Ventilatory support may be invasive (via endotracheal tube or tracheostomy) or non-invasive (via nasal mask or face mask). NIV may be subdivided into positive or negative pressure ventilation (rarely used now).
Positive pressure ventilators
(also called NIV, bi-level, BiPAP (trade name)) deliver volume or pressure support; many different types are available. Bi-level pressure support devices are used extensively and provide ventilation with a higher inspiratory positive airway pressure than expiratory pressure (IPAP and EPAP, the difference in pressure between the two is also called pressure support), selected by the prescriber. They function in several modes, but usually patient-triggered inspiratory support, with provision of an underlying back-up rate that will cut in if the patient fails to breathe. Non-invasive positive pressure support may be provided by specialized portable ventilators or by standard critical care ventilators.
New ‘intelligent’ non-invasive ventilators are becoming available that adjust the ventilation on a breath-to-breath basis. Servo-ventilators (adaptive servo-ventilation, ASV) for Cheyne–Stokes breathing ‘learn’ this ventilation pattern and can increase the pressure support during the hypoventilation phase and decrease it during the hyperventilation phase, effectively ‘ironing out’ the oscillations without leading to over-ventilation and hypocapnia. Volume-assured pressure support ventilation (VAPSV) is where tidal volumes and minute ventilation are monitored and the inspiratory pressure is adjusted to maintain the previous ‘learned’ ventilation. The role of these new ventilators is still being assessed, and they may only be appropriate for certain clinical situations.
Negative pressure ventilators
assist inspiration by ‘sucking out’ the chest wall; expiration occurs through elastic recoil of the lungs and chest wall. Includes devices such as tank ventilators and chest ‘cuirasse’ or ‘shell’ ventilators. The Hayek oscillator is a high-frequency version of the negative pressure cuirasse ventilator. Other devices, such as the rocking bed and ‘pneumobelt’, displace abdominal contents to aid diaphragmatic contraction. Used extensively in the polio epidemics of the 1950s, they are now only very rarely used to manage chronic respiratory failure.
supplies constant positive pressure during inspiration and expiration and is therefore not a form of ventilation but is sometimes mistakenly referred to as such. It provides a ‘splint’ to open the upper airway and collapsed alveoli (thus improving V/Q matching). CPAP is used extensively in the community to treat OSA but also has a role in improving oxygenation in selected patients with acute respiratory failure, e.g. patients with cardiogenic pulmonary oedema, pneumocystis pneumonia (see pp. [link]–[link]), and the obese (see pp. [link]–[link]).
• NIV: non-invasive ventilation, also referred to as non-invasive mechanical ventilation (NIMV)
• NIPPV: non-invasive positive pressure ventilation; confusingly, it is also sometimes interpreted as nasal intermittent positive pressure ventilation and sometimes referred to as ‘NIPPY’, after the name of a particular type of ventilator
• IPAP: inspiratory positive airways pressure
• EPAP: expiratory positive airways pressure, also referred to as positive end expiratory pressure (PEEP)
• BiPAP: bi-level positive airway pressure (IPAP > EPAP), refers to a commercial product but now mistakenly used to refer to similar machines
• CPAP: continuous positive airway pressure (IPAP ≈ EPAP)
• VAPSV : volume-assured pressure support ventilation
• ASV: adaptive servo- (or support) ventilation.
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Antonescu-Turku A, Parthasarathy S. CPAP and bi-level PAP therapy: new and established roles. Respir Care 2010;55:1216–29.Find this resource:
Harris N, Javaheri S. Advanced PAP therapies, in Fundamentals of sleep technology, 2nd edn, Lippincott, Williams and Wilkins, Philadelphia 2012; pp. 444–52.Find this resource:
NIV may be used in an attempt to avoid invasive ventilation and its complications (e.g. upper airway trauma, VAP); alternatively, NIV may represent the ‘ceiling’ of treatment in patients deemed unsuitable for intubation. NIV is not an alternative to invasive ventilation in patients who require this definitive treatment, as it is not sufficiently secure.
Acute exacerbation of COPD
• Consider NIV in patients with an acute exacerbation of COPD who have a respiratory acidosis (pH <7.30) despite initial medical treatment and controlled O2 therapy
• Still often required to rescue patients who have been given too high a concentration of O2 to breath, reduced hypoxic drive, and have become hypercapnic and acidotic; response to NIV can be rapid
• Benefits include reduced mortality and need for intubation, more rapid improvement in physiological outcomes (RR, pH), and symptomatic relief from breathlessness, when compared with standard medical treatment
• NIV only assists ventilation; the pressures used are not enough to take over ventilation due to the high airways resistance
• Invasive ventilation, if deemed appropriate, should be considered, particularly in patients with a severe respiratory acidosis (pH <7.25), as this is associated with treatment failure and increased mortality with NIV alone
• High expiratory pressures (e.g. 6–8cmH2O, PEEP) may help reduce the work of breathing by offsetting intrinsic PEEP but will lessen the IPAP–EPAP difference (thus reducing the ventilation component), unless inspiratory pressures are further increased.
Acute cardiogenic pulmonary oedema
• Use of CPAP via face mask is effective and should be considered in patients who fail to improve with medical management alone
• Bi-level NIV has not been shown to be superior to CPAP, and there is a suggestion of increased MI rates following its use. It may, however, have a role in patients who do not respond to CPAP.
NIV is effective in the treatment of OSA and the overlap syndrome (i.e. raised PaCO2, typically with associated obesity hypoventilation or COPD; see pp. [link]–[link]) when CPAP alone fails to reverse the CO2 retention. NIV is generally recommended as the first choice over CPAP when an acute respiratory acidosis is present, but conversion to CPAP later may be possible when the ventilatory failure has been reversed.
• NIV is the treatment of choice for ventilatory failure resulting from neuromuscular weakness or chest wall deformity
• The pressures used may be adequate to fully take over ventilation, because the chest and lung compliance are often little impaired.
• Immunocompromised patients who develop acute respiratory failure have an extremely high mortality following endotracheal intubation and ventilation
• In immunocompromised patients with pulmonary infiltrates, fever, and hypoxaemic acute respiratory failure, intermittent NIV results in lower intubation rates and hospital mortality when compared with standard treatment
• CPAP is effective in the treatment of pneumocystis pneumonia.
• Use of NIV may result in a reduction in need for intubation, compared with standard medical treatment, although no significant differences in hospital mortality or length of hospitalization have been shown
• CPAP may have a role in improving oxygenation in severe pneumonia
• In patients who would potentially be candidates for intubation, use of NIV or CPAP should not inappropriately delay invasive ventilation and so should only be attempted in an ICU setting.
• There is no evidence to support use of NIV in acute severe asthma, and it should not be used; if ventilation is required, then it should be invasive
• No strong evidence to support use of NIV in exacerbations of bronchiectasis or CF; NIV often used, improving symptoms, and may be useful as a ‘ceiling’ of treatment in patients with severe underlying disease who would not be considered candidates for invasive ventilation
• Bi-level NIV or CPAP may have a role in improving gas exchange following trauma or surgery
• NIV is being increasingly used to aid weaning after invasive ventilation.
Contraindications (some relative) to the use of NIV should be considered in the context of individual patients, e.g. severe hypoxaemia may not be considered a contraindication for NIV in a patient who is unsuitable for invasive ventilation.
Contraindications to NIV
• Cardiac or respiratory arrest
• Impaired consciousness or confusion (relative)
• Severe hypoxaemia
• Copious respiratory secretions
• Haemodynamic instability (relative)
• Facial surgery, trauma, burns, or deformity
• Upper airway obstruction (except from pharyngeal or laryngeal OSA)
• Undrained pneumothorax
• Inability to cooperate or to protect the airway
• Vomiting, bowel obstruction, recent upper GI tract surgery, oesophageal injury.
Plant PK et al. Early use of non-invasive ventilation for acute exacerbations of chronic obstructive pulmonary disease on general respiratory wards. Lancet 2000;355:1931–5.Find this resource:
Royal College of Physicians, BTS, and Intensive Care Society guidelines. Non-invasive ventilation in chronic obstructive pulmonary disease: management of acute type 2 respiratory failure. http://www.rcplondon.ac.uk/sites/default/files/concise-niv-in-copd-2008.pdf.
The decision to start NIV should follow a period of initial standard medical treatment, including appropriate supplementary and controlled O2 therapy; a proportion of patients will improve and will no longer require ventilation. Prior to commencing NIV, a senior doctor should make a decision with the patient and their family regarding suitability for invasive ventilation, should NIV fail, and document this clearly in the medical notes. If the patient is a candidate for invasive ventilation, care must be taken to avoid inappropriate delays in intubation through the use of NIV or CPAP. Liaise with ICU staff early.
Setting up NIV
1. Select an appropriate mask type and size for the patient. Masks may be nasal or oronasal (full face). Nasal masks require clear nasal passages but often allow mouth leaks, particularly in the acutely breathless patient, but may be more comfortable. Full-face masks avoid mouth leakage and are now generally favoured for ventilatory failure
2. Allow the patient to hold the mask to their face prior to attaching the head straps—this may increase confidence and compliance. Mask adjustments are often necessary to minimize air leaks, although some leakage may have to be accepted. Avoid excessive strap tension; one or two fingers should be able to fit under the strap
3. Set up the ventilator. Typical initial pressures for ventilating a patient with hypercapnic respiratory failure due to an exacerbation of COPD would be EPAP 4cmH2O and IPAP 12cmH2O, with a back-up rate of 15/min and inspiratory:expiratory ratio of 1:3 in spontaneous/timed mode. Increase the IPAP in increments of 2cmH2O to a maximum of 20, as tolerated by the patient. Similar settings can be used for patients with hypercapnic respiratory failure resulting from neuromuscular weakness. Increase the EPAP (e.g. to 8 or 10cm) in obese patients with an ‘overlap’ syndrome of COPD and OSA to maintain airway patency during inspiration to allow triggering.
Pressure support ventilators can also be set to provide CPAP by equalizing the IPAP and EPAP; typical pressures range from 5 to 12.5cmH2O. CPAP may improve oxygenation in selected patients with cardiogenic pulmonary oedema or pneumonia.
4. Supplementary O2 concentration (FiO2) should be guided by the underlying disease process and by oximetry monitoring. For many hypercapnic patients with COPD, aiming for O2 saturations between 88% and 92% effectively balances the risks of hypoxia vs hypercapnic respiratory acidosis. By adding O2, you are potentially masking gradual ventilation failure (by deceptively achieving adequate oxygenation) and thus hypercapnia, hence more careful blood gas monitoring will be required. If at all possible, use no, or very little, added O2
5. Patient monitoring should involve assessment of comfort, RR, synchrony with the ventilator, mask leaks, pulse rate, BP, and O2 saturations
6. Arterial or capillary blood gas analysis should be performed after no more than 1h, and again after within an hour if there has been no improvement. Improvement in acidosis and decline in RR after 1 and 4h of treatment are associated with a better outcome. Repeat the blood gas analysis if the clinical condition changes
7. Lack of response may be indicated by a worsening acidosis or persistently abnormal ABGs, or by a reduced conscious level and clinical deterioration. Consider invasive ventilation, if appropriate. The decision to halt NIV depends on the circumstances of the individual patient and should be made by a senior doctor
8. Subsequent management depends on the patient’s response. Optimal duration of NIV is unclear, but it is typically administered for about 3 days in acute respiratory failure. NIV does not need to be continuous; the patient may have breaks for meals and nebulizers. Weaning should be gradual and achieved by increasing the period off NIV, with nocturnal use withdrawn last.
There is no substitute for personally assessing the efficacy of NIV (see Table 57.1). For example, failure to see the lungs inflating can be due to head position (best head position is the so-called ‘sniffing the morning air’ position; produces least pharyngeal resistance). Leaks can be heard. Adjustments can be made; immediately observe the effect. Sometimes, the presence of intrinsic PEEP means significant inspiratory effort is being made (visible intercostal movement) before the ventilator senses inspiration and triggers, thus increasing work of breathing. This can be seen and the EPAP gradually raised, until there is no delay between patient inspiratory effort and the triggering of the ventilator.
Table 57.1 Troubleshooting
Clinical deterioration or worsening respiratory failure
pCO2 remains high (persistent respiratory acidosis)
pO2 remains low (<7kPa), with pCO2 OK
Irritation or ulceration
Dry nose or mouth
Dry sore eyes
Check mask fit
Decongestants, e.g. xylometazoline
Reduce IPAP (or EPAP if already high)
Chest wall deformity and neuromuscular weakness
• NIV has a well-established role in the management of chronic respiratory failure due to chest wall deformity or neuromuscular weakness and has been shown to improve symptoms, gas exchange, and mortality
• Common underlying diagnoses include chest wall deformity and scoliosis, post-polio syndrome, MND, spinal cord injury, neuropathies, myopathies, and muscular dystrophies. The nature of the underlying disease must influence the appropriateness of initiating ventilation; progressive conditions, such as MND, often result in increasing dependence on the ventilator, and the patient and their caregivers should be made aware of this
• NIV is administered at home overnight, and this improves daytime gas exchange. The mechanism for this is unclear; it probably resets the central respiratory drive, although respiratory muscle rest and improved chest wall and lung compliance may also play a part
• Small portable positive pressure ventilators, with either face (usual) or nasal (less often) masks, are used in the majority of cases; negative pressure or abdominal ventilators rarely have a role these days, and their use may be limited by upper airways obstruction
• The decision to introduce overnight NIV is difficult and is based on both symptoms (morning headaches, hypersomnolence, fatigue, poor sleep quality) and evidence of ventilatory failure (daytime hypercapnia (pCO2 >6.0kPa, and/or base excess >3) and/or nocturnal hypoventilation (with O2 saturations <88% on overnight oximetry). Daytime ventilatory failure, however, is often a late feature and is typically preceded by hypoventilation during sleep
• A study in patients with myopathies demonstrated supine inspiratory VC (more sensitive to any diaphragm weakness than sitting or standing) to be an accurate predictor of respiratory reserve; supine inspiratory VC <40% predicted was significantly associated with hypercapnic hypoventilation, and such patients should be considered for treatment with NIV. Supine inspiratory VC <20% was typically associated with daytime respiratory failure, whereas supine inspiratory VC >60% indicated a minimal risk of respiratory complications. Other factors include signs of cor pulmonale or hospital admission with respiratory failure
• Patients with excessive secretions may not be suitable for NIV, although face mask ventilation is possible, even in the setting of bulbar weakness
• Regular follow-up of patients on overnight ventilation is important. Ask about symptoms and compliance, and repeat arterial or capillary blood gas analysis, if indicated. Lack of improvement in gas exchange may reflect non-compliance, excessive air leakage, inadequate pressure support, or progression of underlying disease; consider repeating nocturnal oximetry monitoring on the NIV. Patients with persisting severe hypoxia may benefit from long-term supplementary O2, although this may worsen CO2 retention
• There are significant issues of risk management when prescribing home NIV, particularly rapid access to replacement ventilators, battery back-up facilities, careful reassessment when there is evidence of a deterioration, and appropriate training of both the patient and their carer(s).
Overnight NIV can have a role in patients with central hypoventilation, opiate-induced central apnoea, Cheyne–Stokes respiration, obesity hypoventilation, overlap syndromes of OSA with coexisting COPD or obesity. There is the prospect of further developments in ‘smart’ ventilators, beyond ASV and VAPSV where not only is the pressure support monitored and adjusted, but the level of EPAP required to hold open the pharynx is also adjusted; additional forced oscillation is superimposed on the airflow from the ventilator, and the resultant pressure oscillations enable obstructive episodes (both apnoeas and hypopnoeas) to be distinguished central events. Thus, appropriate inspiratory and expiratory pressures are automatically selected. It is not clear if these new devices work consistently across all aetiologies.
(see p. [link])
Overnight NIV may have a useful role as a ‘bridge’ to transplantation in patients with CF and chronic respiratory failure.
Use of NIV in the management of chronic stable COPD is controversial. Trials have shown conflicting results, although there is some possible benefit in a subgroup of patients with severe hypercapnia, extra nocturnal hypoventilation, and recurrent admissions for worsening ventilatory failure. A recent RCT suggested no overall benefit but may have used suboptimal pressures and interfaces. Further RCTs in this area are ongoing, and the use of the new ‘smart’ ventilator technology may improve the success rate.
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