Deposition and Clinical Impact of Inhaled Particles in the Lung.

Particles suspended in the air we breathe are deposited in the airways as a function of the properties of the particle itself (shape, size and hydration), inspiratory air flow, airway anatomy, breathing environment, and mucociliary clearance. The scientific study of the deposition of inhaled particles in the airways has been conducted using traditional mathematical models and imaging techniques with particle markers. In recent years, the integration of statistical and computer methods, giving rise to a new discipline called digital microfluidics, has led to significant advances. In routine clinical practice, these studies are of great use for optimizing inhaler devices in line with particular characteristics of the drug to be inhaled and the pathology of the patient.

Usefulness of P0.1 in the Follow-Up of Individuals With Air Trapping and Home Noninvasive Ventilation and CPAP.

BACKGROUND: The ventilatory mechanics of patients with COPD and obesity-hypoventilation syndrome (OHS) are changed when there is air trapping and auto-PEEP, which increase respiratory effort. P0.1 measures the ventilatory drive and, indirectly, respiratory effort. The aim of the study was to measure P0.1 in subjects with COPD or OHS on treatment with positive pressure and to analyze their changes in P0.1 after treatment. METHODS: With a prospective design, subjects with COPD and OHS were studied in whom positive airway pressure was applied in their treatment. P0.1 was determined at study inclusion and after 6 months of treatment. RESULTS: A total of 88 subjects were analyzed: 56% were males, and the mean age of 65 ± 9 y old. Fifty-four (61%) had OHS, and 34 (39%) had COPD. Fifty (56%) had air trapping, with an initial P0.1 value of 3.0 ± 1.3 cm H2O compared with 2.1 ± 0.7 cm H2O for subjects who did not have air trapping (P = .001). After 6 months of treatment, subjects who had air trapping had similar P0.1 as those who did not: 2.3 ± 1.1 and 2.1 ± 1 cm H2O, respectively (P = .53). In subjects with COPD, initial P0.1 was 2.9 ± 1.4 cm H2O and at 6 months 2.2 ± 1.1 cm H2O (P = .02). In subjects with OHS, initial P0.1 was 2.4 ± 1.1 cm H2O and at 6 months 2.2 ± 1.0 cm H2O (P = .28). CONCLUSIONS: COPD and air trapping were associated with greater P0.1 as a marker of respiratory effort. A decrease in P0.1 indicates less respiratory effort after treatment.