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Influence of inspired oxygen concentration on PaCO2 during noninvasive ventilation in patients with chronic obstructive pulmonary disease.

Respir Care. 2013 Aug 13;

Authors: Savi A, Maccari JG, Tonietto TF, Antonio AC, de Oliveira RP, Rieder MD, Zignani EC, da Silva EB, Teixeira C

Abstract
BACKGROUND:: The administration of a high inspired oxygen concentration (FIO2) to chronic obstructive pulmonary disease (COPD) patients breathing spontaneously may result in hypercapnia; due to reversal of preexisting regional hypoxic pulmonary vasoconstriction resulting in a greater deadspace. In these patients, during noninvasive ventilation (NIV), the arterial gases behavior was not previously studied.
OBJECTIVES:: To investigate the response of CO2-retaining COPD patients, after acute respiratory crisis stabilization using noninvasive ventilation (NIV), to a high inspired oxygen concentration (FIO2 = 1.0) after having been noninvasively ventilated with FIO2 ≤ 0.50 for a period of time.
DESIGN:: Experimental prospective study.
SETTING:: A 18-bed medical-ICU in a university teaching hospital.
PATIENTS:: CO2-retaining COPD patients recovering from acute respiratory failure using NIV.
INTERVENTIONS:: FIO2 increased to 1.0.
MEASUREMENTS AND MAIN RESULTS:: Seventeen NIV-ventilated CO2-retaining COPD patients were studied both at their baseline FIO2 (0.25 to 0.50), and following a 40-min period of exposure to an FIO2 of 1.0. Mean (±SD) baseline findings were: PaO2 of 101.4 ± 21.7mmHg, PaCO2 of 52.6 ± 10.4mmHg, respiratory rate (RR) of 17.8 ± 3.7breaths/min, tidal volume (VT) of 601 ± 8mL, and Glasgow coma scale (GCS) of 14.8 ± 0.3. Statistical analysis using the paired Student's t-test showed that the PaO2 (290.5 ± 35.7mmHg; p <0.001) increased significantly when the FIO2 was increased to 1.0, but there was no significant change in PaCO2 (51.5 ± 12.3mmHg), RR (17.5 ± 2.8breaths/min), VT (608 ± 8mL) and GCS (14.8 ± 0.3).
CONCLUSION:: These results show that during noninvasive ventilation with an FIO2 sufficient to maintain a normal PaO2, a further increase in FIO2 does not result in an increased PaCO2 in this group of CO2-retaining COPD patients.

PMID: 23942751 [PubMed - as supplied by publisher]

Related Articles

Microbial communities in the respiratory tract of patients with interstitial lung disease.

Thorax. 2013 Aug 14;

Authors: Garzoni C, Brugger SD, Qi W, Wasmer S, Cusini A, Dumont P, Gorgievski-Hrisoho M, Mühlemann K, von Garnier C, Hilty M

Abstract
BACKGROUND: Molecular methods based on phylogenetic differences in the 16S rRNA gene are able to characterise the microbiota of the respiratory tract in health and disease.
OBJECTIVES: Our goals were (1) to characterise bacterial communities in lower and upper airways of patients with interstitial lung disease (ILD) and (2) to compare the results with the microbiota of patients with Pneumocystis pneumonia (PCP) and normal controls.
METHODS: We examined the upper and lower respiratory tract of 18 patients with ILD of whom 5, 6, and 7 had idiopathic interstitial pneumonia (IIP), non-IIP and sarcoidosis, respectively. In addition, six immune-compromised patients with PCP and nine healthy subjects were included as controls. Exclusion criteria were recent bacterial/viral respiratory tract infection, HIV-positivity and subjects receiving antibiotic therapy. Bronchoalveolar lavage fluid and oropharyngeal swabs were simultaneously collected, and microbiota was characterised by ultra-deep 16S rRNA gene sequencing.
RESULTS: The microbiota in lower airways of the majority of patients (30; 90%) primarily consisted of Prevotellaceae, Streptococcaceae and Acidaminococcaceae. α and β diversity measurements revealed no significant differences in airway microbiota composition between the five different groups of patients. Comparison of bacterial populations in upper and lower respiratory tract showed significant topographical discontinuities for 7 (23%) individuals.
CONCLUSIONS: IIP, non-IIP and sarcoidosis are not associated with disordered airway microbiota and a pathogenic role of commensals in the disease process is therefore unlikely. Nevertheless, molecular analysis of the topographical microbiota continuity along the respiratory tract may provide additional information to assist management of individual patients.

PMID: 23945167 [PubMed - as supplied by publisher]

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Mechanisms and impact of the frequent exacerbator phenotype in chronic obstructive pulmonary disease.

BMC Med. 2013;11:181

Authors: Wedzicha JA, Brill SE, Allinson JP, Donaldson GC

Abstract
Exacerbations of chronic obstructive pulmonary disease (COPD) are important events that carry significant consequences for patients. Some patients experience frequent exacerbations, and are now recognized as a distinct clinical subgroup, the 'frequent exacerbator' phenotype. This is relatively stable over time, occurs across disease severity, and is associated with poorer health outcomes. These patients are therefore a priority for research and treatment. The pathophysiology underlying the frequent exacerbator phenotype is complex, with increased airway and systemic inflammation, dynamic lung hyperinflation, changes in lower airway bacterial colonization and a possible increased susceptibility to viral infection. Frequent exacerbators are also at increased risk from comorbid extrapulmonary diseases including cardiovascular disease, gastroesophageal reflux, depression, osteoporosis and cognitive impairment. Overall these patients have poorer health status, accelerated forced expiratory volume over 1 s (FEV1) decline, worsened quality of life, and increased hospital admissions and mortality, contributing to increased exacerbation susceptibility and perpetuation of the frequent exacerbator phenotype. This review article sets out the definition and importance of the frequent exacerbator phenotype, with a detailed examination of its pathophysiology, impact and interaction with other comorbidities.

PMID: 23945277 [PubMed - in process]

An Official American Thoracic Society Proceedings: Work-related Asthma and Airway Diseases. Presentations and Discussion from the Fourth Jack Pepys Workshop on Asthma in the Workplace.

Ann Am Thorac Soc. 2013 Aug;10(4):S17-24

Authors: Tarlo SM, Malo JL, Fourth Jack Pepys Workshop on Asthma in the Workplace Participants

Abstract
Work-related asthma is a common occupational lung disease. The scope of the Fourth Jack Pepys Workshop that was held in May 2010 went beyond asthma to include discussion of other occupational airway diseases, in particular occupationally related chronic obstructive pulmonary disease (COPD) and bronchiolitis. Aspects explored included public health considerations, environmental aspects, outcome after diagnosis, prevention and surveillance, and other work-related obstructive airway diseases. Consistent methods are needed to accurately estimate the comparative burden of occupation-related airway diseases among different countries. Challenges to accomplishing this include variability in health care delivery, compensation systems, cultural contexts, and social structures. These factors can affect disease estimates, while heterogeneity in occupations and workplace exposures can affect the underlying true prevalence of morbidity. Consideration of the working environment included discussion of practical methods of limiting exposure to respiratory sensitizers, methods to predict new sensitizers before introduction into workplaces, the role of legislated exposure limits, and models to estimate relative validity of various ameliorative measures when complete avoidance of the sensitizer is not feasible. Other strategies discussed included medical surveillance measures and education, especially for young individuals with asthma and new workers about to enter the workforce. Medical outcomes after development of sensitizer-induced occupational asthma are best following earlier diagnosis and removal from further exposure, but a subset may be able to continue working safely provided that exposure is reduced under close follow-up monitoring. It was recognized that occupationally related COPD is common but underappreciated, deserving further study and prevention efforts.

PMID: 23952871 [PubMed - in process]