Phrenic Nerve Conduction Time Research Articles

Identification of prolonged phrenic nerve conduction time in the ICU: magnetic versus electrical stimulation

Retrospective study of prospectively collected data to assess the reliability of cervical magnetic stimulation (CMS) to detect prolonged phrenic nerve (PN) conduction time at the bedside. Because PN injuries may cause diaphragm dysfunction, their diagnosis is relevant in intensive care units (ICU). This is achieved by studying latency and amplitude of diaphragm response to PN stimulation. Electrical stimulation (ES) is the gold standard, but it is difficult to perform in the ICU. CMS is an easy noninvasive tool to assess PN integrity, but co-activates muscles that could contaminate surface chest electromyographic recordings. In a first set of 56 ICU patients with suspected PN injury, presence and latency of compound motor action potentials elicited by CMS and ES were compared. With ES as the reference method, CMS was evaluated as a test designed to indicate presence or absence of PN injury. In eight additional patients, intramuscular diaphragm recordings were compared with surface diaphragm recordings and with the electromyograms of possible contamination sources. The sensitivity of CMS to diagnose abnormal PN conduction was 0.91, and specificity was 0.84, whereas positive and negative predictive values were 0.81 and 0.92, respectively. Passing-Bablok regression analysis suggested no differences between the two measures. The correlation between PN latency in response to CMS and ES was significant. The "diaphragm surface" and "needle" latencies were close, and were significantly different from those of possibly contaminating muscles. One hemidiaphragm showed likely signal contamination. CMS provides an easy reliable tool to detect prolonged PN conduction time in the ICU.

Electromyographic tools to assess hemidiaphragm paralysis

Non-invasive measurements of the phrenic nerve conduction time (CT) and diaphragmatic electromyographic response to voluntary inspiratory efforts may help to document an abnormal diaphragmatic function in the presence of hemidiaphragm elevation on chest radiographs. Twenty-one patients were addressed for the diagnosis of abnormal placement and motion of the right (13) or left (8) cupola on chest radiographs. CT was measured by recording the diaphragmatic M-wave evoked by electrical transcutaneous phrenic nerve stimulation. The integrated diaphragmatic surface electromyogram (Edi) was recorded during sniff and Müller manoeuvres. Four patients were followed up during the next 8-16 months. Among the twenty-one patients, five (24%) had a lengthened or absent CT. A right-to-left peak Edi asymmetry was measured in fourteen (67%), including those having abnormal CT. Agreement between side-related radiographic abnormalities and Edi asymmetry was high in the cases of an elevation of the right cupola (12/13, 92%) but poor when the left cupola was suspected (1/8, 13%). Long-term follow-up of Edi asymmetry showed a partial or total recovery. Thus, the combination of measurements of phrenic nerve CT and Edi recordings during voluntary inspiratory efforts confirmed 67% of the radiographic suspicion of diaphragmatic dysfunction.

Change of diaphragm electromyograms in patients with obstructive sleep apnea-hypoventilation syndrome and its significance

Objective To explore change of diaphragm electromyograms in patients with obstructive sleep apnea-hypoventilation syndrome (OSAHS) before and after nocturnal sleep, as well as effective nasal continuous positive airway pressure (n-CPAP) ventilation treatment for more than two months. Methods Diaphragm electromyogram was recorded with chest surface electrodes in 22 patients with moderate and severe OSAHS and 24 normal people, and phrenic nerve conduction time (PNCT) and diaphragm compound muscle action potential (CMAP) provoked by unilateral magnetic stimulation (UMS) were measured for them before and after sleep. Measurements were repeated for five patients with severe OSAHS after effective OSAHS patients before and after nocturnal sleep than that in normal people bilaterally, (8.4±0. 6)ms and (8.4±0. 9)ms vs (7. 3±0. 8)ms and (7. 3±0. 8) ms for the left side; and (8.4±1.3) ms and (8. 9 ± 0. 8) ms vs (7.2 ± 0. 8) ms and (7.2 ± 0. 8 ) ms for the right side ( P < 0. 01 ), respectively ; and amplitude of CMAP was significantly lower in OSAHS patients, (0. 60±0. 20)mV and (0. 64±0. 29)mV vs (0. 98 ± 0. 28)mV and (0. 97±0. 27)mV for the left side; and (0. 53±0. 23)mV and (0. 56±0. 26)mV vs (0. 93 ±0. 29) mV and ( 0. 94 ± 0. 29 ) mV for the right side, respectively ( P < 0. 01 ) ; but no significant significantly shortened bilaterally in five patients with severe OSAHS after effective n-CPAP ventilation treatment for more than two months, (8.6±0. 7)ms vs (7.4±0. 5)ms for the lfet side and (7. 8±0. 6)ms vs (6.4 ± 0. 6) ms for the fight side ( P < 0. 05 ), respectively. Conclusions Both phrenic nerve conduction and diaphragm muscle function are weakened in patients with OSAHA, which may be related to hypoxia and/ or disturbance of sleep structure at night. Key words: Sleep apnea, obstructive; Phrenic nerve; Diaphragm electromyogram

Diaphragm electromyography using an oesophageal catheter: current concepts

The usefulness of diaphragm electromyography recorded from an oesophageal electrode depends on a reliable signal which is free of artefact. The diaphragm EMG (electromyogram) recorded from chest wall surface electrodes may be unreliable because of signal contamination from muscle activity other than the diaphragm. Initially, the oesophageal electrode catheter for human studies had only one electrode pair, which could be difficult to position accurately and was influenced by a change in lung volume. Recently, a multipair oesophageal electrode has been developed which allows a high-quality EMG to be recorded. In the present review, the progress of oesophageal electrode design is outlined. The effects of signal contamination, electrode movement and particularly the effect of change in lung volume on the diaphragm EMG are discussed. The diaphragm EMG, recorded from a multipair oesophageal electrode, is useful to assess neural respiratory drive and diaphragm function in different groups of patients with respiratory disease, including patients with neuromuscular disease and sleep-disordered breathing, and those in the intensive care unit. When combined with cervical and cranial magnetic stimulation, an oesophageal electrode can be used to partition the central respiratory response time and phrenic nerve conduction time.

Diaphragm compound muscle action potential measured with magnetic stimulation and chest wall surface electrodes.

To seek a method to reliably measure phrenic nerve conduction time (PNCT) with magnetic stimulation we investigated two stimulus sites, placing the magnetic coil at the cricoid cartilage (high position) or close to the clavicle (low position). We also compared compound muscle action potential (CMAP) recorded from three different sites: in the sixth to eighth intercostal spaces in the anterior axillary line (Ant-a); in the 8th intercostal space close to the midclavicular line; and with one electrode at the lower sternum and the other at the costal margin. Fourteen normal subjects were studied. The PNCT measured by magnetic stimulation in the high position recorded from (Ant-a) was 7.6+/-0.6 on the left side and 8.4+/-0.7 on the right. The PNCT recorded from all three sites become much shorter when the magnetic coil was moved from the high to the low position. Our results show that PNCT can be accurately measured with magnetic stimulation when care is taken to avoid coactivation of the brachial plexus.

Effect of brachial plexus co-activation on phrenic nerve conduction time

BACKGROUNDDiaphragm function can be assessed by electromyography of the diaphragm during electrical phrenic nerve stimulation (ES). Whether phrenic nerve conduction time (PNCT) and diaphragm electrical activity can be reliably measured...

Diaphragm electromyogram measured with unilateral magnetic stimulation.

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.

Phrenic Nerve and Diaphragm Function Following Open Heart Surgery: A Prospective Study With and Without Topical Hypothermia

In a prospective study, 100 patients undergoing open heart surgery were randomly allocated to receive ice/slush topical hypothermia for myocardial protection (Group I, n = 56) or not (Group II, n = 44). Chest radiographs, diaphragm screening, lung function and phrenic nerve conduction time were assessed pre-operatively and at 1 week and 1 month post-operatively in all patients and subsequently at 3 months, 6 months, 1 year and 2 years in all patients with radiological evidence of diaphragm paralysis. The two groups were similar in terms of age, sex, diabetes and smoking habits. Cardiopulmonary bypass and aortic cross-clamp times were similar in the two groups. Radiological evidence of partial left lower lobe collapse was more frequent in Group I (79 per cent vs. 36 per cent, p < 0.01). Twenty (36 per cent) Group I patients developed unilateral diaphragm paralysis (19 left-sided) compared with none in Group II. Diaphragm paralysis was still present in 19 patients (34 per cent) at 1 month, in five patients (9 per cent) at 1 year and in one patient (2 per cent) at 2 years post-operatively. Phrenic nerve conduction time was recorded in 98 per cent of patients pre-operatively, but was unrecordable on the appropriate side in all 20 patients with diaphragm paralysis 1 week post-operatively. Prolonged phrenic nerve conduction time on the left side was found in a further seven Group I patients 1 week post-operatively. There were no significant differences between the two groups in terms of post-operative arrhythmias, myocardial infarction or mortality.(ABSTRACT TRUNCATED AT 250 WORDS)

Diaphragm paralysis following cardiac surgery: Role of phrenic nerve cold injury

Diaphragm paralysis has been reported radiologically after cardiac surgery with an incidence ranging from 30% to 75% of patients. We studied 100 consecutive patients undergoing open heart operations, half of whom received ice/slush topical hypothermia (group 1) and half of whom did not (group 2). Chest radiology and diaphragm screening were performed at 1 week, 1 month, and every 6 months thereafter in all patients with an elevated diaphragm. Phrenic nerve conduction time was measured in all patients in whom there was radiological evidence of diaphragm paralysis 1 week postoperatively. The two groups were similar in terms of age and sex. Aortic cross-clamp time was less in group 1 (61.5 ± 15.6 minutes) compared with group II (74.4 ± 20.8 minutes), although this difference was not significant. Significant differences, however, were found for radiological evidence of partial left lower lobe collapse (82% in group 1 versus 32% in group 2; p < 0.01) and for radiological evidence of diaphragm paralysis (32% in group 1 versus 2% in group 2; p < 0.001) within the first postoperative week. Unilateral diaphragm paralysis developed in 16 group 1 patients (15 left sided, 1 right sided) compared with only 1 patient in group 2. In these 16 group 1 patients, diaphragm paralysis was still present in 12 (75%) at 1 month and in 5 (31.3%) at 1 year postoperatively. There were no significant differences between the two groups in terms of postoperative arrhythmias, myocardial infarction, or mortality. Phrenic nerve conduction time was found to be a sensitive indicator of phrenic nerve cold injury and recovery. The use of ice/slush topical hypothermia during open heart operations is associated with a high rate of diaphragm paralysis, and its myocardial protective value could be more selectively applied.

Phrenic Neuropathy in Arsenic Poisoning

A patient presented with acute arsenic neuropathy with asymmetric bilateral phrenic nerve involvement. The clinical and roentgenographic observations of phrenic nerve dysfunction were confirmed by prolonged phrenic nerve conduction time. The patient made a significant recovery with d-penicillamine therapy.

Bedside assessment of phrenic nerve function in infants and children

Phrenic nerve damage is widely recognized after cardiac operations and is associated with an increased morbidity and mortality. Retrospective studies in children have estimated a prevalence of phrenic damage of between 0.5% and 2.2%, but all these studies have limited their investigations to patients who have clinical problems postoperatively, and they have all used clinical or radiologic methods to diagnose the damage. These methods are indirect and hard to evaluate, making the accurate early diagnosis of phrenic nerve damage very difficult. Measurement of phrenic nerve conduction time (phrenic latency) allows direct evaluation of phrenic function and integrity, making it potentially much more specific than indirect methods. Using a simplified method of direct phrenic nerve stimulation, we have developed a method of measuring phrenic latency at the bedside in infants and children. A 1 Hz electrical stimulus is applied over the phrenic nerve in the neck and a diaphragmatic electromyogram from the seventh and eighth intercostal spaces is displayed on a storage oscilloscope. Phrenic latency can be measured directly from the screen. Using these methods we have now studied 37 children (aged 2 days to 15 years) before and after cardiac operations. Mean phrenic latency was 5.4 +/- 1.0 msec on the right and 5.4 +/- 1.0 msec on the left. Prolongation of phrenic latency by more than 2 msec was found in seven of 66 postoperative measurements (10.6%). These patients had a substantially worse postoperative course. We believe this technique to be an important contribution to the diagnosis of postoperative phrenic nerve damage, and one that can help in clinical practice to elucidate an important cause of postoperative morbidity and mortality.

Respiratory muscle function in myasthenia gravis.

Global respiratory muscle function and diaphragmatic strength were assessed and compared with quadriceps femoris muscle strength in 17 patients with generalized mild-to-moderate myasthenia gravis and breathlessness. Initial measurements, made 10 h after the last dose of oral anticholinesterase therapy, demonstrated reduced maximal static expiratory (52.4 +/- 26.8% predicted) and inspiratory (54.0 +/- 23.5% predicted) mouth pressures in 16 patients, and reduced quadriceps femoris muscle strength in all cases. Vital capacity (VC) (70.9 +/- 19.0% predicted) was abnormal in 12 patients. Transdiaphragmatic pressure recorded during maximal sniffs (sniff Pdl) was reduced in eight patients, whereas pressure recorded during bilateral phrenic nerve stimulation at 1 Hz (twitch Pdi) was reduced in only three. There was no relationship between the grade of myasthenia or the severity of dyspnea and any of the measurements of respiratory muscle strength. After the administration of edrophonium hydrochloride (Tensilon), there was a significant increase in maximal static expiratory and inspiratory mouth pressures in quadriceps muscle strength and in sniff Pdi. The small increase in VC was not significant, and twitch Pdi increased in only one patient. Phrenic nerve conduction time was normal before and after Tensilon. Two patients with severe long-standing myasthenia showed no improvement in any measurement after Tensilon. We conclude that expiratory and inspiratory muscle weakness was not uncommon in patients with myasthenia gravis. Respiratory muscle strength improved after Tensilon. Vital capacity was a less sensitive measure of respiratory muscle strength than were respiratory mouth pressures and sniff Pdi. Diaphragmatic involvement was not detected by twitch Pdi unless the weakness was severe.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Phrenic nerve stimulation in normal subjects and in patients with diaphragmatic weakness.

Phrenic nerve stimulation is often considered to be difficult and unreliable. The time taken for the phrenic nerves to be located and adequately stimulated was measured in 110 subjects, aged 21-89 years, 26 of whom had diaphragmatic weakness; and phrenic nerve conduction time was recorded in 76 of these individuals. Each phrenic nerve was stimulated transcutaneously in the neck with square wave impulses 0.1 ms in duration at 1 Hz and 80-160 volts while diaphragmatic muscle action potentials were recorded with surface electrodes. The time taken to locate either phrenic nerve ranged from two seconds to 22 minutes (median 10s). Both nerves were located in 83 of the 84 control subjects (99%) and in 21 of the 26 patients with diaphragmatic weakness (81%). Mean (SD) phrenic nerve conduction time in the control subjects was 6.94 (0.77) ms on the right and 6.61 (0.77) ms on the left. A weak relationship was found between conduction time and the subjects' age and height. Four out of 24 patients with diaphragmatic weakness had a prolonged phrenic nerve conduction time. Transcutaneous stimulation of the phrenic nerves was not a time consuming procedure, and it was well tolerated, reproducible, and successful in 95% of subjects.

Effects of phrenic nerve cooling on diaphragmatic function.

The effects of phrenic nerve cooling at 0 degrees C on the nerve and diaphragmatic function were evaluated in dogs. Eleven dogs, anesthetized and mechanically ventilated, were studied. Left diaphragmatic function was assessed by recording the transdiaphragmatic pressure (Pdi) generated during electrical stimulation of the left phrenic nerve at different frequencies (0.5, 30, and 100 Hz). Phrenic nerve stimulations were achieved either directly by electrodes placed around the phrenic nerve above its pericardial course or by intramuscular electrodes placed close to the phrenic nerve endings. Electrical activity of the hemidiaphragm (Edi) was recorded and phrenic nerve conduction time (PNCT) was measured during direct phrenic stimulation. A transpericardial cooling of the nerve, at 0 degrees C, on a length of 1 cm, was performed during 30 min (group A, n = 7) or 5 min (group B, n = 4). After the cooling period, phrenic and diaphragmatic functions were assessed hourly for 4 h (H1-H4). Cooling the phrenic nerve produced a complete phrenic nerve conduction block in all dogs, 100 +/- 10 s after the onset of cold exposure. Conduction recovery time was longer in group A (11 +/- 7 min) than in group B (2 +/- 0.5 min) and PNCT remained increased throughout the study in group A. Furthermore, in group A, Pdi and Edi during direct phrenic stimulation were markedly depressed from H1 to H4. No change in these parameters was noted until H3 during intramuscular stimulation, time at which a significant decrease occurred. By contrast, Pdi and Edi from direct and intramuscular stimulations remained unchanged throughout the study in group B.(ABSTRACT TRUNCATED AT 250 WORDS)

Diaphragmatic Pacing in Infants: Techniques and Results

Phrenic nerve pacing was employed in 8 infants with central hypoventilation syndrome. Their ages ranged from 2.5 to 8.5 months. Preoperative diagnosis was established by demonstrating inadequate ventilatory response to hypercapnia and hypoxia. Percutaneous measurements of phrenic nerve conduction time and diaphragmatic action potentials were performed prior to operation to assess the feasibility of diaphragmatic pacing. A single anterolateral thoracotomy incision was used for both electrode placement in the chest and receiver implantation in the flank. The stimulating electrode was inserted around a segment of intrathoracic phrenic nerve isolated with pleura and perineural blood supply. Follow-up is available on all patients six months to 8 years postoperatively. There were no complications or deaths related to the procedure. In all patients, bilateral phrenic nerve stimulation allowed either marked decrease in or discontinuation of positive-pressure ventilation. Phrenic nerve pacing can be performed safely in infants. It provides an effective alternative method for ventilatory support without the drawbacks of positive-pressure ventilation.

Phrenic and diaphragm function after coronary artery bypass grafting.

We studied respiratory mechanics and phrenic nerve and diaphragm function in 12 patients on the day before and eight to 13 days after coronary artery bypass grafting. The average vital capacity, functional residual capacity, and total lung capacity decreased by 20.5%, 9.5%, and 14.7% respectively after operation. Eleven patients showed less negative maximum inspiratory mouth pressures at any given lung volume after surgery and the magnitude of the change correlated with the reduction in total lung capacity. In 11 of the 12 patients the conduction times of the right and left phrenic nerves did not change substantially after operation and the ratio of inspiratory electrical activity (Edi) of left and right hemidiaphragms was similar before and after the procedure. One patient, however, showed a considerable increase in left phrenic nerve conduction time and a reduction in the left to right Edi ratio postoperatively. In three patients diaphragm function was also assessed by changes in transdiaphragmatic pressure during supramaximal phrenic nerve stimulation and voluntary increase in inspired volume; in none of the three patients did the transdiaphragmatic pressure swings show any significant change in the postoperative period. These data indicate that phrenic nerve paralysis only occasionally accounts for the postoperative loss of lung volume after coronary artery bypass grafting surgery. The mechanism of these abnormalities therefore remains to be determined.

Phrenic nerve conduction time in Guillain-Barré syndrome.

Phrenic nerve conduction was studied in 28 patients with Guillain-Barré syndrome. Conduction time was prolonged in 18 (64.3%) patients and serial studies showed progressive improvement with restoration of normal values in the majority by 12 weeks. The conduction abnormalities had a positive correlation with the extent of the disease, morbidity and mortality. Phrenic nerve conduction time was found to be a more sensitive parameter than vital capacity or median nerve motor conduction velocity in assessing the severity of the disease and predicting impending ventilatory failure.

Phrenic nerve pacing in infants and children: A review of experience and report on the usefulness of phrenic nerve stimulation studies

Nine infants and children, referred for phrenic nerve pacemakers, had measurements of phrenic nerve conduction times and diaphragmatic action potential amplitudes. In these pediatric patients, phrenic nerve conduction times varied from 2.7 to 7.8 msec, were quite reproducible, and were shorter than phrenic nerve conduction times in adults; phrenic nerve conduction time increased with age and with increasing distance between the stimulating electrode and the diaphragm. Diaphragmatic action potential amplitudes varied from 0.08 to 4.1 mV, roughly equivalent to amplitudes in adults, but were variable between patients and within patients on different days. Lower amplitudes were obtained after percutaneous stimulation than after direct phrenic nerve stimulation. Five patients underwent preoperative, percutaneous phrenic nerve stimulation. Strong diaphragmatic contractions allowed us to advise for pacemaker insertion in three patients; weak or absent diaphragmatic contractions allowed us to advise against pacemaker insertion in two patients. Postoperatively, noninvasive measurements of oxygen, carbon dioxide, tidal volume, and diaphragmatic action potential amplitudes have been used to adjust the phrenic nerve pacemaker settings. Phrenic nerve pacemakers have facilitated discharge from the hospital to a home-based ventilation program in six of the seven patients in whom they were inserted. We conclude that phrenic nerve pacing is a practical method of supporting ventilation in carefully selected infants and children. Phrenic nerve stimulation studies are useful in selecting patients for pacing and in adjusting the pacemaker settings.

Phrenic Nerve Function after Pneumonectomy

Using surface electrodes over the lower chest wall, we measured the phrenic nerve conduction time, ie, the time interval between the stimulation of the phrenic nerve in the neck and the onset of the diaphragmatic muscle action potential, in ten patients who had undergone pneumonectomy several years before (mean, eight years) and in 31 control subjects (bilaterally in 19 of them). The mean (+/- SD) value in the control subjects was 7.0 (+/- 0.9) msec, and no value exceeded 10 msec. All the values obtained in the patients were within the control range. We concluded that phrenic nerve function remains normal after pneumonectomy. This method appears to be the most effective means of identifying phrenic nerve involvement in these patients.