Abstract Introduction Premature neonates with bronchopulmonary dysplasia (BPD) often present with both structural and functional impairments in the lung parenchyma and central airways. Determining how much each component—airway or parenchymal disease—contributes to an individual’s respiratory symptoms remains challenging, limiting the precision of patient-specific therapeutic approaches. Ultra-short echo time (UTE) MRI combined with computational fluid dynamics (CFD) simulations enables assessment of regional resistive work of breathing (WOB), while simultaneous measurements of esophageal pressure and nasal flow during MRI provide total resistive and elastic WOB. Components of elevated WOB potentially correlate to distinct BPD phenotypes. Here, we quantify components of WOB and identify elevated components in a subject with BPD vs control. Methods High-resolution 3D UTE MR images were acquired from a healthy respiratory control (post-menstrual age= 42.6 weeks) and a subject with BPD (post-menstrual age= 38 weeks). The control breathed room air, while the BPD subject received oxygen via nasal cannula. During imaging, esophageal pressure (a surrogate for pleural pressure) and nasal flow were recorded. Four respiratory-gated images were retrospectively reconstructed to represent end-expiration, peak-inspiration, end-inspiration, and peak-expiration. Airway surfaces extending from nostrils to second-generation bronchi were segmented from the end-expiration image, and respiratory-gated images were registered to capture airway motion throughout the respiratory cycle. Patient-specific airway anatomy, motion, and airflow rates were used to perform a CFD simulation for each subject, yielding the resistive WOB component of upper airway, trachea, and proximal bronchi (Figure 1A). Esophageal pressure, nasal airflow, and tidal volume data were also used to construct Campbell diagrams and derive total resistive and elastic WOB values. Results WOB components (J/day) in control vs subject with BPD: upper airway resistance 23.8 vs 331.6; tracheal resistance 92.8 vs 471.8; proximal bronchi resistance 50.3 vs 23.0; distal resistance 89.1 vs 48.7; elastic 60.0 vs 1216.4 (Figure 1B). Total WOB was 6.6 times higher in the subject with BPD (2091.5 J/day) compared to the control (316.0 J/day). Conclusion Calculating the components of WOB highlights which multifactorial elements of BPD are causing respiratory impairment and allows for patient-specific treatment plans. This approach identified that reduced lung compliance and elevated central airway resistance, rather than bronchial constriction, drove elevated WOB in this BPD patient, directing potential treatment toward corticosteroids and/or surgical treatment of large airway obstruction, rather than bronchodilators. By identifying the dominant pathophysiologic contributors to respiratory impairment, this integrated MRI-CFD approach enables phenotype-driven, personalized treatment strategies in neonates with BPD. This abstract is funded by: National Institutes of Health R01 HL146689, R01 HL173164
Gunatilaka et al. (Fri,) studied this question.