The call for meaningful patient and family engagement in research has recently gained considerable momentum. This article defines patient and family engagement broadly and specifically in clinical research. Using a multicenter, North American weaning trial as an exemplar, we describe our early experiences as clinical researchers with patient and family engagement. The role of our Patient and Family Advisory Committee in trial design and implementation is illustrated. Through our experiences, we share our insights regarding the perceived opportunities and also highlight some challenges associated with engaging patients and family engagement in critical care research. Although "engagement science" is in its infancy, engaging patients and families in research holds promise as a novel research paradigm that will not only provide new insights into the questions, methods, and outcomes used in ICU research, but it will also make investments in research more accountable and ensure a strong "patient- and family-centered focus" of our research.

The reimbursement for procedures using moderate (conscious) sedation has changed significantly as of January 1, 2017. Due to the increasing use of anesthesia services to provide moderate sedation during endoscopy, the Centers for Medicare & Medicaid Services made the decision to remove work relative value units from many of the services requiring moderate sedation, including the bronchoscopy codes. If a bronchoscopist provides moderate sedation to a patient without using anesthesia services or another qualified provider, that work (and revenue) can be reclaimed by using the relevant codes. An understanding of the recent changes in coding and billing is essential for appropriate reimbursement.

We hypothesized that addressing anxiety and depressive mood disorders will improve chronic cough severity and cough quality of life (CQOL).

Accumulating evidence suggests that extracellular vesicles (EVs) play a role in the pathogenesis of lung diseases. These vesicles include exosomes, ectosomes (ie, microparticles, extracellular vesicles, microvesicles, and shedding vesicles), and apoptotic bodies. Exosomes are generated by inward budding of the membrane (endocytosis), subsequent forming of multivesicular bodies, and release by exocytosis. Ectosomes are formed by outward blebbing from the plasma membrane and are then released by proteolytic cleavage from the cell surface. Apoptotic bodies are generated on apoptotic cell shrinkage and death. Extracellular vesicles are released when the cells are activated or undergo apoptosis under inflammatory conditions. The number and types of released EVs are different according to the pathophysiological status of the disease. Therefore, EVs can be novel biomarkers for various lung diseases. EVs contain several molecules, including proteins, mRNA, microRNA, and DNA; they transfer these molecules to distant recipient cells. Circulating EVs modify the targeted cells and influence the microenvironment of the lungs. For this unique capability, EVs are expected to be a new drug delivery system and a novel therapeutic target.

High-frequency oscillatory ventilation (HFOV) is a unique mode of mechanical ventilation that uses nonconventional gas exchange mechanisms to deliver ventilation at very low tidal volumes and high frequencies. The properties of HFOV make it a potentially ideal mode to prevent ventilator-induced lung injury in patients with ARDS. Despite a compelling physiological basis and promising experimental data, large randomized controlled trials have not detected an improvement in survival with the use of HFOV, and its use as an early lung-protective strategy in patients with ARDS may be harmful. Nevertheless, HFOV still has an important potential role in the management of refractory hypoxemia. Careful attention should be paid to right ventricular function and lung stress when applying HFOV. This review discusses the physiological principles, clinical evidence, practical applications, and future prospects for the use of HFOV in patients with ARDS.

OSA results from the collapse of different pharyngeal structures (soft palate, tongue, lateral walls, and epiglottis). The structure involved in collapse has been shown to impact non-CPAP OSA treatment. Different inspiratory airflow shapes are also observed among patients with OSA. We hypothesized that inspiratory flow shape reflects the underlying pharyngeal structure involved in airway collapse.