Abstract
Vestibulo-mediated cardiovascular control in hazardous situations is important. Our hypothesis is that the prerequisite for sudden infant death syndrome (SIDS) is impaired vestibulo-mediated cardiovascular control. Prematurity is a risk factor for SIDS, and postnatal intermittent hypoxia may contribute to this risk. We studied heart rate (HR) and blood pressure (BP) responses in 10 infants with bronchopulmonary dysplasia (BPD) who were born at 27 ± 2.4 (23–30) wk of gestation. Twenty healthy term infants served as controls. Cardiovascular tests were performed under polysomnographic control during slow-wave sleep (SWS) at a corrected age of 12 ± 3.5 (7–19) wk. Control infants showed biphasic HR and BP responses to side motion with an immediate increase followed by a modest decrease and return to baseline. Compared with the controls, half of the BPD infants had altered BP responses (p < 0.005) without an early increase, followed by a more prominent decrease in BP. BPD infants also presented with a greater variability in BP responses to head-up tilts than did the controls (p < 0.001). In conclusion, these findings suggest that some BPD infants have impaired vestibular sympathoreflex–mediated cardiovascular control. This dysfunction may become critical in life-threatening situations.
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Abbreviations
- BP:
-
blood pressure
- BPD:
-
bronchopulmonary dysplasia
- DBP:
-
diastolic blood pressure
- HFV:
-
high-frequency variability in heart rate
- HR:
-
heart rate
- LFV:
-
low-frequency variability in heart rate
- SBP:
-
systolic blood pressure
- SpO2:
-
arterial oxyhemoglobin saturation
- SWS:
-
slow-wave sleep
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This study was supported by grant number TYH3230 from Helsinki University Hospital, the Sigrid Jusélius Foundation, Finska Läkaresällskapet, and the Foundation for Pediatric Research.
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Viskari, S., Andersson, S., Hytinantti, T. et al. Altered Cardiovascular Control in Preterm Infants with Bronchopulmonary Dysplasia. Pediatr Res 61, 594–599 (2007). https://doi.org/10.1203/pdr.0b013e3180459f43
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DOI: https://doi.org/10.1203/pdr.0b013e3180459f43
