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Review articles

Weaning strategies in problem patients

N Walters, MI Polkey

Weaning usually accounts for approximately 40-50% of the total duration of mechanical ventilation. Approximately twothirds of patients can tolerate withdrawal of ventilation without the need for more gradual weaning, but there are a significant number of patients for whom weaning is difficult. Weaning failure is defined as the failure of a spontaneous breathing trial, or the need for re-intubation within 48 hours of extubation. This article reviews the causes of failure to wean, and outlines a practical approach to dealing with the difficult-to-wean patient. The key to successful weaning combines an approach which optimises ventilation at night, adopts a stepwise approach to reducing ventilatory dependence during the day, and uses non-invasive ventilation as a `bridge' out of the ICU. Having a weaning protocol and ensuring it is initiated in a timely manner is likely to be as important as what is in the protocol.

Keywords: weaning from mechanical ventilation; respiratory muscles; muscle weakness; non-invasive ventilation

Introduction

Respiratory failure may occur because the load on the respiratory muscle `pump' exceeds its capacity, or because problems with the lung parenchyma and/or the pulmonary circulation impair gas exchange or, commonly, a combination of the two. In the UK, over 100,000 patients are admitted to intensive care units (ICUs) each year. Almost two-thirds of patients who are intubated and mechanically ventilated on ICU have pulmonary disease.1 Other indications for mechanical ventilation include neurological disease (such as head injury, Guillain-Barré syndrome or sedation), sepsis and circulatory disease (eg following cardiopulmonary resuscitation). Weaning from mechanical ventilation involves the withdrawal of ventilatory support, which can be done in several ways. Approximately two-thirds of patients can tolerate fairly rapid withdrawal of ventilation without the need for more gradual weaning.2 The most common way to assess whether a patient is ready for extubation is to attempt a trial of spontaneous ventilation, termed a `spontaneous breathing trial' (SBT). If this is tolerated, the question then is whether the patient will tolerate removal of the artificial airway; the patient may need the airway to protect against aspiration or to provide access for tracheal toilet. In a study by Esteban et al, approximately 13% of patients failed extubation despite passing either a 30- or 120- minute SBT;3 there was no significant difference in extubation failure rate between these two groups. Failed extubation has a poor prognosis, with hospital mortality approaching 40% even after adjusting for co-morbidities and illness severity.4 Weaning usually accounts for approximately 40-50% of the total duration of mechanical ventilation.2

extubation. There are many reasons for weaning failure, such as incomplete resolution of the initial condition that necessitated mechanical ventilation or the development of a new problem. Epstein and Ciubotaru reviewed the causes for re-intubation in 74 medical ICU patients. The commonest causes were respiratory failure (28%) and congestive cardiac failure (23%). Aspiration and excessive secretions accounted for 16% cases of re-intubation. Mortality was significantly higher in the groups of patients who were reintubated for `nonairway' reasons (respiratory failure or congestive heart failure) compared to `airway' reasons' (aspiration or upper airway obstruction).4 The three determinants of ventilation that affect failure to wean are shown in Figure 1: 1. Central drive ­ this may be reduced by sedative drugs, sleep or raised intracranial pressure. 2. Respiratory muscle strength ­ can be reduced by critical illness neuromuscular abnormalities, lung hyperinflation,

Central Control Sleep, sedative drugs Capacity of respiratory muscle pump Hyperinflation CINMA Increased load Increase in airway resistance

Reduced chest wall compliance

VENTILATORY SYSTEM MEETS DEMANDS VENTILATORY FAILURE

Aetiology of weaning failure

Weaning failure is defined as the failure of a spontaneous breathing trial, or the need for re-intubation within 48 hours of

JICS Volume 9, Number 2, July 2008

Figure 1 Determinants of ventilation associated with failure to wean.

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Review articles

steroid therapy, or electrolyte disturbance (eg hypophosphataemia or hypomagnasaemia). 3. Increased load ­ such as an increase in airway resistance (bronchospasm, upper airway obstruction) or reduced chest wall compliance (obesity, pleural effusion). The balance between the capacity of the respiratory muscle pump and the load on the respiratory muscles has to match, or ventilatory failure will ensue. Many ICU patients develop critical illness neuromyopathy (termed critical illness neuromuscular abnormalities, CINMA) and this may contribute to weaning problems. Indeed, many studies suggest that CINMA is common. For example Spitzer and colleagues found evidence of CINMA in 62% of `difficult to wean' patients.5 It is increasingly recognised that inactivity is a cause of muscle weakness6 and since patients on mechanical ventilation have, by definition, unloading of the respiratory muscles, it is logical that mechanical ventilation could lead to weakness of these muscles. In animal studies,7 ventilator-induced diaphragmatic dysfunction has been shown to exist after as little as 12 hours of mechanical ventilation. It is characterised by a reduction in the force-generating capacity of the diaphragm and can contribute to weaning problems in ventilated patients. It may be related to mechanical ventilation itself and exacerbated by the use of paralysing agents and steroids. The pathophysiological changes seen include muscle atrophy, structural injury and transformation and remodelling of fibre types. Gayan-Ramirez et al compared continuous mechanical ventilation (CMV), spontaneous breathing and intermittent mechanical ventilation to intermittent spontaneous breathing in anaesthetised and tracheostomised rats.8 They showed that in the group of rats that was continuously mechanically ventilated, there was atrophy of both diaphragm type I and IIx/b fibres. In the spontaneous breathing and intermittently spontaneously breathing groups, there was no change in the diaphragm fibre dimensions or proportions. The contractile properties of the diaphragm were reduced in the groups which were intermittently spontaneously breathing and in those undergoing CMV and the force-frequency curve was , significantly different in the CMV group when compared to the control and spontaneously breathing groups of rats. The results suggest that, in rats, spontaneous breathing, even for short periods, may help to maintain diaphragm function and prevent diaphragm atrophy and down-regulation of key muscle regulatory factors. There was no significant difference between the groups of rats which breathed spontaneously for 20 minutes per day compared to four hours per day. Interestingly key mediators of atrophic signalling, such as the E3 ubiquitin ligase MuRF-1, are expressed in the diaphragms of animals subjected to this type of experiment. Recent data suggest that a similar process occurs in patients who are brain dead in whom (by definition) the brain ceases to drive the respiratory muscles.9 Assessing respiratory muscle function in the ICU setting is problematic.10 Inspiratory muscle strength is conventionally assessed by measuring maximal inspiratory pressures, but since this is dependent on patient aptitude and motivation, it is frequently unreliable or technically impossible in ventilated

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patients.11 Measuring trans-diaphragmatic pressure is an index of diaphragmatic strength; this is done by measuring the difference in pressure between two balloon catheters, one in the stomach and one in the oesophagus, after magnetic stimulation of the phrenic nerve. However, this method is moderately invasive and technically difficult, and may be contra-indicated in some circumstances eg in the presence of oesophageal varices. The relationship between twitch transdiaphragmatic pressure and, for example, length of stay is not straightforward, but this12 and other studies13-17 have confirmed that diaphragmatic weakness is common among critically ill adults and children. In order to assess diaphragmatic function in a non-invasive way, Mills et al postulated that the twitch tracheal tube pressure (pressure change measured at the mouth after phrenic nerve stimulation) could be used to reflect diaphragm strength.18 They performed a study on 14 patients comparing the twitch oesophageal pressure and the twitch tracheal tube pressure in the supine and sitting position. Consistent with previous studies in non ventilated adults,19 this showed that there was a linear relationship between twitch tracheal pressure and twitch oesophageal pressure during supramaximal diaphragmatic stimulation. Although the difference in the twitch pressures was less at low twitch amplitudes it should be remembered that hyperinflation preferentially reduces the oesophageal component of twitch transdiaphragmatic pressure20,21 and that this, combined with true weakness, may make the twitch tracheal pressure difficult to interpret in the critically ill. Critical illness neuromyopathy is common among difficultto-wean patients and affects both the muscle and nerve. It was first described in 195622 and is associated with illness severity, administration of corticosteroids, neuromuscular blocking agents, hyperglycaemia and prolonged ICU stay. Its reported incidence varies from 50-100%. Typically, it is symmetrical and affects proximal muscles. De Jonghe et al23 screened 1,246 ICU patients. Patients without pre-existing neuromuscular disease who were mechanically ventilated for more than seven days were considered (n=332). Of these, 126 were not assessed as they met one of the exclusion criteria, and 111 were not able to be assessed, mostly because they did not regain consciousness. This left 95 patients, of whom 25.3% met the criteria for critical illness neuromyopathy. These patients had a longer mean duration of mechanical ventilation compared to controls, and a trend towards a longer total ICU length of stay (Figure 2). Patients with the acute respiratory distress syndrome (ARDS) are often subject to prolonged mechanical ventilation. Studies have looked at ARDS severity and the degree of impairment of lung function tests post-extubation. There is some evidence that physiological markers of ARDS severity, such as mean pulmonary artery pressure and lung compliance, are associated with worse pulmonary function tests at one year.24 Ghio et al studied lung function (FVC, FEV1, FEV1/FVC, and DLCO) at one year on 41 patients who had been ventilated for ARDS.25 Two-thirds of the patients had impairment of their lung function tests; however, this was mild in more than 70% of these patients, and there was no

Volume 9, Number 2, July 2008 JICS

Review articles

Duration of Mechanical Ventilation ICU-acquired paralysis (n=24) Control (n=71)

(54.5)

ICU Length of Stay ICU-acquired paralysis (n=24) Control (n=71)

(59.0) (34.2)

30

20

10

0

10

20

30

Time before awakening, d

Time after awakening, d

Day 1 Awakening

Figure 2 Duration of mechanical ventilation and length of ICU stay before and after awakening (Taken from De Jonghe et al 23).

correlation with symptoms. They showed that maximum pulmonary artery pressure, lowest thoracic compliance and maximal level of positive end-expiratory pressure (PEEP) correlated with poorer lung function tests. Patients often have a mild restrictive lung defect following ARDS, but the most common finding is a reduction in the carbon monoxide diffusion capacity which may persist longer than the spirometric abnormalities.26

and allowed to breathe either with supplemental oxygen alone or with CPAP at 5 cm H2O.29 The SBT was terminated using objective criteria (ie respiratory rate greater than 35 breaths/min, oxygen saturation <90%). If the patient could breathe for two hours, the team was informed and would make a clinical decision about decannulation/extubation. Unsurprisingly the patients who were in the screening test were extubated faster (Figure 3).

Approach to the patient with weaning difficulties

Step 1 Optimise the clinical condition

Prior to weaning patients, the patient's physical condition should be optimised. This includes maximising respiratory and cardiac function. The patient should be receiving minimal or no sedation and neuromuscular blocking agents should have had time to clear the patient's system. The capacity of the patient to expectorate should be assessed. Ideally, there should be a cough adequate to propel bronchial secretions into the mouth and secretions should not be excessive in volume. Nutrition should be assessed and supplemented where necessary by nasogastric feeding. The role of transfusion to correct anaemia is controversial; while some authorities favour this approach,27 the consensus view is not to transfuse unless the haemoglobin falls below 7 g/dL.28 Where possible, the patient is encouraged to sit out of bed. The patient needs to be psychologically prepared for the next step and family support is invaluable. Lastly it is worth considering how oxygen dependent is the patient? When respiratory muscle weakness is the primary problem, the patient should demonstrate adequate oxygenation without an excessive oxygen requirement, at least while receiving mechanical ventilation.

Step 3 What if the SBT fails?

Figure 3 shows that about 10% of patients will fail the SBT and

continue to require longer-term ventilation. In our practice, we then support the patient maximally at night, aiming to reduce arterial carbon dioxide tension, while trying to extend

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Patients receiving mechanical ventilation (%)

80

60

40

Control (n=151)

20

Intervention (n=149)

0 0 5 10 15 20 25 30

Days after successful screening

Step 2 Spontaneous breathing trial (SBT)

To assess readiness to wean, the patient should have a SBT. In the classic paper on the topic by Ely and colleagues, patients were subjected to daily SBTs by connection to a T-piece

JICS Volume 9, Number 2, July 2008

Figure 3 Kaplan-Meier analysis of the duration of mechanical ventilation after a successful screening test. After adjustment for the severity of illness at base line (as measured by the APACHE II score), age, sex, race, location of the intensive care unit, and duration of intubation before enrollment, a Cox proportional-hazards analysis showed that mechanical ventilation was discontinued more rapidly in the intervention group than in the control group (relative risk of successful extubation, 2.13; 95 per cent confidence interval, 1.55 to 2.92; P<0.001). (Taken from Ely et al29).

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Review articles

ventilatory independence during the day. This philosophy is born of clinical experience and our mechanistic studies of the effect of mechanical ventilation.30 Incremental approaches to extend ventilatory independence are as follows. Initially, it is worth establishing whether the patient is able to tolerate the tracheostomy cuff being deflated and whether they can be satisfactorily ventilated with a machine suitable for domiciliary use overnight. If they can't, the choice is either to attempt weaning again when the patient has improved or, if this seems unlikely, consideration may need to be given to a providing care in a long-term care facility. Next, the tracheostomy tube should be changed to a fenestrated one. The purpose of the fenestrated tube is to facilitate, especially in smaller individuals, the passage of air through the vocal cords so that the patient can use a speaking valve more easily or speak by themselves by digitally occluding the tracheostomy. Use of the voice provides important psychological benefits, facilitates communication with the staff and `rehabilitates' the upper airway. In general the tube should be converted to the smallest size possible, taking into consideration the need for bronchial toilet. Finally, if appropriate assessment shows that the patient cannot safely eat with their tracheostomy in place, then longterm nutrition becomes an issue; converting the nasogastric tube to a PEG tube should be considered for reasons of comfort and also because if the patient eventually progresses to non-invasive ventilation this will facilitate optimal mask fit.

spontaneous breathing compared to the patients who had multiple shorter trials. They also noted that two-thirds of this unselected group was weaned without the need for a specific protocol. Since in the UK, difficult-to-wean patients seem to be more similar to those in Esteban's study, our practice is to perform once daily SBTs.

Step 5 Could non-invasive ventilation be a bridge?

If the patient can be adequately supported on pressure support through a tracheostomy at night, the next step is to try the patient on non-invasive ventilation (NIV) during the day through a face mask with the tracheostomy cuff deflated, a fenestrated inner tube in place and the tracheostomy capped. At this point, NIV may be tried overnight (with or without capnographic assessment). If the patient tolerates this, decannulation to NIV can be reasonably considered. Alternatively, if bronchial toilet is a consideration, a minitracheostomy may need to be inserted, although the utility of this technique is limited by the fact that only the finest suction catheters will pass through a mini-tracheostomy. If the patient does not tolerate the tracheostomy being capped, a decision then needs to be made as to whether the patient will cope better if the tracheostomy, and its associated resistance, is removed. With regards to NIV settings used, pressure control ventilation with IPAP set at least as high as the most recent IPAP on the invasive ventilator +5 cm H2O to overcome the resistance of the tracheostomy tube should be used. The rate should be set at a minimum of 10 breaths per minute. EPAP should be used, especially if there is evidence of atelectasis or if the patient has an underlying respiratory condition such as COPD that will increase intrinsic PEEP .

Step 4 What protocol should be used?

Weaning techniques vary between clinicians. With regard to weaning protocols, Brochard and co-workers31 conducted a randomised trial in three groups of ICU patients who had been intubated for more than 24 hours. They were randomly allocated to be weaned with a T-piece trial, synchronised intermittent mandatory ventilation (SIMV) or pressure support ventilation (PSV). Patients who were not extubated by 21 days or who were re-intubated within 48 hours of initial extubation were regarded as failures to wean. Four hundred and fifty six patients were eligible for the study and 109 entered. When allcause weaning failure was considered, there was a lower , number of failures to wean in the PSV group (23% for PSV 43% for T-piece and 42% for SIMV). Excluding patients who failed to wean for reasons unrelated to the weaning process, this figure became highly significant (8% for PSV 33% for , T-piece and 39% for SIMV). In contrast, Esteban et al2 studied 546 patients in medical and surgical ICUs. One hundred and thirty patients who did not tolerate a two hour trial of spontaneous breathing were allocated to receive either intermittent mandatory ventilation (IMV), PSV, intermittent trials of spontaneous breathing using a T-piece, continuous positive airways pressure (CPAP) interspersed with assistcontrol ventilation or a once-daily trial of spontaneous ventilation interspersed with assist-control ventilation. The patients who were weaned using a once-daily trial of spontaneous ventilation had a significantly shorter time to extubation ­ three times quicker when compared to the IMV group and twice as quick as the PSV group. There was no difference between the groups who had once-daily trials of

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Step 6 What options are available if sputum expectoration is the remaining problem?

When abdominal muscle strength is less than approximately 25% of normal, there is insufficient strength to generate the shearing forces necessary to propel phlegm proximally in the airway.32 Some authorities recommend that this be measured with peak flow,33 although this approach is clearly of limited value in patients with COPD. For many patients, physiotherapy combined with either NIV or intermittent positive pressure breathing is sufficient to facilitate expectoration. A recently re-invented concept is to apply negative pressure after an initial positive pressure.34,35 We compared a mechanical insufflation/exsufflation device to physiotherapy, NIV and exsufflation in patients with congenital myopathy.36 The study found that the neuromuscular disease patients using an insufflation/ exsufflation device produced a higher peak cough flow than an unassisted cough (76% increase compared with 9% in the control group), or one assisted by NIV. Using the device was well tolerated. We made similar observations in patients with motor neurone disease.37 It has yet to be confirmed with a trial whether this device could be used in patients with respiratory muscle weakness post extubation to augment coughing and reduce re-intubation rates, but it is anecdotally used for this purpose in some centres.

Volume 9, Number 2, July 2008 JICS

Review articles

Summary

In conclusion, respiratory muscle weakness is often a contributing factor in patients who are having difficulty weaning from a ventilator, once cardiac and pulmonary function has been optimised. Early weaning reduces the prevalence of ventilator-associated pneumonia and is likely to mitigate the effects of CINMA. The core principles of weaning are to optimise ventilation maximally at night and use a stepwise approach to reducing ventilatory dependence during the day. As soon as possible the patient should be decannulated to NIV which may be useful as a 'bridge' out of the ICU. Having , a weaning protocol and ensuring it is initiated in a timely manner is likely to be as important as what the protocol states. If sputum retention is a problem, it is important to remember that there are mechanical devices to assist with expectoration.

References

1 Hsu C-L, Chen K-Y, Jerng J-S, Yu C-J, Yang P-C. Timing of tracheostomy as a determinant of weaning success in critically ill patients: a retrospective study. Crit Care 2005;9:R46-52. , 2 Esteban A, Frutos F Tobin MJ et al. A comparison of four methods of weaning patients from mechanical ventilation. N Engl J Med 1995;332:345-50. 3. Esteban A, Alia I, Tobin MJ et al. Effect of spontaneous breathing trial duration on outcome of attempts to discontinue mechanical ventilation. Am J Respir Crit Care Med 1999;159:512-18. 4. Epstein SK, Ciubotaru RL. Independent effects of etiology of failure and time to reintubation on outcome for patients failing extubation. Am J Respir Crit Care Med 1998;158:489-93. 5. Spitzer AR, Giancarlo T, Maher L et al. Neuromuscular causes of prolonged ventilator dependency. Muscle Nerve 1992;15:682-86. 6. Fuglevand A, Bilodeau M, Enoka R. Short term immobilization has a minimal effect on the strength and fatigability of a human hand muscle. J Appl Physiol 1995;78:847-55. 7. Decramer M, Gayan-Ramirez G. Ventilator-induced diaphragmatic dysfunction. Am J Respir Crit Care Med 2004;170:1141-42. 8. Gayan-Ramirez G, Testelmans D, Maes K et al. Intermittent spontaneous breathing protects the rat diaphragm from mechanical ventilation effects. Crit Care Med 2005;33:2804-09. 9. Levine S, Nguyen T, Taylor N et al. Rapid disuse atrophy of diaphragm fibers in mechanically ventilated humans. N Engl J Med 2008;358: 1327-35. 10.Polkey MI, Moxham J. Clinical aspects of respiratory muscle dysfunction in the critically ill. Chest 2001;119:926-39. 11.Multz AS, Aldrich TK, Prezant DJ, Karpel JP Hendler JM. Maximal , inspiratory pressure is not a reliable test of inspiratory muscle strength in mechanically ventilated patients. Am Rev Resp Dis 1990;142:529-32. 12 Watson AC, Hughes PD, Harris L et al. Measurement of twitch transdiaphragmatic, esophageal, and endotracheal tube pressure with bilateral anterolateral magnetic phrenic nerve stimulation in patients in the intensive care unit. Crit Care Med 2001;29:1325-31. 13.Polkey MI, Duguet A, Luo YM et al. Anterior magnetic phrenic nerve stimulation: laboratory and clinical evaluation. Intensive Care Med 2000; 26:1065-75. 14.Mills GH, Ponte J, Hamnegård CH et al. Tracheal tube pressure change during magnetic stimulation of the phrenic nerves as an indicator of diaphragm strength on the intensive care unit. Br J Anaesth 2001;87: 876-84. 15.Laghi F Cattapan SE, Jubran A et al. Is weaning failure caused by low, frequency fatigue of the diaphragm? Am J Respir Crit Care Med 2003;167:120-27. , 16.Rafferty GF Greenough A, Manczur T et al. Magnetic phrenic nerve stimulation to assess diaphragm function in children following liver transplantation. Pediatr Crit Care Med 2001;2:122-26.

, 17.Rafferty GF Greenough A, Dimitriou G et al. Assessment of neonatal diaphragm function using magnetic stimulation of the phrenic nerves. Am J Respir Crit Care Med 2000;162:2337-40. 18.Mills GH, Ponte J, Hamnegård CH et al. Tracheal tube pressure change during magnetic stimulation of the phrenic nerves as an indicator of diaphragm strength on the intensive care unit. Br J Anaesth 2001;87: 876-84. 19.Hamnegård CH, Wragg S, Kyroussis D et al. Mouth pressure in response to magnetic stimulation of the phrenic nerves. Thorax 1995;50:620-24. 20.Pengelly LD, Alderson AM, Milic-Emili J. Mechanics of the diaphragm. J Appl Physiol 1971;30:797-805. , 21.Polkey MI, Hamnegård CH, Hughes PD, Rafferty GF Green M, Moxham J. Influence of acute lung volume change on contractile properties of the human diaphragm. J Appl Physiol 1998;85:1322-28. 22.Olsen CW. Lesions of peripheral nerves developing during coma. JAMA 1956;160:39-41. 23.De Jonghe B, Sharshar T, Lefaucheur J-P et al. Paresis acquired in the intensive care unit. A prospective multicenter study. JAMA 2002;288:2859-67. 24. Elliott CG, Rasmusson BY, Crapo RO, et al. Prediction of pulmonary function abnormalities after adult respiratory distress syndrome (ARDS). Am Rev Respir Dis 1987;135:634-38. 25.Ghio AJ, Elliott CG, Crapo RO, et al. Impairment after adult respiratory distress syndrome. An evaluation based on American Thoracic Society recommendations. Am Rev Respir Dis 1989;139:1158-62. 26.Herridge MS, Cheung AM, Tansey CM et al. One-year outcomes in survivors of the acute respiratory distress syndrome. N Engl J Med 2003;348:683-93. 27.Schonhofer B, Wenzel M, Geibel M, Kohler D. Blood transfusion and lung function in chronically anemic patients with severe chronic obstructive pulmonary disease. Crit Care Med 1998;26:1824-28. 28.Dellinger RP Levy MM, Carlet JM et al. Surviving Sepsis Campaign: , international guidelines for management of severe sepsis and septic shock: 2008. Crit Care Med 2008;36:296-327. 29.Ely EW, Baker AM, Dunagan DP et al. Effect on the duration of mechanical ventilation of identifying patients capable of breathing spontaneously. N Engl J Med 1996;335(25):1864-69. 30.Nickol AH, Hart N, Hopkinson N et al. Mechanisms of improvement of respiratory failure in patients with restrictive thoracic disease treated with non-invasive ventilation. Thorax 2005;60:754-60. 31.Brochard L, Rauss A, Benito S et al. Comparison of three methods of gradual withdrawal from ventilatory support during weaning from mechanical ventilation. Am J Respir Crit Care Med 1994;150:896-903. 32.Polkey MI, Lyall RA, Green M et al. Expiratory muscle function in amyotrophic lateral sclerosis. Am J Respir Crit Care Med 1998;158:734-41. 33.Bach JR, Saporito LR. Criteria for extubation and tracheostomy tube removal for patients with ventilatory failure. A different approach to weaning. Chest 1996;110:1566-71. 34.Barach AL, Beck GJ. Mechanical production of expiratory flow rates surpassing the capacity of human coughing. Am J Med Sci 1953;226: 241-48. 35.Barach AL, Beck GJ. Exsufflation with negative pressure. Arch Int Med 1954;93:825-41. 36.Chatwin M, Ross E, Hart N et al. Cough augmentation with mechanical insufflation/exsufflation in patients with neuromuscular weakness. Eur Respir J 2003;21:502-08. 37.Mustfa N, Aiello M, Lyall RA et al. Cough augmentation in amyotrophic lateral sclerosis. Neurology 2003;61:1285-87.

Michael I Polkey Consultant Physician, Royal Brompton

Hospital and National Heart and Lung Institute [email protected]

Nicola Walters Specialist Registrar, Royal Brompton Hospital,

London

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