Prematurity, the Diagnosis of Bronchopulmonary Dysplasia, and Maturation of Ventilatory Control

2021 ◽  
Author(s):  
Daniel Mammel ◽  
James Kemp
Keyword(s):  
Bronchopulmonary Dysplasia ◽  
Ventilatory Control

scholarly journals Title: Prematurity, the Diagnosis of Bronchopulmonary Dysplasia, and Maturation of Ventilatory Control Abbreviated Title: Control of Breathing and the Diagnosis of BPD

2020 ◽  
Author(s):  
Daniel Mammel ◽  
James Kemp
Keyword(s):  
Lung Disease ◽  
Bronchopulmonary Dysplasia ◽  
Ventilatory Support ◽  
Periodic Breathing ◽  
Supplemental Oxygen ◽  
Ventilatory Control ◽  
Plastic Process ◽  
Delayed Maturation ◽  
Parenchymal Lung Disease ◽  
Parenchymal Lung

Infants born before 32 weeks post-menstrual age (PMA) and receiving respiratory support at 36 weeks PMA are diagnosed with bronchopulmonary dysplasia. This label suggests that their need for supplemental oxygen is primarily due to acquired dysplasia of airways and airspaces, and that the supplemental oxygen (O2) is treating residual parenchymal lung disease. However, current approaches to ventilatory support in the first days of life, including artificial surfactant use and lower ventilating pressures have changed the pathology of chronic lung disease, and emerging evidence suggests that immature ventilatory control may also contribute to the need for supplemental oxygen at 36 weeks PMA. In all newborns, maturation of ventilatory control continues ex utero and is a plastic process. Supplemental O2 mitigates the hypoxemic effects of delayed maturation of ventilatory control, as well as reduces the duration and frequency of periodic breathing events. Prematurity is associated with altered and occasionally aberrant maturation of ventilatory control. Infants born prematurely, with or without a diagnosis of BPD, are more prone to long-lasting effects of dysfunctional ventilatory control. Awareness of the interaction between parenchymal lung disease and delayed maturation of ventilatory control is essential to understanding why a given premature infant requires and is benefitting from supplemental O2 at 36 weeks PMA.

scholarly journals Acute and chronic changes in the control of breathing in a rat model of bronchopulmonary dysplasia

2019 ◽  
Vol 316 (3) ◽  
pp. L506-L518 ◽  
Author(s):  
Gary C. Mouradian ◽  
Santiago Alvarez-Argote ◽  
Ryan Gorzek ◽  
Gabriel Thuku ◽  
Teresa Michkalkiewicz ◽  
...  
Keyword(s):  
Control System ◽  
Bronchopulmonary Dysplasia ◽  
Rat Model ◽  
Minute Ventilation ◽  
Control Of Breathing ◽  
Respiratory Morbidity ◽  
Ventilatory Control ◽  
Hyperoxia Exposure ◽  
Age Dependent

Infants born very prematurely (<28 wk gestation) have immature lungs and often require supplemental oxygen. However, long-term hyperoxia exposure can arrest lung development, leading to bronchopulmonary dysplasia (BPD), which increases acute and long-term respiratory morbidity and mortality. The neural mechanisms controlling breathing are highly plastic during development. Whether the ventilatory control system adapts to pulmonary disease associated with hyperoxia exposure in infancy remains unclear. Here, we assessed potential age-dependent adaptations in the control of breathing in an established rat model of BPD associated with hyperoxia. Hyperoxia exposure ([Formula: see text]; 0.9 from 0 to 10 days of life) led to a BPD-like lung phenotype, including sustained reductions in alveolar surface area and counts, and modest increases in airway resistance. Hyperoxia exposure also led to chronic increases in room air and acute hypoxic minute ventilation (V̇e) and age-dependent changes in breath-to-breath variability. Hyperoxia-exposed rats had normal oxygen saturation ([Formula: see text]) in room air but greater reductions in [Formula: see text] during acute hypoxia (12% O2) that were likely due to lung injury. Moreover, acute ventilatory sensitivity was reduced at P12 to P14. Perinatal hyperoxia led to greater glial fibrillary acidic protein expression and an increase in neuron counts within six of eight or one of eight key brainstem regions, respectively, controlling breathing, suggesting astrocytic expansion. In conclusion, perinatal hyperoxia in rats induced a BPD-like phenotype and age-dependent adaptations in V̇e that may be mediated through changes to the neural architecture of the ventilatory control system. Our results suggest chronically altered ventilatory control in BPD.

scholarly journals Ventilatory control in infants, children, and adults with bronchopulmonary dysplasia

2013 ◽  
Vol 189 (2) ◽  
pp. 329-337 ◽  
Author(s):  
Melissa L. Bates ◽  
De-Ann M. Pillers ◽  
Mari Palta ◽  
Emily T. Farrell ◽  
Marlowe W. Eldridge
Keyword(s):  
Bronchopulmonary Dysplasia ◽  
Ventilatory Control

Severe bronchopulmonary dysplasia increases risk for later neurological and motor sequelae in preterm survivors

2006 ◽  
Vol 42 (01) ◽  
pp. 53 ◽  
Author(s):  
Annette Majnemer ◽  
Patricia Riley ◽  
Michael Shevell ◽  
Rena Birnbaum ◽  
Harriet Greenstone ◽  
...  
Keyword(s):  
Bronchopulmonary Dysplasia

Bronchopulmonary Dysplasia Quality of Life Questionnaire

2019 ◽  
Author(s):  
Lysbert Meijer‑Schaap ◽  
Anthony E. J. Dubois ◽  
Boudewijn J. Kollen ◽  
Jet  Tijmens‑van der Hulst ◽  
Bertine M. J. Flokstra‑de Blok ◽  
...  
Keyword(s):  
Quality Of Life ◽  
Bronchopulmonary Dysplasia ◽  
Life Questionnaire ◽  
Quality Of Life Questionnaire

Outpatient Management and Follow-Up of Bronchopulmonary Dysplasia

1984 ◽  
Vol 11 (1) ◽  
pp. 101-122 ◽  
Author(s):  
Beverly L. Koops ◽  
Steven H. Abman ◽  
Frank J. Accurso
Keyword(s):  
Bronchopulmonary Dysplasia ◽  
Outpatient Management

Genomic risk factors for bronchopulmonary dysplasia (BPD) in preterm neonates

2012 ◽  
Vol 224 (07) ◽  
Author(s):  
L Gortner ◽  
P Ahnert ◽  
W Göpel ◽  
P Nürnberg
Keyword(s):  
Risk Factors ◽  
Bronchopulmonary Dysplasia ◽  
Preterm Neonates ◽  
Genomic Risk
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