Acute Respiratory Failure in Chronic Obstructive Pulmonary Disease

Burk, Richard H.

doi:10.1001/archinte.1973.03650120067012

Cited by 46 publications

(5 citation statements)

References 21 publications

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“…Results The geometric mean PD20 FMLP in the patients with chronic bronchitis was 0'06 pmol (95% confidence interval 0-015-0-26), which was significantly lower than that in the control subjects (0-21 pmol (0 02-1P9)). PD20 FMLP in the patients with chronic bronchitis but not age matched controls (p = 0 35) was lower than that found previously in young normal subjects (0 35 pmol (0-07- [1][2][3][4][5][6][7][8]. The return to 95% baseline FEV, occurred after 86(10) minutes in subjects with chronic bronchitis and in 81 (23) minutes in their age matched controls, in both cases being much slower than that seen in young subjects (29(9) minutes).…”

contrasting

confidence: 56%

Effects of inhalation of N-formyl-methionyl-leucyl-phenylalanine in the well elderly and in patients with chronic bronchitis.

Peters

Breslin

Berend

1992

Thorax

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Background Inhalation of the bacterial peptide N-formyl-methionyl-leucyl-phenylalanine (FMLP) produces bronchoconstriction in normal subjects. FMLP thus has a putative role as a mediator of bronchoconstriction associated with bacterial bronchial infection. Methods The effects ofFMLP inhalation were examined in ten subjects with a history of chronic bronchitis and ten age matched control subjects. Each subject inhaled FMLP doses from 0 025 to 0-8

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contrasting

confidence: 56%

Effects of inhalation of N-formyl-methionyl-leucyl-phenylalanine in the well elderly and in patients with chronic bronchitis.

Peters

Breslin

Berend

1992

Thorax

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“…We previously reported that (i) small SRA + cells were detected in PB of all examined cases including healthy volunteers, (ii) multiple organ dysfunction syndrome (including acute respiratory distress syndrome) and acute exacerbation of idiopathic pulmonary fibrosis were systemic consequence with multiple organ injury induce by cytokine abnormality, (iii) large SRA + cells were detected in the PB of these cases and might play important roles in the development of cytokine abnormality . Factors that determine the survival of patients with COPD exacerbation are severity of the lung disease and extrapulmonary problems, such as ischemic heart disease, left ventricular failure, and gastro‐intestinal bleeding . As a result of preliminary examination, we detected large SRA + cells in PB of autopsy cases with severe exacerbation of COPD, and multiple organs of these cases were injured.…”

Section: Discussionmentioning

confidence: 87%

“…11,19 Factors that determine the survival of patients with COPD exacerbation are severity of the lung disease and extrapulmonary problems, such as ischemic heart disease, left ventricular failure, and gastro-intestinal bleeding. 20 As a result of preliminary examination, we detected large SRA þ cells in PB of autopsy cases with severe exacerbation of COPD, and multiple organs of these cases were injured. Monocytes originate from bone marrow and probably remain in circulation for no more than 36 h before migrating into the connective tissue where they increase in size, acquire multiple lysosomes, and become active in phagocytosis.…”

Section: Figurementioning

confidence: 85%

Appearance of large scavenger receptor A‐positive cells in peripheral blood: A potential risk factor for severe exacerbation of chronic obstructive pulmonary disease

Emura

Usuda

Satou

2019

Pathology International

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Fresh peripheral blood (PB) samples from 432 outpatients with stable chronic obstructive pulmonary disease (COPD) were examined. Patients were classified into Group A (large SRA+ cells were undetected) and Group B (large SRA+ cells were detected) and followed‐up for 1 year. Patients were further subdivided according to Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage. Cox proportional hazard model had shown that Gold, Group, home oxygen therapy (HOT), and treatment were significant predictors of severe exacerbation. Six of 353 patients in Group A and 29 of 79 in Group B developed severe exacerbation. The rates of severe exacerbation were significantly higher in Group B patients, GOLD stage 2 than Group A, GOLD stage 2; in Group B, GOLD stage 3 than Group A, GOLD stage 3; and in all of Group B compared with in all of Group A. The Kaplan‐Meier curves of Group B, GOLD stages 1–4, and of all of Group B showed significantly worse rates of severe exacerbation than those of Group A, Gold 1–4, and all of Group A, respectively. The appearance of large SRA+ cells in the PB of patients with stable COPD may represent a useful biomarker for severe COPD exacerbation.

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“…32 The qualification that an elevated Paco2 must be associated with a pH less than 7.35 is important to distinguish patients who chronically have elevated Paco z levels that have been compensated for metabolically.40 In patients with COPD who chronically function with compensated hypoxemia and/or hypcrcarbia, it is important to add to the standard blood gas criteria the qualifier that the clinical status of the patient be rapidly deteriorating. 11 Bone and coworkers 7 defined acute respiratory failure in this group of patients solely on the basis of clinical deterioration of steady state symptoms for hours to days prior to presentation. The indication for endotracheal intubation and mechanical ventilation used in their study was purely clinical and was based on when the patient became stuporous and was unable to cooperate with therapy.…”

Section: Diagnosismentioning

confidence: 99%

Acute Respiratory Failure and Chronic Obstructive Lung Disease

Rosen

1986

Medical Clinics of North America

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The approach to acute respiratory failure in patients with chronic obstructive lung disease (COPD) requires a special understanding of factors regarding diagnosis, patient evaluation, interpretation of laboratory data, and management that is inherent to this group of patients. Although the term COPD as commonly used encompasses a wide variety of patients with the underlying common denominator of limitation of airflow, most of these patients fall into the major categories of chronic bronchitis, asthma, and emphysema. ~1any of these patients manifest an overlap syndrome made up of several or all of the components. The term chronic bronchitis denotes a clinical syndrome characterized by chronic or recurrent bronchial hypersecretion clinically diagnosed by the presence of chronic productive cough with no other cause such as infection, neoplasm, or cardiac disease. The sputum may be mucous, purulent, or eosinophilic in character. 2. 22 The mechanisms of airflow limitation are related to generalized hypcrtrophy and hyperplasia of the mucus-secreting bronchial glands, diffuse inflammation with thickening of the tracheobronchial submucosa, and secretions in the airways. Asthma is characterized by an increased responsiveness of the tracheobronchial tree to various stimuli and is manifested by diffuse narrowing of the airways, which is reversible either spontaneously or as a result of therapy. The airflow limitation results from a combination of mucous plugging of the airways, smooth muscle hypertrophy and constriction, goblet cell hyperplasia, and diffuse mucosal edema. 2 Pulmonary emphysema is defined pathologically as an abnormal enlargement of the airspaces distal to the terminal bronchioles associated with destruction of the alveolar walls. 2 Airflow limitation results from the collapse of small airways due to loss of the elastic recoil of the lung parenchyma, which aids in maintaining the patency of the small bronchioles.

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Acute Respiratory Failure in Chronic Obstructive Pulmonary Disease

Cited by 46 publications

References 21 publications

Effects of inhalation of N-formyl-methionyl-leucyl-phenylalanine in the well elderly and in patients with chronic bronchitis.

Effects of inhalation of N-formyl-methionyl-leucyl-phenylalanine in the well elderly and in patients with chronic bronchitis.

Appearance of large scavenger receptor A‐positive cells in peripheral blood: A potential risk factor for severe exacerbation of chronic obstructive pulmonary disease

Acute Respiratory Failure and Chronic Obstructive Lung Disease

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