Citation

Cohen G, Katz-Salamon M, Malcolm G. J. Physiol. 2012; 590(Pt 23): 6157-6165.

Affiliation

Karolinska Institute;

Copyright

(Copyright © 2012, The Physiological Society, Publisher John Wiley and Sons)

DOI

10.1113/jphysiol.2012.239145

PMID

23006482

Abstract

A resumption of, and escalation in breathing efforts (hyperpnoea) reflexively accelerates heart rate (HR) and may facilitate cardiac and circulatory recovery from apnoea. We analysed whether this mechanism can produce a sustained rise in HR (tachycardia) when a sleeping infant is confronted by mild, rapidly worsening asphyxia, simulating apnoea. Twenty-seven healthy term-born infants aged 1-8 day rebreathed the expired gas for 90s during quiet sleep to stimulate breathing and heart rate. To discriminate cardio-excitatory effects of central respiratory drive, lung inflation, hypoxia, hypercapnia and asphyxia we varied the inspired O2 level and compared temporal changes in response profiles as respiratory sensitivity to hypoxia and asphyxia "reset" after birth. We demonstrate that asphyxia-induced hyperpnoea and tachycardia strengthen dramatically over the 1st week with different time courses and via separate mechanisms. Cardiac excitation by hypercapnia improves first, followed by a slower improvement in respiratory hypoxic drive. A rise in CO2 consequently elicits stronger, longer lasting tachycardia than do moderate increases in respiratory drive or lung expansion. We suggest that without a strong facilitating action of CO2 on the immature heart, respiratory manoeuvres may be unable to reflexively counteract strong vagal bradycardia. This may increase the vulnerability of some infants to apnoea - asphyxia.

Language: en