Pulmonary ventilation function in patients with asthma. A study of mean maximal expiratory volume velocity (flow rate) as determined by a special apparatus.
Explore the source record for details and available documents.
SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Abnormalities in small airways appear to be important in the evolution of chronic obstructive pulmonary disease. Patients with these pathologic lesions may have normal values for airway resistance and forced expiratory volume in one second. Two new tests, the closing volume (CV) and the dependence of maximal flow on density, are believed to be sensitive to abnormalities in the peripheral airways. The CV test detects an increased nonuniformity of changes in volume of pulmonary units. Reduced dependence of flow on density is believed to result from an increase in the peripheral component of the losses of driving pressure which determine maximal expiratory flow. Both tests differentiate smokers with normal conventional spirometric data from age-matched nonsmokers. Although this evidence suggests that these tests can be used to detect abnormalities in small airways, there is very little pathologic confirmation of this belief. The clinical significance of abnormalities in the results of either of these tests in an otherwise normal person has not yet been determined.
We examined the bronchoconstriction produced by airway hypocapnia in normal subjects. Maximal expiratory flow at 25% vital capacity on partial expiratory flow-volume (PEFV) curves fell during hypocapnia both on air and on an 80% helium- 20% oxygen mixture. Density dependence also fell, suggesting predominantly small airway constriction. The changes seen on PEFV curves were not found on maximal expiratory flow-volume curves, indicating the inhalation to total lung capacity substantially reversed the constriction. Pretreatment with a beta-sympathomimetic agent blocked the response, whereas atropine pretreatment did not, suggesting that hypocapnia affects airway smooth muscle directly, not via cholinergic efferents.
Explore the source record for details and available documents.
The potential for introducing bias in studies of pulmonary function by the exclusion of subjects with nonrepeatable measurements was examined in a cohort of Vermont granite workers followed for five years. At each annual survey, a "test failure" was defined as a test in which the two largest forced expiratory volumes in one second (FEV1) differed by more than 200 ml. "Persistent test failure" was defined in terms of 1) the number of test failures for each worker over the six surveys and 2) the difference between the two best efforts at each survey, averaged over all surveys for each worker. The rate of FEV1 loss was estimated for each subject based only on repeatable measurements. It is widespread practice to exclude subjects from analysis who do not perform repeatable lung function tests. The authors found that subjects with persistent test failure were losing FEV1 at a faster rate than subjects without. The results suggest that the application of rigid repeatability criteria may bias epidemiologic findings by the exclusion of many subjects with accelerated loss of lung function.
Explore the source record for details and available documents.
Static and dynamic lung volumes, flow-volume curve in air and after He-O2 were carried out in 5 normal subjects baseline, immediately after rapid infusion of 2 litres of normal saline, and then 15, 30 and 60 min after. At the end of the infusion, a marked reduction of delta MEF50, FVC, FEV1, MEF50, MEF25 and an increase of Viso V and CV/VC were observed in all the subjects. The poor response to He-O2 suggests a predominant increase of small airway resistance after rapid infusion. In the recovery phase, He-O2 tests promptly returned to control values, while an increased CV/VC was detectable until 30 min after the infusion.
The author has investigated the feasibility of DME 25--75/C.V. as a test for the detection of ventilatory disturbances of the small aerial pathways, by comparing the results with those of other tests considered to be very sensitive, such as Vmax 50% and 25% of C.V., Vmax 50% and 25% of C.V. of an air curve and that of a He-O2 mixture (80%--20%), and the isoflow volume. The study was carried out in 90 subjects, divided in two groups in relation to the values obtained by the DME 25--75/C.V., as follows : 44 subjects with bronchial obstruction and 46 subjects showing functional signs of obstruction of the small aerial pathways. The results have indicated that the two populations classified according to this criterium are statistically different also with regard to other tests applied, indicating the feasibility of the test under study, which, compared to other tests, has the advantage of higher sensitivity in relation to the simplicity of the device.
Explore the source record for details and available documents.
The changes in maximum expiratory flow rates after washing out lung air with a helium/oxygen mixture (He/O2, 80 : 20) were measured in 24 patients with chronic irreversible airflow obstruction (FEV1 1.77 +/- SD 0.39 litres; FVC 3.62 +/- 0.59 litres), and in six normal subjects. The percentage increase in flow breathing He/O2 was variable; however, it was similar in normal subjects and in patients with airflow obstruction, and in both groups decreased at low lung volumes. Contrary to previous studies, only three patients with chronic airflow obstruction failed consistently to increase flow rates by greater than or equal to 20% when breathing He/O2 at all lung volumes measured. In six normal subjects and 12 patients with chronic airflow obstruction airway gas viscosity was increased by breathing a neon/oxygen mixture (Ne/O2, 80 : 20). The response to Ne/O2 was again variable (normal subjects delta Vmax.40 4 +/- SD 14%; patients delta Vmax.40 18 +/- 8%). Only two normal subjects and one patient with airflow obstruction consistently reduced their flow rates when breathing Ne/O2. These results indicate either that there is no difference in the distribution of airflow resistance in normal subjects and in patients with chronic airflow obstruction, or that density as well as viscosity is an important determinant of flow in very small airways. In either case, He/O2 breathing is not a good discriminator of the site of airflow obstruction.
Explore the source record for details and available documents.
In an effort to evaluate the relationship between the site of air-flow obstruction and rate of improvement with therapy, we studied 20 asthmatics with spirometry, before and after bronchodilator, using air and 80% helium-20% oxygen (He-O2). Studies were obtained on 3 consecutive days after hospital admission and approximately 18 days after discharge. Greater He-O2 response ([Vmax50(He-O2)--Vmax50(air)]/predicted Vmax50) X 100, was associated with: less cigarette consumption (p less than 0.02), lesser frequency of chronic productive cough (p less than 0.02), more symptom-free intervals (p less than 0.02), and greater frequency of allergic rhinitis (p less than 0.03). Patients with greater He-O2 response (Group 1) reached maximal improvement in air flow by Hospital Day 2, whereas those with a lesser He-O2 response (Group 2) continued to improve throughout the observation period. The Group 1 mean peak expiratory flow rate (PEFR) improved by 24% of predicted per day to maximum, which was significantly greater (p less than 0.025) than the 11% per day rate of improvement of Group 2. The He-O2 response remained relatively stable throughout the course of the study except for 3 patients who dramatically improved their response with therapy. A highly significant correlation, adjusted for regression to the mean, (r = 0.95, p less than 0.0001) was found between mean baseline percent predicted Vmax50 and the mean He-O2 response. After adjustment for regression to the mean, there was no significant relationship between the degree of prebronchodilator He-O2 response and increase in He-O2 response with bronchodilator.(ABSTRACT TRUNCATED AT 250 WORDS)
We hypothesized that contractions of the expiratory muscles carried out to the point of task failure would cause an increase in muscle sympathetic nerve activity (MSNA). We measured MSNA directly in six healthy men during resisted expiration (60% maximal expiratory pressure) leading to task failure with long [breathing frequency (f(b)) = 15 breaths/min; expiratory time (TE)/total respiratory cycle duration (TT) = 0.7] and short (f(b) = 30 breaths/min; TE/TT = 0.4) TE. Both of these types of expiratory muscle contractions elicited time-dependent increases in MSNA burst frequency that averaged +139 and +239%, respectively, above baseline at end exercise. The increased MSNA coincided with increases in mean arterial pressure (MAP) for both the long-TE (+28 +/- 6 mmHg) and short-TE (+22 +/- 14 mmHg) trials. Neither MSNA nor MAP changed when the breathing patterns and increased tidal volume of the task failure trials were mimicked without resistance or task failure. Furthermore, very high levels of expiratory motor output (95% maximal expiratory pressure; f(b) = 12 breaths/min; TE/TT = 0.35) and high rates of expiratory flow and expiratory muscle shortening without task failure (no resistance; f(b) = 45 breaths/min; TE/TT = 0.4; tidal volume = 1.9 x eupnea) had no effect on MSNA or MAP. Within-breath analysis of the short-expiration trials showed augmented MSNA at the onset of and throughout expiration that was consistent with an influence of high levels of central expiratory motor output. Thus high-intensity contractions of expiratory muscles to the point of task failure caused a time-dependent sympathoexcitation; these effects on MSNA were similar in their time dependency to those caused by high-intensity rhythmic contractions of the diaphragm and forearm muscles taken to the point of task failure. The evidence suggests that these effects are mediated primarily via a muscle metaboreflex with a minor, variable contribution from augmented central expiratory motor output.
Explore the source record for details and available documents.
Bronchospasm following exercise is a phenomenon which occurs in most patients with reversible airway disease. The pathophysiologic mechanism leading to this bronchoconstriction with exercise has not yet been defined. Recently, prostaglandins have been implicated in the etiology of asthma. The purpose of this investigation was to determine changes in plasma prostaglandins occurring during exercise-induced asthma. Eight ambulant asthmatics were chosen for baseline pulmonary spirometry and peripheral venous blood prostaglandin E and F levels. The asthmatics were then exercised to 80% of their age-predicted maximal heart rate via a multistage branching treadmill protocol. At 5, 15, and 30 min following exercise, pulmonary spirometry was again performed and peripheral venous blood collected at the indicated times. Clinical bronchospasm as characterized by audible wheezing and greater than 15% decrease in FEV1 and MMEFR was obtained in all of the asthmatics. Peripheral PGE and PGF2alpha determinations following this exercise protocol were not altered significantly: (PGE: 0 min, 238; 5 min, 185; 15 min, 248; 30 min, 256 pg/ml); (PGF2alpha: 0 min, 50; 5 min, 24; 15 min, 25; 30 min, 17 pg/ml) (p less than 0.1). In summary, no significant change in peripheral blood prostaglandin E and F2alpha levels as determined by radioimmunoassay was noted at the time of exercise-induced bronchospasm.
Explore the source record for details and available documents.