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
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.