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Biomedical subjects

M W Elliott

Publications and source records attributed to M W Elliott.

At least 73 records · Page 4Linked to original sources
PubMed1993

An evaluation of P0.1 measured in mouth and oesophagus, during carbon dioxide rebreathing in COPD.

The pressure generated 100 ms after the onset of an occluded inspiratory effort (P0.1) is advocated and used as a measure of respiratory centre drive. We have re-examined P0.1, measured simultaneously in the mouth (Pmo0.1) and the oesophagus (Poes0.1), during carbon dioxide rebreathing, in eight patients with severe chronic obstructive pulmonary disease, to see whether either indicates central respiratory drive. Pmo0.1 was identical to Poes0.1 in 4 out of 61, greater than Poes0.1 in 18 out of 61, and less than Poes0.1 in 39 out of 61 measurements (overall Poes0.1-Pmo0.1, median +0.075, range -0.175 to +1.01 kPa). Within a rebreathing run in an individual patient, there was considerable variability in the relationship Pmo0.1/Poes0.1 (0.89 +/- 0.24), coefficient of variation (CoV%) 14.4 +/- 3.7%), in the end-expiratory oesophageal pressure (0.7 +/- 0.54 kPa, CoV% 105 +/- 106%), and in the time delay between the onset of a fall in oesophageal pressure (Poes) from the end-expiratory level to the beginning of inspiration, defined as starting when mouth pressure (Pmo) fell below atmospheric pressure (129 +/- 25 ms, CoV% 22.5 +/- 5.3%). We conclude that the problem of determining the true onset of inspiratory muscle activity from pressure data, and the likelihood that breaths are taken from different lung volumes, make it unlikely that Poes0.1 accurately represents central respiratory drive during rebreathing in chronic obstructive pulmonary disease. Furthermore, Pmo0.1 differed from Poes0.1 during rebreathing, and their relationship was not constant, so that Pmo0.1 is even less likely to be a useful reflection of central nervous system output or respiratory centre drive in such patients.

Esophagus↗
PubMed1993

Inspiratory muscle effort during nasal intermittent positive pressure ventilation in patients with chronic obstructive airways disease.

Effective intermittent positive pressure ventilation can be achieved noninvasively using a nasal mask, but patient comfort may be compromised and respiratory effort increased unless the trigger threshold is low and the response time of the ventilator short. The effect of nasal ventilation upon inspiratory muscle effort and the functional characteristics of the trigger of a purpose-built ventilator were evaluated in five patients with chronic obstructive airways disease. A measure of inspiratory muscle effort, the average pressure time integral per minute, decreased by at least 80% in four patients and by 50% in one. Only two patients had significant numbers of triggered breaths (17% and 47% of total) during 1 h of ventilation with settings as used at home. Therefore trigger function was evaluated when the patients were made to trigger the ventilator by slowing the control rate. A high resting end-expiratory intrathoracic pressure decreased the effective trigger sensitivity so that a mean (SD) change in oesophageal pressure of 14.8 cmH2O was required to lower mask pressure by 2.4 (0.3) cmH2O and activate the trigger. Even under these conditions of lowest trigger sensitivity inspiratory muscle effort was not increased compared to spontaneous ventilation.

Carbon Dioxide↗
PubMed1992

Pitfalls of bone mineral density evaluation by dual-photon absorptiometry.

Material absorbing photons aligned with the lumbar vertebrae can create falsely elevated measurements of bone mineral density during dual-photon absorptiometry. Three cases illustrating this phenomenon are presented. Although bone mineral density was overestimated in each case, calculated fracture risk was normal in two cases and greatly increased in the third. Photon-absorbing material can create overestimates of bone mineral density during dual-photon absorptiometry, even when a greatly increased fracture risk is computed.

Absorptiometry, Photon↗
PubMed1992

Domiciliary nocturnal nasal intermittent positive pressure ventilation in hypercapnic respiratory failure due to chronic obstructive lung disease: effects on sleep and quality of life.

BACKGROUND: Domiciliary assisted ventilation, using negative or positive pressure devices, is an effective treatment for respiratory failure due to chest wall deformity and neuromuscular disease. Negative pressure ventilators have been used with some success in patients with chronic obstructive lung disease in hospital, but attempts to continue treatment at home have been disappointing. This study evaluates the practicalities of nasal intermittent positive pressure ventilation at home in patients with chronic obstructive lung disease and the effect on sleep and quality of life. METHODS AND RESULTS: Twelve patients with chronic obstructive lung disease and hypercapnic respiratory failure received nasal intermittent positive pressure ventilation at home during sleep. At six months eight were continuing with the ventilation. One patient had died and three had withdrawn because they were unable to sleep with the equipment. Full polysomnography performed during ventilation in patients continuing treatment at six months showed an increase in mean PaO2 of 11% (+2% to +23%) and lower mean transcutaneous carbon dioxide tensions (by -2.7 (-1.3 to -5.1) kPa) overnight compared with spontaneous breathing before the start of nasal intermittent positive pressure ventilation. Total sleep time and sleep efficiency changed during ventilation by +72.5 (+21 to +204) minutes and +5% (-3% to +30%) respectively; sleep architecture and the number of arousals were unchanged. Quality of life did not change but was no worse during ventilation. At one year seven patients were still using the ventilator and PaCO2 and bicarbonate ion concentration during the day had improved further by comparison with the values at six months (change from baseline -1.7 (-2.1 to -0.6) kPa, p less than 0.05, and -6.3 (-11.9 to -4) mmol/l, p less than 0.05). CONCLUSIONS: Nasal intermittent positive pressure ventilation can be used effectively at home during sleep in selected patients with chronic obstructive lung disease. Its future place in management can be established only by formal comparison with long term oxygen therapy.

Female↗
PubMed1992

Short-term use of fluoxetine in asymptomatic obese subjects with sleep-related hypoventilation.

Disordered nocturnal breathing with significant arterial oxygen desaturation and sleep apnoea is a feature of extreme obesity which is often difficult to manage in the short term. We have evaluated the effect of fluoxetine, a centrally acting 5-HT re-uptake inhibitor, on sleep-breathing patterns in asymptomatic extremely obese subjects. A double-blind cross-over study was used to compare fluoxetine (60 mg for three days) to placebo. Eleven obese subjects (ten males, one female, mean weight +/- s.d. 131 +/- 2 kg) slept overnight in a sleep laboratory with the polysomnographic study recorded after an initial acclimatization night. The obese subjects had normal respiratory function and normal fully awake arterial oxygen saturation (%SaO2 97 +/- 1). Marked O2 desaturation was seen in all the subjects during sleep but the average asleep %SaO2 did not differ between the two treatment phases (placebo 90 +/- 5; fluoxetine 92 + 2%). However, fluoxetine significantly increased the minimum %SaO2 recorded during the study night either by abolishing or reducing REM sleep (placebo 73 +/- 2%; fluoxetine 81 +/- 8%; P < 0.05, 95% CI -12.3 to -2.03). Frequent hypopnoea was observed in all subjects in both REM and non-REM sleep whereas apnoea was uncommon. The total apnoea/hypopnoea index fell in six subjects during the fluoxetine night, the largest reduction being seen in the most severely affected. In five of the six the improvement was associated with the abolition of REM sleep. Total sleep time did not differ between the placebo and fluoxetine nights nor did a qualitative assessment of sleep using a visual analogue score.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Inspiratory muscle relaxation rate after voluntary maximal isocapnic ventilation in humans.

We have investigated whether the capacity of the inspiratory muscles to generate pressure and flow during a ventilatory load is related to changes in inspiratory muscle relaxation rate. Five highly motivated normal subjects performed voluntary maximal isocapnic ventilation (MIV) for 2 min. Minute ventilation and esophageal, gastric, and transdiaphragmatic pressures were measured breath by breath. We observed that ventilation, peak inspiratory and expiratory pressures, and inspiratory flow rate declined from the start of the run to reach a plateau at 60 s that was sustained for the remainder of the exercise. In a subsequent series of studies, MIV was performed for variable durations between 15 and 120 s. The normalized maximum relaxation rate of unoccluded inspiratory sniffs (sniff MRR, %pressure loss/10 ms) was determined immediately on stopping MIV. Sniff MRR slowed as the duration of MIV increased and paralleled the decline in inspiratory pressure and ventilation observed during the 2-min exercise. No further slowing in MRR occurred when ventilation became sustainable. We conclude that, during MIV, the progressive loss of ventilation and capacity to generate pressure is associated with the early onset and progression of a peripheral fatiguing process within the inspiratory muscles.

Adult↗
PubMed1991

Sniff esophageal and nasopharyngeal pressures and maximal relaxation rates in patients with respiratory dysfunction.

Sniff esophageal pressure (Pes) and maximal relaxation rate (MRR, percent pressure loss/10 ms) are useful measurements of inspiratory muscle performance, but they require the passage of an esophageal balloon. We have examined the relationship between sniff esophageal and nasopharyngeal pressures (sniff Pes, sniff Pnp) and maximal relaxation rates (Pes MRR, Pnp MRR) in 13 patients with chronic obstructive pulmonary disease (COPD), five with intrapulmonary fibrosis (IPF), and seven with the "shrinking lung syndrome" of systemic lupus erythematosus (SLE). The ratio sniff Pnp/Pes (mean +/- SD) was 0.65 +/- 0.15 in COPD, 0.76 +/- 0.18 in IPF, and 0.91 +/- 0.03 in SLE. The ratio Pnp/Pes MRR was 1.20 +/- 0.2 in COPD, 1.14 +/- 0.12 in IPF, and 1.07 +/- 0.13 in SLE. We confirm that the transmission of pleural pressure to the upper airways during brief dynamic maneuvers is impaired in the presence of airway obstruction and lung fibrosis. We conclude that measurements of sniff Pnp and Pnp MRR are of limited value in patients with abnormal lung mechanics.

Adult↗
PubMed1991

Maximal relaxation rate of inspiratory muscle can be effort-dependent and reflect the activation of fast-twitch fibers.

We have measured the normalized maximal relaxation rate (MRR, % pressure loss/10 ms) of esophageal and transdiaphragmatic pressures in five normal subjects who performed unoccluded shifts from FRC, with the peak pressure varying between 10 and 100% of each subject's maximum. MRR was computed as the maximal rate of decay of pressure divided by the peak pressure, with units of %pressure loss/10 ms. We observed that MRR became progressively faster as sniff peak pressure increased in amplitude above 10% maximum. In four subjects this trend was most marked for sniffs of less than 40% maximal pressure, with little change as peak pressure increased further. In a fifth subject this trend continued across the full range of pressure. Thus, MRR may be an effort-dependent variable during voluntary inspiratory maneuvers. We postulate that sniff MRR becomes faster with increasing peak pressure because of progressive activation of fast-twitch type II muscle fibers. The findings of this study suggest that erroneous conclusions about the significance of slowing of sniff MRR with fatigue may be made if MRR is determined from voluntary efforts with a peak pressure of less than 60% of control maximum, as may occur with fatigue.

Humans↗
PubMed1991

The language of breathlessness. Use of verbal descriptors by patients with cardiopulmonary disease.

The main objective of the present study was to test the hypothesis that patients with cardiopulmonary disease can reliably identify different sensory qualities of their experience of breathlessness. A secondary aim was to examine whether there was any relationship between such specific descriptors of the sensation of breathlessness and a patient's clinical diagnosis. A randomly ordered list of 45 descriptors of breathing discomfort related to exertion was administered on two occasions to 208 patients with cardiopulmonary disease; patients identified the descriptors that applied to their own experience. A total of 169 patients were considered reliable in that their responses were repeatable between questionnaires; there was evidence that an individual's reliability could be assessed by asking repeat questions within a questionnaire. With these patients, individual descriptors generated different degrees of yes and no response and were answered with a variable consistency, suggesting that some questions may be more useful than others in discriminating between the quality of patients' sensations. Overall, patients with obstructive disorders (asthma and chronic obstructive airways disease [COAD]) answered yes more often than those with restrictive or cardiac conditions, possibly reflecting differences in severity of disease. A cluster analysis separated the descriptors into 12 groups which appeared to describe different aspects of breathing discomfort. Relative to their response to other clusters, COAD patients were more inclined to identify distress, asthma patients to indicate wheeziness, restrictive patients to report rapid breathing, and the cardiac group to describe a need to sign. A second cluster analysis separated patients into 12 groups based on responses for the descriptor clusters.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

Domiciliary nocturnal nasal intermittent positive pressure ventilation in COPD: mechanisms underlying changes in arterial blood gas tensions.

The improvement in arterial blood gas tensions following assisted ventilation in chronic obstructive pulmonary disease (COPD) has usually been attributed to the relief of incipient or established respiratory muscle fatigue. The contribution of changes in the load placed upon and the drive to the respiratory muscle pump have not been evaluated. We have investigated the contribution of changes in respiratory muscle strength, the ventilatory response to CO2 and ventilatory function to changes in arterial blood gas tensions in eight patients with severe COPD completing six months domiciliary nasal intermittent positive pressure ventilation. Six patients showed a reduction and two an increase in arterial carbon dioxide tension (PaCO2), median (range) for eight patients, -0.9 kPa (-1.5 to +0.4) (p less than 0.05) and seven showed an improvement in arterial oxygen tension (PaO2), +0.7 kPa (-0.4 to +1.7) (p less than 0.05) during daytime spontaneous breathing. The reduction in PaCO2 was not related to increased inspiratory muscle strength but was correlated with a decrease in gas trapping (Spearman rank correlation coefficient (r(S)) 0.85, p less than 0.05) and in the residual volume (r(s) 0.78, p less than 0.05), suggesting reduced small airway obstruction and, therefore, a reduction in load. The change in PaCO2 also correlated with the increase in ventilation at an end-tidal CO2 of 8 kPa during rebreathing (r(s) -0.76, p less than 0.05) suggesting improved chemosensitivity to CO2. Our data do not support the hypothesis that improvements were due to the relief of muscle fatigue. We suggest that the contribution of changes in load and central drive warrant further investigation.

Female↗
PubMed1990

Non-invasive mechanical ventilation for acute respiratory failure.

The value of mechanical ventilation using intermittent positive pressure ventilation delivered non-invasively by nasal mask was assessed in six patients with life threatening exacerbations of chronic respiratory disease. Median (range) arterial oxygen and carbon dioxide tensions were 4.4 (3.5-7.2) kPa and 8.7 (5.5-10.9) kPa respectively, with four patients breathing air and two controlled concentrations of oxygen. The arterial oxygen tension increased with mechanical ventilation to a median (range) of 8.7 (8.0-12.6) kPa and the carbon dioxide tension fell to 8.2 (6.5-9.2) kPa. Four patients discharged after a median of 10 (8-17) days in hospital were well five to 22 months later. One died at four days of worsening sputum retention and another after five weeks using the ventilator for 12-16 hours each day while awaiting heart-lung transplantation. This technique of mechanical ventilation avoids endotracheal intubation and can be used intermittently. Hypercapnic respiratory failure can be relieved in patients with either restrictive or obstructive lung disease in whom controlled oxygen treatment results in unacceptable hypercapnia. Respiratory assistance can be tailored to individual need and undertaken without conventional intensive care facilities.

Acute Disease↗
PubMed1980

Therapeutic efficacy of vitamin E and selenium in treating hemolytic anemia of owl monkeys (Aotus trivirgatus).

The roles played by vitamin E and by selenium in the anemia of owl monkeys were studied by injecting a mixture of the two antioxidants in 17 anemic monkeys. The result was an increase in mean hemoglobin concentration from 8.6 +/- 2.2 to 11.9 +/- 2.5 g/dl; in 1o of these monkeys with typically elevated numbers of circulating nucleated erythrocytes, the mean number of such cells per 10(2) leukocytes declined from 50.1 +/- 49.9 to 0.6 +/- 1.2. Injections of vitamin E alone in eight monkeys were less consistently effective; selenium administered alone to nine monkeys had no therapeutic effect. Neither anemic nor normal owl monkeys were deficient in serum vitamin E, plasma selenium, erythrocyte glutathione peroxidase or other related erythrocyte enzymes. Oral administration of vitamin E brought about no increase in serum levels of the vitamin, but hemolysis of erythrocytes in dialuric acid decreased from 18.6 +/- 15.8% to 1.0 +/- 0.03%. Selenium therapy brought about increased plasma selenium in two of three experiments, but glutathione peroxidase, which is selenium dependent, did not increase.

Administration, Oral↗