Measuring the mechanical input impedance of the respiratory system with breath-driven flow oscillations.

In recent years, the mechanical input impedance of the respiratory system () determined using the technique known as oscillometry has been gaining traction as a clinical diagnostic tool to complement conventional spirometry. Nevertheless, despite currently approved oscillometry devices being relatively compact and portable, they are still too heavy and bulky to be used in an ambulatory hands-free setting, mostly because of the mass of the motor and power supply. We therefore explored the possibility of using the subject's own respiratory musculature as the power source for creating flow oscillations at the mouth.

Three Alveolar Phenotypes Govern Lung Function in Murine Ventilator-Induced Lung Injury.

Mechanical ventilation is an essential lifesaving therapy in acute respiratory distress syndrome (ARDS) that may cause ventilator-induced lung injury (VILI) through a positive feedback between altered alveolar mechanics, edema, surfactant inactivation, and injury. Although the biophysical forces that cause VILI are well documented, a knowledge gap remains in the quantitative link between altered parenchymal structure (namely alveolar derecruitment and flooding), pulmonary function, and VILI. This information is essential to developing diagnostic criteria and ventilation strategies to reduce VILI and improve ARDS survival.

Cisplatin Pharmacodynamics Following Endobronchial Ultrasound-Guided Transbronchial Needle Injection into Lung Tumors.

Intratumoral delivery of cisplatin by endobronchial ultrasound-guided transbronchial needle injection (EBUS-TBNI) has recently emerged as a therapy for treating peribronchial lung cancers. It remains unclear, however, where best to inject drug into a tumor, and at how many sites, so current cisplatin delivery strategies remain empirical. Motivated by the need to put EBUS-TBNI treatment of lung cancer on a more objective footing, we developed a computational model of cisplatin pharmacodynamics following EBUS-TBNI.

Linking lung function to structural damage of alveolar epithelium in ventilator-induced lung injury.

Understanding how the mechanisms of ventilator-induced lung injury (VILI), namely atelectrauma and volutrauma, contribute to the failure of the blood-gas barrier and subsequent intrusion of edematous fluid into the airspace is essential for the design of mechanical ventilation strategies that minimize VILI. We ventilated mice with different combinations of tidal volume and positive end-expiratory pressure (PEEP) and linked degradation in lung function measurements to injury of the alveolar epithelium observed via scanning electron microscopy. Ventilating with both high inspiratory plateau pressure and zero PEEP was necessary to cause derangements in lung function as well as visually apparent physical damage to the alveolar epithelium of initially healthy mice.

Alveolar leak develops by a rich-get-richer process in ventilator-induced lung injury.

Acute respiratory distress syndrome (ARDS) is a life-threatening condition for which there are currently no medical therapies other than supportive care involving the application of mechanical ventilation. However, mechanical ventilation itself can worsen ARDS by damaging the alveolocapillary barrier in the lungs. This allows plasma-derived fluid and proteins to leak into the airspaces of the lung where they interfere with the functioning of pulmonary surfactant, which increases the stresses of mechanical ventilation and worsens lung injury.

Linking Ventilator Injury-Induced Leak across the Blood-Gas Barrier to Derangements in Murine Lung Function.

Mechanical ventilation is vital to the management of acute respiratory distress syndrome, but it frequently leads to ventilator-induced lung injury (VILI). Understanding the pathophysiological processes involved in the development of VILI is an essential prerequisite for improving lung-protective ventilation strategies. The goal of this study was to relate the amount and nature of material accumulated in the airspaces to biomarkers of injury and the derecruitment behavior of the lung in VILI.