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Biomedical subjects

J Moxham

Publications and source records attributed to J Moxham.

At least 163 records · Page 9Linked to original sources
PubMed1989

Maximal relaxation rates of esophageal, nose, and mouth pressures during a sniff reflect inspiratory muscle fatigue.

Maximal relaxation rate (MRR, % pressure fall/10 msec) of the inspiratory muscles is reduced with fatigue. We have investigated whether MRR of esophageal pressure (Pes) generated by voluntary sniffs is decreased by fatigue, and whether sniff nasopharyngeal (Pnp) and mouth (Pmo) MRR reflect these changes. In 10 normal subjects, control MRR of sniff Pes correlated closely to Pnp MRR (r = 0.977, p less than 0.001) and Pmo MRR (r = 0.947, p less than 0.001). To produce inspiratory muscle fatigue, four highly motivated subjects breathed to exhaustion (3 to 6 min) through a high inspiratory resistance. MRR was determined from 10 sniffs for Pes, Pnp, and Pmo before fatigue, and at intervals up to 10 min after fatigue. The subjects showed a mean decrease in sniff Pes MRR of 33% (range, 20 to 42) immediately after fatigue, which returned exponentially to control values within 3 to 4 min. The mean changes in Pes MRR were reflected by similar changes in Pnp MRR, 32% (range, 18 to 43) and Pmo MRR, 33% (range, 21 to 42). Studies were repeated in the four subjects with closely similar results. We conclude that fatigue of the inspiratory muscles reduces MRR of sniff Pes, and that this is reflected in Pnp and Pmo. Sniff Pes, Pnp, and Pmo MRR measurements may provide a useful method for detecting and monitoring fatigue; Pnp and Pmo have the advantage of being less invasive.

Adult↗
PubMed1989

Diaphragm strength in the shrinking lung syndrome of systemic lupus erythematosus.

The cause of the reduced lung volume in the 'shrinking lung' syndrome of systemic lupus erythematosus (SLE) was investigated in 12 patients with the condition. Nine patients described persistent episodes of pleuritic chest pain. Narrow section (3 mm) computed tomography of the thorax revealed no interstitial fibrosis or significant pleural disease. Assessment of diaphragmatic function using manoeuvres more reliable than the maximal occluded efforts previously used alone to assess respiratory muscle strength, showed that diaphragm strength was unequivocally normal in nine of 12 patients. In three, maximum transdiaphragmatic pressure was moderately reduced, but phrenic nerve stimulation demonstrated that this was due to incomplete activation of the diaphragm during a maximal voluntary effort, rather than to a primary abnormality of the diaphragm. Results of maximum lung recoil pressures and dynamic compliance, and analysis of the 12-s maximum voluntary ventilation, suggested a restriction in chest-wall expansion, although it was not possible to identify the underlying cause of this on the basis of our results. We conclude that the 'shrinking lung' syndrome of SLE is not explained by a primary abnormality of the diaphragm.

Adolescent↗
PubMed1989

The effect of posture and abdominal binding on respiratory pressures.

We examined the effect of posture on the generation of respiratory pressures in 6 highly trained subjects. Transdiaphragmatic pressure was measured at FRC during bilateral percutaneous phrenic nerve stimulation (twitch Pdi) and maximal sniffs (sniff Pdi), with the abdomen bound and unbound. Maximum static inspiratory (PImax) and expiratory (PEmax) mouth pressures were measured with the abdomen unbound. Three postures were examined: seated (Se), semi-supine (30s), and supine (Su). Changes of posture did not significantly alter twitch Pdi. By contrast, sniff Pdi and static mouth pressures were significantly reduced in the Su posture. Abdominal binding significantly increased twitch Pdi only. We conclude that voluntary respiratory manoeuvres requiring activation, recruitment and coordination of different muscle groups are performed better in the Se position. We suggest that posture be standardised for serial comparative measurements of voluntary respiratory pressures in a given subject.

Abdomen↗
PubMed1989

Respiratory muscle weakness and fatigue.

Respiratory muscle weakness can result from a variety of neuromuscular disorders, and it is now possible to identify different patterns of weakness and quantify the extent of this weakness using reliable, sensitive tests of respiratory muscle strength. However the quantification of respiratory muscle 'fatigue' has proved more difficult, and it is now recognized that there is unlikely to be one single index of fatigue, rather a whole sequence of changes that occur in response to loading. It is likely that in practice, a close interplay between respiratory pump capacity, demands on the pump and more especially, adaptive changes in respiratory drive, protect the respiratory muscles from overt peripheral contractile failure, and that the fall in tension following prolonged muscular activity involves many different closely inter-related processes. Investigation of these processes is likely to be more rewarding than attempts to develop a single 'test of fatigue', and may lead to an improved understanding of the role of respiratory muscle dysfunction in ventilatory failure.

Fatigue↗
PubMed1989

The effect of aminophylline on respiratory and limb muscle contractility in man.

The effect of oral aminophylline on respiratory muscle and quadriceps femoris strength was compared with placebo in five normal subjects. A double-blind randomized cross-over protocol, spanning 2-3 wks, was followed. Aminophylline was taken before both placebo and active drug periods to establish correct dosage, to allow tolerance to side-effects to develop, and to keep the two limbs of the study identical and double-blind. Maximal static inspiratory and expiratory mouth pressures at residual volume and total lung capacity, respectively, maximal sniff transdiaphragmatic pressure, maximal voluntary quadriceps femoris contraction force and theophylline levels were measured during placebo and active drug periods. For the group, there were no significant differences between respiratory or quadriceps muscle strength on aminophylline and on placebo although there was a tendency for greater values on aminophylline. Mean theophylline level was 14.6 mg.l-1 (range 8.4-25.0 mg.l-1). We conclude that aminophylline produces no enhancement of skeletal muscle strength, at therapeutic dosage in normal subjects.

Adult↗
PubMed1988

Evaluation of a hand-held spirometer, the Respiradyne, for the measurement of forced expiratory volume in the first second (FEV1), forced vital capacity (FVC) and peak expiratory flow rate (PEFR).

A hand-held spirometer, the Respiradyne (R), was evaluated for the measurement of forced expiratory volume in the first second (FEV1), forced vital capacity (FVC) and peak expiratory flow rate (PEFR) by comparing it with a Vitalograph spirometer (V) and a Wright's peak flow meter (W) in 70 subjects (normals and patients). The results showed close agreement for FEV1; r = 0.99, R = 0.961V + 0.03 X 10(-5) and FVC; r = 0.99, R = 1.003V-0.044. Results for PEFR using the Respiradyne were generally higher than with the peak flow meter; r = 0.98, R = 1.151W-17.576. The Respiradyne is portable and simple to operate and may be suited to use in a variety of non-laboratory situations.

Evaluation Studies as Topic↗
PubMed1988

Performance of transcutaneous PO2 and PCO2 dual electrodes in adults.

Three commercially-available combined PO2-PCO2 electrodes were assessed in vitro, and in adults breathing air, hypoxic and hypercapnic mixtures, for speed of response, correlation with end-tidal gas tensions and drift. Differences in the 90% response time of the individual electrodes were more marked in vitro than in vivo. Changes in end-tidal gas tensions were reflected by proportionate changes in transcutaneous oxygen and carbon dioxide (PtcO2 and PtcCO2) but, in the individual subject, PtcO2 and PtcCO2 were generally poor indicators of the end-tidal values. During steady-state recordings, the PtcO2 signal drifted upwards by more than 12 mm Hg during 140 min in vivo recording in all three electrodes, without changes in either PtcCO2 or end-tidal values. The dual electrodes tested provide non-invasive estimates of qualitative, but not quantitative, change in blood-gas tensions and are likely to have only a limited role to play in adult anaesthetic practice.

Adult↗
PubMed1988

Systemic air embolism during laser bronchoscopy.

We report a case of massive, fatal, systemic gas embolism which occurred during the course of laser bronchoscopic resection of a bronchial carcinoma. The clinical features of systemic air embolism are discussed.

Aged↗
PubMed1988

Diaphragm pacing.

Explore the source record for details and available documents.

Diaphragm↗
PubMed1988

Diaphragm strength in patients with recent hemidiaphragm paralysis.

Eleven patients with unilateral diaphragm paralysis of recent onset were studied to investigate the effect of the paralysis on inspiratory muscle function. Nine of the patients had noticed a decrease in exercise tolerance, which was not explained by any other pathological condition. Hemidiaphragm dysfunction was confirmed by the demonstration of a greatly reduced or absent transdiaphragmatic pressure on stimulation of the phrenic nerve in the neck, by means of surface bipolar electrodes (unilateral twitch Pdi), compared with normal values on the contralateral side. Transdiaphragmatic pressure was 44.6% (9.4%) predicted during a maximal sniff and 30.3% (16.8%) predicted during a maximal static inspiration against a closed airway, confirming diaphragm weakness. Maximum static inspiratory mouth pressures were also low (61.7% (12.7%) predicted), consistent with a reduction in inspiratory muscle capacity. Phrenic nerve conduction time was prolonged on the affected side in nine patients, consistent with phrenic nerve dysfunction, whereas on the unaffected side it was normal. It is concluded that recent hemidiaphragm paralysis causes a reduction in transdiaphragmatic pressure that is associated with a reduction in maximum inspiratory mouth pressure. Phrenic nerve stimulation is a useful technique with which to confirm and quantify hemidiaphragm dysfunction. Measurement of phrenic nerve conduction time provides useful information about the underlying pathology.

Diaphragm↗
PubMed1988

Diaphragm weakness in Charcot-Marie-Tooth disease.

Two patients are described with Charcot-Marie-Tooth disease and chronic peripheral neuropathy. Both had dyspnoea, orthopnoea, and evidence of severe diaphragm weakness. Expiratory muscle function was well preserved and abnormalities of gas exchange during sleep were only minor.

Charcot-Marie-Tooth Disease↗
PubMed1988

Assessment of diaphragm weakness.

Thirty patients with breathlessness and diaphragm weakness were studied by measuring transdiaphragmatic pressures during maximal inspirations to total lung capacity, maximal static inspiratory efforts from residual volume, and maximal sniffs from functional residual capacity. Maximal static respiratory mouth pressures were also recorded, and rib cage and abdominal movements were monitored with pairs of magnetometers. Sniff transdiaphragmatic pressure was abnormally low in all patients and was correlated with transdiaphragmatic pressure during other maneuvers, and with maximal static inspiratory mouth pressures. There was no relationship between the severity of dyspnea and transdiaphragmatic pressure in the group as a whole. The weakest patients had orthopnea and paradoxical inward inspiratory motion of the anterior abdominal wall; measurements suggested that at least 30 cm H2O transdiaphragmatic pressure was required to overcome the hydrostatic pressure of the abdominal contents. By contrast, patients with mild diaphragm weakness had neither orthopnea nor abdominal paradox. Thus, patients with breathlessness and diaphragm dysfunction may have varying degrees of diaphragm weakness that may be difficult to detect clinically; the diagnosis and quantification of diaphragm weakness requires the measurement of transdiaphragmatic pressure.

Adolescent↗
PubMed1988

Hypothyroidism presenting with respiratory muscle weakness.

A 58-yr-old woman presented with recurrent chest infections, breathlessness, and orthopnea. She complained of nonspecific tiredness and aching limbs. A chest radiograph showed an elevated right hemidiaphragm. Thyroid function tests showed her to be severely hypothyroid (T4 = 23 nmol/L; TSH greater than 50 mU/L). Measurement of maximal respiratory mouth pressures (expiratory: 50 cm H2O, normal, 94 +/- 33; inspiratory: 15 cm H2O, normal, 71 +/- 27) suggested global respiratory muscle weakness. Severe bilateral diaphragm weakness was demonstrated by a greatly reduced maximal transdiaphragmatic pressure (Pdi) (Pdi Pimax = 0, normal, 65 +/- 31 cm H2O; sniff Pdi = 25 cm H2O, normal, 121 +/- 25). No Pdi was detectable on stimulation of the right phrenic nerve, whereas, on the left, it was 11 cm H2O (normal 7 to 15 cm H2O). Phrenic nerve conduction time was prolonged to both sides (right, 12 ms, left, 10 ms; normal, less than 9.5 ms). The relaxation rate of Pdi after a maximal sniff and after bilateral phrenic nerve stimulation was abnormally slow (7.4%/10 ms, 6.3%/10 ms, respectively). Three months after starting treatment with thyroxine she had become euthyroid, and phrenic nerve conduction times and Pdi relaxation rates had returned to normal. Maximal respiratory pressures, vital capacity, and maximal voluntary ventilation improved progressively on treatment, although maximal respiratory pressures still had not reached the normal range after six months. We conclude that hypothyroidism may present with breathlessness due to respiratory muscle weakness and/or phrenic nerve neuropathy and is reversible with treatment.

Diaphragm↗
PubMed1988

The value of sniff esophageal pressures in the assessment of global inspiratory muscle strength.

Esophageal pressure generated during a maximal sniff (sniff Pes) was compared with mouth pressure generated during a maximal inspiration against a closed airway (Pimax) as a measure of global inspiratory muscle strength in 61 patients referred for investigation of respiratory muscle function. Transdiaphragmatic pressure (Pdi) was also measured during both maneuvers to compare maximal diaphragmatic strength. Sniff Pes (males, 68 +/- 27 cm H2O; normal greater than 53; females, 66 +/- 21; normal greater than 48) was greater than Pimax (males, 45 +/- 24 cm H2O; normal greater than 42; females, 42 +/- 24; normal greater than 17) in 55 of the 61 patients, both in absolute values and as a percentage of normal. In 36 patients Pimax and sniff Pes were both normal (mean +/- 2 SD), whereas in 13 patients they were both low. In 11 patients, Pimax was low, but sniff Pes was normal. One patient had a reduced sniff Pes but a Pimax at the lower limit of normal. In the 36 patients in whom both Pimax and sniff Pes were normal, Pdi was also normal or only moderately reduced, and in the 13 patients in whom both Pimax and sniff Pes were reduced, Pdi was very low. However, in the group of 11 patients with a low Pimax but a normal sniff Pes, Pdi was normal or only moderately reduced, suggesting that Pimax was falsely low, perhaps because of difficulties with the technique. Conversely, in the single patient with a low sniff Pes but a Pimax just within the normal range, Pdi was very low. We conclude that measurement of esophageal pressure during a maximal sniff is a useful test of inspiratory muscle strength and overcomes the difficulty some patients have in carrying out the Pimax maneuver.

Adolescent↗
PubMed1988

Clinical significance of severe isolated diaphragm weakness.

We studied six patients with isolated bilateral paralysis or severe weakness of the diaphragm, present for 2 to 60 months (mean = 25), to document the clinical and respiratory sequelae of the condition. Severe diaphragm dysfunction was confirmed by the demonstration of the very low maximal transdiaphragmatic pressure (Pdi) generated by either a sniff (13 +/- 6 cm H2O, normal 148 +/- 24) or a static inspiration (11 +/- 8, normal 108 +/- 30) and during bilateral phrenic nerve stimulation (0.8 +/- 2.0, normal 22 +/- 4). Resting arterial blood gases were normal (SaO2 = 95 to 97%) and no oxygen desaturation occurred during maximal exercise on a treadmill. Maximum voluntary ventilation was low and related to PImax (r = 0.89). Overnight sleep monitoring showed that time spent in rapid eye movement sleep was normal (mean 55 +/- 36 min, range 26 to 117 min). Mean maximum increment in transcutaneous CO2 was within normal limits (6 +/- 2 mm Hg, range 3 to 9 mm Hg). Three patients had occasional brief episodes of oxygen desaturation (mean maximal decrease 13 +/- 10%, range 2 to 27%); however, only two of these spent a measurable proportion of total sleep time (TST) with an SaO2 of less than 80% (1% and 3% TST, respectively). No patient has developed any symptoms of nocturnal hypoventilation or chronic respiratory failure during periods of observation of up to five yr. We conclude that bilateral paralysis or very severe weakness of the diaphragm does not of itself lead to respiratory failure unless weakness of other respiratory muscles is present.

Blood Gas Analysis↗