Treatment of allergic bronchopulmonary aspergillosis with inhaled corticosteroids.
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Administration, Inhalation↗
Biomedical subjects
A S Rebuck
Publications and source records attributed to A S Rebuck.
A new method for measuring PCO2 during anaesthesia.
We have evaluated a new method for measuring the oxygenated mixed venous PCO2 (PVCO2) in patients undergoing general anaesthesia. The lungs were inflated with a gas mixture containing 0% carbon dioxide and then 12% carbon dioxide and the expired gas was analysed both before and after a brief period of breath-holding. PVCO2 was estimated from the differences in carbon dioxide concentration before and after the apnoeic period. Simultaneous measurments of PaCO2 were made in blood obtained from radial artery puncture. The range of PaCO2 studied was 3.2--6.13 kPa. The relationship between mixed venous and arterial PCO2 was found to be PaCO2 = 0.87 PVCO2--0.44 (r = 0.91). We conclude that this method for measuring PVCO2 can be used during anaesthesia allowing PaCO2 to be estimated with considerable accuracy.
Adult↗
Effect of isocapnic hypoxia on systolic time intervals in conscious man.
The effects of progressive isocapnic hypoxia on the systolic time intervals were studied in 10 healthy human subjects. We induced hypoxia by a rebreathing method and monitored the arterial oxygen saturation continuously and non-invasively by means of an ear oximeter. Arterial oxygen saturation (SaO2) was allowed to fall to a level of 75 per cent and was then held constant for five minutes. As SaO2 fell, heart rate increased linearly, with a mean increase of 0.83 beats/min per one per cent fall in SaO2. The pre-ejection phase index decreased from a mean of 127.2 ms at full oxygen saturation to 120.1 ms at steady-state hypoxia levels, while the ratio of the pre-ejection phase to left ventricular ejection time decreased from a mean of 0.330 to 0.301. The left ventricular ejection time index increased from 417.4 ms to 429.3 ms, while no statistically significant difference was found in the length of electromechanical systole.
Adult↗
Contribution of rib cage and abdomen-diaphragm to tidal volume during CO2 rebreathing.
In man, there is wide interindividual range in the tidal volume response to CO2. To determine which (rib cage or abdomen-diaphragm) compartment had a greater influence on this range, ventilatory response to CO2 was measured, using Read's method, in eight men and two women seated in a constant-pressure body plethysmograph. Rib cage and abdominal tidal volume was simultaneously measured using magnetometers. Correcting for body size, the tidal volume response of the abdominal compartment was similar in all subjects, whereas that of the rib cage was larger in subjects with high tidal volume response to CO2; a significant correlation was found (P less than 0.01). Rib cage volume displacement lagged behind abdominal in all subjects; phase lag was greatest in the subject with the lowest ventilatory response to CO2. These results suggest that, at high levels of ventilation, a larger volume displacement of the rib cage may reflect a more effective coupling of the diaphragm pressure generator to it or alternatively a reduction in its impedance relative to the abdominal compartment.
Abdominal Muscles↗
Absence of effects of hypoxia on small airway function in humans.
We measured the effects of sustained isocapnic hypoxia (PAO2 = 40--50 Torr; PACO2 = 38--42 Torr) on tests sensitive to small airway function in healthy human subjects. Maximum expiratory flow-volume curves on air, nitrogen-hypoxic, helium-normoxic, and helium-hypoxic mixtures as well as closing volumes while subjects breathed air and a hypoxic mixture were obtained. We then measured total lung capacity (TLC), both plethysmographically and by inert gas dilution, and used the nonplethysmographic method to measure the effects of hypoxia on TLC. In none of these tests were there any statistically significant changes when values obtained during hypoxia were compared with those during normoxia. It is suggested that previous reports that indicated that TLC was increased by hypoxia might have arisen from a plethysmographic artifact.
Adult↗
SCH 1000 in psychogenic asthma.
The effects of a beta 2-sympathomimetic (salbutamol or fenoterol) and the anticholinergic SCH 1000 administered both in combination and with placebo were compared in a double-blind random crossover design. Thirty-three patients with atopic, non-atopic and psychogenic asthma were studied. After inhalation of the sympathomimetic in combination with SCH 1000 or placebo the increase in FEV1 was significantly better for three hours (p less than 0.05) than after inhalation of SCH 1000 alone. There was no difference in the response to SCH 1000 in the atopic or non-atopic groups. However, in patients with a major psychogenic component to their asthma the FEV1 response to SCH 1000 was significantly better (p less than 0.05) than in other asthmatics from four to seven hours past inhalation. These findings suggest that SCH 1000 might be a valuable therapeutic agent in patients with psychogenic asthma.
Aerosols↗
A comparison of the effects of steady-state and progressive hypoxia on the ventilatory and frequency response.
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Adult↗
Influence of rate of induction of hypoxia on the ventilatory response.
1. We have studied the influence of rate of induction of hypoxia on the duration of the phases of the respiratory cycle in seven conscious healthy subjects.2. Nine hypoxic procedures were performed on each subject, comprising three different rates of induction of hypoxia each at three different levels of P(CO2). Ventilation vs. arterial O(2) saturation plots were constructed and patterns of response were analysed in terms of ventilation vs. tidal volume and tidal volume vs. inspiratory duration (T(I)) and vs. expiratory duration (T(E)).3. The highest ventilatory responses were observed during steady-state hypoxia when P(CO2) was held at a level similar to the control mixed venous level; progressive hypoxia at this P(CO2) failed to stimulate ventilation to comparable levels. The ventilatory response was not influenced by rate of induction of hypoxia when P(CO2) was maintained at an end-tidal P(CO2) close to the control level.4. As tidal volume increased in response to hypoxia, T(I) and T(E) shortened. The progressive decrease in cycle duration occurred at all levels of P(CO2) and at all rates of induction of hypoxia, but was most marked under eucapnic conditions during steady state.5. It is concluded that steady-state hypoxia may produce a higher ventilatory response than progressive, non-steady-state hypoxia. Inspiratory time shortens as tidal volume increases irrespective of the rate of induction of hypoxia.
Adult↗
Heart rate response to isocapnic hypoxia in conscious man.
We studied the effect of acute progressive hypoxia on heart rate in conscious healthy subjects. The PCO2 was held constant (+/- 1.5 mmHg) midway between the resting end-tidal and mixed-venous levels. Hypoxia was induced by having the subject rebreathe from a small bag so that the PO2 fell at a rate related to the subject's oxygen consumption. Arterial oxygen saturation (Sao2) was measured continuously during the procedure with an ear oximeter. We found that heart rate (HR) was best fitted to an inverse linear relation to arterial oxygen saturation and a power relation to PO2. The range of deltaHR/deltaSao2 was 0.62-1.46 beats/min per 1% fall in Sao2 (mean +/- SE = 0.98 +/- 0.06). There was no relationship between heart rate and ventilatory responses to hypoxia.
Carbon Dioxide↗
A noninvasive method for measuring the PCO2 of mixed venous blood.
A breath-holding method for measuring the PCO2 of mixed venous blood has been developed. Two gas mixtures, 100 per cent O2 and 12 per cent CO2 in O2, were inspired, and the expired gas was analyzed after 5 and 15 sec of breathholding. The oxygenated mixed venous PCO2 was calculated using an exponential equation. The method was applied in healthy subjects, patients with lung disease, and unconscious mechanically ventilated patients. The mixed venous PCO2 correlated well with arterial PCO2 (r = 0.96), the PCO2 obtained by rebreathing (r = 0.97), and the PCO2 in blood drawn from the pulmonary artery (r = 0.97). The method is noninvasive, has a low coefficient of variance, and allows arterial PCO2 to be estimated by multiplying the breath-holding mixed venous PCO2 by 0.8.
Adult↗
Severe asthma: prevention is better than cure.
Asthmatic patients during sympton-free periods almost invariably have abnormalities in lung mechanics and gas exchange. Tentacious secretions and mucosal thickening exaggerate maldistribution of ventilation and cause flow limitation in small airways. Hence, the maximal expiratory flow volume loop in these patients will show impaired flow rates at low lung volumes and many will show a widened alveolar-arterial O2 tension difference. Preventive treatment should be aimed at reversing these abnormalities. The regular use of inhaled sympathomimetics and oral theophylline preparations is justified in the symptom-free patient whose history suggests that he is susceptible to acute exacerbations. Such patients commonly experience an improved sense of well-being, increased exercise tolerance, and a decrease in the frequency and severity of their acute episodes.
Adrenal Cortex Hormones↗
A mathematical expression to describe the ventilatory response to hypoxia and hypercapnia.
A mathematical expression has been developed to describe the ventilatory responses to changes in arterial oxygen saturation (SaO2) and arterial carbon dioxide tension (PCO2). The derivation is based on the experimental observations: (1) that ventilation is a linear function of PCO2 under isoxic conditions, and (2) that ventilation is a linear function of SaO2 under isocapnic conditions. It is assumed that all functions are continuous and single valued, with the implication that for any given SaO2 and PCO2 there is a unique ventilatory response. The analysis following from these three assumptions has enabled us to derive the following expression for ventilation: VI(SaO2, PCO2) = alpha1 - SaO2 - PCO2 + alpha2 - SaO2 + alpha3 - PCO2 + alpha4 where the alpha's are constants for an individual. This equation, which follows uniquely from the assumption stated, is simpler and contains fewer parameters than previous expressions used to describe ventilation.
Humans↗
A comparison of the bronchodilator activity of Sch 1000 and salbutamol.
The effects of the beta 2-adrenergic agonist, salbutamol, 200 mug, and the cholinergic antagonist, Sch 1000, 40 mug, have been compared in 25 asthmatic patients using a single dose, double-blind, crossover trial design. Salbutamol aerosol produces a greater degree of bronchodilatation than Sch 1000 aerosol during the initial three hours following drug administration. There is no significant difference in the bronchodilator effects of the two drugs in the interval four to eight hours after drug administration. Nonatopic patients showed less difference in bronchodilator response to each of the two drugs than atopic patients. Neither drug showed any significant adverse effect on blood pressure, pulse rate, or electrocardiogram. In six asthmatic patients the effect of the combination of salbutamol, 200 mug, and Sch 1000, 40 mug, was evaluated. The combination produced a longer duration of bronchodilatation than either drug alone when compared to placebo.
Adult↗
Selective tracheobronchial aspiration.
Eighty attempts at placing suction catheters in the left main bronchus were analysed by studying chest radiographs. When angled catheters were used via a tracheostomy tube the success rate was 75%; the rate fell to 15% when straight tubes were used through an orotracheal tube. Assessment and control of the tube length was found to be important to avoid kinking and subsequent obstruction of the catheters.
Bronchi↗
Changes in lung mechanics induced by acute isocapnic hypoxia.
We measured lung mechanics in seven healthy males during acute isocapnic hypoxia (PAO2 = 40-50 Torr; PACO2 = 38-42 Torr). Hypoxia was accompanied by increases in total lung capacity (mean increase +/- SD; 0.40 +/- 0.24 liters; P less than 0.005) functional residual capacity (0.34 +/- 0.25 liters; P less than 0.01) and residual volume (0.56 +/- 0.44 liters; P less than 0.02) in all subjects. Specific conductance of the lung decreased during hypoxia (P less than 0.02). The static deflation pressure-volume curve of the lung was shifted upward during hypoxia in all subjects. Resting end-expiratory recoil pressure of the lung was slightly, but not significantly lower during hypoxtic expiratory lung compliance was greater during hypoxia (0.39 +/- 0.04 l/cmH2O) than control measurements (0.31 +/- 0.05 l/cmH2O; P less than 0.005). No change was noted in dynamic lung compliance. All changes in lung mechanics were reversed within three minutes of reoxygenation. We conclude that acute isocapnic hypoxia increases total lung capacity in man and suggest that this may be due to the effect of hypoxia on the airways and pulmonary circulation.
Adult↗
Workshop on assessment of respiratory control in humans. I. Methods of measurement of ventilatory responses to hypoxia and hypercapnia.
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Humans↗
Ventilatory and waking responses to CO2 in sleeping dogs.
We examined ventilatory and waking responses to hyperoxic hypercapnia in 3 dogs during natural sleep. Progressive hypercapnia was induced by a rebreathing technique, and sleep was determined by electroencephalographic and behavioral criteria. In non-rapid eye movement sleep (high-voltage, slow-frequency electroencephalography) rebreathing continued for 0.99 +/- 0.05 min (mean +/- SE) before arousal occurred, and the alveolar PCO2, at arousal was 54.2 +/- 3.4 mm Hg. In contrast, during rapid eye movement sleep, rebreathing lasted for 1.71 +/- 0.27 min (P less than 0.05) before arousal occurred and the alveolar PCO2 at arousal was 60.3 +/- 4.2 mm Hg (P less than 0.05). Linear regression analysis of breath-by-breath instantaneous minute volume of ventilation, tidal volume, and respiratory frequency against alveolar PCO2 revealed regression coefficients in rapid eye movements sleep that were 14 to 33 per cent of those found in non-rapid eye movement sleep, and correlation coefficients of 0.26 to 0.46, compared to 0.71 to 0.91 in non-rapid eye movement sleep. Thus, the link between CO2 and ventilation appeared to be strong in non-rapid eye movement sleep but considerably disrupted during rapid eye movement sleep. We conclude that centers involved in both waking and ventilatory responses to hypercapnia behave as if they are less aware of or responsive to CO2 in rapid eye movement sleep than in non-rapid eye movement sleep.
Animals↗
Arterial oxygenation and carbon dioxide tensions in the production of hypoxic electroencephalographic changes in man.
1. To investigate the interaction of hypoxaemia and blood PCO2 in the production of cerebral hypoxia, we studied six healthy men in whom acute progressive hypoxia was induced by using a rebreathing technique, while the PCO2 was kept constant. 2. At least two blood PCO2 tensions were studied in each subject. Arterial oxygen saturation was monitored continuously by ear oximetry, calibrated for each subject with arterialized blood. The onset of cerebral hypoxia was identified by the appearance of frontal slow waves (less than 5 Hz) in the electroencephalogram (EEG), which was recorded continuously with the bipolar 10-20 electrode placement system. 3. All subjects developed frontal slow waves during at least one experiment: the EEG changes were similar both within and among subjects, irrespective of the blood PCO2 value. 4. The arterial oxygen saturation at which slow-wave activity first occurred showed a significant inverse linear relationship to the PCO2 value at which hypoxia was induced. 5. The results imply that more profound levels of hypoxia are tolerated with high PCO2 values than with normal or low PCO2 values before hypoxic EEG changes become evident. Thus if eucapnia is maintained, EEG changes suggestive of cerebral hypoxia are unlikely to occur if arterial oxygen saturation remains above 75%.
Adult↗