Search PubMed⌕ Search

Biomedical subjects

J Moxham

Publications and source records attributed to J Moxham.

At least 145 records · Page 8Linked to original sources
PubMed1992

Repetitive stimulation of phrenic nerves in myasthenia gravis.

BACKGROUND: In the investigation of patients with myasthenia gravis, repetitive supramaximal stimulation of an affected peripheral nerve is commonly performed to detect abnormal transmission at the neuromuscular junction. A study was undertaken to determine whether abnormal transmission could similarly be detected during stimulation of the phrenic nerves. METHODS: The phrenic nerves were stimulated supramaximally with surface electrodes in 13 patients with myasthenia gravis and in 16 control subjects (six control patients with diaphragmatic weakness but not with myasthenia and ten normal subjects). The amplitude of diaphragm muscle action potentials was measured with surface electrodes during phrenic nerve stimulation at frequencies of 1-5 Hz for 3-4 seconds. RESULTS: In five patients with myasthenia gravis, a significant decrement (15-43% decrease) occurred in the amplitude of diaphragm muscle action potential during stimulation at 3 Hz. When stimulation frequency was reduced to 1 Hz, diaphragm muscle action potentials returned to their original amplitude within 4-5 seconds. The decrement in the amplitude of the diaphragm muscle action potential was reduced temporarily in three of four patients after the administration of intravenous edrophonium chloride (Tensilon). There was no significant change (< 10% decrease) in the amplitude of diaphragm muscle action potentials during stimulation at increased frequencies either in the 16 control subjects or in eight of the patients with myasthenia gravis. CONCLUSION: A significant reduction in the amplitude of diaphragm muscle action potential occurred in five of 13 patients with myasthenia gravis during phrenic nerve stimulation at 3 Hz but in none of the control subjects. This may be a useful and non-invasive method for identifying patients with myasthenia gravis in whom weakness of the diaphragm is suspected.

Action Potentials↗
PubMed1991

The effects of mild obesity on lung function.

Lung volumes and blood gas tensions were measured in 144 males awaiting coronary artery surgery. Patients were divided into three groups according to their body mass index. Functional residual capacity (FRC), expiratory reserve volume (ERV) and arterial oxygen tension (PaO2) were reduced in the 91 patients with Grade I obesity (mean +/- SD weight, 81.1 +/- 9.0 kg) compared with the results obtained in the 28 patients of normal weight (Grade 0, 70.8 +/- 8.8 kg). The magnitude of the reduction was greater in the Grade II obesity patients (90.1 +/- 8.8 kg, n = 25). Mean values were: FRC 3.45, 3.17, 2.66 l; ERV 1.10, 0.77, 0.59 l and PaO2 11.05, 10.47, 9.99 kPa in patients with Grades 0, I and II obesity respectively. The alveolar-arterial oxygen difference (A-aPO2) was significantly higher in the obese patients. Mean A-aPO2 was 2.47, 3.14 and 3.88 kPa in patients with Grades 0, I and II, respectively. We conclude that obesity, even when mild, significantly impairs lung function.

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

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

Effect of chronic airflow limitation on resting oxygen consumption.

The work of breathing in patients with severe chronic airflow limitation is increased even at rest but little is known about the magnitude of this increase. Resting oxygen consumption (VO2), carbon dioxide production (VCO2), and respiratory quotient (RQ) were measured in 13 patients with severe chronic airflow limitation (mean FEV1 0.78 1, vital capacity 2.1 1) and compared with those of 13 age, weight, and height matched control subjects. Whereas mean RQ was the same in the two groups (0.82), mean VO2 and VCO2 were higher in the patients (+ 18 ml min-1 and + 15 ml min-1 respectively). When VO2 was standardised for body surface area it was 10.9% higher in the patients (p less than 0.05). If the increased resting VO2 in these patients were solely due to increased activity of the respiratory muscles, it would represent a fourfold increase in the oxygen cost of breathing.

Body Surface Area↗
PubMed1990

Effect of acute hypercapnia on limb muscle contractility in humans.

The effect of acute hypercapnia on skeletal muscle contractility and relaxation rate was investigated. The contractile force of fresh and fatigued quadriceps femoris (QF) and adductor pollicis (AP) was studied in normal humans by use of electrical stimulation. Maximum relaxation rate from stimulated contractions was measured for both muscles. Acute hypercapnia led to a rapid substantial reduction of contraction force. The respiratory acidosis after 9% CO2 was breathed for 20 min [mean venous blood pH 7.26 and end-tidal PCO2 (PETCO2) 65.1 Torr] reduced 20- and 100-Hz stimulated contractions of QF to 72.8 +/- 4.4 and 80.0 +/- 5.1% of control values, respectively. After 8 and 9% CO2 were breathed for 12 min, AP forces at 20- and 50-Hz stimulation were also reduced. Twitch tension of AP was reduced by a mean of 25.5% when subjects breathed 9% CO2 for 12 min [mean arterialized venous blood pH (pHav) 7.25 and PETCO2 66 Torr]. Over the range of 5% (pHav 7.38 and PETCO2 47 Torr) to 9% CO2, there was a linear relationship between twitch tension loss and pHav, arterialized venous blood PCO2, and PETCO2. Acute respiratory acidosis (mean PETCO2 61 Torr) increased the severity of low-frequency fatigue after intermittent voluntary contractions of AP. At 20 min of recovery, twitch tension was 63.2 +/- 13.4 and 46.8 +/- 16.4% of control value after exercise breathing air and 8% CO2, respectively. Acute hypercapnia (mean PETCO2 65.1 and 60.5 Torr) did not alter the maximum relaxation rate from tetanic contractions of fresh QF and from twitch tensions of AP.

Acidosis, Respiratory↗
PubMed1989

Respiratory muscle weakness in the Lambert-Eaton myasthenic syndrome.

Respiratory muscle function was assessed in six patients with the Lambert-Eaton myasthenic syndrome. Five had histologically proved small cell carcinoma of the lung; the sixth later developed metastases from an unknown primary site. Two patients had ventilatory failure, one without respiratory symptoms; another, who had emphysema, had dyspnoea and orthopnoea. The remaining three patients had no respiratory symptoms. Four patients had limb muscle weakness as judged by the maximal voluntary contraction of the quadriceps muscle (range for all subjects 32-100% predicted). Transdiaphragmatic pressure (Pdi) was measured during a maximal unoccluded sniff (Pdi: sniff), a maximal sustained inspiratory effort against a closed airway (Pdi: Pimax), and phrenic nerve stimulation (Pdi: twitch). Mild to moderate diaphragmatic weakness was present in all six patients in proportion to the degree of leg weakness (Pdi: sniff 30-64% predicted; r = 0.6; Pdi:Pimax 6-69% predicted, r = 0.8); this was associated with very low or absent Pdi:twitch during phrenic nerve stimulation. Four patients had weakness of the expiratory muscles. Improvement in muscle strength was documented in two patients after tumour chemotherapy and specific treatment with 3,4-diaminopyridine and prednisolone; one patient was still alive five years from first diagnosis. It is concluded that the respiratory muscles may be implicated in this condition more often than has previously been recognised. As the lack of mobility may cause respiratory symptoms to be minimised, the presence of respiratory muscle weakness may remain undiagnosed unless formal measurement of respiratory muscle function is made.

Autoimmune Diseases↗
PubMed1989

Twitch pressures in the assessment of diaphragm weakness.

To assess the value of phrenic nerve stimulation in the investigation of diaphragm function, transdiaphragmatic pressures were measured in 20 healthy subjects and in 15 patients with diaphragm weakness, during unilateral and bilateral transcutaneous phrenic nerve stimulation at 1 Hz at functional residual capacity (twitch Pdi). Diaphragm function was initially assessed by measuring transdiaphragmatic pressure during a voluntary manoeuvre, the maximal sniff (sniff Pdi); normal readings were confirmed in the control subjects (102-157 (normal greater than 98) cm H2O in the 10 men, 79-102 (normal greater than 70) cm H2O in the 10 women) and reduced values were found in the 15 patients with diaphragm weakness (7.5-90 cm H2O in the 13 men, 23 and 53 cm H2O in the two women). Twitch Pdi during bilateral phrenic nerve stimulation ranged from 8.8 to 33 cm H2O in the control subjects and from 3.1 to 27 cm H2O in the 10 patients in whom a measurement could be obtained. Bilateral twitch Pdi correlated with sniff Pdi both in the control subjects and in the patients with diaphragm weakness (r = 0.75). Only four patients had a bilateral twitch Pdi below the lowest value seen in the control group, including the three with the lowest sniff Pdi (3.1-8.5 cm H2O). These results indicate that transdiaphragmatic pressure recorded during bilateral phrenic nerve stimulation discriminated between control subjects and patients with known weakness of the diaphragm only when this was severe.

Adult↗
PubMed1989

Lung function after coronary artery surgery using the internal mammary artery and the saphenous vein.

Lung volumes and arterial blood gas tensions in patients undergoing coronary artery surgery were compared in 77 patients given an internal mammary artery graft (group 1) and 33 patients given a saphenous vein graft only (group 2). Patients in both groups developed a severe restrictive ventilatory defect after surgery, more pronounced in those receiving an internal mammary artery graft. Mean (SEM) vital capacity in groups 1 and 2 was reduced to 36% (1.2%) and 45% (2.0%) of preoperative values on the second postoperative day (1.56 and 1.85 1 respectively), with some recovery by day 4 to 56% (1.2%) and 63% (2.1%) of preoperative values. The mean (SEM) arterial oxygen tension was 7.34 (0.13) kPa for group 1 and 7.46 (0.20) kPa for group 2 on day 2, rising to 8.39 (0.13) and 9.01 (0.23) kPa on day 4. Analgesic requirements were greater in the group receiving an internal mammary artery graft. Possible explanations for the differences between the effects of the two grafts include the higher frequency of pleurotomy, the placing of pleural drains, and additional surgical trauma when internal mammary artery grafts are used.

Adult↗
PubMed1989

Physiotherapy after coronary artery surgery: are breathing exercises necessary?

One hundred and ten men undergoing coronary artery bypass grafting took part in a prospective randomised study comparing three physiotherapy protocols. All patients were taught self supported huffing and coughing by a physiotherapist and encouraged to move about. This comprised the sole treatment for the 37 control patients (group 3). Additional physiotherapy included breathing exercises for the 35 patients in group 1 and use of an incentive spirometer for the 38 patients in group 2. Functional residual capacity (FRC) was measured daily at the bedside until the fifth postoperative day and arterial blood gas tensions were measured on the second and fourth postoperative days. After surgery patients developed a severe restrictive ventilatory defect and profound arterial hypoxaemia. There were no differences between the three groups. Mean FRC on day 2 was 1.90 litres (61% of the preoperative value), increasing to 2.32 1 by day 5 (76% of the preoperative value). The mean arterial oxygen tension was 7.37 kPa on day 2 and 8.58 kPa on day 4. Four patients in group 1, two in group 2, and five in group 3 developed a chest infection. It is concluded that the addition of breathing exercises or incentive spirometry to a regimen of early mobilisation and huffing and coughing confers no extra benefit after uncomplicated coronary artery bypass grafting.

Breathing Exercises↗
PubMed1989

The measurement of inspiratory muscle strength by sniff esophageal, nasopharyngeal, and mouth pressures.

Sniff esophageal pressure (Pes) is a useful measurement of global inspiratory muscle strength, although it does require passage of an esophageal balloon. We investigated the relationship between nasopharyngeal pressure (Pnp) or pressure within the mouth (Pmo) and Pes during a maximal sniff from FRC without a noseclip. We measured Pes, Pnp, and Pmo simultaneously in 10 normal volunteers, and in 12 patients with inspiratory muscle weakness. In both groups, Pnp and Pmo were slightly less but very close to Pes. In normal volunteers, the mean ratio Pnp/Pes was 0.92 +/- 0.006 (mean +/- SE) and Pmo/Pes was 0.95 +/- 0.006. Regression analysis showed Pes = 4.57 + 1.05 Pnp (r = 0.995, p less than 0.001) and Pes = 0.74 + 1.05 Pmo (r = 0.994, p less than 0.001). Similar relationships between Pnp, Pmo, and Pes were found over a wide range of pressures generated by submaximal sniffs in normal subjects. In patients, the mean ratio Pnp/Pes was 0.90 +/- 0.02 and Pmo/Pes was 0.87 +/- 0.03. Regression analysis showed Pes = 5.12 + 1.0 Pnp (r = 0.949, p less than 0.001) and Pes = 11.2 + 0.882 Pmo (r = 0.936, p less than 0.001). We conclude that Pnp and Pmo predict Pes during a maximal sniff in both normal subjects and in patients with inspiratory muscle weakness. Sniff Pnp and/or Pmo may provide a useful and less invasive method of measuring maximal inspiratory pressures during a sniff.

Adult↗