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Delayed chemoreceptor responses in infants with apnoea.

M Katz-Salamon¹

¹Dept for Women's and Child Health, Karolinska Institute, Elevhemmet H1O2, S-171 76 Stockholm, Sweden. miriam.katz-salamon@ks.se

Archives of Disease in Childhood

|February 24, 2004

Summary

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.

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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.

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