Non-invasive ventilation

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Chapter 33 Non-invasive ventilation

Non-invasive ventilation (NIV) is a valuable therapeutic option in the management of acute and chronic respiratory failure – for some diagnoses it is the preferred option. Successful use of NIV in acute respiratory failure (ARF) was first published in 1936,¹ and the use of NIV predates the introduction of laryngoscopy (early 1900s) and the widespread use of positive-pressure mechanical ventilation (MV) via an endotracheal tube (1950s).²

NIV is defined as ventilatory support without an (invasive) endotracheal airway. It has an increasingly important role in the short-term management of readily reversible ARF,^3,⁴ and in chronic respiratory failure due to obstructive sleep apnoea (OSA) and neuromuscular disease.

NIV may be achieved either through the delivery of positive airway pressure (P_ao) or the application of a negative-pressure generator to the chest (‘chest box’ or cuirass) or body (‘iron lung’). A conceptual framework is shown in Figure 33.1. This chapter deals primarily with the use of positive-pressure NIV to treat ARF.

Figure 33.1 Conceptual non-invasive ventilation paradigm. See text for definitions.

Negative-pressure generators may be used for the management of acute or chronic respiratory disease.⁵ Major limitations to the use of negative-pressure generators include the induction of OSA, lack of fractional inspired oxygen (FiO₂) control, equipment bulk and size.⁶ However, external negative-pressure generators suit some patients with chronic respiratory failure, particularly as there is no oral or nasal prosthesis.

The clinical efficacy of NIV depends upon: (1) the mode used; and (2) the nature and severity of the underlying respiratory disorder. Correctly applied, NIV can reduce morbidity and mortality, whereas inappropriate application may delay definitive therapy and adversely affect outcome. An understanding of the physiologic rationale for NIV will assist the clinician in understanding the indications and benefits, and predict the side-effects of the various NIV modes.^7,⁸ Many of the general issues regarding ventilation are discussed in Chapter 27, and this chapter will focus on those issues specific to NIV.

PHYSIOLOGY OF NIV

The physiological benefits of NIV are similar to those of invasive ventilatory support. The application of NIV can reverse many of the physiologic and mechanical derangements associated with respiratory failure through:

• augmentation of alveolar ventilation (

) to reverse respiratory acidosis and hypercarbia

• alveolar recruitment and increased FiO₂ to reverse hypoxia

• reduction in work of breathing (W_mus) to reduce or prevent respiratory muscle insufficiency

• stabilisation of the chest wall in the presence of chest trauma or surgery

• reduction in left ventricular (LV) afterload that may lead to an improved cardiac function

The respiratory effort (pressure–volume work) required to achieve a desired minute volume () may be viewed as the summation of the individual forces that must be overcome to generate inspiratory flow, namely: elastic work (or ‘stretch’; W_el), flow-resistive work (airflow obstruction; W_res), and threshold work (W_thres). Since the volume component is constant the equation of motion can be written as:

See Chapter 27 for a more detailed explanation.

With the addition of a device for ventilatory support, the respiratory muscle effort (P_mus) required by the patient is equivalent to the difference between the applied P_ao and the total work required to maintain .

This relationship may be rearranged into its individual components, as follows:

where E is the respiratory elastance (inverse of compliance), V is the volume of gas, R is the respiratory and circuit flow-resistance, is the inspiratory flow rate and PEEP_i is the sum of the extrinsic and intrinsic PEEP (≈P_thres).

It is important to remember that breathing via a circuit will create additional airflow resistance (R) adding to breathing work (P_mus), and thus attention to circuit design is important (see below).

PEEP_i is absent in the healthy lung, but common in the presence of tachypnoea, airflow obstruction and dynamic hyperinflation. This threshold load must be counterbalanced by an equivalent amount of inspiratory effort before inspiratory flow can commence. Since threshold load impedes inspiration it will also impede the onset (triggering) of inspiratory support modes (inspiratory positive airway pressure (IPAP) and pressure support ventilation (PSV)).

Respiratory failure occurs when the forces opposing inspiration – namely elastic (P_el), resistive (P_res) and threshold (PEEP_i) work – exceed the respiratory muscle effort (P_mus) required to maintain . Hypermetabolic states (e.g. trauma, sepsis) increase basal , whereas pulmonary and chest wall diseases increase respiratory workload, and neuromuscular disease impairs respiratory muscle effort. NIV may prevent respiratory failure by counterbalancing the respiratory workload and/or reducing respiratory muscle effort, and thus maintain .

Although all invasive MV modes may be delivered non-invasively, four are commonly described: continuous positive airway pressure (CPAP); PSV; bilevel or biphasic positive airway pressure (BiPAP); and pressure- or volume-limited intermittent positive-pressure ventilation. Other modes under investigation include high-frequency and proportional assist ventilation.

All NIV modalities utilise closed (or semiclosed) circuits and are thus capable of controlling and delivering high FiO₂. This is an important mechanism by which NIV improves oxygenation, independently of other mechanisms discussed below.

CONTINUOUS POSITIVE AIRWAYS PRESSURE

CPAP is a form of NIV because it provides respiratory support even though the P_ao applied is constant throughout the respiratory cycle. This mode can address a number of objectives of ventilatory support, namely:

1 reduction in the work of breathing by:

• alveolar recruitment leading to reduction in elastic work

• reducing threshold load created in the presence of PEEP_i

2 reversing hypoxia through alveolar recruitment and reduction of intrapulmonary shunt

3 reduction of LV transmural pressure (afterload)^9,¹⁰

INSPIRATORY POSITIVE AIRWAY PRESSURE AND PSV

Positive inspiratory airway pressure, without expiratory pressure (e.g. PSV or IPAP), provides respiratory support by reducing both the elastic and resistive components of respiratory work. This may result in:

• augmentation of tidal volume (V_T) and reduction in PaCO₂

• reduction in P_mus with reduction or prevention of respiratory muscle insufficiency

• induction of pulmonary surfactant release through alveolar inflation above resting tidal volume ¹¹

BILEVEL POSITIVE AIRWAY PRESSURE (BPAP)

BPAP allows separate settings for inspiratory (IPAP) and expiratory (EPAP) airway pressure levels, and is conceptually similar to PSV plus CPAP. Respiratory frequency is usually determined by the spontaneous rate but may be time-cycled and independent of patient effort. In some patients BPAP may not be as effective in reducing P_mus as the combination of PSV plus CPAP.^2,¹²

CONTROLLED VENTILATION

NIV may also be administered as volume- or pressure-limited MV applied via a mask (instead of an endotracheal airway).

PATIENT–VENTILATOR INTERACTION

This is discussed in Chapter 27, and subdivided into: (1) triggering of inspiration; (2) inspiration; and (3) cessation of inspiration. The only aspect that is specific to NIV arises from mask leaks that may interfere with the ability to sense the end of expiration because there is continued ‘expiratory’ gas flow.

NON-INVASIVE VENTILATION EQUIPMENT

Equipment design varies according to NIV mode and purpose (e.g. critical care or domiciliary setting), and significant variation in performance characteristics have been documented.^12,¹³ The important characteristics of an efficient NIV circuit include:

• High gas flow that can match the peak inspiratory airflow. Mechanisms to generate high flows include a pressurised gas supply, a gas turbine or a jet Venturi mechanism. A continuous-flow device often imposes less circuit work than a demand flow device.

• An expiratory resistor capable of maintaining the desired PEEP, yet offering a low resistance to expiratory flow to reduce fluctuations in the desired P_ao. This may be a threshold resistor or flow resistor. The optimal position for the expiratory valve is as close to the patient’s airway as possible.

• Minimal-length, wide-bore tubing to reduce turbulence and flow resistance.

• A flow or pressure sensor for identifying inspiratory effort, and triggering positive inspiratory pressure support (e.g. PSV or IPAP).

• Ability to control and deliver a wide range of FiO₂.

• Other desirable features include the facility to humidify inspired gases and nebulise drugs, and the provision for pressure relief safety valves, battery back-up, apnoea back-up support, acoustic suppression and monitoring of volume and P_ao. These features are less important for domiciliary (long-term) NIV equipment.

Many mask designs are also available and the optimal design depends upon the purpose and mode of NIV and patient anatomy and preference. These include intranasal, nasal, oronasal, full-face and helmet (full-head) masks. Desirable features of a mask include light-weight and transparent materials providing a comfortable air-tight seal with minimal dead space and separate inspiratory and expiratory ports to minimise airflow turbulence and rebreathing.^13,¹⁴ In lung model studies, expiratory ports over the nasal bridge reduce dead space,¹⁵ which may prove to be clinically advantageous.

Mask discomfort, arising from the mask seal, air leaks, humidification or claustrophobia, is a common cause of poor compliance with NIV. Masks that cover nose and mouth tend to produce more reliable and constant P_ao because they are unaffected by mouth breathing, a common problem in the critically ill patient. Nasal masks are less restrictive on the patient’s ability to talk, eat/drink and expectorate and have a higher compliance in longer-term and domiciliary applications. To compensate for air leaks effectively, nasal masks should be used with circuits capable of rapidly augmenting and delivering high flows > 100 l/min.

Fibreoptic bronchoscopy can be easily, and often safely, performed during NIV. In addition to the usual precautions regarding fibreoptic bronchoscopy, an orofacial mask with at least two ports is required. One of these can be modified to allow a simple valve for insertion of the bronchoscope, and the other used for NIV. Provided there is adequate NIV flow reserve during suction, this can be performed during all modes of NIV. This technique may allow both diagnostic and therapeutic bronchoscopy without intubation in critically ill patients.

COMPLICATIONS AND ASSESSMENT OF EFFICACY

Contraindications and complications specific to NIV are listed in Table 33.1. Most patients requiring NIV should be managed in a critical care ward with appropriately trained medical and nursing staff. Although the development of sophisticated, portable, non-invasive ventilators makes iteasy to provide NIV in any environment, its benefits may diminish outside the critical care environment.^16,¹⁷

Table 33.1 Contraindications and complications of non-invasive ventilation

Contraindications

• Respiratory arrest

• Unprotected airway (coma, sedation)

• Upper-airway obstruction

• Inability to clear secretions

• Untreated pneumothorax

• Marked hameodynamic instability

Complications

• Mask discomfort, patient intolerance

• Facial or ocular abrasions

• Nasal congestion, sinus pain

• Oronasal dryness

• ↑ Intraocular pressure (particularly in patients with glaucoma)

• ↑ Intracranial pressure (particularly in patients with neurotrauma)

• ↓ Blood pressure (if hypovolaemic)

• Aspiration pneumonia (rare)

• Aerophagy and gastric distension (uncommon; routine gastric decompression is unnecessary)

Following the application of NIV reversal of hypoxia, and transient reduction in respiratory rate and effort are commonly observed irrespective of the underlying disease. Although these are important goals of respiratory support, they are a poor guide to the true efficacy of NIV. More reliable clinical measures of NIV efficacy include reversal of hypercarbia and sustained improvement in respiratory function. Efficacy of NIV should be assessed using outcomes such as rates of compliance, intubation, nosocomial pneumonia and mortality.

NON-INVASIVE VENTILATION AND ACUTE RESPIRATORY FAILURE ^2,^16,¹⁸

CARDIOGENIC PULMONARY OEDEMA (CPO)^2,^8,¹⁹

CPO is a common cause of severe reversible ARF. Since the 1930s, a number of investigators have documented the therapeutic benefits of all modes of NIV – particularly CPAP – in the treatment of CPO. CPO leads to an increase in elastic workload (P_el) and, to a less extent, resistive workload (P_res) as a consequence of diastolic LV dysfunction, an increase in lung water and impaired surfactant function. CPAP reverses hypoxia, recruits alveoli and reduces intrapulmonary shunt and LV afterload. Redistribution of extravascular lung water from alveoli to the interstitial space is aided by recruitment of alveoli and surfactant production.

Over 20 prospective randomised controlled trials of NIV in CPO have consistently demonstrated physiologic improvements in hypoxic and hypercapnic respiratory failure, and a significant reduction in the need for intubation, hospital length of stay and improved survival (95% confidence interval (CI) relative risk (RR) = 0.38–0.90).¹⁹ Even though the majority of these patients were managed in a critical care setting the average duration of respiratory support was much shorter for NIV (9 ± 11 hours) than those who required MV.²⁰

The optimal mode of NIV in CPO appears to be CPAP alone. The optimal P_ao level remains to be resolved, although 10 cmH₂O appeared to be safe and effective in the majority of subjects. Whilst the addition of a differential inspiratory pressure (e.g. bilevel ²¹ and PSV^22,²³) appears to be as effective as CPAP, it does not appear to provide an additional outcome benefit¹⁹ and may increase the rate of myocardial infarction^24,²⁵ (95% CI RR 0.92–2.42).¹⁹ Bilevel NIV and CPAP have equivalent impact on respiratory parameters, but may have different effects on myocardial function.^24,²⁵ CPAP reduces preload and afterload^9,¹⁰ and myocardial catecholamine release²⁶ but the cyclical P_ao (of bilevel NIV) may cause preload and afterload to rise and fall during respiration.^2,²⁷

Current evidence supports the routine use of mask CPAP in moderate or severe CPO as standard therapy and as the first-line option for respiratory support.^16,²⁸

ACUTE RESPIRATORY FAILURE IN CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)

COPD patients have an elevated resistive work (P_res), often coupled with an elevated basal and elastic work (P_el) as a result of the pre-existing parenchymal damage. Threshold load (PEEP_i) is frequently present as a result of airflow obstruction, and is exacerbated during ARF by further increased W_res and respiratory rate. Reversible ARF is a common complication of COPD.

Both CPAP and PSV reduce P_mus in intubated COPD patients weaning from MV. The importance of NIV in hypercapnic ARF is now supported by at least 14 well-performed prospective randomised controlled studies ^18,²⁹^–³¹ in over 600 patients. Most investigators have demonstrated a low incidence of side-effects and a significant decrease in intubation rates and in-hospital mortality.³¹ The meta-analysis of NIV trials reveals significant reductions in mortality (95% CI RR = 0.35–0.76) and the need for intubation (95% CI RR = 0.33–0.53) – the number of patients needed to avoid intubation or death were as few as 4 and 10 respectively.³² Risk reduction appears to be proportional to the severity of respiratory acidosis.³³ The incidence of nosocomial pneumonia is lower with NIV³⁴^–³⁶ and this may explain some of the mortality reduction associated with NIV.³⁶ Nevertheless, mask intolerance, nursing workload and failure rates are greater than those reported with NIV in CPO.²

Current evidence supports the use of NIV in hypercapnic ARF as a component of standard therapy in COPD subjects. This is supported by many respiratory medicine societies throughout the world,^16,^28,³⁷ that ‘patients hospitalised for exacerbations of COPD with rapid clinical deterioration should be considered for noninvasive positive pressure [ventilatory support] to prevent further deterioration in gas exchange, respiratory workload and the need for endotracheal intubation’.¹⁶

All modes of NIV have been shown to be effective but there are no comparative trials that address the question of optimal mode or pressure level.¹⁶ Patients with ARF arising predominantly from airflow obstruction (P_res) and/or threshold load are likely to respond to CPAP. Most patients also have reduced alveolar ventilation, marked hypercapnia or respiratory muscle insufficiency and are therefore likely to benefit from the addition of inspiratory support, i.e. PSV, IPAP or non-invasive positive-pressure ventilation (NIPPV).

NIV is indicated in the presence of respiratory acidosis (pH < 7.37) or persistent breathlessness.^32,³⁸ These patients should be managed in a critical care setting where appropriate equipment and skill are available² and reported outcomes appear better.^17,³² The level of inspiratory support (usually 5–15 cmH₂O) should be titrated to improve , as indicated by improvement in tidal volume and pH, and reductions in respiratory rate and PaCO₂. Low levels of CPAP (4–8 cmH₂O) should be titrated to minimise the patient effort required to trigger inspiratory assistance and the FiO₂ titrated to reverse hypoxia.

Early predictors of NIV success in COPD patients include the pH and PaCO₂, but not the PaO₂, response within the first 2 hours of therapy.^32,³⁹ Predictors of NIV failure include mask intolerance, severe acidosis (pH < 7.25), tachypnoea (> 35/min), impaired conscious state and poor clinical response to initial therapy.³⁹ Prior to the commencement of NIV the clinician should develop a clear management strategy for those patients who fail a trial of NIV.

Although reported success rates are high (70–90%), NIV failure (i.e. intubation) appears to increase with the severity of respiratory acidosis.^32,³⁸ For the poorly compliant patient, reassurance and explanation together with a trial of different size and/or type of mask, or initiation with lower pressure settings, and brief periods off NIV will sometimes assist. Low-dose anxiolytic drugs may be beneficial where anxiety is a recurrent precipitant of tachypnoea, but should be used with extreme caution because of their respiratory-depressant side-effects.

Late failure (> 48 hours) occurs in 10–20% of patients ^18,^30,³⁹ despite an initial improvement with NIV. This group of patients has a high mortality risk.⁴⁰ Whether their worse outcome is related to the severity of their underlying disease, or from delayed initiation of MV, remains unclear.

ASTHMA

Asthma is an acute inflammatory lung disease that increases resistive (P_res) and threshold (PEEP_i) respiratory work. Physiological and clinical improvement has been demonstrated in acute asthmatics with the application of CPAP ⁴¹^–⁴³ and bilevel NIV.⁴³^–⁴⁵ One randomised controlled trial of bilevel NIV titrated over 30 minutes resulted in significant improvement in forced expiratory volume in 1 second (FEV₁) and a lower hospital admission rate.⁴⁶

The clinical role of NIV in the management of acute asthma and the benefit of differential inspiratory pressure, if any, remains to be clarified. We have found 5 cmH₂O CPAP to be effective in moderate to severe asthma not responding to continuous inhaled bronchodilators. Nebulised drugs can be effectively delivered even in the presence of a high-flow NIV circuit.⁴⁷ Controlled clinical studies with robust end-points are awaited.

ACUTE LUNG INJURY (ALI) AND ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)

Like CPO, ALI leads to increase in elastic workload (P_el) and, to a lesser extent, resistive workload (P_res) arising from an increase in alveolar–capillary permeability, the release of inflammatory mediators and impaired surfactant function. In contrast to CPO there is little supportive evidence for NIV in ALI and ARDS. Even though the addition of PEEP is important during MV for ALI or ARDS and NIV has a lower prevalence of nosocomial pneumonia,³⁴^–³⁶ current data do not support the routine use of NIV in undifferentiated hypoxaemic ARF.^48,⁴⁹

Despite numerous clinical reports of successful use of NIV in the setting of community-acquired pneumonia (without COPD) and other forms of ALI, the failure rate remains high.^31,^48,⁵⁰^–⁵³ This may reflect the differences in duration, severity and the pathophysiology of pneumonia, ALI and ARDS compared to CPO. Some studies showing apparent benefit have failed to exclude patients with CPO⁵⁴ or COPD^55,⁵⁶ – specific subgroups known to benefit from NIV.

PNEUMONIA IN THE IMMUNOCOMPROMISED PATIENT

MV is associated with high morbidity and mortality risks in immunocompromised patients.⁵⁶^–⁵⁸ These patients may benefit from NIV² through a reduction in intubation and MV,^56,⁵⁷ but it is unclear whether this translates into improved hospital survival^56,⁵⁸ or not.^36,⁵⁷ Whether NIV simply avoids a high-morbidity therapy (i.e. MV)³⁴ or selects those with a more readily reversible form of ARF and those more likely to survive is unclear. Nevertheless it seems reasonable, based on the current data, to offer NIV to these patients.¹⁶ Once again, clear guidelines need to be established for the management of those patients who fail a trial of NIV and those in whom MV is deemed inappropriate or futile.

POSTOPERATIVE AND POSTTRAUMATIC ARF

ARF in postoperative and trauma patients may arise from a number of reversible pathological processes associated with increases in elastic workload (P_el) and impaired respiratory muscle function, including dependent atelectasis, impaired chest wall mechanics, poor cough, nosocomial infection, aspiration pneumonitis and non-respiratory trauma or sepsis.

Mask CPAP consistently improves physiological parameters (e.g. oxygenation and respiratory rate) and reduces the risk of intubation in general surgical ⁵⁹ and cardiothoracic patients⁶⁰ with mild postoperative hypoxic respiratory failure, but evidence for an outcome benefit is lacking. It is possible that the addition of inspiratory support (PSV or BiPAP) may improve survival in certain subgroups, such as postoperative lung resection.⁶¹ Many of these patients have underlying COPD, and extrapolation of these results to non-COPD patients awaits further study.

Mask CPAP has been shown to be superior to MV in patients with isolated severe chest trauma,^62,⁶³ but the exact role of NIV is unclear. NIV is contraindicated in the presence of other significant injuries such as neurotrauma and intracranial hypertension and in the presence of an untreated pneumothorax.

NIV-ASSISTED WEANING

As a result of the demonstrable benefits of NIV in COPD and the widespread use of invasive PSV to assist weaning from MV, NIV has also been recommended to expedite weaning from MV by allowing early extubation,⁶³ and to treat failed or accidental extubation. The putative advantages relate to reduction in the duration and the risks of MV (e.g. nosocomial pneumonia).

For COPD patients, once again, there appears to be a survival benefit,⁶⁴ but this is less clear in other groups,⁶⁵ where controlled studies do not support an overall benefit.¹⁶ Although NIV is an option for early weaning it is not a substitute for strategies to improve early access to NIV (to reduce the need for MV) and improve weaning success (to reduce the risk of premature extubation).

NIV AND CHRONIC RESPIRATORY DISEASE

NIV is an important modality for short-term assistance and long-term treatment of severe chronic respiratory failure associated with obstructive and central sleep apnoea syndromes,^16,⁶⁶ and chronic hypoventilation syndromes associated with extrapulmonary disease such as neuromuscular disease,⁶⁷ and thoracic deformities.⁶⁸ There appears to be less benefit in chronic parenchymal lung disease, such as (stable) COPD and cystic fibrosis.⁶⁹

These patients may require short-term MV or NIV in a critical care environment for respiratory support during an acute illness or as an aid to perioperative care. NIV (plus minitracheostomy for secretion removal) may improve outcome compared to intubation and MV ⁷⁰ but failure rates appear to be higher than in acute hypercapnic COPD.⁷¹ Alternatively these conditions may be first diagnosed during admission for treatment of severe ARF and, following recovery, will require assessment for long-term NIV.

NIV AND SLEEP APNOEA SYNDROMES ^72,⁷³

Moderate or severe OSA results in nocturnal hypoventilation and episodic hypoxia that can lead to pulmonary and systemic hypertension, cardiac failure, and daytime hypercapnia and somnolence. Many of these complications can be arrested or reversed through the appropriate use of nocturnal CPAP.^16,^66,⁷⁴ Patients with suspected sleep apnoea require accurate assessment by a respiratory physician, including sleep studies, prior to the routine use of domiciliary CPAP. Occasionally bilevel or controlled ventilation will be needed when there is inadequate central respiratory drive. In many patients respiratory drive will improve, and they can then be managed with CPAP after a period of bilevel or controlled ventilation.

Intercurrent illness, surgery or the use of sedatives and opioid analgesics will increase the frequency and duration of hypopnoea, apnoea and hypoxia. CPAP should be available even for those patients who do not require admission to a critical care ward.

NIV AND CHRONIC HYPOVENTILATION SYNDROMES

Domiciliary NIV (predominantly using inspiratory support modes or NIPPV) should be considered in all patients presenting with severe chronic respiratory failure due to neuromuscular disease.^67,^69,⁷⁵ Early referral and consideration of domiciliary NIV are recommended because of improved outcomes^67,⁷⁶ and quality of life. In cystic fibrosis patients it may have a role simply as a bridge to organ transplantat.^57,⁶⁸ In direct contrast to the role of NIV in acute exacerbations of COPD, there is little or no benefit of domiciliary NIV in the presence of stable COPD,^16,^37,^71,⁷⁷ unless one of the former conditions coexists.