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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have used the CT transthoracic scan to measure regional lung density in vivo, as our previous studies have shown that this correlates with the increase in size of distal air spaces, which is a defining characteristic of emphysema. We have studied 32 patients with chronic airflow limitation (FEV1, 15 to 68% predicted) caused by chronic bronchitis and emphysema (synonym, COPD), with a wide range of arterial PO2 (38 to 90 mm Hg) and PCO2 (32 to 63 mm Hg) while breathing air at rest. We could find no significant relationships between the extent of emphysema (as assessed in vivo by the EMI number defining the lowest fifth percentile of the CT density histogram of the lung fields) and either arterial blood gas tensions, mean pulmonary arterial pressure, cardiac output, or calculated total pulmonary vascular resistance while at rest (n = 32) or during supine leg exercise (n = 29). We conclude that the extent of emphysema does not correlate with the clinical or pathologic features of the "pink and puffing" (i.e., mild hypoxemia, no CO2 retention, no pulmonary hypertension, etc.) or "blue and bloated" (i.e., hypoxemia, CO2 retention, pulmonary hypertension) pattern of patients with COPD nor to the spectrum of hemodynamic and gas exchange abnormalities that commonly occur in patients between these two extreme examples. Thus, "pink puffers" should not be equated with "the emphysematous" pattern of this disease. Although these clinicophysiologic patterns remain valid as descriptions, they do not relate to the extent of underlying emphysema in COPD.
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PMID:Pulmonary hemodynamics, gas exchange, and the severity of emphysema as assessed by quantitative CT scan in chronic bronchitis and emphysema. 272 56

In view of the common findings that patients with pulmonary disease exhibit larger maximal exercise hyperpnea (Vmax) than their maximal voluntary ventilation (MVV), the limiting factor for the exercise loading in these patients has been considered to be excessive hyperventilation. Recently, plasma potassium released from exercising muscle has been found to effectively stimulate arterial chemoreceptors. This effect is further potentiated by the presence of hypoxia. Since patients often become hypoxemic by exercise loading, it was suspected that potassium may play a role to limit exercising capacity due to excessive stimulation of the peripheral chemoreceptors. In 1975, Kawakami et al. reported that in response to exercise loading emphysematous type patients exhibited higher potassium and lactic acid concentration than the bronchitic and mixed type COPD patients. Their findings, together with breathlessness often seen in the emphysema may be further evidence supporting the inference mentioned above.
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PMID:[On the role of potassium as a limiting factor for exercise hyperpnea]. 274 71

Trends in COPD morbidity and mortality were investigated among the population of Tecumseh, Michigan, for the period 1959 to 1987. COPD was mentioned on the death certificates of 11% (102) of deceased men and 13% (24) of deceased women. Forty-one percent of these deaths was attributed to COPD as the underlying cause and the remainder to COPD as a contributory cause. Usage of diagnostic terms changed during the course of the study; emphysema was mentioned on 81% of certificates completed prior to 1968, whereas COPD was entered on 77% of the certificates written after 1978. Proportional mortality rates of COPD increased from 8% during 1959 to 1967 to 13.3% during 1979 to 1987 among men, and from 2.7% during the earlier years to 4.3% during the later years among women. Death rates for COPD and for all causes combined increased among men from the early 1960s to the late 1970s, then declined. Death rates for all causes combined were stable among women, but COPD death rates may have increased. Prevalence rates for chronic bronchitis were lower at the third examination than at the second in both sexes. Prevalence of obstructive airway disease was highest at the first and lower at the second and third examinations in men but not in women. Agreement between study diagnoses of COPD and entry of COPD on death certificates was poor. COPD was recorded on the death certificate for only 21% of men and only 6% of women who had COPD diagnosed at a study examination.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Trends in COPD morbidity and mortality in Tecumseh, Michigan. 278 59

The diagnosis of emphysema has been associated with changes in the appearance of the pressure-volume (P-V) curve: reduced maximal recoil pressure, increased lung volume, and a shift in the position of the curve to the left. In our clinical practice, we have observed that patients with chronic obstructive lung disease (COPD) commonly had P-V curves with reduced maximal elastic recoil that are difficult to classify according to the classic description of the P-V curve in emphysema. In order to study the variability of P-V curves, we studied 39 cigarette smokers attending a pulmonary clinic (age, 61 +/- 1 yr; smoking history, 45 +/- 3 pack-years; mean +/- SEM) and compared them with 20 patients with alpha-1-antitrypsin deficiency (AATD) (age, 41 +/- 2 yr; 13 smokers with a smoking history of 17 +/- 2 pack-years, and seven nonsmokers). Subjects underwent spirometry, lung volume, and diffusing capacity measurements as well as static deflation P-V curves. To characterize the P-V curves, we used transpulmonary pressure at 90% of TLC (PL90) as a measure of overall recoil and specific compliance (Csp) as a measure of the slope of the initial part of the P-V curve. The curves of non-AATD smokers were classified into three groups: 13 had PL90 greater than or equal to 80% predicted (Group I), 13 had PL90 less than 80% predicted and Csp greater than or equal to 0.08 (Group II), and 13 had PL90 less than 80% predicted and Csp less than 0.08 (Group III).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pressure-volume curves in smokers. Comparison with alpha-1-antitrypsin deficiency. 278 62

The normal respiratory function of the larynx has been described in detailed reports in both the otolaryngology and the respiratory physiology literature. The role of the posterior cricoarytenoid muscle in vocal cord abduction has been shown to be paramount in laryngeal respiratory function. However, only in recent reports has attention been directed toward disordered laryngeal function as evidenced in pulmonary disorders, such as asthma, or in association with underlying pulmonary disorders, such as asthma (ROAD) or emphysema (COPD). In this article, cases will be presented to demonstrate the role of disordered laryngeal function appearing as pulmonary disease and associated with various degrees of underlying pulmonary disease. The effect on pulmonary function tests and the role of treatment will be discussed.
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PMID:Laryngeal dysfunction and pulmonary disorder. 308 69

453 patients aged over 40 hospitalized with severe COPD, a mean age of 66 years and mean FEV1 of 1.24 litres (49% predicted) were prospectively followed up for 5 years (341) and 10 years (195) respectively. 5-year survival was 47%, while 10-year survival was severely limited despite uniform therapy (23%). Average survival was only 4.4 years. Of the 15 prognostic factors considered, initial FEV1, body-weight, smoking behavior, diagnosis of bronchial asthma or emphysema, finding of p pulmonale and reversibility of bronchodilation had a significant influence on survival. The average decrease in FEV1 per year was only 28 ml in the surviving patients. It was lowest in those with FEV1 reversibility of more than 105 ml after bronchodilation. A maximum increase of FEV1 of more than 485 ml during the initial hospitalization, together with stopping smoking, were the next two important factors in FEV1 decrease. Mean annual NO2 concentration at home did not correlate significantly with survival and FEV1 decrease.
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PMID:[Course and prognosis of chronic obstructive lung disease over 5 and 10 years]. 317 77

Patterns of radioaerosol deposition in patients with COPD may be interpreted on the basis of derangements in convective ventilation. Thus, in patients with asthma, central deposition is consistently associated with increased airway resistance, in the absence of acute attack, indicating that in this condition major airways are usually the site of bronchial constriction. In patients with chronic bronchitis, inhomogeneous and spotty deposition patterns are strongly associated with indexes of uneven and wasted ventilation and may be explained on the basis of destruction or obstruction of peripheral airways. Spotty deposition is ascribed to very uneven convective ventilation reduced to a limited number of air streams, as opposed to the normal situation of a very high number of air streams giving rise to the uniform pattern of radioaerosol deposition. Patients with emphysema show less distinctive patterns of deposition and may resemble those of the patients with asthma and chronic bronchitis. Nevertheless, the deposition features are very useful to better characterize the patient even in the emphysematous group. From the practical point of view, the features of aerosol deposition provide useful information for evaluation and treatment of the patient with COPD. They may also prove useful to better define and characterize the different disease entities grouped as COPD.
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PMID:Imaging of ventilation in chronic obstructive pulmonary disease. 329 73

The importance of proteases and protease inhibitors for the pathogenesis of pulmonary emphysema and chronic bronchitis of the horse is described. Endogenous elastases from neutrophil granulocytes and macrophages, which probably provoke emphysema in the human being, are not relevant in horse emphysema. Exogenous elastases from different species of streptomyces may be responsible for emphysema generation in this species. Part of the exogenous elastases are poorly or not inhibited at all by the equine blood protease inhibitors especially by alpha 1-protease inhibitors. A disorder similar to genetic alpha 1-protease inhibitor deficiency in the human being could not be found in the horse. Proteases and protease inhibitors are probably also relevant for the pathogenesis of chronic bronchitis. Neutral proteases from neutrophil granulocytes may be relevant as initiators or amplifiers of an inflammation in the human being and in the horse. Under physiological conditions the proteases are controlled by the secretory protease inhibitor called HUSI-1 in the human being. In contrast, the horse lacks a protease inhibitor proper to secretion in its respiratory ducts. Protease activity, which correlates with the degree of the COPD, was detected in equine inflamed tracheobronchial secretions. This finding is useful in diagnostic evaluation of the individual disease.
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PMID:[Proteases and protease inhibitors of possible clinical relevance in COPD of horses]. 332

In this study, functional evolution over ten years was evaluated in 13 patients with early emphysema. The diagnosis was made on the basis of a decrease in single-breath DCO (55 +/- 14 percent predicted, mean +/- 1 SD), a loss of elastic recoil (CL,st = 0.76 +/- 0.25 L/cm H2O), and only minor airway obstruction (FEV1 = 87 +/- 13 percent predicted, Sgaw = 0.09 +/- 0.04 cm H2O-1.s-1), and compatible chest radiographs. During the ten years, there was a decrease in FEV1 of 0.89 +/- 0.40 L p less than 0.001), with a range of 0.20 to 1.55 L (which could not clearly be related to smoking habits or to initial lung function), a decrease in elastic recoil (p less than 0.05, with a decrease of Ptp, TLC by 6 +/- 7 cm H2O; p approximately equal to 0.05), an increase in TLC of 0.46 +/- 0.80 1 (p approximately equal to 0.05), and in RV/TLC of 9 +/- 3 percent (p less than 0.001). The resistance of the upstream segment (ratio Ptp/Vmax) increased slightly but generally remained within normal limits. In conclusion, patients with early emphysema resemble those with classic COPD, with a mean yearly decline in FEV1 similar to that in COPD.
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PMID:Early emphysema. Ten years' evolution. 339 13

We studied the acute effect of a single, oral dose of 200 mg almitrine and of placebo on arterial blood gas tensions, ventilation, gas exchange and pulmonary mechanics in 28 patients with chronic obstructive bronchitis and emphysema (COPD), 20 patients with bronchial asthma and 10 patients with interstitial lung disease. Almitrine significantly increased PaO2 in COPD, had a borderline effect in bronchial asthma and no effect in lung fibrosis. In all groups of patients almitrine significantly increased minute ventilation and decreased arterial carbon dioxide tension (PaCO2). Placebo had no effect on arterial oxygen tension (PaO2) and PaCO2 in any of the groups. Therefore, despite similar effects on ventilation, the improvement of arterial PO2 by almitrine depends on the underlying disease.
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PMID:The acute effect of a single oral dose of 200 mg almitrine on gas exchange in patients with chronic obstructive bronchitis and emphysema, bronchial asthma and lung fibrosis. 369 32


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