomenon seen in hypoxic newborn and premature infants: to wit, a brief hyperventilatory response followed by hypoventilation and apnea. [2]In many ways, the newborn or premature infant is similar to the authors' [1]rabbit-with-epidural-anesthesia model. Obviously, the blood pressure of the newborn or premature infant is much lower than that in an older child or adult. At the same time, infants exhibit primarily parasympathetic tone; this is seen in their exaggerated bradycardic responses to laryngoscopy, anesthetics, and succinylcholine, and in the absence of hypotension after pharmacologic sympathectomy with spinal or epidural anesthesia. These similarities between the rabbit-with-epidural-anesthesia model and the newborn or premature infant led me to wonder whether there might be a common mechanism for hypoxic apnea and a role for blood pressure augmentation, adrenergic agonists, or vagolytics in the prevention or treatment of infant apnea.
Unfortunately, the methods chosen by the authors do not allow us to determine whether the critical factor in hypoxic apnea is the level of sympathetic tone or simply the absolute blood pressure. It would be interesting to see whether hypoxic apnea occurs in rabbits in which hypotension is induced by a nonsympatholytic mechanism (hypovolemia, sodium nitroprusside) as well as mechanisms involving blockade of the sympathetic system (trimethaphan, epidural anesthesia). Similarly, it would be interesting to see whether hypoxic apnea could be avoided in rabbits undergoing epidural anesthesia using nonsympathomimetic interventions (volume loading, vagolytics) rather than administration of adrenergic agonists. Although it is certainly possible that the critical factor is oxygen delivery to the brain, as mediated by arterial oxygen content and arterial blood pressure, the authors' [1]methods do not rule out the possibility of specific, sympathetic modulation of respiratory drive mediated through the thoracic sympathetic system.
The authors [1]are to be commended for shedding light on the issue of unexpected cardiorespiratory arrest in patients undergoing spinal or epidural anesthesia. At the same time, their work raises provocative questions about apnea in infants and control of respiratory drive.
Joel B. Gunter, M.D.
Associate Professor; Clinical Anesthesia and Pediatrics; Department of Anesthesiology; University of Cincinnati; Cincinnati, Ohio;gunterjb@email.uc.edu
(Accepted for publication July 7, 1998.)
