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Editorials

Chest. 2015;147(6):1447-1448. doi:10.1378/chest.14-3171

Club cells are nonciliated epithelial cells found mainly in bronchioles as well as basal cells found in large airways. They have been ascribed several protective roles, including airway repair after injury, secretion of antiinflammatory and immunomodulatory proteins, and detoxification.1 The study by Gamez et al2 in this issue of CHEST (see page 1467) reports a reduction in the number of club cells in bronchial biopsy specimens from patients with COPD compared with matched normal smokers, suggesting that these cells may normally have a protective role against the development of airway obstruction. Ablation of club cells in transgenic mice results in squamous metaplasia of the airways with impaired epithelial cell regeneration and peribronchiolar fibrosis reminiscent of the changes seen in COPD airways.3

Chest. 2015;147(6):1448-1450. doi:10.1378/chest.14-2745

Ventilator-associated pneumonia (VAP) is one of the most common infections in patients who are mechanically ventilated and is frequently due to infection by antibiotic-resistant bacteria. Mortality, hospital lengths of stay, and health-care costs are typically greater among patients with respiratory failure complicated by VAP compared with patients who do not develop VAP.1 Moreover, we know that the administration of inappropriate initial antibiotic therapy for VAP, usually due to the presence of multidrug-resistant bacteria as the causative pathogens, is associated with greater hospital mortality and longer hospital lengths of stay.2

Chest. 2015;147(6):1450-1452. doi:10.1378/chest.15-0077

Idiopathic pulmonary fibrosis (IPF) is the most common subtype of interstitial lung disease (ILD) and disproportionately affects older adults.1 The pathogenesis of IPF in some patients has been linked to shortening of chromosomal ends, or telomeres, which is regulated by both genetic and environmental factors.2,3 Since telomeres erode with each cycle of cell replication, this genomic timepiece provides a surrogate measure of molecular age and, thus, provides a biologic explanation for the increased incidence of IPF in older patients.

Point and Counterpoint

Chest. 2015;147(6):1453-1455. doi:10.1378/chest.15-0273

Approximately 20% of Americans spend time in an ICU around the time of their death, and most deaths follow a decision to limit life-sustaining therapies.1,2 Many factors contribute to treatment limitation decisions, including patient prognosis, expected benefits and burdens of available treatments, and patient preferences. Because many patients in the ICU lack decision-making capacity, a surrogate decision-maker often speaks on behalf of the patient and collaborates with the treating physician to determine treatment goals.

Chest. 2015;147(6):1455-1457. doi:10.1378/chest.15-0275

At first, it seems that physicians might have a responsibility to recommend goals of care for dying patients in the ICU. I suggest this is mistaken. Not only do physicians usually have no such responsibility to recommend goals, it is even a mistake if they do. Usually, the next of kin or other surrogate is the decision-maker in such cases, but regardless of whether it is a still-competent patient or a surrogate, many bad things can happen if physicians try to recommend treatment goals. If surrogates decide, they should pursue what the patient would have wanted, if known, and otherwise what is in the patient’s best interest.

Chest. 2015;147(6):1457-1458. doi:10.1378/chest.15-0274

In his Counterpoint editorial, Dr Veatch1 argues that physicians cannot presume to know what is best for patients, that recommendations can sway patients’ decisions about medical treatments, and, therefore, recommendations may result in decisions that are not in patients’ best interests. Not surprisingly, we share considerable ground on each of these points. I, too, acknowledge that there are challenges determining what is best for patients, and I recognize the risk of misleading surrogates with recommendations. However, when a patient lacks decisional capacity, has no advance directive, and is in the process of dying, clinical decisions require thoughtful integration of medical facts and patient values. The physician has access to the medical facts by virtue of his training, and he comes to know the patient’s values through discussion with a surrogate. The physician is the most appropriate person to integrate these factors into a recommended plan of care.

Chest. 2015;147(6):1458-1459. doi:10.1378/chest.15-0276

Dr Hutchison,1 supporting physician recommendations, cites ambiguous data implying French and Canadian surrogates prefer physician participation and > 40% of Americans prefer no recommendations. He claims physicians should make recommendations based on their beliefs about patients’ authentic values.

Commentary: Ahead of the Curve

Chest. 2015;147(6):1460-1466. doi:10.1378/chest.15-0278

Infectious disease epidemics in the past have given rise to psychologic and emotional responses among health-care workers (HCWs), stemming from fear of infection during patient care. Early experiences in the AIDS epidemic provide an example where fear of contagion resulted in differential treatment of patients infected with HIV. However, with a deeper understanding of AIDS pathogenesis and treatment, fear and discrimination diminished. Parallels exist between early experiences with AIDS and the present outbreak of Ebola virus disease in West Africa, particularly regarding discussions of medical futility in seriously ill patients. We provide a historical perspective on HCWs’ risk of infection during the provision of CPR, discuss physicians’ duty to treat in the face of perceived or actual HCW risk, and, finally, present the protocols implemented at the National Institutes of Health to reduce HCW risk while providing lifesaving and life-sustaining care.

Original Research: COPD

Chest. 2015;147(6):1467-1476. doi:10.1378/chest.14-1174

BACKGROUND:  Club cell secretory protein (CCSP) is a protective biomarker associated with annual decline in lung function. COPD progression results from an imbalance between injury and repair initially triggered by cigarette smoking.

OBJECTIVE:  We investigated the effect of CCSP as a therapeutic strategy to restore the balance between injury and repair in COPD simultaneously, validating an ex vivo air-liquid interface (ALI) culture of human bronchial epithelial cells.

METHODS:  Endobronchial biopsy specimens (EBBs) were obtained from 13 patients with COPD, eight smokers, and eight control subjects. Morphometric analysis of the initial EBBs was performed. ALI cultures derived from the same EBBs were exposed to cigarette smoke extract (CSE) with or without exogenous recombinant human CCSP (rhCCSP) supplementation. CCSP and IL-8 concentrations were assessed at steady state and after CSE exposure.

RESULTS:  Morphometric analysis of the initial EBBs showed increased cell density but decreased immunostaining of CCSP+ cells in EBBs of patients with COPD (P = .03 vs control subjects). At steady state, lower CCSP (P = .04) and higher IL-8 levels (P < .0001) were found in COPD ALI epithelium. Exogenous rhCCSP supplementation dampened CSE-induced IL-8-release in patients with COPD and returned to levels similar to those of smokers and control subjects (P = .0001). A negative correlation was found between IL-8-release in ALI and CCSP+ cell density in initial biopsy specimens (P = .0073).

CONCLUSIONS:  In vitro, rhCCSP exogenous supplementation can reverse CSE-induced IL-8 release in biopsy specimens from patients with COPD, indicating a potential use of this strategy in vivo.

Chest. 2015;147(6):1477-1484. doi:10.1378/chest.14-1368

BACKGROUND:  COPD is a leading cause of death and disability in the United States. Patients with COPD are at a high risk of nutritional deficiency, which is associated with declines in respiratory function, lean body mass and strength, and immune function. Although oral nutritional supplementation (ONS) has been associated with improvements in some of these domains, the impact of hospital ONS on readmission risk, length of stay (LOS), and cost among hospitalized patients is unknown.

METHODS:  Using the Premier Research Database, we first identified Medicare patients aged ≥ 65 years hospitalized with a primary diagnosis of COPD. We then identified hospitalizations in which ONS was provided, and used propensity-score matching to compare LOS, hospitalization cost, and 30-day readmission rates in a one-to-one matched sample of ONS and non-ONS hospitalizations. To further address selection bias among patients prescribed ONS, we also used instrumental variables analysis to study the association of ONS with study outcomes. Model covariates included patient and provider characteristics and a time trend.

RESULTS:  Out of 10,322 ONS hospitalizations and 368,097 non-ONS hospitalizations, a one-to-one matched sample was created (N = 14,326). In unadjusted comparisons in the matched sample, ONS use was associated with longer LOS (8.7 days vs 6.9 days, P < .0001), higher hospitalization cost ($14,223 vs $9,340, P < .0001), and lower readmission rates (24.8% vs 26.6%, P = .0116). However, in instrumental variables analysis, ONS use was associated with a 1.9-day (21.5%) decrease in LOS, from 8.8 to 6.9 days (P < .01); a hospitalization cost reduction of $1,570 (12.5%), from $12,523 to $10,953 (P < .01); and a 13.1% decrease in probability of 30-day readmission, from 0.34 to 0.29 (P < .01).

CONCLUSIONS:  ONS may be associated with reduced LOS, hospitalization cost, and readmission risk in hospitalized Medicare patients with COPD.

Chest. 2015;147(6):1485-1493. doi:10.1378/chest.14-1693

BACKGROUND:  Quantitative analysis of high-resolution chest CT scan (QCT) is an established method for determining the severity and distribution of lung parenchymal destruction in patients with emphysema. Diffusing capacity of the lung for carbon monoxide (Dlco) is a traditional physiologic measure of emphysema severity and is probably influenced more by destruction of the alveolar capillary bed than by membrane diffusion per se. We reasoned that Dlco should correlate with tissue volume from QCT.

METHODS:  A total of 460 patients with upper-lobe-predominant emphysema were enrolled in the study. The mean (SD) of percent predicted values for FEV1, total lung capacity, and Dlco were 30.6% (8.0%), 129.5% (18.1%), and 6.7% (13.1%), respectively. QCT was performed using custom software; the relationship between Dlco and various metrics from QCT were evaluated using Pearson correlation coefficients.

RESULTS:  On average, whole-body plethysmography volumes were higher by 841 mL compared with QCT-calculated total lung volume. However, there was a strong correlation between these measurements (r = 0.824, P < .0001). Dlco correlated with total lung volume (r = 0.314, P < .0001), total tissue volume (r = 0.498, P < .0001), and percentage of lung with low density (−950 Hounsfield units) (r = −0.337, P < .0001).

CONCLUSIONS:  In patients with severe emphysema, Dlco correlates best with total tissue volume, supporting the hypothesis that pulmonary capillary blood volume is the main determinant of Dlco in the human lung. The relationships between Dlco and various anatomic metrics of lung parenchymal destruction from QCT inform our understanding of the relationship between structure and function of the human lung.

Original Research: Critical Care

Chest. 2015;147(6):1494-1502. doi:10.1378/chest.14-1687

BACKGROUND:  Ventilator-associated pneumonia (VAP) remains a common complication in critically ill surgical patients, and its diagnosis remains problematic. Exhaled breath contains aerosolized droplets that reflect the lung microbiota. We hypothesized that exhaled breath condensate fluid (EBCF) in hygroscopic condenser humidifier/heat and moisture exchanger (HCH/HME) filters would contain bacterial DNA that qualitatively and quantitatively correlate with pathogens isolated from quantitative BAL samples obtained for clinical suspicion of pneumonia.

METHODS:  Forty-eight adult patients who were mechanically ventilated and undergoing quantitative BAL (n = 51) for suspected pneumonia in the surgical ICU were enrolled. Per protocol, patients fulfilling VAP clinical criteria undergo quantitative BAL bacterial culture. Immediately prior to BAL, time-matched HCH/HME filters were collected for study of EBCF by real-time polymerase chain reaction. Additionally, convenience samples of serially collected filters in patients with BAL-diagnosed VAP were analyzed.

RESULTS:  Forty-nine of 51 time-matched EBCF/BAL fluid samples were fully concordant (concordance > 95% by κ statistic) relative to identified pathogens and strongly correlated with clinical cultures. Regression analysis of quantitative bacterial DNA in paired samples revealed a statistically significant positive correlation (r = 0.85). In a convenience sample, qualitative and quantitative polymerase chain reaction analysis of serial HCH/HME samples for bacterial DNA demonstrated an increase in load that preceded the suspicion of pneumonia.

CONCLUSIONS:  Bacterial DNA within EBCF demonstrates a high correlation with BAL fluid and clinical cultures. Bacterial DNA within EBCF increases prior to the suspicion of pneumonia. Further study of this novel approach may allow development of a noninvasive tool for the early diagnosis of VAP.

Chest. 2015;147(6):1503-1509. doi:10.1378/chest.14-2599

BACKGROUND:  Adaptive support ventilation (ASV) is a closed loop mode of mechanical ventilation (MV) that provides a target minute ventilation by automatically adapting inspiratory pressure and respiratory rate with the minimum work of breathing on the part of the patient. The aim of this study was to determine the effect of ASV on total MV duration when compared with pressure assist/control ventilation.

METHODS:  Adult medical patients intubated and mechanically ventilated for > 24 h in a medical ICU were randomized to either ASV or pressure assist/control ventilation. Sedation and medical treatment were standardized for each group. Primary outcome was the total MV duration. Secondary outcomes were the weaning duration, number of manual settings of the ventilator, and weaning success rates.

RESULTS:  Two hundred twenty-nine patients were included. Median MV duration until weaning, weaning duration, and total MV duration were significantly shorter in the ASV group (67 [43-94] h vs 92 [61-165] h, P = .003; 2 [2-2] h vs 2 [2-80] h, P = .001; and 4 [2-6] days vs 4 [3-9] days, P = .016, respectively). Patients in the ASV group required fewer total number of manual settings on the ventilator to reach the desired pH and Paco2 levels (2 [1-2] vs 3 [2-5], P < .001). The number of patients extubated successfully on the first attempt was significantly higher in the ASV group (P = .001). Weaning success and mortality at day 28 were comparable between the two groups.

CONCLUSIONS:  In medical patients in the ICU, ASV may shorten the duration of weaning and total MV duration with a fewer number of manual ventilator settings.

TRIAL REGISTRY:  ClinicalTrials.gov; No.: NCT01472302; URL: www.clinicaltrials.gov

Chest. 2015;147(6):1510-1522. doi:10.1378/chest.14-3161

OBJECTIVE:  This study aimed to determine whether inhaled prostaglandins are associated with improvement in pulmonary physiology or mortality in patients with ARDS and assess adverse effects.

METHODS:  The following data sources were used: PubMed, EMBASE, CINAHL, Cochrane Central Register of Controlled Trials, Cochrane Database of Systematic Reviews, reference lists, conference proceedings, and ClinicalTrials.gov. Studies selected included randomized controlled trials and nonrandomized studies. For data extraction, two reviewers independently screened titles and abstracts for eligibility. With regard to data synthesis, 25 studies (two RCTs) published over 21 years (1993-2014) were included. The PROSPERO registration number was CRD42014013180.

RESULTS:  One randomized controlled trial showed no difference in the change in mean Pao2 to Fio2 ratio when comparing inhaled alprostadil to placebo: 141.2 (95% CI, 120.8-161.5) to 161.5 (95% CI, 134.6-188.3) vs 163.4 (95% CI, 140.8-186.0) to 186.8 (95% CI, 162.9-210.7), P = .21. Meta-analysis of the remaining studies demonstrated that inhaled prostaglandins were associated with improvement in Pao2 to Fio2 ratio (16 studies; 39.0% higher; 95% CI, 26.7%-51.3%), and Pao2 (eight studies; 21.4% higher; 95% CI, 12.2%-30.6%), and a decrease in pulmonary artery pressure (−4.8 mm Hg; 95% CI, −6.8 mm Hg to −2.8 mm Hg). Risk of bias and heterogeneity were high. Meta-regression found no association with publication year (P = .862), baseline oxygenation (P = .106), and ARDS etiology (P = .816) with the treatment effect. Hypotension occurred in 17.4% of patients in observational studies.

CONCLUSIONS:  In ARDS, inhaled prostaglandins improve oxygenation and decrease pulmonary artery pressures and may be associated with harm. Data are limited both in terms of methodologic quality and demonstration of clinical benefit. The use of inhaled prostaglandins in ARDS needs further study.

Chest. 2015;147(6):1523-1529. doi:10.1378/chest.14-0663

OBJECTIVE:  The objective of this study was to develop a mechanism of discovering misdirection into the airway of naso/orogastric (NG) tubes before they reach their full depth of placement in adults.

METHODS:  A prospective, observational study was performed in humans, evaluating both the self-inflating bulb syringe (SIBS) and a colorimetric CO2 detector. A prospective convenience sample of 257 NG tube placements was studied in 199 patients in medical ICUs of a tertiary care medical center. Findings were compared to a “standard” (ie, end tidal CO2 results of a capnograph and the results of a chest radiograph performed at the completion of the tube placement).

RESULTS:  On the first tube placement attempt in any patient, the SIBS had a sensitivity of 91.5% and a specificity of 87.0% in detecting nonesophageal placement, while the colorimetric device exhibited 99.4% sensitivity and 91.3% specificity. On subsequent insertions, the SIBS showed 95.7% sensitivity and 100% specificity, while the colorimetric device exhibited 97.8% sensitivity and 100% specificity. The colorimetric device was eight times more expensive than the SIBS.

CONCLUSIONS:  The SIBS and the colorimetric CO2 detector are very good at detecting NG tube malpositioning into the airway, although the colorimetric device is slightly more sensitive and specific. Neither method adds substantial time or difficulty to the insertion process. The colorimetric device is substantially more expensive. The decision as to which method to use may be based on local institutional factors, such as expense.

Chest. 2015;147(6):1530-1538. doi:10.1378/chest.14-2005

BACKGROUND:  COPD seems related to poor outcome in patients with ventilator-associated pneumonia (VAP). However, many patients in the ICU with COPD do not require intubation but can also develop pneumonia in the ICU. We, therefore, compared the characteristics and outcomes of patients with ICU-acquired pneumonia (ICUAP) with and without underlying COPD.

METHODS:  We prospectively assessed the characteristics, microbiology, systemic inflammatory response, and survival of 279 consecutive patients with ICUAP clustered according to underlying COPD or not. The primary end point was 90-day survival.

RESULTS:  Seventy-one patients (25%) had COPD. The proportion of VAP was less frequent in patients with COPD: 30 (42%) compared with 126 (61%) in patients without COPD (P = .011). Patients with COPD were older; were more frequently men, smokers, and alcohol abusers; and more frequently had previous use of noninvasive ventilation. The rate of microbiologic diagnosis was similar between groups, with a higher rate of Aspergillus species and a lower rate of Enterobacteriaceae in patients with COPD. We found lower levels of IL-6 and IL-8 in patients with COPD without previous intubation. The 90-day mortality was higher in patients with COPD (40 [57%] vs 74 [37%] in patients without COPD, P = .003). Among others, COPD was independently associated with decreased 90-day survival in the overall population (adjusted hazard ratio, 1.94; 95% CI, 1.11-3.40; P = .020); this association was observed only in patients with VAP but not in those without previous intubation.

CONCLUSIONS:  COPD was independently associated with decreased 90-day survival in patients with VAP but not in those without previous intubation.

Chest. 2015;147(6):1539-1548. doi:10.1378/chest.14-2454

BACKGROUND:  ARDS is a heterogeneous syndrome that encompasses lung injury from both direct and indirect sources. Direct ARDS (pneumonia, aspiration) has been hypothesized to cause more severe lung epithelial injury than indirect ARDS (eg, nonpulmonary sepsis); however, this hypothesis has not been well studied in humans.

METHODS:  We measured plasma biomarkers of lung epithelial and endothelial injury and inflammation in a single-center study of 100 patients with ARDS and severe sepsis and in a secondary analysis of 853 patients with ARDS drawn from a multicenter randomized controlled trial. Biomarker levels in patients with direct vs indirect ARDS were compared in both cohorts.

RESULTS:  In both studies, patients with direct ARDS had significantly higher levels of a biomarker of lung epithelial injury (surfactant protein D) and significantly lower levels of a biomarker of endothelial injury (angiopoietin-2) than those with indirect ARDS. These associations were robust to adjustment for severity of illness and ARDS severity. In the multicenter study, patients with direct ARDS also had lower levels of von Willebrand factor antigen and IL-6 and IL-8, markers of endothelial injury and inflammation, respectively. The prognostic value of the biomarkers was similar in direct and indirect ARDS.

CONCLUSIONS:  Direct lung injury in humans is characterized by a molecular phenotype consistent with more severe lung epithelial injury and less severe endothelial injury. The opposite pattern was identified in indirect lung injury. Clinical trials of novel therapies targeted specifically at the lung epithelium or endothelium may benefit from preferentially enrolling patients with direct and indirect ARDS, respectively.

Original Research: Transplantation

Chest. 2015;147(6):1549-1557. doi:10.1378/chest.14-0631

BACKGROUND:  Human telomere disease consists of a wide spectrum of disorders, including pulmonary, hepatic, and bone marrow abnormalities. The extent of bone marrow and liver abnormalities in patients with interstitial lung disease (ILD) and short telomeres is unknown.

METHODS:  The lung transplant clinic established a prospective protocol to identify short telomeres in patients with ILD not related to connective tissue disease or sarcoidosis. Patients with short telomeres underwent bone marrow biopsies, liver biopsies, or both as part of the evaluation for transplant candidacy.

RESULTS:  One hundred twenty-seven patients met ILD categorization for inclusion. Thirty were suspected to have short telomeres, and 15 had the diagnosis confirmed. Eight of 13 (53%) patients had bone marrow abnormalities. Four patients had hypocellular marrow associated with macrocytosis and relatively normal blood counts, which resulted in changes to planned immunosuppression at the time of transplant. Four patients with more severe hematologic abnormalities were not listed because of myelodysplastic syndrome (two); monoclonal gammopathy of unclear significance (one); and hypocellular marrow, decreased megakaryocyte lineage associated with thrombocytopenia (one). Seven patients underwent liver biopsies, and six had abnormal liver pathology. These abnormalities did not affect listing for lung transplant, and liver biopsies are no longer routinely obtained.

CONCLUSIONS:  Subclinical bone marrow and liver abnormalities can be seen in patients with ILD and short telomeres, in some cases in the absence of clinically significant abnormalities in peripheral blood counts and liver function tests. A larger study examining the implication of these findings on the outcome of patients with ILD and short telomeres is needed.

Chest. 2015;147(6):1558-1565. doi:10.1378/chest.14-1543

BACKGROUND:  Hypersensitivity pneumonitis (HP) is an inhaled antigen-mediated interstitial lung disease (ILD). Advanced disease may necessitate the need for lung transplantation. There are no published studies addressing lung transplant outcomes in HP. We characterized HP outcomes compared with referents undergoing lung transplantation for idiopathic pulmonary fibrosis (IPF).

METHODS:  To identify HP cases, we reviewed records for all ILD lung transplantation cases at our institution from 2000 to 2013. We compared clinical characteristics, survival, and acute and chronic rejection for lung transplant recipients with HP to referents with IPF. We also reviewed diagnoses of HP discovered only by explant pathology and looked for evidence of recurrent HP after transplant. Survival was compared using Kaplan-Meier methods and Cox proportional hazard modeling.

RESULTS:  We analyzed 31 subjects with HP and 91 with IPF among 183 cases undergoing lung transplantation for ILD. Survival at 1, 3, and 5 years after lung transplant in HP compared with IPF was 96%, 89%, and 89% vs 86%, 67%, and 49%, respectively. Subjects with HP manifested a reduced adjusted risk for death compared with subjects with IPF (hazard ratio, 0.25; 95% CI, 0.08-0.74; P = .013). Of the 31 cases, the diagnosis of HP was unexpectedly made at explant in five (16%). Two subjects developed recurrent HP in their allografts.

CONCLUSIONS:  Overall, subjects with HP have excellent medium-term survival after lung transplantation and, relative to IPF, a reduced risk for death. HP may be initially discovered only by review of the explant pathology. Notably, HP may recur in the allograft.

Original Research: Sleep Disorders

Chest. 2015;147(6):1566-1573. doi:10.1378/chest.14-2114

BACKGROUND:  Increased CO2 chemosensitivity and augmented exercise ventilation are characteristic of patients with heart failure (HF) with central sleep apnea (CSA). The aim of this study was to test the hypothesis that decreased end-tidal CO2 by cardiopulmonary exercise testing predicts CSA in patients with HF.

METHODS:  Consecutive ambulatory patients with New York Heart Association II to III HF were prospectively evaluated by CO2 chemosensitivity by rebreathe, cardiopulmonary exercise testing, and polysomnography (PSG). Subjects were classified as having either CSA (n = 20) or no sleep apnea (n = 13) by PSG; a central apnea-hypopnea index (AHI) ≥ 5 was used to define CSA. Subgroups were compared by t test or Mann-Whitney test and data summarized as mean ± SD. P < .05 was considered significant.

RESULTS:  At rest, subjects with CSA had higher central CO2 chemosensitivity (Δminute ventilation [V. e]/Δpartial pressure of end-tidal CO2 [Petco2], 2.3 ± 1.0 L/min/mm Hg vs 1.6 ± 0.4 L/min/mm Hg, P = .02) and V. e (15 ± 7 L/min vs 10 ± 3 L/min, P = .02) and lower Petco2 (31 ± 4 mm Hg vs 35 ± 4 mm Hg, P < .01) than control subjects. At peak exercise, the ventilatory equivalents per expired CO2 (V. e/V. co2) was higher (43 ± 9 vs 33 ± 6, P < .01) and Petco2 lower (29 ± 6 mm Hg vs 36 ± 5 mm Hg, P < .01) in subjects with CSA. In addition, CO2 chemosensitivity, peak exercise V. e/V. co2, and Petco2 were independently correlated with CSA severity as quantified by the AHI (P < .05). Peak exercise Petco2 was most strongly associated with CSA (OR, 1.29; 95% CI, 1.08-1.54; P = .01; area under the curve, 0.88).

CONCLUSIONS:  In patients with HF and CSA, ventilatory drive is increased while awake at rest and during exercise and associated with heightened CO2 chemosensitivity and decreased arterial CO2 set point.

Chest. 2015;147(6):1574-1581. doi:10.1378/chest.14-1498

BACKGROUND:  Mechanisms of decreased exercise capacity in patients with hypertrophic cardiomyopathy (HCM) are not well understood. Sleep-disordered breathing (SDB) is a highly prevalent but treatable disorder in patients with HCM. The role of comorbid SDB in the attenuated exercise capacity in HCM has not been studied previously.

METHODS:  Overnight oximetry, cardiopulmonary exercise testing, and echocardiographic studies were performed in consecutive patients with HCM seen at the Mayo Clinic. SDB was considered present if the oxygen desaturation index (number of ≥ 4% desaturations/h) was ≥ 10. Peak oxygen consumption (V. o2peak) (the most reproducible and prognostic measure of cardiovascular fitness) was then correlated with the presence and severity of SDB.

RESULTS:  A total of 198 patients with HCM were studied (age, 53 ± 16 years; 122 men), of whom 32% met the criteria for the SDB diagnosis. Patients with SDB had decreased V. o2peak compared with those without SDB (16 mL O2/kg/min vs 21 mL O2/kg/min, P < .001). SDB remained significantly associated with V. o2peak after accounting for confounding clinical variables (P < .001) including age, sex, BMI, atrial fibrillation, and coronary artery disease.

CONCLUSIONS:  In patients with HCM, the presence of SDB is associated with decreased V. o2peak. SDB may represent an important and potentially modifiable contributor to impaired exercise tolerance in this unique population.

Original Research: Asthma

Chest. 2015;147(6):1582-1590. doi:10.1378/chest.14-3105

BACKGROUND:  The growing epidemics of obesity and asthma are major public health concerns. Although asthma-obesity links are widely studied, the effects of weight loss on asthma severity measured by airway hyperresponsiveness (AHR) have received limited attention. The main study objective was to examine whether weight reduction reduces asthma severity in obese adults with asthma.

METHODS:  In a prospective, controlled, parallel-group study, we followed 22 obese participants with asthma aged 18 to 75 years with a BMI ≥ 32.5 kg/m2 and AHR (provocative concentration of methacholine causing a 20% fall in FEV1 [PC20] < 16 mg/mL). Sixteen participants followed a behavioral weight reduction program for 3 months, and six served as control subjects. The primary outcome was change in AHR over 3 months. Changes in lung function, asthma control, and quality of life were secondary outcomes.

RESULTS:  At study entry, participant mean ± SD age was 44 ± 9 years, 95% were women, and mean BMI was 45.7 ± 9.2 kg/m2. After 3 months, mean weight loss was 16.5 ± 9.9 kg in the intervention group, and the control group had a mean weight gain of 0.6 ± 2.6 kg. There were significant improvements in PC20 (P = .009), FEV1 (P = .009), FVC (P = .010), asthma control (P < .001), and asthma quality of life (P = .003) in the intervention group, but these parameters remained unchanged in the control group. Physical activity levels also increased significantly in the intervention group but not in the control group.

CONCLUSIONS:  Weight loss in obese adults with asthma can improve asthma severity, AHR, asthma control, lung function, and quality of life. These findings support the need to actively pursue healthy weight-loss measures in this population.

Chest. 2015;147(6):1591-1598. doi:10.1378/chest.14-2689

BACKGROUND:  Obesity is associated with poor asthma control, increased asthma morbidity, and decreased response to inhaled corticosteroids. We hypothesized that obesity would be associated with decreased bronchodilator responsiveness in children and adolescents with asthma. In addition, we hypothesized that subjects who were obese and unresponsive to bronchodilator would have worse asthma control and would require more asthma controller medications.

METHODS:  In the Study of African Americans, Asthma, Genes, and Environments (SAGE II) and the Genes-environments and Admixture in Latino Americans (GALA II) study, two identical, parallel, case-control studies of asthma, we examined the association between obesity and bronchodilator response in 2,963 black and Latino subjects enrolled from 2008 to 2013 using multivariable logistic regression. Using bronchodilator responsiveness, we compared asthma symptoms, controller medication usage, and asthma exacerbations between nonobese (< 95th% BMI) and obese (≥ 95th% BMI) subjects.

RESULTS:  The odds of being bronchodilator unresponsive were 24% (OR, 1.24; 95% CI, 1.03-1.49) higher among obese children and adolescents compared with their not obese counterparts after adjustment for age, race/ethnicity, sex, recruitment site, baseline lung function (FEV1/FVC), and controller medication. Bronchodilator-unresponsive obese subjects were more likely to report wheezing (OR, 1.38; 95% CI, 1.13-1.70), being awakened at night (OR, 1.34; 95% CI, 1.09-1.65), using leukotriene receptor inhibitors (OR, 1.33; 95% CI, 1.05-1.70), and using inhaled corticosteroid with long-acting β2-agonist (OR, 1.37; 95% CI, 1.05-1.78) than were their nonobese counterpart. These associations were not seen in the bronchodilator-responsive group.

CONCLUSIONS:  Obesity is associated with bronchodilator unresponsiveness among black and Latino children and adolescents with asthma. The findings on obesity and bronchodilator unresponsiveness represent a unique opportunity to identify factors affecting asthma control in blacks and Latinos.

Chest. 2015;147(6):1599-1609. doi:10.1378/chest.14-0258

BACKGROUND:  Secretory phospholipases A2 (sPLA2) initiate the biosynthesis of eicosanoids, are increased in the airways of people with severe asthma, and induce mucin hypersecretion. We used IL-13-transformed, highly enriched goblet cells and differentiated (ciliary cell-enriched) human bronchial epithelial cell culture to evaluate the relative contribution of ciliated and goblet cells to airway sPLA2 generation and response. We wished to determine the primary source(s) of sPLA2 and leukotrienes in human airway epithelial cells.

METHODS:  Human bronchial epithelial cells from subjects without lung disease were differentiated to a ciliated-enriched or goblet-enriched cell phenotype. Synthesis of sPLA2, cysteinyl leukotrienes (cysLTs), and airway mucin messenger RNA and protein was measured by real-time-polymerase chain reaction and an enzyme-linked immunosorbent assay, and the localization of mucin and sPLA2 to specific cells types was confirmed by confocal microscopy.

RESULTS:  sPLA2 group IIa, V, and X messenger RNA expression was increased in ciliated-enriched cells (P < .001) but not in goblet-enriched cells. sPLA2 were secreted from the apical (air) side of ciliated-enriched cells but not goblet-enriched cells (P < .001). Immunostaining of sPLA2 V was strongly positive in ciliated-enriched cells but not in goblet-enriched cells. sPLA2 released cysLTs from goblet-enriched cells but not from ciliated-enriched cells, and this result was greatest with sPLA2 V (P < .05). sPLA2 V increased goblet-enriched cell mucin secretion, which was inhibited by inhibitors of lipoxygenase or cyclooxygenase (P < .02).

CONCLUSIONS:  sPLA2 are secreted from ciliated cells and appear to induce mucin and cysLT secretion from goblet cells, strongly suggesting that airway goblet cells are proinflammatory effector cells.

Original Research: Pulmonary Vascular Disease

Chest. 2015;147(6):1610-1620. doi:10.1378/chest.14-1678

BACKGROUND:  Inflammation may contribute to the pathobiology of pulmonary arterial hypertension (PAH). Deciphering the PAH fingerprint on the inflammation orchestrated by dendritic cells (DCs) and T cells, key driver and effector cells, respectively, of the immune system, may allow the identification of immunopathologic approaches to PAH management.

METHODS:  Using flow cytometry, we performed immunophenotyping of monocyte-derived DCs (MoDCs) and circulating lymphocytes from patients with idiopathic PAH and control subjects. With the same technique, we performed cytokine profiling of both populations following stimulation, coculture, or both. We tested the immunomodulatory effects of a glucocorticoid (dexamethasone [Dex]) on this immunophenotype and cytokine profile. Using an epigenetic approach, we confirmed the immune polarization in blood DNA of patients with PAH.

RESULTS:  The profile of membrane costimulatory molecules of PAH MoDCs was similar to that of control subjects. However, PAH MoDCs retained higher levels of the T-cell activating molecules CD86 and CD40 after Dex pretreatment than did control MoDCs. This was associated with an increased expression of IL-12p40 and a reduced migration toward chemokine (C-C motif) ligand 21. Moreover, both with and without Dex, PAH MoDCs induced a higher activation and proliferation of CD4+ T cells, associated with a reduced expression of IL-4 (T helper 2 response) and a higher expression of IL-17 (T helper 17 response). Purified PAH CD4+ T cells expressed a higher level of IL-17 after activation than did those of control subjects. Lastly, there was significant hypomethylation of the IL-17 promoter in the PAH blood DNA as compared with the control blood.

CONCLUSIONS:  We have highlighted T helper 17 cell immune polarization in patients with PAH, as has been previously demonstrated in other chronic inflammatory and autoimmune conditions.

Original Research: Pulmonary Procedures

Chest. 2015;147(6):1621-1628. doi:10.1378/chest.14-1704

BACKGROUND:  Bronchoscopy in patients with space-occupying brain lesions is anecdotally felt to carry a high risk of neurologic complications.

METHODS:  We conducted a retrospective cohort study of patients with evidence of a malignant, space-occupying brain lesion who were referred for flexible or rigid bronchoscopy or endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA). The primary outcome of interest was the incidence of neurologic complications following the procedures in these patients.

RESULTS:  Of the 103 enrolled patients, flexible bronchoscopy was performed in 41, rigid bronchoscopy in 12, and EBUS-TBNA in 50. Among these patients, 41 (40%) had evidence suggestive of increased intracranial pressure on imaging. Among all study patients, none (95% CI, 0-0.035) had neurologic, procedure-specific, or sedation-specific complications, and the level of care was not escalated in any of these patients.

CONCLUSIONS:  On the basis of our findings, we recommend that procedures such as flexible or rigid bronchoscopy or EBUS-TBNA in patients with malignant space-occupying brain lesions should be considered reasonably safe as long as neurologic findings are stable.

Chest. 2015;147(6):1629-1634. doi:10.1378/chest.14-1701

BACKGROUND:  The clinical course of patients with malignant pleural effusions (MPEs) varies. The decision to undertake “definitive therapy” (pleurodesis, indwelling pleural catheter [IPC], or both) for MPEs is decided on a case-by-case basis. Identifying factors that predict definitive therapy may help guide early initiation of treatment. The aim of the study was to identify clinical, laboratory, and radiologic predictors associated with clinicians’ prescription of definitive therapy for patients with MPE.

METHODS:  A multicenter, observational study was conducted over 55 months involving tertiary centers in Perth, Western Australia, Australia, and Lleida, Spain. Demographic, clinical, radiologic, biochemical, and histologic data and the treatments received were recorded. Logistic regression was performed to determine the variables useful for predicting definitive therapy.

RESULTS:  Data of 540 patients (365 from Perth and 184 from Lleida) were analyzed; 537 fulfilled the criteria of an MPE. Definitive therapy was used in 288 patients (53.6%): 199 received a pleurodesis and 89 an IPC. Univariate analysis of the combined cohort revealed that definitive therapy was more likely if the effusion has low pH, either as a continuous variable (OR, 30.30; P < .01) or with a pH cutoff of < 7.2 (OR, 2.09; P = .03); was large (> 50% of hemithorax) (OR, 2.75; P < .01); or was associated with mesothelioma (OR, 1.83; P < .01). Following multivariate analysis, low pleural pH (OR, 37.04; P < .01), large effusions (OR, 3.31; P < .01), and increasing age (OR 1.02, P = .01) were associated with the use of definitive therapy.

CONCLUSIONS:  Patients with MPE with an effusion of low pleural fluid pH and large size on radiographs at first presentation are more likely to be treated with pleurodesis and/or IPC.

Original Research: Bronchiectasis

Chest. 2015;147(6):1635-1643. doi:10.1378/chest.14-1961

BACKGROUND:  Although viral infections are a major cause of exacerbations in patients with chronic airway diseases, their roles in triggering bronchiectasis exacerbations in adults remain unclear. Therefore, we prospectively investigated the incidence and clinical impacts of viral infection in adults with bronchiectasis exacerbations.

METHODS:  The study cohort of 119 adults with bronchiectasis was followed up prospectively for 12 months. Nasopharyngeal swabs and sputum samples were assayed for 16 respiratory viruses, using polymerase chain reaction assays. Symptoms, spirometry, quality of life, bacterial cultures, and inflammatory markers were assessed during steady-state bronchiectasis and exacerbations.

RESULTS:  A total of 100 exacerbations were captured from 58 patients during 1-year follow-up. Respiratory viruses were found more frequently in nasopharyngeal swabs and sputum during bronchiectasis exacerbations (49 of 100, 49.0%) than during steady state (11 of 58, 18.9%; P < .001). The most common viruses found in patients experiencing exacerbations were coronavirus (19 of 65, 39.2%), rhinovirus (16 of 65, 24.6%), and influenza A/B viruses (16 of 65, 24.6%). Virus-positive exacerbations were associated with a greater increase in markers of systemic and airway inflammation (serum IL-6 and tumor necrosis factor-α; sputum IL-1β and tumor necrosis factor-α) compared with virus-negative exacerbations, but the differences in spirometric indexes, quality of life, and bacterial density were unremarkable. In receiver operating characteristics analysis, serum interferon-γ-induced protein 10 yielded an area under curve of 0.67 (95% CI, 0.53-0.77; P = .018). Furthermore, a greater proportion of patients with virus-positive exacerbations received IV antibiotics.

CONCLUSIONS:  Prevalence of viral infections, detected by polymerase chain reaction assay, is higher in cases of bronchiectasis exacerbations than in steady-state bronchiectasis, suggesting that respiratory viruses play crucial roles in triggering bronchiectasis exacerbations. The potential mechanisms of virus-induced bronchiectasis exacerbations merit further investigations.

TRIAL REGISTRY:  ClinicalTrials.gov; No.: NCT01801657; www.clinicaltrials.gov

Original Research: Cardiovascular Disease

Chest. 2015;147(6):1644-1650. doi:10.1378/chest.14-2414

BACKGROUND:  Recent findings suggest that patients with atrial fibrillation (AF), in addition being at thromboembolic risk, are at risk of myocardial infarction (MI). Our aim was to investigate predictors of MI and cardiovascular death in a cohort of patients with AF who were taking anticoagulants.

METHODS:  We prospectively followed up 1,019 patients with AF for a median of 33.7 months (3,223 person-years). All patients were treated with oral vitamin K antagonists. Primary outcome was a composite end point of cardiovascular events (CVEs) including fatal/nonfatal MI, cardiac revascularization, and cardiovascular death.

RESULTS:  The mean age of the patients was 73.2 years, and 43.8% were women. At follow-up, 111 CVEs (3.43%/y) had occurred: 47 fatal-nonfatal MI/revascularization and 64 cardiovascular deaths. In addition, 31 stroke/transient ischemic attacks (0.96%/y) were recorded. Patients experiencing CVEs were older (P < .001) and had a higher prevalence of metabolic syndrome (MetS) (P = .005), heart failure (P = .001), and prior cardiac (P < .001) and cerebrovascular events (P < .001). On a Cox proportional hazard analysis, age (hazard ratio [HR], 1.083; 95% CI, 1.053-1.113; P < .001), smoking (HR, 2.158; 95% CI, 1.193-3.901; P = .011), history of cerebrovascular (HR, 1.704; 95% CI, 1.119-2.597; P = .013) and cardiac (HR, 1.658; 95% CI, 1.105-2.489; P = .015) events, MetS (HR, 1.663; 95% CI, 1.107-2.499; P = .014), heart failure (HR, 1.584; 95% CI, 1.021-2.456; P = .040), and male sex (HR, 1.499; 95% CI, 1.010-2.223; P = .044) predicted CVEs.

CONCLUSIONS:  Patients with AF still experience a high rate of CVEs despite receiving anticoagulant treatment. MetS is a common clinical feature in patients with AF, which increases the risk of CVEs. A holistic approach is needed to reduce the cardiovascular risk in patients with AF.

TRIAL REGISTRY:  ClinicalTrials.gov; No.: NCT01882114; URL: www.clinicaltrials.gov

Chest. 2015;147(6):1651-1658. doi:10.1378/chest.14-2099

BACKGROUND:  The risk of ischemic stroke/thromboembolic events after an intracranial hemorrhage (ICH) in patients with atrial fibrillation (AF) who are on warfarin treatment is poorly characterized. The aim of this study was to assess the association between the risk of ischemic stroke/thromboembolic events and ICH.

METHODS:  Linkage of three Danish nationwide administrative registries in the period between 1999 and 2012 identified patients with AF on warfarin treatment. Event-rate ratios of stroke/thromboembolic events, major bleeding, and all-cause mortality stratified by ICH were calculated, and Cox proportional hazard models were used to compare event rates among ICH survivors. A matched OR was calculated for ICH occurrences within 0 to 3 months relative to the 3 to 6 months prior to a stroke/thromboembolic event. A rate ratio of claimed warfarin prescriptions in a 3-month period pre- and post-ICH was also calculated.

RESULTS:  We studied 58,815 patients with AF (median age, 72.6 years; 60% men). When compared with the non-ICH group, the ICH group was at increased risk for stroke/systemic embolism/transient ischemic attack (TIA) (rate ratio, 3.67; 95% CI, 3.12-4.31) and mortality (rate ratio, 5.55; 95% CI, 5.20-5.92), but not for major bleeding (rate ratio, 1.06; 95% CI, 0.81-1.39). The matched OR of ICH occurrences prior to a stroke/systemic embolism/TIA was 4.33 (95% CI, 2.44-8.15). The rate ratio of claimed warfarin prescriptions post- and pre-ICH event was 0.28 (95% CI, 0.24-0.33).

CONCLUSIONS:  In this large-scale study of patients with AF treated with warfarin, first-time ICH was associated with an increased rate of ischemic stroke/systemic embolism/TIA and mortality compared with the non-ICH group. There was a decrease in the warfarin-prescription purchase rate in the post-ICH period compared with pre-ICH, which may partly explain the excess risk.

Recent Advances in Chest Medicine

Chest. 2015;147(6):1659-1670. doi:10.1378/chest.14-1313

This review article describes two protocols adapted from lung ultrasound: the bedside lung ultrasound in emergency (BLUE)-protocol for the immediate diagnosis of acute respiratory failure and the fluid administration limited by lung sonography (FALLS)-protocol for the management of acute circulatory failure. These applications require the mastery of 10 signs indicating normal lung surface (bat sign, lung sliding, A-lines), pleural effusions (quad and sinusoid sign), lung consolidations (fractal and tissue-like sign), interstitial syndrome (lung rockets), and pneumothorax (stratosphere sign and the lung point). These signs have been assessed in adults, with diagnostic accuracies ranging from 90% to 100%, allowing consideration of ultrasound as a reasonable bedside gold standard. In the BLUE-protocol, profiles have been designed for the main diseases (pneumonia, congestive heart failure, COPD, asthma, pulmonary embolism, pneumothorax), with an accuracy > 90%. In the FALLS-protocol, the change from A-lines to lung rockets appears at a threshold of 18 mm Hg of pulmonary artery occlusion pressure, providing a direct biomarker of clinical volemia. The FALLS-protocol sequentially rules out obstructive, then cardiogenic, then hypovolemic shock for expediting the diagnosis of distributive (usually septic) shock. These applications can be done using simple grayscale machines and one microconvex probe suitable for the whole body. Lung ultrasound is a multifaceted tool also useful for decreasing radiation doses (of interest in neonates where the lung signatures are similar to those in adults), from ARDS to trauma management, and from ICUs to points of care. If done in suitable centers, training is the least of the limitations for making use of this kind of visual medicine.

Contemporary Reviews in Critical Care Medicine

Chest. 2015;147(6):1671-1680. doi:10.1378/chest.14-1733

Acute exacerbations of asthma can lead to respiratory failure requiring ventilatory assistance. Noninvasive ventilation may prevent the need for endotracheal intubation in selected patients. For patients who are intubated and undergo mechanical ventilation, a strategy that prioritizes avoidance of ventilator-related complications over correction of hypercapnia was first proposed 30 years ago and has become the preferred approach. Excessive pulmonary hyperinflation is a major cause of hypotension and barotrauma. An appreciation of the key determinants of hyperinflation is essential to rational ventilator management. Standard therapy for patients with asthma undergoing mechanical ventilation consists of inhaled bronchodilators, corticosteroids, and drugs used to facilitate controlled hypoventilation. Nonconventional interventions such as heliox, general anesthesia, bronchoscopy, and extracorporeal life support have also been advocated for patients with fulminant asthma but are rarely necessary. Immediate mortality for patients who are mechanically ventilated for acute severe asthma is very low and is often associated with out-of-hospital cardiorespiratory arrest before intubation. However, patients who have been intubated for severe asthma are at increased risk for death from subsequent exacerbations and must be managed accordingly in the outpatient setting.

Contemporary Reviews in Sleep Medicine

Chest. 2015;147(6):1681-1690. doi:10.1378/chest.14-2078

OSA is a common, often chronic, condition requiring long-term therapy. Given the prevalence of OSA, as well as its significant health-related sequelae, a range of medical and surgical treatments have been developed and used with varying success depending on individual anatomy and patient compliance. Although CPAP is the primary treatment, many patients cannot tolerate this treatment and require alternative therapies. In this clinical scenario, surgery is often warranted and useful. Surgical management is aimed at addressing obstruction in the nasal, retropalatal, and retroglossal/hypopharyngeal regions, and many patients have multiple levels of obstruction. This review presents a comprehensive overview of research findings on a wide spectrum of surgical approaches currently used by sleep clinicians when other therapeutic modalities fail to achieve positive outcomes.

Medical Ethics

Chest. 2015;147(6):1691-1696. doi:10.1378/chest.14-2046

Since 1986, the Emergency Medical Treatment and Labor Act (EMTALA) has imposed an obligation on hospitals and physicians to evaluate and stabilize patients who present to a hospital ED seeking care. Available sanctions for noncompliance include fines, damages awarded in civil litigation, and exclusion from Medicare. EMTALA uses several terms that are familiar to physicians (eg, “emergency medical condition,” “stabilize,” and “transfer”), but the statutory definitions do not map neatly onto the way in which these terms are used and understood in clinical settings. Thus, there is potential for a mismatch between a physician’s on-the-spot professional judgment and what the statute demands. We review what every physician should know about EMTALA and answer six common questions about the law.

Topics in Practice Management

Chest. 2015;147(6):1697-1703. doi:10.1378/chest.14-2954
FREE TO VIEW

Extracorporeal membrane oxygenation (ECMO) is a temporary technique for providing life support for cardiac dysfunction, pulmonary dysfunction, or both. The two forms of ECMO, veno-arterial (VA) and veno-venous (VV), are used to support cardiopulmonary and pulmonary dysfunction, respectively. Historically, ECMO was predominantly used in the neonatal and pediatric populations, as early adult studies failed to improve outcomes. ECMO has become far more common in the adult population because of positive results in published case series and clinical trials during the 2009 influenza A(H1N1) pandemic in 2009 to 2010. Advances in technology that make the technique much easier to implement likely fueled the renewed interest. Although exact criteria for ECMO are not available, patients who are good candidates are generally considered to be relatively young and suffering from acute illness that is believed to be reversible or organ dysfunction that is otherwise treatable. With the increase in the use in the adult population, a number of different codes have been generated to better identify the method of support with distinctly different relative value units assigned to each code from a very simple prior coding scheme. To effectively be reimbursed for use of the technique, it is imperative that the clinician understands the new coding scheme and works with payers to determine what is incorporated into each specific code.

CME Resource Center

Chest. 2015;147(6):1704-1705. doi:10.1378/chest.15-0394

As seen in this CME online activity (available at http://journal.cme.chestnet.org/home-niv-copd), COPD is a common and debilitating disease and is currently the third leading cause of death in the United States. The role of noninvasive ventilation (NIV) in the management of severe, hypercapnic COPD has been controversial. However, it was concluded that current data would support the following recommendations. Patients with COPD with a waking Paco2 > 50 to 52 mm Hg, an overnight Paco2 > 55 mm Hg, or both who are symptomatic and compliant with other therapies should be eligible for NIV. In addition, multiple previous hospital admissions for COPD exacerbation, requiring noninvasive/invasive mechanical ventilation, strongly suggest a need for chronic NIV. Patients with COPD with a BMI > 30 kg/m2 respond particularly well to this therapy. When the decision is made to start NIV, this treatment is probably best initiated during a short hospitalization, although this can be accomplished in the clinic, home, or sleep laboratory if well-trained clinicians are available. Newer modes of NIV such as volume-assured pressure support, particularly with autotitrating expiratory positive airway pressure (EPAP), may create the opportunity for home NIV initiation easier for less experienced physicians. Regardless of the mode selected, inspiratory pressures must be in the 20 to 25 cm H2O range to meaningfully increase tidal volume, reduce work of breathing, and, importantly, reduce waking arterial Paco2. EPAP is currently set at 4 to 5 cm H2O, although future technologies may allow this to be individualized to maximally reduce auto-positive end expiratory pressure. The NIV device should have a backup rate although it is controversial as to whether this should be set at a high (18-20 breaths/min) vs a low (8-10 breaths/min) rate. The proper use of NIV in appropriately chosen patients with COPD can improve quality of life and increase survival. Ongoing studies are assessing if the frequency of future hospitalizations can be reduced with NIV. Thus, NIV should be strongly considered in any patients with COPD meeting the criteria described here.

Pectoriloquy

Chest. 2015;147(6):1706. doi:10.1378/chest.14-2791
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It is the story deciphered that transcriptionists quote.
Familiar words fill the pages of our daily progress note.
Meaning and emphasis of a crafted, collective expectation,
To influence administrators and payers with subtle manipulation.
However, some medical words rarely appear in this written chatter.
Whether due to tricky spelling or pronunciation does not matter.
Borborygmi, bradykinesia, and horriplation,
Not to mention micturition or lachrymation.
Trichotillomania, singultus, and rarely defecation,
But post-op patients worry us with their eructation.
Some words we hope to never see; munchausen and hoarder,
Chronic low back pain and oppositional defiant disorder.
Another word that leaves us terribly uneasy is psychopath.
But not nearly as much as operating on a bad vasculopath.
Plenty of other strange words comprise our medical jargon,
Makes the cost of medical school seem almost like a bargain.
While most words leave us longing for discharge planners to hear our plea,
The one word we simply never see is that of good old pectoriloquy.

Chest. 2015;147(6):1707. doi:10.1378/chest.14-2716
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I’m in the ER in gown and jeans. The curtain
of my cubicle is open. I chat with a young woman
in street clothes sitting on her bed. Her curtain is open.
She has two sons and smiles as she describes them.
One likes football, the other baseball.
She has migraines. She is thinking brain tumor.
I have a persistent pain that feels as if I got punched
in the chest just left of center. I’m thinking
it’s from the four feet of snow I shoveled and then,
this spring, from the seven yards of mulch.
I am thinking tumor-wrapped aorta
or peanut-shaped plaque in a coronary artery.
In the ER cubicle across from mine, a surgeon
talks to a man about the softball-sized growth
on the man’s inner thigh. The curtain is open.
The surgeon wants to admit him.
The man asks the ER nurse to call his girlfriend
to let her know he won’t be coming home tonight.
He wants to go out for a smoke.
He wants me to see the growth on his leg.
I glance at it out of respect.
“It’s like a car accident,” the ER nurse says,
“where you should, but don’t want to, look away.”
The man talks about a past heart attack, how,
while pushing a mower, his left side went numb.
“I felt like I had pins and needles in me,” he says.
Soon, attendants arrive and roll him away
on his bed with wheels.
After an EKG, a blood test, and chest X-rays,
I learn I have inflamed cartilage where ribs
meet breastbone. I am Paul Bunyan
and embarrassed to be here among the sick.
I drive home repeating the word “costochondritis.”
In the kitchen, I empty the dishwasher
and note the marvelous colors and designs on plates,
the glorious curves of goblets, and outside,
on the deck rail, the magnificent music of a wren.
Later, in bed, with my hand, I trace the lovely,
warm, and steady thigh of my sleeping wife.

Selected Reports

Chest. 2015;147(6):e199-e204. doi:10.1378/chest.14-0757

Internal fixation of the ribs has been shown in numerous studies to decrease complications following traumatic rib fractures. Anterior injuries to the chest wall causing cartilaginous fractures, although rare, can cause significant disability and can lead to a variety of complications and, therefore, pose a unique clinical problem. Here, we report the surgical technique used for four patients with internal fixation of injuries to the cartilaginous portions of the chest wall treated at our center. All patients had excellent clinical outcomes and reported improvement in symptoms, with no associated complications. Patients who have injuries to the anterior portions of the chest wall should be considered for internal fixation of the chest wall when the injuries are severe and can lead to clinical disability.

Ultrasound Corner

Chest. 2015;147(6):e205-e207. doi:10.1378/chest.14-0967
FREE TO VIEW

A 39-year-old woman, gravida 4, para 0, at 10 weeks’ gestation was admitted to the obstetrics ward for fever, dysuria, back pain, and a dry cough that she had for 3 weeks. Medical history was significant for pituitary microadenoma, nephrolithiasis status after lithotripsy, and three prior spontaneous abortions. She worked in a daycare center, was married, and denied a history of excessive alcohol use, cigarette smoking, or illicit drugs. Because of her history of nephrolithiasis, the patient was started on ceftriaxone for presumed urinary tract infection. At the time of admission, she was noted to have a temperature of 38.2°C, BP of 112/61 mm Hg, heart rate of 111 beats/min, and an oxygen saturation breathing ambient air of 100%. Admission chest radiograph was not done to prevent radiation exposure to the fetus. Laboratory results were notable for a WBC count of 8 and an unremarkable urinalysis.

Chest Imaging and Pathology for Clinicians

Chest. 2015;147(6):e208-e214. doi:10.1378/chest.14-2237

A male lifelong nonsmoker aged 58 years with no prior asbestos exposure complained of gradual worsening breathlessness over 3 months. This was associated with abdominal and leg swelling and a 2-kg weight loss. He had no fever, night sweats, hemoptysis, joint pain, rash, abdominal pain, chest pain, or orthopnea. The patient had no recent travel or contact with pulmonary TB. He had stage I left-side testicular seminoma treated with left-sided radical orchidectomy 10 years previous and recently received a diagnosis of Child’s B alcoholic liver cirrhosis. His hepatitis B and C screen result was normal.

Pulmonary, Critical Care, and Sleep Pearls

Chest. 2015;147(6):e215-e219. doi:10.1378/chest.14-2402

A 43-year-old man with antisynthetase syndrome was seen in our pulmonary clinic for worsening dyspnea. He was recently diagnosed with antisynthetase syndrome because he had nonspecific interstitial pneumonitis on a surgical lung biopsy and polymyositis associated with anti-Jo-1 and anti-SSA-52 autoantibodies. Along with his worsening dyspnea, he also had a dry cough, lower extremity edema, and abdominal distension. He had gained 11 kg over 1 month. He had been taking prednisone 40 mg daily 2 months prior, which had been recently weaned to 20 mg daily. He had also been on mycophenolate mofetil but had recently discontinued it on his own.

Chest. 2015;147(6):e220-e223. doi:10.1378/chest.14-2148

A 52-year-old white man presented to a pulmonary clinic for evaluation of a 2.3 × 1.7 cm lung nodule. The patient had originally presented to his cardiologist for palpitations. The palpitations were described as a “fluttering” sensation, occurring daily, more often at rest, but not associated with syncope. At the time, he denied dyspnea, paroxysmal nocturnal dyspnea, or orthopnea. The patient had a coronary artery calcium scoring test done, which revealed a lobulated, well-circumscribed, smoothly marginated lower lobe nodule, and he was sent to a pulmonary clinic for further evaluation. The patient denied shortness of breath, chest pain, cough, wheezing, or hemoptysis. He denied fatigue, night sweats, or weight loss. He had a 1 pack-year smoking history and stopped cigarettes 30 years ago but still smoked two to three cigars monthly. His family history was only significant for early coronary artery disease. He was an avid marathon runner who worked as an athletic equipment manager for a prominent sports team in Arizona.

Chest. 2015;147(6):e224-e227. doi:10.1378/chest.14-1540

A 29-year-old man with a history of oculocutaneous albinism presented to the ED complaining of progressive dyspnea on exertion. One month prior to admission, the patient had begun to experience worsening dyspnea provoked by routine household activities. Additionally, he had developed a nonproductive cough, exacerbated by cold weather. He denied associated chest pain, hemoptysis, fever, chills, or night sweats. He denied any new exposures or sick contacts in the recent past. A review of systems was significant for a history of epistaxis and frequent bruising. Born in Honduras, he had immigrated to the United States approximately 10 years prior to his presentation to our facility. Furthermore, there was no family history of albinism, bleeding disorders, or pulmonary disease.

Correspondence

Chest. 2015;147(6):e228-e229. doi:10.1378/chest.15-0159
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ResponseResponse ONLINE EXCLUSIVES
Chest. 2015;147(6):e229. doi:10.1378/chest.15-0219
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Chest. 2015;147(6):e230. doi:10.1378/chest.15-0198
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Chest. 2015;147(6):e231. doi:10.1378/chest.15-0189
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Chest. 2015;147(6):e232. doi:10.1378/chest.15-0253
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ResponseResponse ONLINE EXCLUSIVES
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Chest. 2015;147(6):e234-e235. doi:10.1378/chest.15-0184
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ResponseResponse ONLINE EXCLUSIVES
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Chest. 2015;147(6):e236-e237. doi:10.1378/chest.14-3118
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ResponseResponse ONLINE EXCLUSIVES
Chest. 2015;147(6):e237. doi:10.1378/chest.15-0165
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Chest. 2015;147(6):e238. doi:10.1378/chest.15-0204
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  • CHEST Journal
    Print ISSN: 0012-3692
    Online ISSN: 1931-3543