Inspiratory gas flow induced by cardiac systole.

This study was made to quantify the inspiratory gas flow pulse produced by cardiac systole. Ten adults (9 men, 1 woman; age 24-65 yr) were studied, of whom two had respiratory muscle weakness. The inspiratory flow pulse commenced 50-60 msec after the R wave of the ECG and lasted 106 (SD22) msec. In eight subjects seated and breathing through a mouthpiece, the flow pulse reached a peak of 120 (SD 58) ml sec-1 and displaced a volume of 6.6 (SD 2.3) ml (range 3.6-9.9 ml). Similar results were obtained using a nasal mask. By adding an external airway resistance, the effective intrathoracic pressure responsible for inspiratory flow was estimated to be -0.21 (SD 0.03) cm H2O. Duplicate studies showed little variation in pulse volume. The mechanism of the inspiratory gas flow pulse and its contribution to gas exchange is discussed.

Estimating alveolar surface area during life.

Alveolar surface area (Sa) may be derived from measurements of total lung capacity (TLC) and mean linear intercept (Lm), an estimate of average airspace size. Because the index of pulmonary distensibility, K, is a function of Lm, we were able to derive Lm from ln K using their respective age regressions and estimated Sa in 147 healthy subjects. K was obtained from exponential analysis of static pressure-volume data. TLC was measured in a body plethysmograph. As an estimate of airspace size, the value used for Lm was shown to be appropriate for the air-inflated lung at TLC. In 95 men (mean age 40 +/- 16 SD years), Sa was 118 (SD 22) m2 and in 52 women (mean age 38 +/- 17 SD years) it was 91 (SD 18) m2 and Sa decreased with age (P less than 0.001). In a morphometric study, Thurlbeck (Am. Rev. Respir. Dis. 95: 765-773, 1967) obtained smaller values for Sa (owing to the use of a smaller lung volume) and a similar decrease in Sa with age as that found here. Providing a standardised methodology is used for measurement of K, the present method allows a reasonable estimate of Sa to be obtained during life.

Effect of the chest wall and blood volume on pulmonary distensibility.

To determine the reason for increased pulmonary distensibility in excised lungs, we performed deflation pressure-volume (PV) studies in 24 dogs. Exponential analysis of PV data gave K, an index of distensibility. Lung volume was measured by dilution of neon. Compared with measurements obtained in the supine position, with the chest closed, and with esophageal pressure (Pes) to obtain transpulmonary pressure, K was not changed significantly with the chest strapped, with pleural pressure to obtain transpulmonary pressure, or with the chest open. From displacement of PV curves obtained in the supine position and with the chest closed or open, we estimated that Pes was 0.18 kPa greater than average lung surface pressure. An increase in K in the prone and head-up positions was attributed to a traction artifact decreasing Pes. Exsanguination increased K and produced a relative increase in gas volume. These results show that overall pulmonary distensibility is unaffected by an intact chest wall. An increase in K and gas volume after exsanguination probably reflects a decreased pulmonary blood volume, with collapse of capillaries increasing the alveolar volume-to-surface ratio.

Decreased pulmonary distensibility and pulmonary barotrauma in divers.

Pulmonary distensibility, lung volume and conductance were measured in 14 men (mean age 22 (SD 3) years) who suffered pulmonary barotrauma (PBT) during shallow water diving. Exponential analysis of static pressure-volume date obtained during deflation of the lungs gave K, and index of distensibility. The pulmonary conductance-recoil pressure (GL-PL) relationship was also obtained during deflation. Total lung capacity (TLC) was measured in a body plethysmograph or by nitrogen washout. The results were compared with 34 male nonsmokers and 10 healthy male divers. Mean lung volumes and FEV1 did not differ significantly in the three groups. In the PBT group K was decreased and recoil pressure was increased; the slope of the regression of GL and PL was decreased indicating stiffer airways. Decreased K reflects a decreased airspace size. Smaller airspaces increase the surface component of recoil pressure which increases the stress in tissue fibres. Relatively stiff airways may magnify the elastic stresses in peribronchial alveolar tissue increasing the possibility of rupture of alveolar walls with interstitial gas dissection.

Lung volume and distensibility in insulin-dependent diabetes mellitus.

The effect of insulin-dependent diabetes mellitus on pulmonary function was studied in 22 diabetic nonsmokers (11 men) with a mean age of 40 yr (SE, 4 yr) and no history of cardiorespiratory disease. Exponential analysis of static pressure-volume data obtained during deflation of the lungs gave the exponent K, an index of pulmonary distensibility. In the diabetic subjects, mean values for total lung capacity, functional residual capacity, VC, and FEV1 were similar to predicted values. Diffusing capacity, K, and in K did not differ significantly from corresponding values in healthy subjects. The regression of in K on age was significant (R = 0.52; p less than 0.01) and similar to that obtained for 124 healthy subjects. The findings show that insulin-dependent diabetes mellitus does not affect pulmonary function. This study does not support the routine testing of lung function in otherwise well diabetic nonsmokers.

Management of fibrosing alveolitis with polymyositis dermatomyositis.

A 38-year-old man with polymyositis-dermatomyositis developed acute life-threatening fibrosing alveolitis. We report a two year follow-up of this patient, during which control of alveolitis was obtained using prednisolone, and was maintained with the addition of cyclophosphamide. Relapse of myositis responded to increased prednisolone. Serial measurements of vital capacity and transfer factor assisted management of alveolitis, but changes in vital capacity preceded changes in transfer factor, and were more convenient to perform during frequent outpatient review.

Decreased pulmonary distensibility in fibrosing alveolitis and its relation to decreased lung volume.

The relation between pulmonary distensibility, lung volume, and elastic recoil pressure was examined in 45 patients (38 men) with cryptogenic fibrosing alveolitis (mean age 61 (SD 14) years). Exponential analysis of static pressure-volume data obtained during deflation of the lungs gave the exponent K, an index of the distensibility of the remaining inflatable lung tissue. Total lung capacity (TLC) was measured in a body plethysmograph or by nitrogen washout. The results were compared with values obtained in 147 healthy subjects (95 men), of mean age 39 (SD 16) years. Fibrosing alveolitis decreased K by 0.62 (SEM 0.04) kPa-1. This decrease was approximately equal to 2 SD of the regression of log K on age in healthy subjects. TLC was decreased to a mean of 70% (SD 14%) predicted in the patients with fibrosing alveolitis. Lung recoil pressure at maximum inspiration was about twice the expected value and regression analysis showed that most of this increase was related to the decreased K rather than to the decreased TLC. In the men with fibrosing alveolitis the regression of height standardised TLC (TLC/Ht3) on K was significant (p less than 0.02); the regression slope was similar to that for 95 healthy men, but was displaced to a smaller lung volume. The dependence of TLC/Ht3 on K is consistent with the close relation between K and peripheral airspace size found in normal lungs. In fibrosing alveolitis decreased pulmonary distensibility probably reflects a decrease in airspace size, whereas most of the decrease in lung volume reflects the loss of inflatable tissue in the fibrotic process.

Rate of increase in pulmonary distensibility in a longitudinal study of smokers.

To examine the hypothesis that an abnormally rapid increase in pulmonary distensibility occurs in cigarette smokers, 39 adult smokers (24 men), mean age 47 (SD 8) years, who were not disabled were studied on two occasions over a mean interval of 3.5 (SD 0.5) years. Exponential analysis of static pressure-volume data obtained during deflation of the lungs gave the exponent K, an index of distensibility. Total lung capacity (TLC) was measured in a body plethysmograph. At entry into the longitudinal study means values for K and static recoil pressure in the 39 smokers available for follow up were similar to those obtained in the original group of 101 smokers (73 men), mean age 42 (SD 11) years, in the cross sectional study. Over the interval of the study, ln K and TLC increased and FEV1 decreased at rates greater than those found in a previous longitudinal study of 34 non-smokers (24 men), mean age 42 (SD 15) years. In the longitudinal study of smokers the observed changes in K and in recoil pressure over the interval of study were greater than the values obtained from the regression slopes found in the cross sectional study of smokers. On the basis of the regression model used previously in the longitudinal study of non-smokers, the age coefficient for ln K was greater than that found in the non-smokers (p less than 0.01). The regression model also showed that the slope of ln K on age increased in older subjects. Because K is related to peripheral airspace size, a rapid rate of increase in K identifies smokers in whom airspace size is increasing abnormally rapidly. In this study the rate of increase in K and the variation between subjects was sufficient to explain the magnitude of the increased pulmonary distensibility found in cigarette smokers who present with emphysema.

Chronic eosinophilic pneumonia in a patient with ataxia telangiectasia.

The first reported case of chronic eosinophilic pneumonia in a patient with ataxia telangiectasia is described. The patient displayed the immunoglobulin deficiencies and abnormalities of lymphocyte numbers characteristic of ataxia telangiectasia. Treatment with corticosteroids led to a dramatic recovery. The proposed pathogenetic mechanisms of chronic eosinophilic pneumonia are discussed in the light of the immunological abnormalities associated with ataxia telangiectasia.

Malignant asthma presenting as right heart failure.

Studies are reported of four patients (all lifetime non-smokers) who presented with right heart failure as a consequence of unrelieved asthmatic airways obstruction. These patients demonstrated severe airways obstruction with crackles on auscultation and hypercapnia. As shown here, such a presentation, without the usual pattern of dyspnoea and wheeze, tends to obscure the diagnosis and delays effective treatment. In three of the patients, treatment to relieve airways obstruction improved gas exchange, and the heart failure resolved. In the remaining patient, improvement was limited, and death ensued from respiratory failure. In patients who present with right heart failure, a relationship with airways obstruction and respiratory failure should be considered and assessed by objective tests. Delays in the effective treatment of these patients may result in the progression of their disease to a stage at which airways obstruction no longer responds to medical therapy.

A longitudinal study of pulmonary distensibility in healthy adults.

To assess changes in pulmonary distensibility with age in a longitudinal study, 34 healthy non-smoking adults were examined on two or more occasions over an interval of 6.0 +/- 1.8 yr (mean +/- SD). Exponential analysis of static pressure-volume data obtained during deflation of the lungs gave the exponent, K, an index of distensibility. Total lung capacity (TLC) was measured in a body plethysmograph and increased over the interval of study. The results were compared with findings in a previous cross-sectional study of 124 subjects. At entry into the longitudinal study, mean values for K and static recoil pressure were similar to those obtained for subjects in the cross-sectional study. Over the interval of study, K increased more in subjects with higher values for K (older subjects) supporting the use of a logarithmic analysis of K on age. Using a statistical model which allowed for a variable number of observations and for variance of K between subjects, the increase in ln K with age was similar to that found in the cross-sectional study. From the relationship between K and the average size of airspaces (mean linear intercept, Lm) demonstrated previously in excised lungs, it is shown that the reported increase in Lm with age suffices to explain the increase in K with age in intact subjects.

Pulmonary distensibility and ventilatory function in smokers.

To define the increase in pulmonary distensibility preceding the development of emphysema, we studied 101 cigarette-smoking volunteers, 73 males and 28 females between the ages of 18 yr and 60 yr (mean 42 yr), who were not disabled. A single exponential function fitted to deflation static pressure-volume data gave the exponent K, an index of distensibility. Total lung capacity (TLC) was measured with a body plethysmograph. Values for VC, FEV1 and mid-expiratory flow were only slightly less than values obtained in nonsmokers. K was increased in smokers and increased with age at a greater rate than in nonsmokers, but smokers were unevenly affected. In relation to height, TLC was increased in male smokers and the increase was directly related to the increase in K. The findings show that increased pulmonary distensibility may be identified in smokers without airway obstruction. Because K is directly related to the size of peripheral airspaces, increased pulmonary distensibility in smokers implies an increase in the size of airspaces caused by an action of cigarette smoke, and taking place in asymptomatic subjects.

Large lungs after childhood asthma: a consequence of enlarged airspaces.

The long-term effects of asthma on lung volume were investigated in 18 asthmatic patients during periods of remission from airway obstruction; ten had developed asthma in childhood (before 8 years of age) and eight after the age of 18 years. Subjects whose asthma began in childhood had an increased total lung capacity (TLC) on average; adult-onset asthmatics had normal mean lung volumes. Exponential analysis of static pressure-volume curves in these subjects showed that the childhood-onset asthmatics had lungs of increased distensibility, while adult-onset asthmatics had lungs of normal distensibility. In a further ten adults selected for having had asthma in the past and an increased vital capacity, all had developed asthma in childhood, had lungs of increased distensibility and an increased TLC. Increased distensibility and an increased TLC were closely associated within individuals. The close relationship between distensibility and the size of peripheral air spaces demonstrated in mammalian lungs, suggests that asthma in childhood may increase TLC and distensibility because of an increase in the size of peripheral airspaces.

Chronic airflow obstruction. Evolution of disordered function in cigarette smokers.

Measurements of the mechanical behaviour of the lung, which reflect lung structure, have been used to elucidate the evolution of chronic airflow obstruction in male cigarette smokers and subjects with pulmonary emphysema. The exponent K, from a single exponential function fitted to static pressure-volume data, is an index of lung distensibility directly related to the size of peripheral airspaces. Elastic recoil pressure is inversely related to K. Conductance measured during forced and interrupted deflations of the lungs reflects the dimensions of airways. K increased abnormally with age in smokers suggesting an increase in the airspace size caused by the effects of cigarette smoke which probably acts by intensifying elastase activity in lung tissue. Decreased conductance implying narrowing of airways is found in young smokers, but conductance rises and airways become more distensible in older smokers. A progressive increase in K (with decrease in recoil pressure) and a decrease in conductance are responsible for the advancement of severe airflow obstruction in cigarette smokers.