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Biomedical subjects

T J Clark

Publications and source records attributed to T J Clark.

At least 109 records · Page 6Linked to original sources

Cigarette smoking in asthma.

A survey was performed of smoking habits and respiratory symptoms of 106 asthmatic patients attending a hospital out-patient clinic. A quarter of the patients were currently smokers and a further quarter were ex-smokers. Less than a third of the smokers complained of symptoms of wheeze or dyspnoea after smoking. Asthmatic smokers had a much higher prevalence of chronic cough but their lung function appeared no lower than non-smokers. Ten asthmatic smokers were selected to contrast their acute bronchial response to smoking a currently marketed cigarette with that of ten asymptomatic smokers. Only four of ten asthmatic patients and two of ten asymptomatic smokers developed acute airway narrowing after smoking despite changes in venous blood nicotine levels which confirmed cigarette smoke inhalation. Many more asthmatic patients smoke than might be expected from the known instability of their airways. Our failure to show frequent and substantial airway reactivity to cigarette smoke in these patients suggests either that cigarette smoke may not be as acutely irritant as might be anticipated or that some asthmatic patients acquire tolerance to it. The effects of chronic cigarette consumption could be demonstrated even in this small sample which suggests that asthmatic patients should be advised to stop smoking, especially as many clinicians expect asthma and smoking to be a rare coincidence.

Adult↗

Practical importance of a preceding full inhalation or exhalation upon the measurement of airway resistance.

1. Airway resistance was measured close to functional residual capacity before and after a full inhalation of total lung capacity, as well as before and after a full exhalation to residual volume. 2. The effects of these volume manoeuvres upon airway resistance (and associated lung volume) were determined in four resting normal male subjects and in six normal men during experimentally induced bronchoconstriction after breathing an air/histamine mist from a Wright's nebulizer. 3. In four men the duration of the effect of a full inhalation upon airway resistance after induced bronchoconstriction was assessed separately. 4. Neither a full inhalation nor a full exhalation altered airway resistance under normal conditions. However, a full inhalation reduced airway resistance in the presence of bronchoconstriction and this effect lasted for a period of 45 s. Even with bronchoconstriction, a full exhalation had no effect on airway resistance. 5. Account must therefore be taken of the potential reduction in airway resistance which may result from a full inhalation, particularly when indirect measurements of airway function which involve a full inhalation, such as forced spirometry, are used to assess airway obstruction.

Airway Resistance↗

Evaluation of methods used to estimate inhaled dose of carbon monoxide.

We have compared estimation of alveolar carbon monoxide measured either as end-expired or mixed-expired carbon monoxide tension with two spectrophotometric estimations of venous blood carboxyhaemoglobin (COHb). Estimation of mixed-expired carbon monoxide proved more convenient for patients than the end-expired method, and this estimation of carbon monoxide exposure discriminated between non-smokers and smokers as well as measurements of COHb. The technique is bloodless, economical, and simple to perform. It should prove a valuable method for validating reported smoking habits of people attending smoking advisory centres and for epidemiological surveys of smoking.

Carbon Monoxide↗

Comparison of normal and asthmatic circadian rhythms in peak expiratory flow rate.

A computer technique (cosinor analysis) has been used to evaluate circadian rhythms in airway calibre in normals and asthmatics. Two hundred and twenty-one normal subjects recorded peak expiratory flow rate (PEFR) at home four times a day for seven days. Rhythm detection was statistically significant in 145 of them (65.6%) who showed a mean amplitude of 8.3% of individual mean PEFR (+/- SD 5.2%). Amplitude was independent of age, sex, atopy, family history of asthma, and smoking habit. Fifteen of them were also studied three times a day for five days in the laboratory with flow-volume loops. Eleven showed significant PEFR rhythms at home. No single measurement from the flow-volume loop showed periodicity in as many of them but rhythms were now also detected in the other four normal subjects in some components of the loop. Fifty-six asthma patients were studied with a similar protocol of PEFR measurement and compared with the 145 rhythmic normal subjects. Mean phases of the normal and asthmatic rhythms were not significantly different with acrophases (peak of rhythm cycle) at 1557 and 1526 respectively. The mean asthmatic amplitude was, however, significantly greater at 50.9%. Nocturnal asthma, therefore, probably represents an exaggeration of a normal circadian rhythm in airway calibre. The amplitude of the PEFR rhythm is an index of bronchial lability and is thus valuable in monitoring asthma patients. An amplitude of greater than 20% should be a useful screening test for asthma.

Adolescent↗

Cigarette smoke inhalation and the acute airway response.

The acute airway response to smoking varying numbers (one to four) of identical cigarettes in rapid succession and smoking single cigarettes of differing tar/nicotine yields was assessed repeatedly in 13 healthy smokers. The airway response was variable, indicating airway narrowing consistently in only three subjects. There appeared no difference between forced spirometry and measurement of airway resistance in detecting the airway response. No relationship was observed between the airway response and amount of smoke inhaled into the lungs as measured either by changes in venous blood nicotine or percentage carboxyhaemoglobin. When five smokers inhaled smoke directly from a cigarette acute airway narrowing was consistently observed. A normal smoking pattern consisting of an initial drag of smoke into the mouth, followed after a pause by inhalation of smoke diluted with air, did not consistently cause airway narrowing although similar amounts of smoke as the direct drag were inhaled as assessed by changes in venous blood nicotine. The manner of smoke inhalation affects the relative concentrations of the different constituents of smoke reaching the lungs and also appears to be the main determinant of the acute airway response to smoking, which was unrelated to the number of cigarettes smoked or the tar content of the smoke. This suggests that patterns of smoke inhalation may influence the pathogenesis of bronchial disease associated with smoking.

Adult↗

Bronchial disease in ulcerative colitis.

Ten patients with ulcerative colitis, all of whom were non-smokers, presented with a productive cough. In six, the chest radiography was normal and cough was the only symptom; three of these patients had a minor obstructive ventilatory defect on testing. Four patients complained of exertional dyspnoea and had both an abnormal chest radiograph with bilateral pulmonary shadows and a mixed obstructive and restrictive ventilatory defect. Bronchial epithelial biopsies from four patients (two with and two without pulmonary shadows) revealed basal reserve cell hyperplasia, basement membrane thickening, and submucosal inflammation, changes more usually associated with cigarette smoking. Inhaled beclomethasone diproprionate relieved cough in seven patients. The occurrence of airway epithelial disease in association with ulcerative colitis raises the possibility of a systemic mechanism affecting both bronchial and colonic epithelium. It does not seem likely that sulphasalazine was the cause of the pulmonary syndrome in these subjects.

Adult↗

Maximal expiratory flow volume curves in workers exposed to asbestos.

We have studied 40 workers with varying industrial exposure to asbestos, using routine spirometry and maximal expiratory flow volume curves (MEFVC). Abnormalities of MEFVC were common and seen in those with normal spirometry and total lung capacity. The high incidence of abnormal MEFVC suggests that air flow dysfunction in small airways may follow prolonged asbestos exposure. Our findings support, therefore, the idea that asbestos exposure may cause an obstruction to airflow arising particularly in small airways, and that one of the common functional abnormalities attributable to asbestos exposure is airways obstruction.

Adult↗

Acute effects of smoking a single cigarette on the airway resistance and the maximal and partial forced expiratory flow volume curves.

The acute airway response to smoking a single cigarette was assessed in eight symptom-free male smokers. The changes in airway function were determined using a computer analysis of maximal and partial expiratory flow volume curves together with measurement of airway resistance. The amount of smoke inhaled was assessed by measuring levels of nicotine in venous blood. When the results of all studies were analysed for the group as a whole only small and inconsistent changes in airway function were observed after smoking a cigarette, although all the subjects appeared to inhale the smoke. Although the group showed inconsistent changes, one subject exhibited a change on all four occasions in the studies using the maximal and partial expiratory flow volume curves. This was seen particularly for Vmax50 and Vmax40 obtained from the maximal and partial expiratory flow volume curves respectively. There appeared to be no difference between the two manoeuvres in their sensitivity to smoke-induced change. One subject showed a response to smoking when airways resistance was measured but this was on only one of two occasions. It is therefore possible that certain smokers are more susceptible to inhaled cigarette smoke and such individuals may be those who develop chronic airflow obstruction. The absence of a group effect was attributed to any smoking response being smaller than the other factors which affect measurements of airway function.

Adult↗

Does sleep cause nocturnal asthma?

The effects of sleep interruption and deprivation were studied in 21 patients with nocturnal asthma. Seven patients were awakened at 0200 on three consecutive night and exercised for 15 minutes. This produced no significant improvement in the overnight fall in peak expiratory flow rate (PEFR) compared with a control night of uninterrupted sleep. In a second study in five patients PEFR was measured at two-hourly intervals to estimate the time of onset of the nocturnal fall in PEFR. On three subsequent nights they were awakened and exercised one hour before this time. This also failed to prevent a fall in PEFR by 0600. Eleven patients, who had followed a similar protocol to the second study, were kept awake until after 0300 or later, and PEFR was observed hourly. Six of them (group A) sustained their usual fall in PEFR while awake, proving that sleep was not responsible for their nocturnal asthma. Five patients (group B) showed little fall in PEFR until they were allowed to sleep, when an appreciable fall was noted on waking at 0600. When sleep deprivation was repeated in two patients in group B, however, they sustained falls in PEFR while still awake. We conclude that the circadian rhythm in PEFR is often in phase with the timing of sleep but sleep does not cause nocturnal asthma. Disruption of sleep therefore has no apparent value in the treatment of nocturnal asthma.

Adolescent↗

A comparison of salbutamol given by pressure-packed aerosol or nebulization via IPPB in acute asthma.

Salbutamol was given by pressure-packed aerosol or nebulizer via IPPB to patients with acute asthma to compare the effectiveness of these methods of inhalation. The results show that both methods produce significant bronchodilatation even in patients admitted with moderately severe asthma (FEV1 about 38% predicted) but a slightly greater improvement may be achieved by IPPB nebulization. Our findings indicate that supervised inhalation of a pressure-packed aerosol of salbutamol may be useful for the initial treatment of asthmatic attacks but confirm the marginal advantage of IPPB nebulization, which should be reserved for patients unable to inhale from a pressure-packed aerosol or failing to respond to its treatment.

Acute Disease↗

Spirometry in healthy men: a correlation with smoking and with mild symptoms.

Symptoms, smoking history, and variates taken from the forced expiratory manoeuvre were studied in a group of 271 healthy men attending a mass radiography unit. It was found that correlation of the forced expiratory ratio (FEV1/FVC) with the presence of mild or moderate respiratory symptoms was at least as satisfactory as that of technically more complicated measurements such as MEF50 and MEF75. In asymptomatic individuals those differences associated with smoking were the same for FEV1/FVC as for MEF75. Asymptomatic abnormalities of lung function were not observed. Simple measurements such as FEV1/FVC can therefore provide as much information from a forced expiratory manoeuvre to screen for early airways obstruction as MEF50 and MEF75.

Adolescent↗

Pulmonary and pleural lesions in rheumatoid disease.

Lung and pleural involvement in rheumatoid disease is reviewed and discussed. Attention is drawn to the male preponderance, to the frequency with which lung infections occur in rheumatoid patients and to some problems posed in them by infection with mycobacteria. Pleural effusion, pulmonary nodules and fibrosing alveolitis are familiar in association with rheumatoid arthritis. Less familiar associations include upper lobe fibrosis, 'shrinking lung' and mixed pleural and pulmonary involvement. It is suggested that rheumatoid patients display a wider range of intrathoracic disease than seems generally appreciated.

Adrenal Cortex Hormones↗

Asthma: analysis of sudden deaths and ventilatory arrests in hospital.

The incidence of episodes of unexpected ventilatory arrest, some of which led to sudden death, was studied in 1169 consecutive hospital admissions for asthma. Of the most acute cases, 458 were initially managed in a special care unit where only one ventilatory arrest occurred. A further nine cases of arrest, three of which proved fatal, happened on general wards. Accepted clinical criteria of a severe attack were not present in those episodes occurring outside the unit, which were apparently mild attacks. The risk of sudden death could not be related to the severity of the attack but it did correlate with the presence of excessive diurnal variation in peak expiratory flow rate (PEFR). Special treatment of patients with this sign might reduce mortality.

Asthma↗

Diurnal variation of asthma.

We have studied possible aetiological factors in the large diurnal variation in peak expiratory flow rate seen in some asthmatics. This phenomenon occurred in both atopic and non-atopic patients. It could not be attributed to recumbency in bed at night or to allergy to the house dust mite in bedding. Circadian variation in asthmatic shift workers was intimately related to sleep and virtually independent of solar time. Treatment tends to lose its effect as it is discontinued during sleep and this increases the apparent diurnal variation in many patients. Excessive circadian variation may be an important factor in sudden asthma deaths. The importance of effective nocturnal medication is stressed.

Asthma↗