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Published on: December 26, 2013
Delayed chemoreceptor responses in infants with apnoea
1Dept for Women's and Child Health, Karolinska Institute, Elevhemmet H1O2, S-171 76 Stockholm, Sweden. miriam.katz-salamon@ks.se
Insights
Infants with apnoea of infancy (AOI) show impaired chemoreceptor responses, indicating abnormal respiratory control. This study reveals deficits in CO2 and O2 responses, contributing to the pathogenesis of AOI.
Area of Science:
- Neonatal physiology
- Respiratory control
- Chemoreception
Background:
- Apnoea of infancy (AOI) is a condition characterized by pauses in breathing.
- The underlying mechanisms of AOI are not fully understood, but abnormal respiratory control is suspected.
Purpose of the Study:
- To investigate the role of chemoreceptor function in the development of apnoea of infancy.
- To test the hypothesis that AOI is caused by a deficit in chemoreception.
Main Methods:
- 112 infants were studied: 43 healthy controls, 28 with periodic breathing or central apnoea (PBCA), and 41 with obstructive apnoea (OA).
- Chemoreceptor responses to hypercapnia (CO2) and hyperoxia (O2) were measured.
- Ventilatory response strength and reaction time were analyzed.
Main Results:
- Control infants exhibited the strongest and fastest CO2 responses.
- Infants with PBCA and OA showed significantly weaker and slower CO2 responses.
- All infants had similar O2-induced ventilation decreases, but apnoeic infants had longer response times.
Conclusions:
- Inappropriate central respiratory control is a key factor in the development of apnoea of infancy.
- Chemoreceptor deficits contribute to the pathogenesis of AOI.
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% CO2 in air) for 6-8 minutes and hyperoxia (100% O2) for 60 seconds were expressed in terms of response strength and reaction time. Age at birth (gestational week 37-41) and age at test (2-34 postnatal weeks) were comparable across groups (median, min-max value). A total of 70 CO2 and 71 O2 tests were analysed.
Results:
The strongest and fastest CO2 responders were control infants: their median increase in ventilation was 291%/kPaCO2 and their reaction time 16 breaths. In infants with PBCA and OA, the increase in ventilation was 41% and 130%/kPaCO2, and reaction time 64 and 54 breaths, respectively. There was a significant negative correlation between CO2 response strength and response time. In response to hyperoxia there was a comparable decrease in ventilation in all infants (12-20%), but a significantly longer response time in infants with apnoea (20 v 12 breaths). There was no correlation between the response strength and response time to O2 and CO2.
Conclusion:
An inappropriate central control of respiration is an important mechanism in the pathogenesis of apnoea of infancy.
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