Exhaled Breath Condensate (EBC) Collection and Analysis in Mechanically Ventilated ICU Patients: Monitoring of the Influence of Various Tidal Volumes on Lung Inflammatory Biomarkers

INTRODUCTION:

Airway inflammation plays a key role in many airway diseases. Non invasive methods to study these inflammatory processes and to monitor airway diseases are in high demand. Stimulating interest is in breath analysis, such as the analysis of exhaled breath condensate (EBC), a technique of sampling the epithelial lining fluid of the lung (ELF), as an even easier way to assess airway inflammation (1,2). The appeal of EBC lies in its ability to collect non-invasively a wide range of nonvolatile molecules from the respiratory tract, the fact that it can be repeated frequently within short intervals without adverse events and that collection devices can be used in a wide range of settings including intensive care units (3,4,5,6).

Analysis of EBC could not be limited to patient monitoring and understanding mechanisms of pulmonary disease. It also could become a useful tool for monitoring and screening for healthy individuals for possible early pulmonary tissue damage (6,7). There is a special need for more data on intra-subject and day-to-day variation, both essential for the decision as to whether a biomarker can serve as a research tool or even has the potential for disease monitoring in clinical practice (7).

It has been recognized for some time that mechanical ventilation may induce lung injury and inflammation (8,9,10). Recent experimental and clinical data suggest that in healthy lungs, mechanical ventilation with tidal volume ranging between 7 and 12 ml/kg in the absence of positive end-expiratory pressure may lead to endothelial, extracellular matrix and peripheral airways damage without major inflammatory response, which further worsen with higher tidal volumes (15,34). Several mechanisms may explain damage to the lung structure induced by mechanical ventilation: regional over distension, 'low lung volume' associated with tidal airway closure, and inactivation of surfactant (15).

High tidal volume ventilation has been shown to result in increased mortality while low tidal volume ventilation is regarded as a lung protective strategy in ALI, ARDS (11,12,13,35).