M Green

Imperial College London, Londinium, England, United Kingdom

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Publications (113)615.64 Total impact

  • M I Polkey · J Moxham · M Green

    No preview · Article · Feb 2011 · European Respiratory Journal

  • No preview · Article · Nov 2006 · Revue des Maladies Respiratoires
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    ABSTRACT: Although breathlessness is common in chronic heart failure (CHF), the role of inspiratory muscle dysfunction remains unclear. We hypothesised that inspiratory muscle endurance, expressed as a function of endurance time (Tlim) adjusted for inspiratory muscle load and inspiratory muscle capacity, would be reduced in CHF. Endurance was measured in 10 healthy controls and 10 patients with CHF using threshold loading at 40% maximal oesophageal pressure (Poes(max)). Oesophageal pressure-time product (PTPoes per cycle) and Poes(max) were used as indices of inspiratory muscle load and capacity, respectively. Although Poes(max) was slightly less in the CHF group (-117.7 (23.6) v -100.0 (18.3) cm H(2)O; 95% CI -37.5 to 2.2 cm H(2)O, p = 0.1), Tlim was greatly reduced (1800 v 306 (190) s; 95% CI 1368 to 1620 s, p<0.0001) and the observed PTPoes per cycle/Poes(max) was increased (0.13 (0.05) v 0.21 (0.04); 95% CI -0.11 to -0.03, p = 0.001). Most of this increased inspiratory muscle load was due to a maladaptive breathing pattern, with a reduction in expiratory time (3.0 (5.8) v 1.1 (0.3) s; 95% CI 0.3 to 3.5 s, p = 0.03) accompanied by an increased inspiratory time relative to total respiratory cycle (Ti/Ttot) (0.43 (0.14) v 0.62 (0.07); 95% CI -0.3 to -0.1, p = 0.001). However, log Tlim, which incorporates the higher inspiratory muscle load to capacity ratio caused by this altered breathing pattern, was >/=85% predicted in seven of 10 patients. Although a marked reduction in endurance time was observed in CHF, much of this reduction was explained by the increased inspiratory muscle load to capacity ratio, suggesting that the major contributor to task failure was a maladaptive breathing pattern rather than impaired inspiratory muscle endurance.
    Full-text · Article · Jun 2004 · Thorax
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    ABSTRACT: Impaired respiratory muscle endurance (RME) could reduce exercise tolerance and contribute to ventilatory failure. The aim of the present study was to develop a clinically-feasible method to measure RME using negative-pressure inspiratory-threshold loading. It was hypothesized that endurance time (tlim) could be predicted by normalizing oesophageal pressure-time product (PTP) per total breath cycle (PTPoes) for maximum oesophageal pressure (Poes,max); the load/capacity ratio. The corresponding mouth pressures, PTPmouth and Pmouth,max were also measured. The RME test was performed on 30 healthy subjects exposed to the same target pressure (70% of Poes,max). Eight patients with systemic sclerosis/interstitial lung disease were studied to assess the validity and acceptability of the technique. Normal subjects showed a wide intersubject variation in tlim (coefficient of variation, 69%), with a linear relationship demonstrated between log tlim and PTPoes/Poes,max (r=0.88). All patients with systemic sclerosis/interstitial lung disease had normal respiratory muscle strength, but six out of eight had a reduction in RME. In conclusion, endurance time can be predicted from the load/capacity ratio, over a range of breathing strategies; this relationship allows abnormal respiratory muscle endurance to be detected in patients. Oesophageal and mouth pressure showed a close correlation, thus suggesting that the test could be applied noninvasively.
    Full-text · Article · Mar 2002 · European Respiratory Journal
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    ABSTRACT: Anecdotal observations suggest that low frequency fatigue, as judged by a fall in twitch tension, is more difficult to achieve in the diaphragm than nonrespiratory muscle but this hypothesis has not previously been directly tested. We studied 7 subjects by performing incremental repetitive contraction loading protocols of the diaphragm and quadriceps. We measured twitch transdiaphragmatic pressure (Tw Pdi) and twitch quadriceps tension (Tw Q) during both muscle contraction and relaxation phases during the run. Unpotentiated and potentiated Tw Pdi and Tw Q were measured before and at 20, 40, and 60 minutes after the run. During the run, greater activation of the quadriceps was achieved; for example, at 70% of maximal voluntary effort the interpolated Tw Q was 12.5% of the relaxation phase Tw Q (implying activation of 87.5%) compared with 29.4% (i.e., 70.6% activation) for the diaphragm (p = 0.05). A significantly greater fall in Tw Q than Tw Pdi was observed (unpotentiated Tw Pdi at 20 minutes 94% baseline versus Tw Q 59% baseline, p = 0.007). Low frequency fatigue in humans is more difficult to generate in the diaphragm than in the quadriceps muscle due in part to reduced central activation.
    No preview · Article · Feb 2002 · Beiträge zur Klinik der Tuberkulose
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    ABSTRACT: Diaphragm strength can be assessed from twitch gastric (TwPgas), twitch oesophageal (TwPoes), and twitch transdiaphragmatic pressure (TwPdi) in response to phrenic nerve stimulation. This requires the passage of balloon catheters, which may be difficult. Changes in pressure measured at the mouth during phrenic nerve stimulation avoid the need for balloon catheters. We hypothesized that pressures measured at the tracheal tube during phrenic stimulation, could also reflect oesophageal pressure change as a result of isolated diaphragmatic contraction and, therefore, reflect diaphragm strength. We aimed to establish the relationship between twitch tracheal tube pressure (TwPet), TwPoes, and TwPdi in patients in the supine and sitting positions. The phrenic nerves were stimulated magnetically bilaterally, in 14 ICU patients while supine and on another occasion while sitting up at 45 degrees. In the sitting position mean TwPoes was 9.1 cm H2O and TwPet 11.3 cm H2O (mean(SD) difference -2.2 (SD 1.5)). In the supine position mean TwPoes was 8.1 cm H2O and TwPet 9.9 cm H2O (mean difference -1.8 (2.2)). The difference between TwPoes and TwPet was less at low twitch amplitude; less than +/- 1 cm H2O below a mean twitch height of 8 cm H2O supine and 10 cm H2O sitting. Sitting TwPet was related to TwPoes r2=0.93 and TwPdi r2=0.65 (P<0.01). Supine TwPet was related to TwPoes r2=0.84 and TwPdi r2=0.83 (P<0.01). The mean within occasion coefficient of variation while sitting was TwPet=13.3%, TwPoes=13.9%, TwPdi=11.2%, and supine TwPet=11.6%, TwPoes=14.6%, TwPdi=11.8%. We conclude that TwPet reflects TwPoes during diaphragmatic stimulation and is worthy of further study to establish its place as a guide to the presence of respiratory muscle strength and fatigue.
    Full-text · Article · Jan 2002 · BJA British Journal of Anaesthesia
  • I M Stell · M I Polkey · P J Rees · M Green · J Moxham
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    ABSTRACT: The aim of this study was to measure inspiratory pressure-generating capacity in patients presenting with acute asthma, as it has been suggested that inspiratory muscle fatigue may contribute to breathlessness and acute respiratory failure. Descriptive study. Emergency departments of two inner-city hospitals. Fifty-one patients with acute asthma, and 45 patients without respiratory disease who served as control subjects. Measurements and results: Maximum inspiratory pressure-generating capacity was measured soon after presentation by the sniff nasal inspiratory pressure (SNIP) method. The mean (SD) SNIP was 110 cm H(2)O (23 cm H(2)O) in men with asthma (mean for control subjects, 126 cm H(2)O [25 cm H(2)O]; p < 0.05) and 80 cm H(2)O [24 cm H(2)O] in women with asthma (mean for control subjects, 105 cm H(2)O (26 cm H(2)O); p < 0.01). In a second study of simultaneous SNIP and intrathoracic pressure measurements in a group of patients with acute asthma (n = 10) and control subjects (n = 11), the effect of airways obstruction on SNIP was assessed. The measurement of sniff esophageal pressure was more negative than SNIP by approximately 16% in asthmatic patients and by 4% in control subjects. Taking account of the likely effect of airways obstruction on SNIP, the reduction in inspiratory pressure-generating capacity that was observed in these patients with moderately severe acute asthma was minor and was consistent with the modest hyperinflation observed. This study did not find evidence of inspiratory muscle weakness or fatigue in patients with moderately severe acute asthma presenting to the emergency department.
    No preview · Article · Sep 2001 · Chest
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    ABSTRACT: In normal subjects, at submaximal inspiratory volumes, the carbon monoxide gas transfer (TLCO) is reduced, but the CO transfer coefficient (KCO) is higher than would be predicted at total lung capacity (TLC). Similar changes have also been observed in patients with severe isolated diaphragm weakness. The TLCO tends to be reduced, but relatively less than the TLC and thus when the TLCO is corrected for alveolar volume (VA), the KCO is raised (Laroche et al, 1988). Therefore, in clinical practice, a raised KCO is often taken as a feature of respiratory muscle weakness, but no studies have examined the effects of combined inspiratory and expiratory muscle weakness. We compared the lung function data in a retrospective review of 6 patients with isolated inspiratory muscle weakness [IMW: mean sniff oesophageal pressure, sniff Poes, -32 cm H2O, mean Cough Pgas 157 cm H2O] and 5 patients with combined inspiratory and expiratory muscle weakness [IMW & EMW: mean sniff Poes, -39 cm H2O, mean Cough Pgas 48 cm H2O]. All these patients had primary neuromuscular diseases without evidence of airways disease, as judged by the flow-volume loops, and had no evidence of parenchymal disease on chest x-ray. We also studied 6 normal subjects expiring to only 50% of expiratory reserve volume and inspiring to only to 50 % of inspiratory capacity, thus mimicking the IMW & EMW group. The mean (SD) results are shown as % predicted: IMW IMW & EMW NORMALS TLC 62.7 ± 6.9 80.9 ± 13.0 RV 89.7 ± 9.4 157.4 ± 48.6 TLCO 65.4 ± 13.7 58.0 ± 11.9* 80.0 ± 7.7* VA 51.7 ± 7.7 71.9 ± 14.6 70.4 ± 4.9 KCO 136.7 ± 27.4 85.5 ± 9.4* 115.3 ± 7.9*. *TLCO and KCO were different in the combined inspiratory and expiratory muscle weakness group and normals (P<0.05), although the VA was similar in the two groups. We confirm that an elevated KCO is a feature of isolated inspiratory muscle weakness, whereas in patients with combined inspiratory and expiratory muscle weakness, which is less common, the KCO is likely to be mildly reduced rather than increased. The mechanism for this is unclear.
    No preview · Article · Dec 2000
  • N. Hart · A.H. Nickol · M. Green · J. Moxham · M.I. Polkey
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    ABSTRACT: In contrast to the clinical measurement of respiratory muscle strength (RMS), few techniques are currently available for the measurement of respiratory muscle endurance (RME) and thus the measurement of RME has been limited. However measurement of RMS does not assess how the respiratory muscles will cope when an increased load is placed on the system and previous studies have shown that, in some clinical conditions, RME can be impaired despite normal strength [Mancini et al. JAmCollCardiol. 1994. 24:972-81; Leith DE and Bradley M. JAP. 1976. 41(4): 508-16]. Previously we have shown that endurance time is a function of the oesophageal load/capacity ratio [Hart et al. Thorax. 1999. 54(3): A74]. We hypothesised that this relationship would be constant over a wide range of duty cycles and endurance times (TLim). We studied 24 healthy subjects using a negative pressure loading device. The load was the same (70% of maximum negative oesophageal pressure, Poesmax) and there was no restriction placed on the pattern of breathing. We measured TLim and oesophageal pressure (Poes) and calculated pressure time product for Poes (PTPoes). A simple regression plot of Log PTPoes/Poesmax (load/capacity ratio) against Log TLim, with 95% confidence bands, was obtained. We conclude that use of this relationship will allow diction of abnormal RME in patients. (Graph Presented).
    No preview · Article · Dec 2000
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    ABSTRACT: Anterior magnetic stimulation (aMS) of the phrenic nerves is a new method for the assessment of diaphragm contractility that might have particular applications for the clinical assessment of critically ill patients who are commonly supine. We compared aMS with existing techniques for measurement of diaphragm weakness and fatigue in 10 normal subjects, 27 ambulant patients with suspected diaphragm weakness and 10 critically ill patients. Laboratory and intensive care unit of two university hospitals. Although aMS was not demonstrably supramaximal in normal subjects, the mean value of twitch transdiaphragmatic pressure (Tw Pdi) obtained at 100% of stimulator output, 23.7 cmH2O, did not differ significantly from that obtained with bilateral supramaximal electrical stimulation (ES), 24.9 cmH2O, or bilateral anterior magnetic phrenic nerve stimulation (BAMPS), 27.3 cmH2O. A fatiguing protocol produced a 20 % fall in aMS-Tw Pdi and a 19% fall in BAMPS-Tw Pdi; the fall in aMS-Tw Pdi correlated with the fall in BAMPS-Tw Pdi (r2 = 0.84, p = 0.03) indicating that aMS can detect diaphragm fatigue. In ambulant patients aMS agreed closely with existing measures of diaphragm strength. The maximal sniff Pdi correlated with both the aMS-Tw Pdi (r2 = 0.60, p < 0.0001) and the BAMPS-Tw Pdi (r2 = 0.65, p < 0.0001) and the aMS-Tw Pdi was a mean (SD) 2.2 (4.3) cmH2O less than BAMPS-Tw Pdi. In addition, aMS correctly identified diaphragm dysfunction in patients studied on the ICU. We conclude that aMS is of clinical value for the investigation of suspected diaphragm weakness.
    No preview · Article · Sep 2000 · Intensive Care Medicine
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    ABSTRACT: The function of the diaphragm and other respiratory muscles during exercise in chronic obstructive pulmonary disease (COPD) remains controversial and few data exist regarding respiratory muscle pressure generation in this situation. The inspiratory pressure/time products of the oesophageal and transdiaphragmatic pressure, and the expiratory gastric pressure/time product during exhaustive treadmill walking in 12 patients with severe COPD are reported. The effect of noninvasive positive pressure ventilation during treadmill exercise was also examined in a subgroup of patients (n=6). During free walking, the inspiratory pressure/time products rose early in the walk and then remained level until the patients were forced to stop because of intolerable dyspnoea. In contrast, the expiratory gastric pressure/time product increased progressively throughout the walk. When patients walked the same distance assisted by noninvasive positive pressure ventilation, a substantial reduction was observed in the inspiratory and expiratory pressure/time products throughout the walk. When patients walked with positive pressure ventilation for as long as they could, the pressure/time products observed at exercise cessation were lower than those observed during exercise cessation after free walking. It is concluded that, in severe chronic obstructive pulmonary disease, inspiratory muscle pressure generation does not increase to meet the demands imposed by exhaustive exercise, whereas expiratory muscle pressure generation rises progressively. Inspiratory pressure support was shown to substantially unload all components of the respiratory muscle pump.
    Full-text · Article · May 2000 · European Respiratory Journal
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    AC Watson · ML Harris · N Hart · M Green · J Moxham

    Full-text · Article · Mar 2000 · Critical Care
  • A.C. Watson · N. Hart · M.L. Harris · M. Green · J. Moxham
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    ABSTRACT: We hypothesised that critically ill patients who fail weaning trials may do so because they have weak respiratory muscles, and therefore insufficient capacity to deal with the increased load imposed on them by self-ventilation. Twitch transdiaphragmatic pressure (TwPdi) was measured to quantitate inspiratory muscle capacity.A subsequent weaning trial was 'successful' if the patient self-ventilated for 2 hours,and 'unsuccessful' if not.During weaning,transdiaphragmatic pressure (Pdi) and duty cycle (Ti/Ttot) were measured.Pressure time index of the diaphragm, PTI(Pdi) was calculated as meanPdi/TwPdi x Ti/Ttot, and used as an indicator of load. 12 ICU patients were studied (6M, 6F), average ICU stay 24 days (range 14-39). Mean baseline TwPdi was 8.35cm H2O (range 3.75-11.42) in the 3 patients who failed weaning, and 11.36cm H20 (range 3.03-18.52) in the 9 who succeeded.In the failure group, mean PTI(Pdi) was 0.05 (range 0.02-0.05) at 1 min, and 0.12 (range 0.06-0.16) at the end of the trial. In the successful group, mean PTI(Pdi) was 0.12 (range 0.05-0.24) at 1min, and 0.13 (range 0.05-0.22) at 120 min.Therefore,although initial load was lower in the failure group, it increased progressively over time.We conclude that increasing load on weak respiratory muscles may contribute to failure of self-ventilation.
    No preview · Article · Dec 1999
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    ABSTRACT: The quantification of RME has proven difficult due to the influence of a variety of physiological variables (e.g. inspiratory time) on endurance time (Tlim). In this study, we used an inspiratory threshold loading method and hypothesised that endurance time (Tlim) is dependent on the load/capacity ratio. We studied 6 healthy subjects during 3 separate endurance runs using a negative pressure loading device(Chen et al. ERJ 1998;12:208-11). In each run the load was the same (70% of maximum oesophageal pressure, Poes max) and there was no restriction placed on the pattern of breathing. We measured Tlim (mean endurance time for all endurance runs was 325.4s ±192.08s) and oesophageal pressure and calculated pressure time product for Poes (PTPoes), as an indicator of work performed. A plot of log PTPoes/Poesmax (load/capacity ratio) against time for each endurance run was obtained: Regression Plot 95% Confidence Bands (Graph Presented) We conclude that use of this "nomogram" may allow assessment of RME even when subjects vary their breathing strategy.
    No preview · Article · Dec 1999
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    P D Hughes · M I Polkey · J Moxham · M Green
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    ABSTRACT: Diaphragm paralysis is a recognized complication of neuralgic amyotrophy that causes severe dyspnoea. Although recovery of strength in the arm muscles, when affected, is common, there are little data on recovery of diaphragm function. This study, therefore, re-assessed diaphragm strength in cases of bilateral diaphragm paralysis due to neuralgic amyotrophy that had previously been diagnosed at the authors institutions. Fourteen patients were recalled between 2 and 11 yrs after the original diagnosis. Respiratory muscle and diaphragm strength were measured by volitional manoeuvres as maximal inspiratory pressure and sniff transdiaphragmatic pressure. Cervical magnetic phrenic nerve stimulation was used to give a nonvolitional measure of diaphragm strength: twitch transdiaphragmatic pressure. Only two patients remained severely breathless. Ten of the 14 patients had evidence of some recovery of diaphragm strength, in seven cases to within 50% of the lower limit of normal. The rate of recovery was variable: one patient had some recovery after 2 yrs, and the rest took 3 yrs or more. In conclusion, in most patients with diaphragm paralysis due to neuralgic amyotrophy, some recovery of the diaphragm strength occurs, but the rate of recovery may be slow.
    Preview · Article · Mar 1999 · European Respiratory Journal
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    ABSTRACT: The purpose of this study was to establish the phrenic nerve conduction time (PNCT) for magnetic stimulation and further assess the relatively new technique of anterior unilateral magnetic stimulation (UMS) of the phrenic nerves in evaluating the diaphragm electromyogram (EMG). An oesophageal electrode was used to record the diaphragm compound muscle action potential (CMAP) elicited by supramaximal percutaneous electrical phrenic nerve stimulation (ES) and UMS from eight normal subjects. The oesophageal electrode used for recording the CMAP was positioned at the level of the hiatus and 3 cm below. The diaphragm CMAP was also recorded from chest wall surface electrodes in five subjects. All of the phrenic nerves could be maximally stimulated with UMS. A clear plateau of the amplitude of the CMAP was achieved for the right and left phrenic nerves. The mean amplitudes of the CMAP recorded from the oesophageal electrode were, for the right side, 0.74+/-0.29 mV (mean+SD) for ES and 0.76+/-0.30 mV for UMS with maximal power output, and for the left side 0.88+/-0.33 mV for ES and 0.80+/-0.24 mV for UMS. PNCT measured by the oesophageal electrode with ES and UMS with maximal output were, for the right side, 7.0+/-0.8 ms and 6.9+/-0.8 ms, respectively, and for the left side 7.8+/-1.2 ms and 7.7+/-1.3 ms, respectively. However, the CMAP recorded from chest wall surface electrodes with UMS was unsuitable for the measurement of PNCT. The results suggest that unilateral magnetic stimulation of the phrenic nerves combined with an oesophageal electrode can be used to assess diaphragmatic electrical activity and measure the phrenic nerve conduction time.
    Full-text · Article · Mar 1999 · European Respiratory Journal
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    ABSTRACT: The purpose of this study was to establish the phrenic nerve conduction time (PNCT) for magnetic stimulation and further assess the relatively new technique of anterior unilateral magnetic stimulation (UMS) of the phrenic nerves in evaluating the diaphragm electromyogram (EMG).An oesophageal electrode was used to record the diaphragm compound muscle action potential (CMAP) elicited by supramaximal percutaneous electrical phrenic nerve stimulation (ES) and UMS from eight normal subjects. The oesophageal electrode used for recording the CMAP was positioned at the level of the hiatus and 3 cm below. The diaphragm CMAP was also recorded from chest wall surface electrodes in five subjects.All of the phrenic nerves could be maximally stimulated with UMS. A clear plateau of the amplitude of the CMAP was achieved for the right and left phrenic nerves. The mean amplitudes of the CMAP recorded from the oesophageal electrode were, for the right side, 0.74±0.29 mV (mean±sd) for ES and 0.76±0.30 mV for UMS with maximal power output, and for the left side 0.88±0.33 mV for ES and 0.80±0.24 mV for UMS. PNCT measured by the oesophageal electrode with ES and UMS with maximal output were, for the right side, 7.0±0.8 ms and 6.9±0.8 ms, respectively, and for the left side 7.8±1.2 ms and 7.7±1.3 ms, respectively. However, the CMAP recorded from chest wall surface electrodes with UMS was unsuitable for the measurement of PNCT.The results suggest that unilateral magnetic stimulation of the phrenic nerves combined with an oesophageal electrode can be used to assess diaphragmatic electrical activity and measure the phrenic nerve conduction time.
    Preview · Article · Jan 1999 · European Respiratory Journal
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    ABSTRACT: The purpose of the study was to compare electrical stimulation (ES) and cervical magnetic stimulation (CMS) of the phrenic nerves for the measurement of the diaphragm compound muscle action potential (CMAP) and phrenic nerve conduction time. A specially designed esophageal catheter with three pairs of electrodes was used, with control of electrode positioning in 10 normal subjects. Pair A and pair B were close to the diaphragm (pair A lower than pair B); pair C was positioned 10 cm above the diaphragm to detect the electromyogram from extradiaphragmatic muscles. Electromyograms were also recorded from upper and lower chest wall surface electrodes. The shape of the CMAP measured with CMS (CMS-CMAP) usually differed from that of the CMAP measured with ES (ES-CMAP). Moreover, the latency of the CMS-CMAP from pair B (5.3 +/- 0.4 ms) was significantly shorter than that from pair A (7.1 +/- 0.7 ms). The amplitude of the CMS-CMAP (1.00 +/- 0.15 mV) was much higher than that of ES-CMAP (0.26 +/- 0.15 mV) when recorded from pair C. Good-quality CMS-CMAPs could be recorded in some subjects from an electrode positioned very low in the esophagus. The differences between ES-CMAP and CMS-CMAP recorded either from esophageal or chest wall electrodes make CMS unreliable for the measurement of phrenic nerve conduction time.
    No preview · Article · Jan 1999 · Journal of Applied Physiology
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    ABSTRACT: In the supine patient diaphragm contractility can be assessed by measuring the twitch transdiaphragmatic pressure (Tw Pdi) elicited by bilateral anterior magnetic stimulation of the phrenic nerves in the neck (BAMPS) (Mills et al AJRCCM 1996;154: 1099). A limitation of this technique is that it requires two magnets and two coils with a consequent increase in costs and complexity. It has recently been reported that stimulation of the phrenic nerves using a single coil placed anteriorly over the upper sternum can also activate the diaphragm (aMS) (Similowski et al JAP 1997:82;1190). This technique is potentially attractive since it would allow assessment of diaphragm contractility in the supine position with only one magnet and coil. To further evaluate aMS we investigated whether it could detect diaphragm fatigue. 5 healthy subjects were studied and Tw Pdi was measured as the mean of 10 stimuli before, and 20, 40 and 60 minutes after, a protocol (2 minutes of maximal isocapnic hyperpnea;MVV) known to induce low frequency diaphragm fatigue (Polkey et al ERJ 1997,10:1859). Data are presented in the figure; both techniques identified a fall in Tw Pdi at 20 minutes after MVV in 4 of 5 subjects. In the fifth aMS showed a fall of 2.1 cm H2O (13%) while BAMPS showed a rise of 0.8 cm H2O (4%). A statistically significant relationship was observed between the %fall in BAMPS Tw Pdi and the %fall in aMS Tw Pdi (r=0.66, p<0.01). (Graph Presented) We conclude that aMS can be used to demonstrate diaphragm fatigue but that, as with other stimulation techniques, caution should be exercised in the interpretation of results if the change is numerically small.
    No preview · Article · Dec 1998
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    ABSTRACT: Diaphragm paralysis is one cause of unexplained breathlessness; its recognition is therefore clinically useful. Diaphragm and phrenic nerve function can be assessed by recording the EMG from chest wall surface electrodes after electrical phrenic nerve stimulation (ES) or unilateral magnetic stimulation of the phrenic nerve (UMS). Both these methods have limitations; UMS may generate complex waveforms due to the contribution of upper thoracic muscles whereas the phrenic nerve may be difficult to locate with ES. The oesophageal electrode is less influenced by other muscles but in diaphragm paralysis it may be difficult to position a conventional single pair electrode at the diaphragm and an absent response to phrenic nerve stimulation may result simply from poor positioning. We therefore designed a novel multipair esophageal electrode; the electrode consisted of four electrode pairs with a total span of 17 cm and was therefore long enough to encompass the esophageal hiatus. Seven patients with diaphragm paralysis (two bilateral and five unilateral), as judged from pressure measurements, were studied . The catheter was fixed with the proximal electrode 40 cm away from nose. Five UMS stimulations were performed and the EMG was simultaneously recorded from four electrode pairs. All the patients were successfully assessed in less man 20 minutes. No EMG response was recorded in the two patients with bilateral diaphragm paralysis or in the non-functioning phrenic nerves whereas a good quality EMG was recorded in the 5 functioning hemidiaphragms. The amplitude of the EMG and phrenic nerve conduction time for the functioning hemidiaphragm were 1.16±0.29 mV (mean±SD) and 7.6±1.5 ms, respectively, which is within normal limits for our laboratory. We conclude that multipair esophageal electrode recording combined with UMS is a rapid and reliable technique for the diagnosis of the diaphragm paralysis.
    No preview · Article · Dec 1998

Publication Stats

3k Citations
615.64 Total Impact Points

Institutions

  • 2011
    • Imperial College London
      Londinium, England, United Kingdom
  • 1997-2004
    • Royal Brompton and Harefield NHS Foundation Trust
      • Respiratory Medicine
      Harefield, England, United Kingdom
  • 2002
    • Royal Berkshire NHS Foundation Trust
      Reading, England, United Kingdom
  • 2000
    • Sahlgrenska University Hospital
      Goeteborg, Västra Götaland, Sweden
  • 1994-1998
    • National Heart, Lung, and Blood Institute
      베서스다, Maryland, United States
  • 1995-1997
    • The Kings College
      Бесемер, Alabama, United States
  • 1985-1996
    • King's College London
      • Division of Asthma, Allergy and Lung Biology
      Londinium, England, United Kingdom
  • 1993
    • The Heart Lung Center
      Londinium, England, United Kingdom