Gasping and other cardiorespiratory patterns during sudden infant deaths

Citation
Cf. Poets et al., Gasping and other cardiorespiratory patterns during sudden infant deaths, PEDIAT RES, 45(3), 1999, pp. 350-354
Citations number
24
Categorie Soggetti
Pediatrics,"Medical Research General Topics
Journal title
PEDIATRIC RESEARCH
ISSN journal
00313998 → ACNP
Volume
45
Issue
3
Year of publication
1999
Pages
350 - 354
Database
ISI
SICI code
0031-3998(199903)45:3<350:GAOCPD>2.0.ZU;2-L
Abstract
To gain information on the cardiorespiratory changes occurring immediately before sudden infant death (SLD), recordings of heart rate and chest wall i mpedance were analyzed in nine infants who had died at a median age of 4.8 mo (range 1-6 mo) while attached to a memory monitor. Postmortem diagnoses were sudden infant death syndrome in seven infants and mild bronchopulmonar y dysplasia in two infants. Primary cause of the monitor alarm was bradycar dia in all but two infants. Heart rate fell to less than or equal to 15 bpm 7.5 min (range 1.4-25.2 min) after the first alarm; then was no indication of heart block or ventricular tachycardia. Apnea (>20 s) began 0.3 to 13.7 min (median 2.7 min) after this alarm in five infants and 7 to 20 s before it in three infants; in the remaining infant, stimulation occurred before any apnea. Gasping was already present at the time of the first monitor ala rm in three infants and occurred within 2.7 min after it in a further four infants. One infant only began to gasp 13 min after the first monitor alarm . The duration of gasping ranged from 3 s to 11 min in those five infants i n whom it was not interrupted by resuscitation. The latter was given to thr ee infants 4, 21, and 228 s after the monitor alarm but had no effect on th e ongoing decrease in heart rate. Since gasping only occurs if Pao(2) is < 5-15 mm Hg, it is most likely that the seven infants who gasped at or short ly after the first monitor alarm were already severely hypoxemic at that ti me. This hypoxemia developed in the absence of prolonged central apnea. The role of other mechanisms potentially resulting in severe hypoxemia, such a s upper airway obstruction or rebreathing, remains to be determined.