Amanda's NICU ED Blogs

Bronchopulmonary dysplasia (BPD) remains one of the most challenging chronic conditions we encounter in the NICU, affecting approximately40% of infants born before 28 weeks’ gestation. As nurses caring for these infants, understanding the evolving nature of BPD and how to optimize respiratory support is crucial for improving outcomes.
Modern BPD is no longer simply a consequence of ventilator injury, it’s adevelopmental lung disordercharacterized by impaired alveolar and vascular growth, variable airway disease, and a highly heterogeneous clinical presentation. The infants we care for may present with very different pathophysiologic “phenotypes,” and each requires a unique approach to support, assessment, and prevention of deterioration.
A key principle in managing established BPD is thatventilatory strategies differ fundamentally from those used in acute RDS. While we minimize ventilator exposure in early lung disease, infants with established or severe BPD often requiremoresupport, not less, to maintain gas exchange and allow growth and lung repair.
Key Ventilator Settings for Severe BPD:
Tidal volume:10–15 mL/kg (higher to overcome dead space)
Respiratory rate:12–20 breaths/min (slower to allow complete exhalation)
Inspiratory time:0.5–1.0 seconds (longer for “slow” lung units)
PEEP:7–12 cmH₂O (individualized; higher for malacia)
SpO₂ target:92–95% (especially with pulmonary hypertension)
These parameters reflect a physiologic approach that aims for stability, growth, and reduced energy expenditure rather than rapid weaning. Ventilatory management strategies can be further individualized by recognizing the BPD phenotype of a patient.
Bronchopulmonary dysplasia (BPD) is not a single disease it’s a heterogeneous spectrum of injury and abnormal development. Every infant’s lung is a mixture of damage, repair, and adaptation. Recognizing the phenotype(s) helps the NICU team individualize respiratory care, anticipate complications, and guide nursing priorities.
Over the last decade, advanced imaging, pulmonary function testing, and collaborative multicenter research have helped definefive overlapping pulmonary phenotypesof BPD. Most infants demonstratemore than one phenotype, and their pattern may evolve over time as the lungs grow or experience new insults.
Pathophysiology:Simplified, enlarged alveoli and abnormal septation decrease surface area for gas exchange. Compliance is poor and ventilation–perfusion matching is uneven.
Imaging:Heterogeneous chest X-ray with alternating areas of atelectasis and hyperinflation; CT shows simplified or cystic parenchyma.
Clinical clues:
Oxygen dependency despite moderate support
Coarse crackles or diminished breath sounds
Poor growth even when FiO₂ seems stable
Ventilator approach:Moderate to higher tidal volumes (10–15 mL/kg) and longer inspiratory times to recruit slow lung units; PEEP titrated to prevent collapse.
Nursing focus:Gentle handling, frequent position changes to optimize aeration, monitor for fatigue during cares, and advocate for adequate nutrition to support lung repair.
Pathophysiology:Excess extracellular matrix and fibroblast activity create stiff, poorly compliant lungs. This is often a consequence of over-distention or inflammation.
Imaging:Diffuse streaking or reticulation on X-ray/CT; ultrasound “B-lines.”
Clinical clues:
Elevated PaCO₂ with minimal visible retractions (“stiff lung”)
Increased peak pressures on the ventilator
Ventilator approach:Optimize PEEP to keep alveoli open; avoid excessive volumes. Some infants benefit from cautious steroid therapy.
Nursing focus:Watch for rising CO₂ or tiring despite minimal movement; coordinate with the team to minimize stress and maintainconsistentpositioning.
To be clear “consistent” doesn’t meanimmobile— it meansavoiding frequent or abrupt position changes that cause derecruitment. When a baby with stiff lungs is movedrapidlyor placed flat after being prone or side-lying, their alveoli can collapse quickly, leading to:
Immediate desaturations and increased FiO₂ needs
Elevated work of breathing until recruitment is restored
Possible hemodynamic instability if pulmonary pressures rise
So, in these infants, nurses aim for:
Gentle, deliberate repositioning(every few hours, not every few minutes).
Predictable, supportive posturessuch as prone or side-lying, to optimize lung expansion without sudden changes.
Time to settle and re-recruitafter position changes before increasing stimulation.
This approach provides stability in oxygenation and minimizes episodes of “chasing” desats that come from frequent handling.
Pathophysiology:Narrowing and remodeling of bronchioles cause air trapping and hyperinflation.
Imaging:Flattened diaphragms, hyperlucent fields, or mosaic attenuation on CT.
Clinical clues:
Wheezing or prolonged expiratory phase
Hyperinflation on CXR
Desaturation with agitation or feeding
Ventilator approach:Lower rates (12–20 bpm), longer expiratory times, and individualized PEEP to prevent air-trapping; bronchodilators may help.
Nursing focus:Observe for increased WOB during care, monitor chest rise symmetry, suction gently to avoid dynamic collapse, and communicate trends in tolerance or agitation.
Pathophysiology:Tracheomalacia or bronchomalacia leads to dynamic airway collapse during exhalation or agitation.
Imaging/Testing:Dynamic bronchoscopy or CT showing >50% airway collapse.
Clinical clues:
Expiratory stridor or “barking” cough
Sudden desaturations when crying, suctioning, or coughing (“BPD spells”)
Dramatic improvement with higher PEEP or when calm
Ventilator approach:Higher baseline PEEP (10–12 cm H₂O or more) to stent airways open; slower weaning pace.
Nursing focus:Prevent agitation, maintain adequate PEEP during circuit breaks, and use calming, consistent care routines to avoid airway collapse.Establish predictable care routines (e.g., temperature → reposition → assessment→ suction → diaper → feed), use slow deliberate movements, reduce environmental stressors, and coordinate suctioning and repositioning with respiratory therapy to promote stability.
Pathophysiology:Vascular remodeling, endothelial dysfunction, and impaired angiogenesis result in pulmonary hypertension (BPD-PH).
Testing:Echocardiography, BNP, or cardiac MRI.
Clinical clues:
Labile oxygen saturations, cyanotic “spells,” or desats with crying/stooling
Signs of right heart strain on echo
Ventilator approach:Maintain higher SpO₂ targets (92–95%) and stable FiO₂ to prevent pulmonary hypertensive crises. Pulmonary vasodilators and evaluate for pulmonary vein stenosis.
Nursing focus:Avoid hypoxemia and hypercarbia, minimize stress during cares, monitor for edema or hepatomegaly, and collaborate closely with cardiology.
Most infants with severe or evolving BPD havemixed phenotypesfor example, parenchymal + vascular or small-airway + malacia. The dominant phenotype may shift as inflammation resolves, growth accelerates, or new complications arise.
The nurse’s role is to interpret these evolving patterns at the bedside: noticing which interventions (positioning, PEEP, suctioning, oxygen titration) make the biggest difference. This ongoing observation informs real-time adjustments and ensures that care is truly phenotype-guided and individualized rather than protocol-driven.

Elshenawy et al, 2024
For many infants with severe or established BPD, prolonged mechanical ventilation becomes necessary to support growth and neurodevelopment. When ongoing invasive ventilation is required beyond the early postnatal period,tracheostomy placement may be considered. This decision iscomplex and highly individualized.
A recent multicenter review foundsubstantial variability in the timing, indications, and outcomes of tracheostomy among centers, reflecting differences in institutional culture, family perspectives, and available resources . There is no universally accepted “optimal timing.” Instead, each decision should be grounded inshared decision-makinginvolving the family, neonatology, pulmonology, otolaryngology, nursing, respiratory therapy, and developmental specialists.
Key Considerations in Decision-Making:
Clinical trajectory:Is the infant progressing toward stability or experiencing recurrent decompensations despite maximal support?
Pulmonary phenotype:Infants with significant airway malacia or severe parenchymal disease may be more likely to benefit from a secure airway and chronic ventilatory support.
Potential benefits:Improved comfort and stability, facilitation of growth, decreased sedation needs, and enhanced neurodevelopment through increased interaction and mobility.
Risks and burdens:Tracheostomy carries risks of infection, accidental decannulation, and chronic airway complications. Families may also face high caregiver demands, frequent medical visits, and psychosocial stressors.
Because of these competing factors, the conversation about tracheostomy should begin early and evolve gradually, allowing families time to understand the rationale, ask questions, and meet other caregivers who have navigated similar decisions. Nurses play a vital role in this process by translating complex medical information into meaningful context, recognizing parental emotions, and advocating for alignment between family values and care goals.
Ultimately, the goal is not only to prolong survival but to enhance the child’s quality of life and developmental potential, ensuring that each decision reflects both the medical realities and the family’s hopes for their infant’s future .

Understanding where an infant falls within thecontinuum of BPD carehelps predict clinical needs, guide multidisciplinary interventions, and anticipate recovery trajectory.
Characteristics:
Severe respiratory lability and desaturations
Poor ventilator synchrony
Hemodynamic instability or bradycardia
Fluid overload/anasarca
High sedation requirements
Nursing Priorities:
Minimize stimulation and cluster care thoughtfully
Monitor for pulmonary hypertension and early “BPD spells”
Maintain strict fluid balance
Document tolerance to changes in ventilator settings
Provide consistent family support through critical periods
Characteristics:
Achieved cardiopulmonary stability
Stable ventilator and oxygen needs
Beginning to wean sedation
Tolerating enteral feeds
Nursing Priorities:
Gradually introduce developmental activities
Monitor for feeding intolerance
Engage therapy services early
Prepare for tracheostomy or gastrostomy discussions
Increase family participation in care
Characteristics:
Stable oxygenation and gradual ventilator weaning
Increasing activity tolerance
Demonstrated linear growth and appropriate weight gain
Often managed via tracheostomy (but not always)
Nursing Priorities:
Promote developmental milestones
Support family learning complex care (e.g. gastrostomy tube & tracheostomy)
Ensure consistent routines and developmental stimulation
Monitor growth trends and correlate with ventilator changes
Characteristics:
Adequate respiratory reserve and home readiness
Sustained interaction with environment
Improving neurodevelopment and tone
Transitioning to home ventilator or noninvasive support
Nursing Priorities:
Continue family teaching for home care
Facilitate discharge coordination with home services
Support family confidence and readiness
Maintain developmental therapies and community connection

Elshenawy et al, 2024
Physiologic values only tell part of the story. Aholisticapproach helps identify when support is sufficient or when it’s not.
Signs of Adequate Support:
Comfortable work of breathing at rest
Ability to engage in care and play
Consistent weight gain (>15 g/kg/day)
Calm demeanor without heavy sedation
Stable oxygen requirements
Signs of Inadequate Support:
Increased work of breathing with routine care
Poor feeding tolerance or oral aversion
Stalled growth or weight loss
Frequent desaturations or “BPD spells”
Escalating agitation or sedation needs
These episodes of acute desaturation may stem fromairway collapse, pulmonary hypertensive crisis, infection, or mucus plugging.
Nursing Actions:
Check airway patency– suction, assess ETT/trach position.
Optimize positioning– prone or side-lying often improves oxygenation.
Assess ventilator synchrony– adjust sedation or communicate with the team if dyssynchrony persists.
Apply phenotype-specific strategies:
Increase PEEP for airway malacia.
Provide supplemental oxygen for PH crises.
Use manual breaths or recruitment for atelectasis.
Infants with severe BPD may spendmonths on ventilation, but neurodevelopment continues in parallel.
Your role includes:
Coordinating care to preserve calm, awake periods.
Advocating for developmental positioning and kangaroo care.
Facilitating parent–infant bonding despite equipment.
Promoting positive oral experiences to prevent aversion.
Documenting progress in therapy and growth milestones.
As infants move through the phases of BPD, ventilatory needs shift. Nursing observation is essential to guide this progression:
Document tolerance to ventilator weaning attempts.
Note work of breathing with activities.
Correlate growth trends with ventilator adjustments.
Communicate observed patterns and triggers to the interdisciplinary team.
Caring for infants with severe BPD requires a deep understanding of disease heterogeneity, phenotype-driven care, and phase-based progression. Our goal is not simply to wean ventilator settings, it’s to support physiologic stability, growth, and neurodevelopment.
By recognizing phenotypes, anticipating triggers, and advocating for individualized support, NICU nurses play a vital role in helping these infants move from survival to thriving. Remember: in BPD,adequate and stable support that promotes growth is more valuable than rapid weaning.
Your skilled assessment, advocacy, and compassion make you the bridge between complex technology and the delicate process of healing. 🌿

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Amanda
© 2025 This content is for educational purposes and should complement, not replace, your unit's policies and procedures.
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References:
Elshenawy, S., Abman, S. H., & Keszler, M. (2024).Understanding the evolving phenotypes of bronchopulmonary dysplasia: Toward personalized respiratory management in preterm infants.Seminars in Perinatology, 48(4), 151872.https://doi.org/10.1016/j.semperi.2024.151872
O’Connor, M. J., Colletti, C., McGrath-Morrow, S. A., & Collaco, J. M. (2021).Phenotypes of bronchopulmonary dysplasia in children and their clinical relevance.Early Human Development, 163, 105482.https://doi.org/10.1016/j.earlhumdev.2021.105482
Özkan, H., Köksal, N., & Yalaz, M. (2022).Bronchopulmonary dysplasia: Where are we now?Turkish Archives of Pediatrics, 57(4), 385–390.https://doi.org/10.5152/TurkArchPediatr.2022.22249
McKinney, R. L., Napolitano, N., Levin, J. J., Kielt, M. J., Abman, S. H., Cuevas Guaman, M., Rose, R. S., Courtney, S. E., Matlock, D., Agarwal, A., Leeman, K. T., Sanlorenzo, L. A., Sindelar, R., Collaco, J. M., Baker, C. D., Hannan, K. E., Douglass, M., Eldredge, L. C., Lai, K., … Keszler, M. (2022).Ventilatory strategies in infants with established severe bronchopulmonary dysplasia: A multicenter point prevalence study.The Journal of Pediatrics, 242, 248–252.https://doi.org/10.1016/j.jpeds.2021.10.036
Gibbs, K., Jensen, E. A., Alexiou, S., Munson, D., & Zhang, H. (2019).Ventilation strategies in severe bronchopulmonary dysplasia.NeoReviews, 21(4), e226–e237.https://doi.org/10.1542/neo.21-4-e226
Lantos, J., Ferretti, E., & Abman, S. H. (2023).Tracheostomy in infants with severe bronchopulmonary dysplasia: Ethical and clinical considerations.Biomedicines, 11(9), 2572.https://doi.org/10.3390/biomedicines11092572
Gilfillan, M., & Bhandari, V. (2023). Pulmonary phenotypes of bronchopulmonary dysplasia in the preterm infant.Seminars in perinatology,47(6), 151810.https://doi.org/10.1016/j.semperi.2023.151810

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