Biomedical subjects
A H Campbell
Publications and source records attributed to A H Campbell.
Brief upper airway (laryngeal) dysfunction.
We describe in six men, recurrent episodes recurring over months or years, of sudden, brief complete obstruction to respiration followed by dyspnoea with loud inspiratory stridor lasting two to five minutes. Attacks occurred during wakefulness and/or sleep. In one patient an episode was witnessed endoscopically: the initial obstruction was seen to be caused by complete laryngeal closure. The false vocal cords then opened, but the vocal cords remained adducted and caused inspiratory stridor. The similarity of the attacks described by the other patients suggests that they were all caused by laryngeal closure. Furthermore, they could simulate the episodes by voluntarily adducting their vocal cords. The symptoms were usually preceded by a sensation of throat irritation and in four cases symptoms of upper respiratory infection were present. Associated features present in some of the patients included post-nasal discharge, snoring, sleep apnoea and gastro-oesophageal reflux. None was hypocalcaemic. Although stimulation of laryngeal receptors is known to produce reflex laryngeal closure, cough is the usual response during wakefulness. Treatment aimed at reducing upper airway irritation and voluntary inhibition of coughing appeared successful in reducing the incidence and severity of the episodes. Recognition of the condition is important as it may be confused with other causes of acute dyspnoea and it appears to respond to specific management.
A comparative study of atropine methonitrate, salbutamol, and their combination in airways obstruction.
Dose-response relationships of the cholinergic antagonist, atropine methonitrate, and the beta-adrenergic agonist, salbutamol, were examined by cumulative dose techniques. A wet aerosol, 1.5 mg atropine methonitrate produced a maximum response. The response to 200 microgram of salbutamol from a pressurised aerosol was close to maximum. Secondly, the bronchodilator response of salbutamol microgram was compared with atropine methonitrate 2 mg and placebo in 18 asthmatic patients in a randomised crossover study. In 11 of them the bronchodilator response of the combination of salbutamol and atropine methonitrate was evaluated. Atropine methonitrate produced a similar peak bronchodilator effect to salbutamol, but its effect was more prolonged, the response being significantly greater at four and six hours than with salbutamol. The combination of drugs produced a significantly greater and more lasting bronchodilatation than either of the drugs alone. Despite mild side effects, atropine methonitrate, either alone or in combination with an adrenergic drug, appears to have a place in the treatment of sever reversible airway obstruction not adequately controlled by conventional treatment.
Acute changes of lung volumes and lung mechanics in asthma and in normal subjects.
Lung volumes, pulmonary mechanics, and specific airway conductance (sGaw) were studied before and 15 minutes after 200 microgram of aerosol salbutamol in nine asthmatics undergoing mild spontaneous exacerbations of their disease and in five normal subjects. In addition, three of the normal subjects were studied after voluntarily breathing at high lung volumes for one minute. The normal subjects and four of the asthmatics showed no overall changes in lung volumes or pressure-volume (PV) curves after salbutamol, even though airway dilatation was produced in the asthmatic subjects. In another five asthmatics, salbutamol induced a significant fall in the total lung capacity (TLC) in three, and in the residual volume and functional residual capacity in all five. There was a significant displacement of the PV curve downwards and to the right in all five, with increased lung compliance (Cl stat) in two. The fall in TLC could be accounted for by the increase in lung elasticity. There is reason to believe that this change in lung mechanics could be due to the reversal of asthma-induced stress relaxation. Sustained breathing at high lung volume is known to cause stress relaxation of the lung. However, this breathing pattern did not alter the PV curve or TLC in two of three normal subjects, which is consistent with stress relaxation being rapidly reversible. The other normal subject had an acute shift of the PV curve upwards and to the left after breathing at high lung volume. It has been concluded that stress relaxation is usually rapidly reversed but that in some individuals it may only be slowly reversed. This more persistent form of stress relaxation may contribute to the acute changes of TLC found in some asthmatics.
Sputum eosinophilia in chronic bronchitis and asthma.
The occurrence of sputum eosinophilia was investigated in 115 patients with chronic bronchitis and asthma. They were clinically divided into four groups; those with asthma only, those with asthma of equal or greater duration than chronic bronchitis, those with chronic bronchitis recently complicated by asthma and those with chronic bronchitis only. Although sputum eosinophilia was more common in the asthmatic groups there was no significant difference between the groups in the degree of sputum eosinophilia. When the groups were subdivided on the basis of methacholine and isoprenaline response (asthma subgroup, greater than or equal to 20% response to isoprenaline or greater than or equal to 40% response to methacholine; chronic-bronchitis subgroup, less than 10% response to isoprenaline plus less than 20% response to methacholine), there was a significant difference between the groups in the degree of sputum eosinophilia. However, sputum eosinophilia still occurred in the chronic bronchitics. In the asthmatic patients, there appeared to be no difference in the degree of sputum eosinophilia in those with positive skin tests, or on steroid medication, compared with those with negative skin tests or not on steroids.¿
Follow-up of past tuberculosis, its value and limitations.
Recently the policy of life-long follow-up of tuberculous patients has been questioned, particularly for those who have taken adequate chemotherapy. To assess the value of follow-up at a chest clinic, the relapse rate of approximately 3000 male patients was examined and found to be 0.51 percent annually during the last eight years. It was 0.46 percent amongst those treated prior to the introduction of prolonged chemotherapy, 0.55 percent anually amongst those prescribed at least 18 months chemotherapy. No relapses would have been missed if all the patients had been followed for five years after ceasing chemotherapy and only selected groups subsequently. The selected groups included, those not prescribed adequate chemotherapy in the past, those suspected of irregularity of drug intake, alcoholics and those with atypical or resistant organisms. It was concluded that patients adequately treated with chemotherapy need not be followed up after five years.
Letter: Mortality from asthma and bronchodilator aerosols.
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Mortality from asthma and bronchodilator aerosols.
The mortality rate from asthma in Australia had a transcient rise between 1960 to 1967. There was a remarkably high correlation between the sales of pressurized adrenergic aerosols in each of the four most populated States and the corresponding asthma mortality rate for two triennia, 1961 to 1963 and 1964 to 1966. This relationship was not found after 1966. From 1965 to 1966, Australians were warned repeatedly of the possible dangers of over-usage of the adrenergic aerosols. The sales pattern of the aerosols altered, showing a slackening of the rate of increase of sales in 1966 and 1967. This and other evidence suggests that the warnings may have reduced the prevalence of over-usage of the aerosols and that before this, over-usage of the adrenergic aerosols could have caused the epidemic of asthma deaths.
Increased upper airway resistance in patients with airway narrowing.
The mean air flow resistance of the orolaryngeal (upper) airway was significantly increased in 7 of 11 patients with chronic airway obstruction, when compared with 6 controls. All the patients had noisy respiration with harsh breath sounds audible by auscultation over the larynx. The increase in resistance was greater during expiration than during inspiration. Since 4 patients had normal upper airway resistance, the signs were not invariably associated with upper airway narrowing and presumably could arise also in the chest. When increased, upper airway resistance was usually more than half the total airway resistance. It is suggested that this increase could only be due to narrowing of the glottis, probably by muscle activity. This narrowing may have had the same function as expiration through pursed lips. On the other hand, when present, the increased resistance through the upper airway during inspiration is unlikely to have had a useful function.
Isolation and hormone-responsiveness of intact cells from a transplantable osteogenic sarcoma in the rat.
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Respiratory mechanics in airways obstruction associated with inspiratory dyspnoea.
Inspiratory muscle strength and the flow and elastic pressure opposing inspiration were measured in seven patients with severe airways obstruction who found inspiration difficult at rest. A comparison was made of measurements obtained from seven normal subjects and five patients with airways obstruction not experiencing inspiratory dyspnoea at rest. Measurements were also obtained when inspiratory dyspnoea was induced in the normal subjects by adding an inspiratory resistance or by voluntarily increasing lung volume. Compared with the controls the inspiratory muscle strength of the patients was reduced but was not significantly less than that of the patients without inspiratory dyspnoea. The pressure required to produce inspiratory flow was significantly greater when inspiratory dyspnoea was present (P = 0-01). However, there was considerable overlap in the pressures of those with and without inspiratory dyspnoea. A better relationship was obtained when muscle strength was considered. The ratio of inspiratory muscle strength to the pressure required to produce flow was 0-24 +/- 0-07 (mean +/- SD) in patient with inspiratory dyspnoea, 0-10 +/- 0-03 in patients without inspiratory dyspnoea, and 0-033 +/- 0-019 in normal subjects. There was no overlap between the two patient groups. The ratios of the normal subjects were increased when inspiratory dyspnoea was induced and, with the exception of two cases, were all above those obtained when inspiratory dyspnoea was absent. Inspiratory dyspnoea was experienced with lower ratios in the normals than in the patients with airways obstruction.
Relationship of constitutional factors and cigarette smoking to decrease in 1-second forced expiratory volume.
A 5-year prospective survey of 34 subjects with mild chronic bronchitis revealed marked individual variation in the annual rate of decrease in the forced expiratory volume in 1 sec. The mean annual decrease in the 1-sec forced expiratory volume was 0.046 +/- 0.057 liter. Although the annual decrease in the 1-sec forced expiratory volume was greater among smokers (0.056 +/- 0.061 liter per year) than non- and ex-smokers (0.016 +/- 0.021 liter per year; P less than 0.005), differences in tobacco consumption did not account for the individual variation. This variation was related, instead, to 3 phenomena believed to indicate the presence of host susceptibility to chronic bronchitis. These phenomena were bronchial reactivity to methacholine, ventilatory responsiveness to isoproterenol, and sputum eosinophilia. The correlation between the rate of decrease in 1-sec forced expiratory volume and the degree of methacholine reactivity was 0.76 (P less than 0.001); the correlation between the decrease in 1-sec forced expiratory volume and ventilatory responsoveness to isoproterenol was 0.45 (P less than 0.01). Deterioration of 1-sec forced expiratory volume was appreciably greater among those with sputum eosinophilia (0.062 +/- 0.06 liter per year) than among thse without eosinophilia (0.017 +/- 0.033 liter per year P less than 0.01). The progression of abnormality appeared to depend on an interaction between cigarette smoking and individual susceptibility. Even minimal tobacco consumption led to serious ventilatory deterioration when methacholine reactivity was high, whereas heavy smoking produced little effect on the decrease in 1-sec forced expiratory volume when methacholine reactivity was slight.
Care and management of patients in respiratory failure.
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The effect of chest physiotherapy upon the FEV1 in chronic bronchitis.
Chest physiotherapy, including posturing the patient head downwards while the chest is percussed and vibrated, was used in the treatment of patients with an exacerbation of chronic bronchitis. In seven patients the mean FEV declined from 1.38 litres plus or minus 0.39 to 1.25 litres plus or minus 0.37 after postural drainage and percussion (P less than 0.001). Twenty minutes later the FEV rose to 1.37 litres plus or minus 0.33. The mean decline in the FEV1 was prevented by prior administration of salbutamol. The fall in the FEV1 did not occur in 10 patients who received the postural tipping without chest percussion. Also it was not induced by coughing every two minutes during posturing. It was considered that the fall in FEV1 after chest physiotherapy was due to bronchoconstriction caused by the chest percussion or vibration, particularly in patients with bronchoconstriction under basal conditions. The induced bronchoconstriction counter-balanced any improvement of the FEV due to freeing the airways of sputum, but in two patients with moderate to copious sputum an improvement of the FEV1 was repeatedly obtained in measurements made 20 minutes after the physiotherapy when the bronchoconstriction had presumably subsided. Although the immediate decline in FEV1 was not large, it is considered inadvisable to employ chest percussion and vibration in sick patients unless a bronchodilator is administered previously.