Introduction. Preterm infants frequently require mechanical ventilation, which may have detrimental effects. One of the main forms of ventilator-induced lung injury (VILI) is pneumothorax (PTX), air leakage into the pleural cavity. Preterm infants are frequently ventilated with high frequency oscillatory ventilation (HFOV) to prevent VILI. Clinical detection of VILI is delayed due to lack of a method for continuous monitoring of lung ventilation. 

Hypothesis. Chest wall dynamics is a simple indicator of lung expansion and air distribution within the lungs during HFOV.

Objectives. This study explores the relationship between airway pressure and chest wall motion during HFOV, under physiological and pathophysiological conditions, defines a model that describes this relationship, and investigates whether asymmetric ventilation can be observed in chest wall motion dynamics.

Methods. 5 rabbits were ventilated with HFOV at various frequencies. Heart rate, blood pressure, pulse oximetry, endotracheal tube pressure and chest wall accelerations were continuously monitored. A tube was inserted into the right pleural space, to allow for controlled PTX development.

Results. Chest wall motion was asymmetrical under physiological conditions, with right chest wall accelerations greater than the left. Onset of PTX caused a significant drop in chest wall accelerations. Lack of correlation was observed between monitored hemodynamic parameters and measured chest wall motion. A linear relationship was observed between endotracheal tube pressure and chest wall accelerations, both at baseline and PTX. Most of the acceleration signals energy appeared in the imposed ventilation basic frequency. The last two observations suggest that non-linear elements played a minor role. Bode plots of the system transfer function reveal that the system switches from a second to a first order system within the tested frequency range.

Conclusions. The observed asymmetry in chest wall motion suggests high chest wall compliance in small animals and raises the possibility of monitoring asymmetric ventilation and pathologies. The feasibility of PTX detection by monitoring chest wall motion was established. The current difficulty in early clinical diagnosis of PTX by means of monitored hemodynamic parameters was confirmed. The linear transfer function between endotracheal tube pressure and chest wall accelerations and the low order of the system led to development of a simple analytical model that suggests that the behavior is dominated by the resistance to flow and the compliance of the lungs and chest wall. The model adequately describes the relationship between airway pressure and chest wall motion during HFOV and simulates the effects of PTX.