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Ventilation inhomogeneity in CDH infants – A new attitude within a simulation study

Stankiewicz Barbara, Mierzewska-Schmidt Magdalena, Górczyńska Krystyna, Pałko Krzysztof J., Baranowski Artur, Kozarski Maciej, Darowski Marek

Biocybernetics and Biomedical Engineering

2021

Vol. 41, no. 4

1378--1389

Congenital Diaphragmatic Hernia (CDH) is a serious newborn defect requiring mechanical ventilation. Initial ventilation settings should take into account the severity of lungs inhomogeneity (LI), but it is not assessed in everyday clinical practice. We present a new LI index that can be easily determined at the bedside. It is based on a comparison of resistive-elastic properties of lungs and defined as a ratio of time constants T1 T2_1 of gas flows in both lungs (T1 = R1∙C1, T2 = R2∙C2). We hypothesised that T1 T2_1 index increase causes a rise of lungs impedance (Z) and requires elevation of peak inspiratory pressure (PIP), mean airway pressure (MAP), and work of breathing (WOB). Infant hybrid (numerical-physical) respiratory simulator and a ventilator were used to simulate conventional ventilation of homogeneous and inhomogeneous lungs, and to measure PIP, MAP and WOB. A high correlation was found between Z, WOB, PIP, MAP and the T1T2_1 index (r = 0.9, P < 0.001). The increase of T1T2_1 index from 1 to 20 resulted in significant rise of WOB, PIP and MAP, e.g. at RR = 60 bpm, the WOB (1.05 → 1.49∙J_l), PIP (15.2 →20.5 cmH2O) and MAP (6.8 → 8.4 cmH2O), P < 0.005. It seems that T1T2_1 index could be used for prediction of PIP and MAP required to achieve effective ventilation in CDH infants; it also may affect the choice of ventilation strategy (CMV or HFV) as well as ventilator settings on CMV. We show how the relationships between WOB, PIP, MAP and the T1T2_1

Epithelial cell damage due to airway reopening – an experimental investigation

Kuraszkiewicz B.

Biocybernetics and Biomedical Engineering

2007

Vol. 27, no. 4

49-58

Airway collapse and reopening due to mechanical ventilation exerts mechanical stress on airway walls and injures surfactant - compromised lungs. The reopening of a collapsed airway was modeled experimentally by progression of a semi-infinite bubble in a narrow fluid-occluded channel. The extent of injury caused by bubble progression to pulmonary epithelial cells lining the channel was evaluated. Counter intuitively, cell damage increased with decreasing opening velocity. The presence of pulmonary surfactant, Infasurf, completely abated the injury. These results support the hypotheses that mechanical stresses associated with airway reopening injure pulmonary epithelial cells and that pulmonary surfactant protects the epithelium from this injury.