Hypoxia Reinforces Laryngeal Reflex Bradycardia in Infants

Abstract

The laryngeal chemoreflex involves bradycardia, apnea, swallowing and peripheral vasoconstriction. This reflex was studied in twelve infants, aged 5 days-28 weeks, who had sustained an apparent life-threatening event or were siblings of infants who had died of the sudden infant death syndrome. The bradycardic and apneic components of the reflex were found to be significantly, and sometimes powerfully, reinforced when elicited by pharyngeal water instillation during acute, mild hypoxia (transcutaneous PO2 4.6-8.3 kPa). Apnea duration during normoxia was 0.7-15 sec, and during hypoxia 2-30 sec. Heart rate change ranged from +26% to -21% during normoxia, as compared with -4% to -63% during hypoxia. The percentage change in heart rate was found to inversely correlate with the transcutaneous PO2-level prevailing when the reflex was elicited. The conclusion is that there is a significant reinforcement of the cardiorespiratory adjustments when the laryngeal reflex is activated during simultaneous excitation of the peripheral arterial chemoreceptors. One infant, showing a particularly strong increase of the cardiorespiratory response to laryngeal receptor stimulation during hypoxia, later died of sudden infant death syndrome.

Nicotine Attenuates the Ventilatory Response to Hypoxia in the Developing Lamb

“…from laryngeal stimulation, may lead to severe bradycardia. An augmentation of this reflex interaction has been shown in infants who subsequentl y died of SIDS (47). Similar augmentation of reflex brad ycardia has experimentally been produced by stimulation of the chemoreceptors with nicotine (15).…”

Impaired Cardiorespiratory Recovery after Laryngeal Stimulation in Nicotine-Exposed Young Lambs

“…sympathetic activation, increased alertness, and augmented peripheral chemoreceptor and baroreceptor sensory discharge. The clinical importance of these escape and defense mechanisms are supported by observations that infants who are at risk for life-threatening events are also less able to recover from LCR-induced reflex apnea and bradycardia (5,6) In this study, we tested the hypothesis that long-term postnatal exposure to nicotine attenuates and prolongs recovery from apnea and bradycardia in response to LCR stimulation. This notion was based on our previous observations that postnatal nicotine exposure leads to an attenuation of cardiorespiratory defense mechanisms to hypoxia (7).…”

Prolonged Hypoxemia Enhances and Acute Hypoxemia Attenuates Laryngeal Reflex Apnea in Young Lambs

“…Others have shown that acute hypoxemia preceding laryngeal stimulation results in a reinforced cardiorespiratory response that may be fatal (2,5). They postulated that this combination may be a possible mechanism for SIDS.…”

“…CB denervation significantly increased the apnea response after laryngeal stimulation in 2-to 4-wk-old lambs, but this response remained unchanged in younger lambs, suggesting that a mature CB function plays a role in limiting reflex apnea caused by laryngeal water stimulation (14). However, it has been postulated that acute hypoxia preceding apnea induces a positive feedback that reinforces suppression of breathing, a mechanism that may play a role in the etiology of SIDS (2,5,20). Recently, there has been much interest in the study of peripheral chemoreceptor function in infancy because of a possible relationship between hypoxic exposure, CB malfunction, and the SIDS (2 1-23).…”