Gait speed is used increasingly to predict function and future well-being among healthy elderly people as well as for those with long-term medical conditions. When selecting outcome measures such as walking speed, it is important to include the circumstances under which the measurement is made to avoid bias and ensure accurate recommendations. We completed a retrospective chart review of walking test results from patients with chronic lung disease to demonstrate the practical implications of reporting gait speed from either a standing or walking start. In this cohort of 99 patients (55 with COPD), gait speed from a standing start underestimated usual gait speed (difference = 6.1 m/min [5.3-6.9 m/min]) with poor agreement (8 m/min [6.6-9.4 m/min]) between the two methods of reporting speed. The standing start speed incorrectly identified some patients as at higher risk for poor health. In a practical example, gait speed from a standing start produced 11 false-negative evaluations of the ability to complete a road crossing at usual speed. We present walking speeds using both methods, which illustrate the importance of construct validity and measurement protocol.

Tobacco exposure results in various changes to the airways and lung parenchyma. Although emphysema represents the more common injury pattern, in some individuals, cigarette smoke injures alveolar epithelial cells and other lung cells, resulting in diffuse infiltrates and parenchymal fibrosis. Smoking can trigger interstitial injury patterns mediated via recruitment and inappropriate persistence of myeloid and other immune cells, including eosinophils. As our understanding of the role of cigarette smoke constituents in triggering lung injury continues to evolve, so does our recognition of the spectrum of smoking-related interstitial lung changes. Although respiratory bronchiolitis-interstitial lung disease, desquamative interstitial pneumonia, pulmonary Langerhans cell histiocytosis, and acute eosinophilic pneumonia have a well-established association with tobacco use, its role and impact on idiopathic pulmonary fibrosis, combined pulmonary fibrosis and emphysema, and connective tissue disease-related interstitial lung diseases is still ambiguous. Smoking-related interstitial fibrosis is a relatively newly appreciated entity with distinct histopathologic features but with unclear clinical ramifications. Increased implementation of lung cancer screening programs and utilization of CT scans in thoracic imaging have also resulted in increased identification of "incidental" or "subclinical" interstitial lung changes in smokers, the ensuing impact of which remains to be studied.

Previously, we and other investigators have described reversible loss of lung elastic recoil in patients with acute and persistent, moderate-to-severe, chronic, treated asthma who never smoked, and its adverse effect on maximal expiratory airflow. In four consecutive autopsies, we reported the pathophysiologic mechanism(s) has been unsuspected mild, diffuse, middle and upper lobe centrilobular emphysema.

Cough originates from stimulation of structures innervated by the vagus nerve, including the airways and distal esophagus. Arnold nerve reflex describes the induction of cough by stimulation of the external auditory canal, which is innervated by the auricular branch of the vagus. Historically, the prevalence of this reflex has been reported in the range of 2% to 3% on the basis of studies of outpatients in otolaryngology practices, but has not been investigated in healthy volunteers or in patients with chronic cough.

Cough is common in pulmonary TB and other chronic respiratory infections. Identifying features that predict whether pulmonary TB is the cause would help target appropriate individuals for rapid and cost-effective screening, potentially limiting disease progression and preventing transmission to others.

Alpha-1 antitrypsin deficiency (AATD) is characterized by low serum levels of or dysfunctional alpha-1 proteinase inhibitor. In the lung parenchyma, this results in a loss of protection against the activity of serine proteases, particularly neutrophil elastase. The resultant imbalance in protease and antiprotease activity leads to an increased risk for the development of early-onset emphysema and COPD. As in traditional smoke-related COPD, the assessment of the severity and disease progression of lung disease in AATD is conventionally based on lung function; however, pulmonary function tests are unable to discriminate between emphysema and airways disease, the two hallmark pathologic features of COPD. CT imaging has been used as a tool to further characterize lung structure and evaluate therapeutic interventions in AATD-related COPD. Moreover, recent advances in quantitative CT have significantly improved our assessment of the lung architecture, which has provided investigators and clinicians with a more detailed evaluation of the extent and severity of emphysema and airways disease in AATD. In addition, serial CT imaging measures are becoming increasingly important, as they provide a tool to monitor emphysema progression. This review describes the principles of CT technology and the role of CT imaging in assessing pulmonary disease progression in AATD, including the effect of therapeutic interventions.

We designed and conducted this multicenter randomized active-controlled open-label trial to evaluate the efficacy of acupuncture, auricular point pressing, and nicotine replacement therapy (NRT) on tobacco cessation in the Chinese population.

Relative risk (RR) and number needed-to-treat (NNT) are frequently time-dependant measures. We performed a systematic review and meta-analysis to assess whether trial duration influenced the relative and absolute risk of worsening in randomized controlled trials (RCTs) comparing combination therapy (CT) of pulmonary arterial hypertension (PAH)-specific therapies vs monotherapy (MT).

Lung-protective ventilation (LPV) has become the cornerstone of management in patients with ARDS. A subset of patients is unable to tolerate LPV without significant CO2 elevation. In these patients, permissive hypercapnia is used. Although thought to be benign, it is becoming increasingly evident that elevated CO2 levels have significant physiological effects. In this narrative review, we highlight clinically relevant end-organ effects in both animal models and clinical studies. We also explore the association between elevated CO2, acute cor pulmonale, and ICU mortality. We conclude with a brief review of alternative therapies for CO2 management currently under investigation in patients with moderate to severe ARDS.

Return of spontaneous circulation after cardiac arrest results in a systemic inflammatory state called the post-cardiac arrest syndrome, which is characterized by oxidative stress, coagulopathy, neuronal injury, and organ dysfunction. Perturbations in oxygenation and ventilation may exacerbate secondary injury after cardiac arrest and have been shown to be associated with poor outcome. Further, patients who experience cardiac arrest are at risk for a number of other pulmonary complications. Up to 70% of patients experience early infection after cardiac arrest, and the respiratory tract is the most common source. Vigilance for early-onset pneumonia, as well as aggressive diagnosis and early antimicrobial agent administration are important components of critical care in this population. Patients who experience cardiac arrest are at risk for the development of ARDS. Risk factors include aspiration, pulmonary contusions (from chest compressions), systemic inflammation, and reperfusion injury. Early evidence suggests that they may benefit from ventilation with low tidal volumes. Meticulous attention to mechanical ventilation, early assessment and optimization of respiratory gas exchange, and therapies targeted at potential pulmonary complications may improve outcomes after cardiac arrest.