Problems with nasal CPAP machines.
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Humans↗
Biomedical subjects
L G Olson
Publications and source records attributed to L G Olson.
Differences in the symptoms of men and women with obstructive sleep apnoea.
In order to determine whether the clinical features of obstructive sleep apnoea (OSA) are the same in men and women we reviewed the records of 22 women with OSA. The women were matched with 44 men of similar age (+/- 5 years) and frequency of respiratory events (less than or equal to 15/hr, 16-40/hr, 41-70/hr and greater than 70/hr). The degree of daytime somnolence was similar in men and women. Women are more likely than men to complain of morning fatigue and morning headache, and less likely to report restless sleep or to have been told of apnoea during sleep. Difficulty initiating sleep (DIS) was twice as common in women as in men (p less than 0.05). Most of these differences were also seen when women and men who snored but did not have OSA were compared. Arterial hypertension was less common in women (3/22) than in men (18/44), (p less than 0.001). More striking than the differences between men and women in the prevalence of single symptoms was the existence of a subgroup of women (9/22) with no complaint of either apnoea, choking arousals or restless sleep, and normal blood pressure, complaining only of fatigue and morning headache, and in three cases DIS as well. We concluded that OSA may be commoner in women than previous reports suggest, and that the clinical features may be misleading in women.
Adult↗
Frusemide antagonises exercise-induced but not histamine-induced bronchospasm.
Frusemide has recently been shown to antagonise exercise-induced bronchospasm, an action attributed to blockade of chloride channels in the bronchial epithelium. In order to test the hypothesis that frusemide non-specifically antagonises bronchospasm, we tested the bronchial reactivity to inhaled histamine in ten subjects aged 22 to 35 years, after nebulising 30 mg of frusemide, and after nebulising the frusemide vehicle (water at pH 9.1). The geometric mean (histamine PD20) after inhalation of the solution was 0.6 mumol and after frusemide was 0.45 mumol. The mean difference in PD20 between control and frusemide was -0.50 mumol (frusemide test more reactive) but this change was not statistically significant. We conclude that nebulised frusemide does not antagonise histamine-induced bronchospasm, and that the ability of frusemide to block exercise-induced bronchospasm may be specific to that stimulus.
Administration, Inhalation↗
Long-term acceptance of continuous positive airway pressure in obstructive sleep apnea.
We studied the long-term acceptability of nasal continuous positive airway pressure (CPAP) treatment in 168 consecutive patients, 147 with obstructive sleep apnea (OSA) and 21 with snoring. Follow-up was between 1.5 and 78 months. At latest follow-up 107 of 168 (64%) were still using CPAP. Acceptance of CPAP was least for patients with snoring alone (6 of 21 persisted) and best for patients with both excessive daytime somnolence and severe hypoxemia (minimum SaO2 less than 75%), of whom 40 of 45 (89%) persisted with treatment. Patients with excessive daytime somnolence but without severe hypoxemia were less tolerant of CPAP (39 of 71, 55%, persisted) than patients with no symptoms of excessive somnolence but with severe hypoxemia (21 of 30, 70%, persisted). The most common reasons for discontinuing CPAP were intolerance of the mask (26 of 61), the inconvenience of treatment (16 of 61), and the lack of symptomatic benefit from treatment (10 of 61). We concluded that long-term acceptance of CPAP was difficult to predict in advance but that it was most likely in patients with the most severe sleep apnea. Because intolerance of the mask and inconvenience were the most common reasons for ceasing treatment, improvements in the design of CPAP systems and careful patient training may improve the acceptability of CPAP substantially.
Female↗
Patterns of use of chest physiotherapy in a teaching hospital.
Studies of chest physiotherapy in medical patients have consistently shown benefit only in patients who produce large amounts of sputum. Among surgical patients systematically repeated maximal inspiration is the only procedure that clearly reduces the incidence of post-operative pulmonary complications. Rationalization of the use of physiotherapy requires data on the pattern of its use. To obtain such data an audit was conducted on the use of physiotherapy in patients discharged from Royal Newcastle Hospital in October 1989. It was suspected that respiratory physicians would account for the bulk of chest physiotherapy. All patients admitted under respiratory physicians and random samples of patients admitted under other physicians and under surgical specialists were surveyed. Chest physiotherapy was ordered in 13/44 (30%) patients cared for by respiratory physicians, 5/45 (11%) other medical patients and 11/48 (23%) surgical patients (P = 0.049). Chest physiotherapy was ordered in 28 of 29 instances for conditions in which it is of no proven benefit. From the total numbers of medical and surgical patients it was estimated that 71% of chest physiotherapy referrals in October 1989 were for non-medical patients. About half of all referrals were initiated by junior medical staff. Much of the chest physiotherapy performed in the hospital was unlikely to have been of major clinical value and patients with respiratory illnesses were minor consumers of chest physiotherapy. Attempts to reduce wasteful overuse of chest physiotherapy may be most effective if directed at physiotherapists. If medical staff are targeted it would be essential to reach those attached to surgical units.
Drainage, Postural↗
Lack of airway response to nasal irritation in normal and asthmatic subjects.
Twenty two subjects (10 normals, nine asthmatics and three who had suggestive histories for asthma but normal bronchial histamine challenges) underwent nasal challenges with logarithmic incremental doses of histamine or saline on alternate days. Nasal resistance (measured by posterior rhinometry), and forced expiratory volume in one second (FEV1) were assessed after each dose of nasal histamine or placebo. After each nasal challenge (maximum nasal dose of 250 micrograms of histamine or doubling of nasal resistance) bronchial responsiveness was measured with a bronchial histamine challenge. Despite significant changes in nasal resistance with nasal histamine (p less than 0.01) there was no significant change in the forced expiratory volume in one second, or in bronchial responsiveness. We were unable to demonstrate nasobronchial reflexes initiated by acute irritation of the nasal mucosa with histamine in either normal subjects or in those with mild to moderate asthma.
Adolescent↗
Estimation of the probability of disturbed breathing during sleep before a sleep study.
We have investigated the ability of a statistical model developed from clinical data and questionnaire responses to predict disturbance of breathing during sleep. Data from 100 consecutive patients referred for sleep study for suspected sleep apnea were used to develop the model using logistic regression analysis. For each subject, the model predicted the probability of having an apnea-hypopnea index (AHI) greater than 15; this probability was compared with the AHI measured from sleep study. A probability cutoff point (= 0.15) was decided on that minimized the number of subjects with false-negative predictions. Four terms--apneas observed by bed partner, hypertension, body mass index, and age--were found to contribute significantly to the model with observed apneas being by far the most predictive term of the four (adjusted odds ratio 19.7). When the model was tested to estimate the probability of an AHI greater than 15 for 105 patients from a second group of consecutive patients referred for sleep study, the model correctly classified 33 of 36 patients with a measured AHI greater than 15 (sensitivity = 92%) and 35 of 69 patients with a measured AHI less than or equal to 15(specificity = 51%). This study shows that analysis of clinical features of patients presenting with suspected sleep apnea may reduce the need for sleep studies by about one-third yet still lead to the identification of the great majority of patients with abnormal breathing during sleep.
Female↗
Urinary uric acid:creatinine ratio, serum erythropoietin, and blood 2,3-diphosphoglycerate in patients with obstructive sleep apnea.
A noninvasive, inexpensive method of excluding significant sleep-associated hypoxemia would be desirable for patients being investigated and treated for obstructive sleep apnea (OSA). Sixty-eight such patients provided specimens before and after sleep studies for estimation of urinary uric acid:creatinine ratio (UA:Cr), serum erythropoietin (EPO), and blood 2,3-diphosphoglycerate (2,3-DPG). Mean (SD) morning 2,3-DPG was higher in 26 patients with overnight hypoxemia than in 42 normoxemic patients (2.54 [0.46] versus 2.24 [0.44] mmol/L; p = 0.01). Neither overnight change nor absolute values of serum EPO or urinary UA:Cr were significantly different between hypoxemic and normoxemic groups. There was a diurnal variation in serum EPO in normoxemic patients (P.M. EPO = 14.8 [7.1] mU/ml; A.M. EPO = 10.7 [7.1] mU/ml; p less than 0.05) but not in hypoxemic patients. Eighteen hypoxemic patients were restudied after using nasal continuous positive airway pressure (nCPAP) for at least 4 wk. Seven normoxemic patients not using nCPAP were restudied after a similar time. There were no significant differences between pretreatment and posttreatment nights in absolute values or percentage overnight change of blood 2,3-DPG or serum EPO in either group. In the hypoxemic (nCPAP) group, overnight change in urinary UA:Cr was lower on the second night (p = 0.04); there was no significant change in the control group. We conclude that although urinary UA:Cr, serum EPO, and 2,3-DPG may be physiologically related to hypoxemia, none of these measures can be used to predict accurately the presence of moderate nocturnal hypoxemia in patients with OSA or in monitoring the effect of their therapy.
2,3-Diphosphoglycerate↗
Preventing and dealing with scientific fraud in Australia.
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Australia↗
Nasal histamine challenges in symptomatic allergic rhinitis.
Twenty subjects (seven with perennial allergic rhinitis, seven with symptomatic seasonal allergic rhinitis, and six normal control subjects) underwent assessment of nasal sensitivity to histamine. Nasal resistance was measured by posterior rhinometry under control conditions and after log incremental doses of histamine solution pipetted into the nose (0.5 to 5000 micrograms). Allergic subjects exhibited a twofold rise of nasal resistance with doses of 0.5, 5, or 50 micrograms of histamine, whereas the nasal resistance in normal subjects remained unchanged until 500 or 5000 micrograms of histamine had been administered. Nasal reactivity to histamine was not correlated with symptoms on the day of testing but was correlated with the number of positive wheals to skin prick testing. It was concluded that nasal resistance is more sensitive to histamine in subjects with allergic rhinitis than in normal control subjects and that this difference may be used as the basis of a diagnostic test.
Administration, Intranasal↗
Influence of muscle activity on the elastance of the upper airway of rabbits.
This study sought to assess the effect of variations in upper airway muscle activity on upper airway pressure-volume properties. Upper airway elastance, closing pressure, and reserve volume were measured in the isolated upper airways of anesthetized rabbits under control conditions and after administration of gallamine (2 mg/kg iv) or after 10 min of spontaneous respiration of 7% CO2 in O2. Administration of gallamine to seven animals was associated with a fall in reserve volume from 0.94 +/- 0.24 to 0.69 +/- 0.17 (95% confidence interval) ml (P less than 0.01) and of closing pressure from -7.53 +/- 0.23 to -5.75 +/- 1.05 cmH2O (P less than 0.01), but airway elastance did not change significantly. Hypercapnia in seven animals was associated with a rise in elastance from 7.06 +/- 0.91 to 7.67 +/- 0.86 cmH2O/ml (P less than 0.001) and in reserve volume from 0.68 +/- 0.06 to 0.86 +/- 0.13 ml (P less than 0.05). Closing pressure also changed from -5.88 +/- 0.94 to -7.92 +/- 1.85 cmH2O. This change was correlated with the change in reserve volume but not with the change in elastance. In three animals exposed to hypercapnia, return to room air breathing was associated with return of elastance, reserve volume, and closing pressure to control levels. It is concluded that muscle activity in the upper airway affects both the size and elastance of the airway, but the dominant mechanism by which upper airway muscles increase the resistance of the upper airway to collapse is by increasing airway volume.
Airway Resistance↗
Pressure-volume properties of the upper airway of rabbits.
In 10 anesthetized rabbits the upper airway cephalad of the vocal cords was isolated from the distal airway and sealed. Static deflation pressure-volume data were recorded from the isolated upper airway. The relationship between pressure and volume in the upper airway was a straight line; the correlation coefficient (r) ranged from 0.97 to 1.00. The following quantities were derived from the data: the pressure-volume ratio (upper airway elastance, cmH2O/ml), the pressure in the airway at airway closure (closing pressure, cmH2O), and the airway volume at zero airway pressure (reserve volume, ml). Mean upper airway elastance was 8.13 +/- 1.45 [95% confidence intervals (CI)] cmH2O/ml, closing pressure was -6.93 +/- 1.53 (95% CI) cmH2O, and reserve volume was 0.74 +/- 0.15 (95% CI) ml. There was no significant correlation between elastance and closing pressure (r = 0.47, P greater than 0.1), but closing pressure and reserve volume were significantly correlated (r = 0.77, P less than 0.01). Pressure-volume data recorded from newly dead animals exhibited the same linear relationship between pressure and volume observed in living animals. It is concluded that the pressure-volume properties of the isolated upper airway of the rabbit can be expressed as a single value for airway elastance, that estimation of pressure-volume properties over part of the volume range is representative of the whole volume range, and that pressure-volume properties are determined by passive elastic properties of the airway tissues. It appears that the resistance of the upper airway to collapse by negative intraluminal pressure is more dependent on the initial size of the airway than on its elastance.
Airway Resistance↗
Performance of the Hudson Multi-Vent oxygen mask.
The performance of the Hudson Multi-Vent oxygen mask was assessed by attaching it to a model of a head and generating varying inspiratory flows of oxygen through the mouth and nasal orifices. The oxygen concentration that was delivered by the mask varied with the inspiratory flow rate at all oxygen concentrations. This effect was proportionately similar at all levels of set oxygen concentration: about 50% of the increment of inspired oxygen was lost as the inspiratory flow rate increased from 20 L/min to 100 L/min. The performance of the mask was not affected by the route (oral or nasal) of inspiratory flow. Rotation of the mask in the coronal plane produced marked changes in delivered oxygen concentration; with the oxygen concentration set at 50%, and the inspiratory flow rate at 40 L/min, the delivered oxygen concentration was 45% when the mask was parallel to the coronal plane of the model, was 41% when it was angled 10 degrees towards the face, and was 27% when it was angled 10 degrees away from the face. The measurement of oxygen concentrations at different points inside the mask confirmed that the oxygen-enriched gas is directed in a localized stream in the centre of the mask, and that air is entrained through the large ports that are sited at the sides of the mask to satisfy inspiratory flow. The measurement of inspired oxygen concentrations in 12 hospital inpatients confirmed that the model reflected accurately the performance of the mask when used in a routine way. We conclude that, in clinical use, the Hudson Multi-Vent mask is unlikely to deliver the set oxygen concentration, and that the delivered oxygen concentration is not predictable.
Equipment Design↗
Non-muscular factors in upper airway patency in the rabbit.
The hypothesis tested in these experiments was that factors other than contraction of upper airway muscles influence the resistance of the upper airway to collapse. The intra-luminal pressures required to close and re-open the upper airway were measured in the isolated upper airways of anesthetised rabbits. The level of activity in upper airway muscles manipulated by ventilation with 100% O2 or 7% CO2 and by muscle paralysis with gallamine. During ventilation with 100% O2 closing pressure was -10.34 +/- 0.53 cm H2O (mean +/- 95% c.i., n = 23) and re-opening pressure was -3.15 +/- 0.51 cm H2O. Ventilation with 7% CO2 changed the closing pressure to -11.63 +/- 0.67 cm H2O (P less than 0.05) and re-opening pressure to -3.81 +/- 0.67 cm H2O (NS). In 10 animals muscle paralysis with gallamine (2 mg/kg i.v.) did not significantly alter closing or re-opening pressures during ventilation with 100% O2, and did not abolish the ability of ventilation with 7% CO2 to augment collapse resistance. In 6 animals death was followed by a fall in closing and re-opening pressures to 30-60% of the values recorded in paralysed animals. We conclude that in this preparation active muscle contraction is not the main source of resistance to airway closure or of the proclivity of the closed airway to re-open.
Airway Obstruction↗
The nasal response to exercise and exercise induced bronchoconstriction in normal and asthmatic subjects.
Two studies were carried out to test the hypothesis that the fall and recovery of nasal resistance after exercise in asthmatic and non-asthmatic subjects are related to the development of bronchoconstriction after exercise. In study 1 nasal resistance (posterior rhinomanometry) and specific airway resistance (sRaw) were measured before challenge and one, five, 10 and 30 minutes after four minutes of exhausting legwork exercise in nine asthmatic subjects and nine age matched healthy subjects. One minute after exercise there was a reduction in nasal resistance of 49% (SD 15%) from baseline in the healthy subjects and of 66% (17%) in the asthmatic subjects. This response and the subsequent return of nasal resistance to baseline values did not differ significantly between the two groups despite a substantial difference in the change in sRaw, an increase of 74% (45%) in the asthmatic subjects 10 minutes after exercise, and no change in the non-asthmatic subjects. In study 2, nasal and specific airway resistances were monitored according to the same measurement protocol in six subjects with increased airway reactivity. Subjects exercised on two occasions, wearing a noseclip, once while breathing cold, dry air and once while breathing warm, humid air. The fall in nasal resistance was similar under both conditions (to 47% and 39% of baseline), through sRaw rose only after cold air inhalation (to 172% of baseline). The results indicate that the nasal response to exercise is not related to bronchial obstruction in asthmatic subjects after exercise or to the temperature or humidity of the air inspired through the mouth during exercise.
Adult↗
Airway secretions influence upper airway patency in the rabbit.
The hypothesis tested in these experiments was that the properties of the upper airway mucosal surface may be important in reopening of the closed airway, and that mucosal surface properties may depend on airway secretions. The intraluminal pressures required to close and reopen the upper airways were measured in the isolated upper airways of anesthetized rabbits. Atropine (0.1 mg/kg i.v.), given to reduce the volume of upper airway secretions, had no effect on closing or on reopening pressures. Stimulation of upper airway secretions in 6 animals with methacholine (0.2 mg/kg subcutaneously) changed closing pressures from -10.63 +/- 0.57 to -16.91 +/- 0.60 cm H2O (p less than 0.05) but made the airway less likely to reopen, changing reopening pressures from -3.45 +/- 0.48 to -2.12 +/- 0.39 cm H2O (p less than 0.04), and caused frequent failure of the airway to reopen spontaneously. Filling the upper airways with saline to mimic the hydrostatic forces present in the mucus-filled airway caused both closing and reopening pressures to become more negative. We conclude that reopening pressure is influenced by the secretions lining the airway surface, and, therefore, that airway closure and airway reopening may be substantially independent.
Airway Obstruction↗
Aminophylline in acute asthma.
It is widely believed that theophylline is a valuable addition to beta-agonists in the treatment of asthma. This is true when beta-agonists are given in low doses, but available evidence suggests that theophylline adds little or nothing to the effect of maximal doses of beta-agonists. Clinical trials, albeit some with limitations, in acute asthma support the view that theophylline confers no benefit on patients treated with high-dose beta-agonists. As theophylline is a difficult drug to use safely, and its toxicity is serious, its use should be confined to unusual circumstances, and the dose should be small.
Adrenergic beta-Agonists↗
Effect of a dopamine antagonist on ventilation during sustained hypoxia in mice.
To test the hypothesis that dopamine accumulated in the carotid body limits hyperventilation during acclimatization to sustained hypoxia, we administered the dopamine antagonist droperidol to mice undergoing acclimatization to an inspired O2 fraction (FIo2) of 0.1. Twelve mice were exposed to hypoxia for 10 days and ventilation in 10% O2 and in 7% CO2 in air were measured daily by a plethysmographic method. Under both conditions ventilation increased during acclimatization to hypoxia: ventilation in 10% O2 increased from 39.4 +/- 3.8 (mean +/- SE) ml/min before exposure to sustained hypoxia to 72.2 +/- 4.2 ml/min after 3 days of continuous hypoxia, and ventilation in 7% CO2 in air at the same time increased from 113.2 +/- 5.4 ml/min to 140.0 +/- 5.6 ml/min. Twelve mice were exposed to FIo2 of 0.1 for 10 days and received droperidol (300 micrograms/kg intraperitoneally) before exposure to sustained hypoxia and on the 2nd, 4th, and 8th days of continuous hypoxia. Before exposure to sustained hypoxia, droperidol increased ventilation in 10% O2 from 40.1 +/- 2.5 ml/min to 72.5 +/- 5.2 ml/min, but after 2, 4, and 8 days of continuous hypoxia droperidol caused an acute fall in ventilation (ventilation in 10% O2 after droperidol on day 2: 49.1 +/- 3.1 ml/min, on day 4: 44.4 +/- 3.7 ml/min, and on day 8: 27.8 +/- 3.4 ml/min). Two days after the animals were returned to room air, ventilation in 10% O2 again increased in response to droperidol. We conclude that dopamine in the carotid body does not limit ventilatory responses to hypoxia during acclimatization to sustained hypoxia.
Animals↗