Composite flow-volume curves matched at total lung capacity in the study of density dependence of maximal expiratory flows.
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Methacholine tests are widely used as a diagnostic aid for asthma. Their strength has been reputed to be the high sensitivity and very infrequent occurrence of false-negative test results (ie, high negative predictive value). There are 2 commonly used methods that have been outlined by the American Thoracic Society. These methods were thought to give equivalent results. However, in 3 investigations in which we have compared the 2 methods, we have demonstrated a marked lack of comparability. In subjects with borderline to mild airway responsiveness (tidal breathing, methacholine PC20 >2 mg/mL), the 5 deep inhalations required of the dosimeter method produce marked bronchoprotection in some subjects with asthma. The result of this bronchoprotection is that in 55 subjects with asthma, 50% of those whose tidal breathing PC20 value was greater than 2 mg/mL and 25% of the total had negative methacholine challenge results. This indicates that the standardized dosimeter method has an unacceptable loss of diagnostic sensitivity. We recommend that the dosimeter method not be performed as outlined by the American Thoracic Society and that methacholine should be administered by means of submaximal inhalations or tidal breathing.
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Various radiological methods for estimating lung volume depend on anatomical correlation with the volume of the thorax. It is not possible to derive general factors for correcting these methods and the accuracy and reliability can be improved only by introducing individual corrections. It must also be remembered that radiometric calculations of gas volume and lung capacity depend on the assumption that there is a fixed relationship between these. This, however, is untrue for a whole series of patho-physiological circumstances. Because of these problems, we describe our own radiometric method.
The authors studied in 50 healthy subjects the cilindroid and the planimetric method for the radiological measurement of TLC. Both methods proved to be accurate, but the first showed a better relation with the pletismographic measurements; in both methods the individual variability was very limited (5 divided by 6%). In a screening protocol comprising double-projection chest X-ray, the radiological measurement of TLC seems to be very useful to evaluate with simplicity and realiability its values and its variations in time.
The ventilatory capacity, total lung capacity and transfer factor with their respective subdivisions have been measured on 254 healthy British boy and girl twins aged 8-16 yrs. The logarithmic regression relationships of lung function on stature have been compared with those on sitting height and on stature plus indices of body muscle and fat. The regressions on stature and on sitting height describe the results with similar precision, but stature is marginally better; either index may be used as the reference variable. For the description of inspiratory capacity and of all indices which include this volume (e.g. vital capacity, total lung capacity and transfer factor), additional precision is secured by adding to the regression equation on stature a term for fat-free mass or body mass divided by the square of the stature; for the description of functional residual capacity, the inclusion of a term for % body fat similarly reduces the variance about the regression equation. The difference in lung function between boys and girls is smaller when the function is related to stature than to sitting height. It is further reduced when fat-free mass/sature and % body fat are also included in the prediction equations. The equations may be used to obtain reference values for indices of lung function in similar subjects.
INTRODUCTION: Liquid lung fixing through the trachea to a pressure of 25 cmH2O is currently accepted to be ideal. However, some studies do not seem to confirm that assumption. MATERIAL AND METHODS: The lungs of Fischer rats were filled with fixing liquid to four different pressures: 20 cm, 25 cm, 30 cm and 35 cmH2O. The fixed lungs were processed for inspection under a light microscope for morphometric study. The following variables were recorded: lung volume, tissue volume, air volume, internal alveolar surface (IAS), alveolar chord to measure the size of the distal air space, and the number of alveoli. Statistical comparisons were performed. RESULTS: Lung volume increased with insufflation pressure, with significant differences related to pressure increases from 20 cm to 25 cm and from 30 cm to 35 cmH2O. Air volume did not change, although tissue volume changed when pressure increased from 20 cm to 30 cmH2O and from 30 cm to 35 cmH2O. The increase of tissue volume was related to extravasation of interstitial fixer. The number of alveoli increased with pressure from 20 to 30 cm and from 30 to 35 cmH2O. IAS increased with pressure from 20 cm and all the other pressures. Alveolar chord, which is related to size of alveoli, decreased significantly as pressure increased from 20 cm to 25 cm. CONCLUSION: A pressure of 25 cmH2O is ideal for liquid fixing of lung volumes. With lower pressures the lung is partially distended and with higher pressures the fluid can pass into the interstitial space.
An increased TLC has been reported during exacerbations of asthma, but the methods used (helium, dilution, plethysmography) have been subsequently found unreliable in the assessment of lung volumes in patients with obstructive lung disease. To address this problem, we measured TLC (TLC-XR) from posteroanterior and lateral chest roentgenograms obtained during exacerbations (E) of asthma and after recovery (R) using planimetry in 12 asthmatic subjects. At recovery, TLC was also measured by plethysmography or by helium dilution for comparison with the radiographic measurement. The plethysmographic measurements were made with a panting frequency less than 1 Hz to allow for airway obstruction. A chest radiologist also used independent radiologic measurements of hyperinflation (lung height, diaphragmatic arc height, rib counts) to assess lung volumes. Mean FEV1 during E was 1.43 +/- 0.38 L, and significant improvement occurred at R (FEV1 = 2.81 +/- 0.58 L, p less than 0.05). Of the independent radiologic variables measured, only an increase in lung height distinguished the two sets of radiographs. Mean TLC-XR (E) (6.01 +/- 1.62 L) was significantly greater than mean TLC-XR (R) (5.44 +/- 1.17 L, p less than 0.05). TLC measured radiographically at recovery was strongly correlated (r = 0.94) with TLC measured by plethysmography or helium dilution. We conclude that acute reversible increases in TLC do occur during exacerbations of asthma and that these changes are only readily detected by formal planimetry.
OBJECTIVE: Quality control in the clinical pulmonary function laboratory has been well developed for spirometry and diffusing capacity but not for the measurement of TLC. The purpose of the present study was to test two approaches to this problem. First, we compared TLC by body plethysmography (TLCb) with a value predicted from TLC measured by multibreath helium dilution (TLCm). Concordance between the measured and predicted values would imply the validity of the measurements. Second, we measured the test-retest variability of TLCb, TLCm and TLC measured by single breath helium dilution (TLCs) to assess the consistency of the measurements. METHODOLOGY: We performed a prospective study of 815 veterans. RESULTS: The prediction of TLCb from TLCm improved (r2 increased from 0.44 to 0.64) when FEV1/FVC and the difference between TLCm and TLCs were added to the model. The coefficient of variation for test-retest of TLCs, TLCm and TLCb were 8.9, 7.1 and 5.4%, respectively. Of all tests, 5.9% were inconsistent based on pathophysiology or measurement error and attributed mostly to TLCm. CONCLUSIONS: Prediction of TLCb from TLCm was not sufficiently accurate as to be useful for quality control. Comparison of TLCs, TLCm and TLCb may be useful for determining the internal data validity.
BACKGROUND: It is well established that patients with longstanding weakness of the respiratory muscles have a reduction in lung distensibility. Although this occurs in most patients without any radiographic changes suggesting parenchymal lung disease, it has been attributed to the development of microatelectasis. METHODS: A high resolution computed tomographic (CT) scanner was used in eight patients with traumatic tetraplegia and six patients with generalised neuromuscular disorders to look for areas of atelectasis. With the patient in the supine posture scans of 1 mm thickness were obtained at total lung capacity at intervals of 1 cm from the apex to the base of the lung. RESULTS: Vital capacity, total lung capacity, and inspiratory muscle strength were reduced to a mean of 59.5%, 73.9%, and 51.1% of predicted values, respectively. Static expiratory lung compliance was decreased in 12 of the 14 patients and averaged 69.1% of the predicted value. The CT scans revealed only small areas of atelectasis in one tetraplegic patient and in one patient with a generalised neuromuscular disorder; no parenchymal abnormality was seen in the other 12 patients. CONCLUSIONS: In many patients with chronic weakness of the respiratory muscles the reduced lung distensibility does not appear to be caused by microatelectasis. It might be related to alterations in elasticity of the lung tissue.
A computerized system has been developed to analyze the parameters that can be derived from the nitrogen washout curve. Analog signals for air flow, volume, and nitrogen concentration are entered either on-line or off-line into a 24,000 mini-computer. The program calculates vital capacity, total lung capacity, and residual volume, as well as the slope of phase III, closing volume in liters, total lung capacity, residual volume, closing capacity, closing volume/vital capacity ratio, and closing capacity/total lung capacity ratio. Validation tests showed excellent correlation between hand- and computer-calculated values of closing volume(r=0.864), vital capacity (r=0.997), total lung capacity (r=0.991), and slope of phase III (R=0.926). We concluded that the computerized system for analysis of the expired nitrogen washout curve is as reliable as hand calculations and is immeasurably faster.
BACKGROUND: Chronic heart failure causes disturbances in ventilation and pulmonary gas transfer that participate in limiting peak exercise oxygen uptake (VO(2p )). The beta-adrenergic receptor blocker carvedilol improves left ventricular (LV) function and not VO(2p). This study was aimed at investigating the pulmonary response to changes in LV performance produced by carvedilol in patients with chronic heart failure. METHODS: Twenty-one patients with New York Heart Association class II to III heart failure were randomly assigned (2 to 1) to carvedilol (25 mg twice daily, n = 14) or placebo (n = 7) for 6 months. Rest forced expiratory volume (FEV(1)), vital capacity, total lung capacity, carbon monoxide diffusing capacity, its alveolar-capillary membrane component, pulmonary venous and transmitral flows (for monitoring changes in LV end-diastolic pressure), LV diastolic and systolic dimensions, stroke volume, ejection fraction, and fiber shortening velocity were measured at baseline and at 3 and 6 months. VO(2p), peak ratio of dead space to tidal volume (VD/VT(p)), ventilatory equivalent for carbon dioxide production (VE/VCO(2)), and VO(2) at anaerobic threshold (VO(2at)) were also determined. RESULTS: FEV(1), vital capacity, total lung capacity, carbon monoxide diffusing capacity, and the alveolar-capillary membrane component were impaired in chronic heart failure compared with 14 volunteers and did not vary with treatment. Carvedilol reduced end-diastolic pressure, end-diastolic diameter, and end-systolic diameter and increased ejection fraction, stroke volume, and fiber shortening velocity without affecting VO(2p), VO(2at), VD/VT(p), or VE/VCO(2) at 3 and 6 months. Placebo did not produce significant changes. CONCLUSIONS: In chronic heart failure carvedilol ameliorates LV function at rest and does not significantly affect ventilation and pulmonary gas transfer or functional capacity. These results suggest that improvement in cardiac hemodynamics with carvedilol does not reverse pulmonary dysfunction. Persistent lung impairment might have some role in the failure of carvedilol to improve exercise performance.
Lung function tests (i.e., spirometry, flow volume, and body plethysmography) were performed in 213 patients (age 6-21 years, mean 11.3 years) with hemodynamically significant congenital heart defects: atrial septal defect, ventricular septal defect (VSD), tetralogy of Fallot, aortic stenosis and coarctation of the aorta. We measured lung vital capacity, total lung capacity (TLC), residual volume (RV), the percentage ratio of the latter two measurements (%RV/TLC), maximal expiratory flow rates at 25% and 50% of vital capacity, and specific airway conductance. Pulmonary restriction dominated in patients with tetralogy of Fallot; pulmonary hyperinflation was more frequent in patients with VSD and coarctation of the aorta; and obstruction of the airways was observed most frequently in patients with tetralogy of Fallot. In conclusion, we found a range of pathologic lung function parameters in patients with hemodynamically significant congenital heart defects.
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