2004
DOI: 10.1136/adc.2003.030957
|View full text |Cite
|
Sign up to set email alerts
|

Delayed chemoreceptor responses in infants with apnoea

Abstract: Aims: To test the hypothesis that apnoea of infancy (AOI) is due to a deficit in chemoreception. Methods: Tests were performed on 112 infants: 43 healthy control infants, 28 infants with periodic breathing or central apnoea (PBCA), and 41 infants with obstructive apnoea (OA) on overnight polysomnography. Chemoreceptor responses to hypercapnia (4% and 6% CO 2 in air) for 6-8 minutes and hyperoxia (100% O 2 ) for 60 seconds were expressed in terms of response strength and reaction time. Age at birth (gestational… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
2
1

Citation Types

0
15
0

Year Published

2006
2006
2022
2022

Publication Types

Select...
6
2

Relationship

0
8

Authors

Journals

citations
Cited by 38 publications
(16 citation statements)
references
References 33 publications
0
15
0
Order By: Relevance
“…Changes in arterial O 2 pressure levels [caused by chronic hypoxemia at birth (30) or hypoxia-induced changes in arterial CO 2 (31)] may determine the sensitivity to hypoxia, which interferes with postnatal readjustment of the chemoreflex. This statement could, however, be subject to criticism as there is no evidence that the changes in transcutaneous O 2 are closely related to arterial O 2 pressure [with a slower response time for transcutaneous O 2 , in particular (7,32)], whereas another study showed that PaO 2 varied broadly with SpO 2 and that the latter accurately reflected the simultaneous PaO 2 (33). Moreover, borderline hypoxemia could exist without a decrease in saturation (10).…”
Section: Discussionmentioning
confidence: 99%
“…Changes in arterial O 2 pressure levels [caused by chronic hypoxemia at birth (30) or hypoxia-induced changes in arterial CO 2 (31)] may determine the sensitivity to hypoxia, which interferes with postnatal readjustment of the chemoreflex. This statement could, however, be subject to criticism as there is no evidence that the changes in transcutaneous O 2 are closely related to arterial O 2 pressure [with a slower response time for transcutaneous O 2 , in particular (7,32)], whereas another study showed that PaO 2 varied broadly with SpO 2 and that the latter accurately reflected the simultaneous PaO 2 (33). Moreover, borderline hypoxemia could exist without a decrease in saturation (10).…”
Section: Discussionmentioning
confidence: 99%
“…It has been further suggested that infants with central SAH events may have depressed or delayed ventilation responses to hypercarbia and possibly hypoxemia regardless of their apnoeic severity. In order to meet homoeostatic demands, the respiratory control mechanisms in the brain stem must be able to detect and respond to changes in arterial carbon dioxide and oxygen levels in a rapid manner [1,2]. The strength and timing of the ventilation response can then have confounding effects.…”
Section: Discussionmentioning
confidence: 99%
“…The clinical symptoms and PSG characteristics of SAH for infants differ from those in children and adults [1,2]. Infantile SAH usually results from congenital facial anomalies and neurological abnormalities that involve muscle tone and upper airway control [2,3]. Unlike children and adults, SAH in an infant can present a unique threat to life, such as sudden infant death syndrome and premature apnoea.…”
Section: Introductionmentioning
confidence: 98%
See 1 more Smart Citation
“…Oxygen causes ventilatory depression in mature mammals [26], and may yield similar potentiation effects to those found here. However, the present study focused on the early post-natal period during which ventilatory depression may be aggravated by other sources of respiratory instability, in particular immaturity of the central chemoreceptors [27].…”
Section: Methodological Considerationsmentioning
confidence: 99%