EIT based pulsatile impedance monitoring during spontaneous breathing in cystic fibrosis.

OBJECTIVE

Evaluating the lung function in patients with obstructive lung disease by electrical impedance tomography (EIT) usually requires breathing maneuvers containing deep inspirations and forced expirations. Since these maneuvers strongly depend on the patient's co-operation and health status, normal tidal breathing was investigated in an attempt to develop continuous maneuver-free measurements.

APPROACH

Ventilation related and pulsatile impedance changes were systematically analyzed during normal tidal breathing in 12 cystic fibrosis (CF) patients and 12 lung-healthy controls (HL). Tidal breaths were subdivided into three inspiratory (In1, In2, In3) and three expiratory (Ex1, Ex2, Ex3) sections of the same amplitude of global impedance change. Maximal changes of the ventilation and the pulsatile impedance signal occurring during these sections were determined (▵I and ▵I ). Differences in ▵I and ▵I among sections were ascertained in relation to the first inspiratory section. In addition, ▵I /▵I was calculated for each section.

MAIN RESULTS

Medians of changes in ▵I were  <0.05% in all sections for both subject groups. Both groups showed a similar pattern of ▵I changes during tidal breathing. Changes in ▵I first decreased during inspiration (In2), then increased towards the end of inspiration (In3) and reached a maximum at the beginning of expiration (Ex1). During the last two sections of expiration (Ex2, Ex3) ▵I changes decreased. The CF patients showed higher variations in ▵I changes compared to the controls (CF:  -426.5%, HL:  -158.1%, coefficient of variation). Furthermore, ▵I /▵I significantly differed between expiratory sections for the CF patients (Ex1-Ex2, p  <  0.01; Ex1-Ex3, p  <  0.001; Ex2-Ex3, p  <  0.05), but not for the controls. No significant differences in ▵I /▵I between inspiratory sections were determined for both groups.

SIGNIFICANCE

Differences in ▵I changes and in ▵I /▵I between both subject groups were speculated to be caused by higher breathing efforts of the CF patients due to airway obstruction leading to higher intrathoracic pressures, and thus to greater changes in lung perfusion.