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Chapter | 15 |
c0075 Respiratory management in neurological
rehabilitation
Anne Bruton

patients are susceptible to respiratory infections through

CONTENTS
immobility or aspiration (see Table 15.1). As respiratory
Introduction 319 dysfunction can be life-threatening, it makes sense for
Respiratory assessment 319 every physiotherapist to be competent to conduct an
assessment of the respiratory system, to be aware of the
Arterial blood gases 319 common problems with which patients present, and to
Pulse oximetry and capnometry 321 have a basic toolkit of interventions designed to manage
Vital capacity 321 such problems. This chapter will cover the areas of respi-
Peak cough flow 322 ratory assessment, problem recognition and respiratory
physiotherapy management in neurological patients.
Inspiratory/expiratory pressures 323
Sniff test 323
Respiratory problems associated with RESPIRATORY ASSESSMENT
neurological conditions 323 s0030
Physiotherapy management of specific
A comprehensive respiratory assessment as outlined in p0450
problems 324
Box 15.1 is only possible in a patient in a stable situation.
Problem 1: Breathlessness/dyspnoea 324 If any ‘red flags’ are noticed (see Box 15.2), the assessment
Problem 2: Sputum retention and atelectasis 324 may need to be adapted and shortened. Although it is gen-
Problem 3: Hypoventilation 326 erally recognized that neurological disease may result in
respiratory dysfunction, its presentation in such patients
Problem 4: Respiratory failure 327
Respiratory physiotherapy management may be atypical, because of wider effects of the underlying
post brain injury 328 condition (Polkey et al., 1999). The tests starred (*)
in Box 15.1 will now be described further in relation to
Management of brain injury patients
neurological patients.
requiring invasive ventilation 328

Arterial blood gases s0035

INTRODUCTON Arterial blood gas (ABG) sampling is performed to obtain p0455
s0025
accurate measures of arterial oxygen (PaO2), arterial car-
p0445 Respiratory problems are not confined to respiratory bon dioxide (PaCO2), and blood acidity/alkalinity (pH);
patients. Every patient has the potential to develop respi- these variables combined with body temperature allow
ratory dysfunction. This is particularly true for patients for calculation of bicarbonate (HCO3) and arterial oxygen
with neurological disorders. As well as problems with saturation (SaO2). Both PaO2 and PaCO2 can be affected
reduced central drive or neuromuscular weakness asso- by respiratory muscle weakness. Mild weakness leads to
ciated with pathology and trauma, many neurological slight hypoxaemia (low oxygen i.e. PaO2 <8 kPa/<60

© 2011 Elsevier Ltd.

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t0010 Table 15.1 Clinical course for some neurological conditions commonly associated with respiratory problems

DISORDER CLINICAL CURSE PREVALENCE OF RESPIRATORY INVOLVEMENT

CNS
Multiple sclerosis Relapsing Pulmonary function impaired in 63%; respiratory failure or
infection causes death in 5%

Parkinson’s disease Slowly progressive Pneumonia accounts for 20% of deaths, possibly from
bulbar or upper airway muscle involvement and impaired
cough

Spinal cord
Trauma Permanent High lesions (C1–3) usually require long-term ventilation

Motor neurone
Postpolio syndrome Very slowly progressive Respiratory impairment usually only in those with initial
respiratory muscle involvement

Motor neurone disease Progressive Death almost uniformly due to respiratory complications

Motor nerves
Guillain-Barré syndrome Slowly reversible Respiratory failure in 28%

Charcot–Marie–Tooth Very slowly progressive 96–100% have prolonged phrenic nerve conduction; 30%
have vital capacity <80% predicted

Neuromuscular junction
Myasthenia gravis Reversible Aspiration pneumonia gives rise to crises with 6% mortality

Botulism Slowly reversible 8% mortality due to respiratory failure

Muscle
Duchenne muscular dystrophy Progressive Respiratory failure is major cause of death

(Adapted from Aboussouan 2005, with permission.) Au6

b0010 Box 15.1 Elements of a respiratory assessment

p0010 General end-of-bed observations: Palpation checking for – tracheal centrality; chest pulsations/
Breathing pattern, cyanosis, distress, accessory muscle use, tenderness/depressions/bulges/movements/scars; tactile/
swallowing, speech pattern, posture. vocal fremitus
Percussion –to detect chest resonance/dullness
p0020 History (from patient/relatives/friends):
Past medical history, history of present complaint, recent Auscultation – to listen for presence/absence normal or
symptoms (cough/sputum/chest tightness/breathlessness), added lung sounds.
smoking history, environmental exposures (pollution/ Current general status: p0055
occupational), family health history, travel history, social Body temperature, blood pressure, pulse rate, fluid balance,
history, drug history. blood chemistry, intracranial pressure.
p0030 Clinical examination: Respiratory bedside/laboratory testing: p0065
Inspection – hands (finger clubbing, tremor, temperature); Chest X-rays/other imaging, sputum culture, arterial blood gases
chest shape; breathing rate, depth, frequency, symmetry (ABGs)*, pulse oximetry and capnometry*, lung function Au7
(left:right) and regularity; sputum (quantity, colour, smell); tests (e.g. vital capacity)*, peak cough flow*, inspiratory/
cough competence expiratory pressures* (mouth/sniff/transdiaphragmatic).

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b0015 Box 15.2 Respiratory ‘red flags’

• General (e.g. chest pain/haemoptysis) – always need oxygen saturation below 90%. Can be difficult to detect
further investigation because of potential to indicate reliably in artificial lighting
serious pathology • Altered mental status – agitation/drowsiness. Acute
• Breathlessness or inability to talk in complete sentences at confusion with breathlessness may indicate severe
rest – breathlessness may be of sudden onset or gradual. If hypoxaemia (or sepsis/metabolic disturbance)
related to muscle weakness, it may initially be more • Exhaustion and shallow breathing – may follow a period
apparent at night when lying down/sleeping of ‘distressed’ breathing, when work of breathing
• Accessory muscle use while at rest – normal breathing overwhelms the patient and fatigue leads to ventilatory
requires minimal effort, so use of additional muscles (e.g. failure
sternocleidomastoid) indicates respiratory distress • Altered arterial blood gases – hypoxaemia with
• Weak cough or inability to clear secretions – suggests hypercapnia indicates ventilatory failure
weakness of expiratory muscles • Vital capacity falling below 15 mL/kg body weight
• Cyanosis (dusky or bluish tinge to skin) – seen round lips/ indicates respiratory muscle weakness requiring ventilator
tongue ¼ central cyanosis. Usually only occurs once support (Polkey et al., 1999).
arterial oxygen tension falls below 8 kPa (60 mmHg), and

mmHg) and hypocapnia (low carbon dioxide, i.e. (e.g. overnight). This can be useful because patients with
PaCO2<4.7 kPa/<35 mmHg); severe weakness causes respiratory muscle weakness may develop nocturnal
hypercapnia (high carbon dioxide, i.e. PaCO2 >6kPa/ hypoventilation, leading to elevated carbon dioxide levels
>45 mmHg), but only when muscle strength is <40% not initially detectable during the day.
predicted (ATS 2002). However, ABG derangement is a
late feature in neuromuscular disease, so normal results
are compatible with significant weakness of the respira-
Vital capacity s0045

Au1 tory muscles (Hutchinson & Whyte, 2008). Patients with Vital capacity (VC) is the volume change at the mouth p0465
established respiratory failure from neuromuscular weak- between full inspiration and complete expiration (see Fig-
ness will show hypoxaemia and a compensated respira- ure 15.1). VC can be measured using conventional spi-
tory acidosis (raised PaCO2 and HCO3 with a normal or rometers or recorded from equipment used to measure
mildly reduced pH). static lung volumes and their subdivisions. Guidelines
for measurement have been published by the American
Thoracic Society/European Respiratory Society task force
s0040 Pulse oximetry and capnometry
(Wanger et al., 2005).
p0460 Pulse oximetry and capnometry provide non-invasive Ideally, the VC manoeuvre is performed with the p0470
measures of blood oxygenation and alveolar carbon diox- patient using a mouthpiece and wearing a nose clip. In
ide. Transcutaneous pulse oximetry estimates oxygen satu- patients with neuromuscular weakness, assistance may
ration (SpO2) of capillary blood, based on the absorption be required to provide a seal around the mouthpiece, or
of light from light-emitting diodes positioned in a finger a facemask may be substituted. It is important that
clip or adhesive strip probe. SpO2 indicates the oxygen patients understand they must completely fill and empty
bound to haemoglobin, while PaO2 indicates the oxygen their lungs. The largest value from at least three acceptable
dissolved in the plasma. Normal SpO2 is 95–98%, but manoeuvres (with a rest of 1 minute between man-
patients with very low levels of haemoglobin (normal oeuvres) is used.
¼11–18 g/dl) can have 100% saturation. Pulse oximetry Normal values are calculated from the patient’s age, p0475
can help to identify problems such as atelectasis and height and gender. A normal VC, with no significant fall
pneumonia; however, it only measures oxygenation, not when supine, means that respiratory muscle weakness is
ventilation. It is possible to have normal oxygen satura- unlikely. However, muscle weakness in conditions such
tion while carbon dioxide is rising. Capnometry measures as myasthenia gravis can fluctuate significantly. Generally,
carbon dioxide at the end of expiration, known as it is only when muscle force is reduced to less than 50%
end-tidal carbon dioxide (ETCO2). It is expressed as a of predicted that a decrease in VC can be observed. A fall
percentage or in kPa/mmHg. In patients with normal in VC by more than 15–20% when the patient lies supine
lungs and normal ventilation/perfusion ratios, ETCO2 specifically suggests weakness of the diaphragm.
equates to PaCO2. Normal values are around 5–6%, In acute neuromuscular disorders the VC and oxygen p0480
which equates to 4.7–6.0 kPa (35–45 mmHg). Both pulse saturation should be rechecked at frequent intervals. A
oximetry and capnometry permit continuous monitoring VC <1 L in an adult (<15 mL/kg), a fall in VC by more

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f0010 Figure 15.1 Lung volumes and capacities in neurological disease. (From Aboussouan LF. Respiratory disorders in neurologic
diseases. Leve Clin J Med 2005; 72:511–520. Reprinted with permission. Copyright # 2005 Cleveland Clinic. All rights reserved.)

than 50% on serial testing, or onset of bulbar palsy are all The recent joint guidelines from the British Thoracic p0490
indications to involve the intensive care unit (Hutchinson Society (BTS) and Association of Chartered Physiothera-
Au2 & White, 2008). In chronic neuromuscular disorders, pists in Respiratory Care for respiratory physiotherapy
monitoring can be less frequent, but a serial fall in VC (Bott et al., 2009), include a guide for recording PCF
(particularly a fall below 1.2–1.5 L or <40–50% of pre- in patients with neuromuscular weakness. It can be
dicted) indicates a need for further respiratory assessment measured through either a mouthpiece or face mask
Au2 (Hutchinson & Whyte, 2008). attached to a peak flow meter and expressed in litres/
minute or litres/second. The patient should be instructed
to breathe in as deeply as possible and cough hard into
s0050 Peak cough flow
the device. PCF is expected to be higher than peak expi-
p0485 A normal cough requires the ability to generate sufficient ratory flow, but in patients with bulbar dysfunction, this
inspiratory and expiratory power and a functional glottis. difference is not seen – potentially offering a way to
Ability to cough effectively is therefore compromised by monitor the onset of bulbar involvement (Boitano,
either inspiratory or expiratory muscle weakness. However, 2006).
expiratory muscle weakness has greater impact as mild to PCF is dependent on effort and lung volume, with p0495
moderate expiratory muscle weakness can result in a weak cooperation being essential. The largest value from at least
cough, even if inspiration is normal (Boitano, 2006). In three acceptable attempts is usually recorded. Normal PCF
some neurological disorders, such as bulbar type motor is around 360 to 840 l/minute (Hutchinson & Whyte, Au2
neurone disease (MND; see Ch. 8), a functional glottis 2008). Airway clearance becomes impaired and the risk
may be absent. Formal cough assessment requires the inser- of serious infection increases when PCF<160 L/minute,
tion of gastric balloons and is conducted in specialized so in chronic progressive conditions, airway clearance
laboratories, but cough strength can be assessed at the bed- techniques should be taught before these levels are
side using peak cough flow (PCF). PCF is a measure of max- approached (Tzeng & Bach, 2000). It has been suggested
imal airflow generated during a cough manoeuvre. It that any neuromuscular patients with a PCF<270
provides a global indicator of cough strength that correlates L/minute should be considered at risk of respiratory
well with the ability to clear secretions. complications.

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s0055 Inspiratory/expiratory pressures of inspiratory muscle strength. Peak nasal pressure is

measured in one occluded nostril during a maximal sniff,
p0500 Guidelines for testing the respiratory muscles have been performed from relaxed end-expiration through the other
published by the American Thoracic Society (2002). open nostril. Portable commercial systems are available
Inspiratory and expiratory pressures are recorded to assess for measuring SNIP at the bedside. Patients should be
respiratory muscle strength, but should be viewed as encouraged to make maximal efforts, with a rest between
indices of global respiratory muscle output rather than sniffs. Most patients achieve a plateau within 5–10
as direct measures of their contractile properties (ATS, attempts. A sniff test is not suitable in patients with nasal
2002). Mouth and nasal pressures can be recorded at the congestion, which leads to falsely low values (Fitting,
bedside using hand-held pressure meters. These volitional 2006).The sniff is easily performed by most patients,
bedside tests are simple, portable and inexpensive; but requires little practice and is relatively reproducible. It is
their accuracy and reliability has been questioned because therefore a useful voluntary test for evaluating diaphragm
of their dependence on maximal effort and their signifi- strength in the clinical setting, giving equal or greater pres-
cant learning effect. Non-volitional tests such as phrenic sures than PImax. However, SNIP and PImax are not
nerve stimulation are more reliable, but are expensive interchangeable and should be considered as comple-
and confined to specialist centres. menting one another for the assessment of inspiratory
p0505 Measurement of the maximum static inspiratory pres- muscle strength.
sure generated at the mouth (PImax), or the maximum There are reference values for SNIP in adults (Uldry & p0525
static expiratory pressure (PEmax), are the classic voli- Fitting, 1995) and children (Rafferty et al., 2000). Surpris-
tional tests of respiratory muscle strength. PImax can be ingly, SNIP is similar in children and adults, despite a
more sensitive to respiratory muscle weakness than VC, large difference in respiratory muscle mass. Values of max-
because decreases in respiratory muscle strength occur imal SNIP greater than 70 cmH2O (males) or 60 cmH2O
before decreases in lung volume can be identified. (females) are unlikely to be associated with significant
p0510 Patients are normally seated and noseclips are not inspiratory muscle weakness (Hutchinson & Whyte, Au2
required. Careful instruction and encouraged motivation 2008). The SNIP test appears particularly suited to neuro-
are essential. Measurements require maximal inspiratory muscular weakness because it obviates the use of a
or expiratory efforts against a quasi occlusion. The pres- mouthpiece and because it is easily mastered by most
sure must be maintained for at least 1.5 seconds, so that patients. However, assessment of severe muscle weakness
the maximum pressure sustained for 1 second can be should not rely on SNIP alone, but should include other
recorded. The maximum value of three manoeuvres that tests such as PImax, vital capacity, nocturnal oximetry or
vary by less than 20% is usually recorded, but some ABGs (Fitting, 2006).
authors have recommended that more measures are
needed to reach a true maximum, and even low variability
between measures may not guarantee that maximal efforts RESPIRATORY PROBLEMS s0065
have been made (Aldrich & Spiro, 1995). Although sim- ASSOCIATED WITH NEUROLOGICAL
ple in principle, the manoeuvres are difficult for many
patients and require a good seal around the mouthpiece. CONDITIONS
Low values may therefore be due to true muscle weakness,
or a submaximal effort, or air leaks, e.g. in the case of At a simplistic level, the mechanics of the respiratory sys- p0530
facial muscle weakness. The sniff is an alternative tem function as a pump to drive air into the body, analo-
manoeuvre that is more natural and easier for most gous to the heart pumping blood around the body. The
patients (see section on Sniff test). four essential elements of the pump are intact central neu-
p0515 The normal ranges for PImax and PEmax are wide, so rological drive, neural pathways, thoracic cage and respira-
that values in the lower quarter of the normal range are tory muscles. The respiratory system is only effective when
compatible both with normal strength and with mild or there is a balance between the load on the system and the
moderate weakness.In adults a PImax of more than 80 capacity of the respiratory pump to overcome this load
cmH2O in males, or 70 cmH2O in females, excludes clin- (Polkey et al., 1995). Respiratory load is determined by
ically significant respiratory muscle weakness (Hutchin- the lung, thoracic and airway mechanics; respiratory capac-
Au2 son & Whyte, 2008). ity is the neuromusculoskeletal competence.Problems arise
either from an increase in load (e.g. excessive secretions or
bronchoconstriction) or from a decrease in capacity (e.g.
s0060 Sniff test neuromuscular pathology) or from a combination of both.
p0520 A sniff is a short, sharp voluntary inspiratory manoeuvre Common relevant neurological problems are reduced air-
involving contraction of the diaphragm and other inspira- way protection and respiratory muscle weakness:
tory muscles. Sniff nasal inspiratory pressure (SNIP) • Reduced airway protection (through reduced u0345
has been proposed as a volitional, non-invasive measure consciousness or bulbar/upper airwayweakness) – may

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current physiotherapy practice include: positioning, relaxa-

t0015 Table 15.2 Primary respiratory muscles and their
tion and various forms of breathing retraining (e.g. pursed
level of innervations
lip breathing, Papworth breathing, Buteyko breathing) as
well as complementary therapies such as acupuncture;
RESPIRATORY MUSCLES SPINAL LEVEL
however, there is a lack of evidence for effectiveness of
Sternomastoids C1–C3 any of these techniques in neurological patients. An over-
view of dyspnoea in neurological conditions has recently
Diaphragm C3–C5 been published (Murtagh et al., 2006).
Scalenes C3–C8 Oxygen therapy for dyspnoea s0080
Parasternal intercostals T1–T5 Even in patients with primary respiratory conditions, the p0560
use of oxygen to relieve breathlessness is controversial.
Interosseus intercostals T1–T11 In patients with neuromuscular weakness, although low
External/internal abdominal obliques T6–T12 flow oxygen is commonly prescribed and may relieve
some symptoms and hypoxia, it usually results in a fur-
Transversus abdominis T7–L1 ther increase in arterial CO2 and may therefore aggravate
other symptoms. It should therefore be avoided or used
with extreme caution in this group (Bott et al., 2009).
lead to aspiration and/or infection, which in turn can
lead to breathlessness/dyspnoea, sputum retention and Problem 2: Sputum retention and atelectasis s0085
atelectasis (literally ‘airlessness’,collapse of lung tissue In patients with neurological disorders, an ineffective p0565
preventing alveolar gas exchange) cough is the main reason for sputum retention. Recent
u0350 • Respiratory muscle weakness (see Table 15.2) or evidence-based guidelines on airway clearance techniques
fatigue (through original pathology, immobility or gave 10 recommendations for various patient populations
acquired disorders) – may lead to inability to ventilate (ACCP, 2006). However, only three of these recommen- Au3
and/or inability to cough which in turn can lead to dations related specifically to patients with neuromuscular
breathlessness/dyspnoea, sputum retention, atelectasis, weakness (i.e. manual cough assist (MCA), mechanical
hypoventilation (inadequate ventilation, often related cough assist and expiratory muscle strength training)
to reduced rate or depth of respiration) and respiratory and none were supported by any robust evidence (Haas
failure. et al., 2007).
p0545 Some of these problems will be discussed further in the Box 15.3 provides the indicators of atelectasis or respi- p0570
next section on physiotherapy management. ratory infection. Airway clearance therapy can be divided
into techniques: to augment inspiration, to augment expi-
ration/cough, and to mobilize/remove secretions (see
s0070 Physiotherapy management of Box 15.4 for a list of techniques in common clinical use).
specific problems
Augmenting inspiration s0090
s0075 Problem 1: Breathlessness/dyspnoea
Inspiration can be augmented through thoracic expansion p0575
p0550 Dyspnoea occurs with mismatching of muscular effort rel- exercises in those who can perform them voluntarily, or
ative to ventilation. It is a subjective sensation that is by ‘air stacking’ which can be achieved under volition by
poorly related to objective tests of respiratory function. glossopharyngeal breathing (see Bott et al., 2009 for a
Dyspnoea occurs in airways obstruction, increased neural description), or by the use of a manual resuscitator bag
effort relative to muscular function (as occurs in neuro- or ventilator. Its effectiveness depends on ability to
muscular weakness), and excessive breathing response rel-
ative to metabolic demand. Dyspnoea can be an unreliable
symptom, but marked dyspnoea only when lying flat is
typical of isolated diaphragm paralysis, as is breathlessness Box 15.3 Indicators of atelectasis or infection b0020
on immersion in water.
p0555 Once any treatable cause for breathlessness has been Rising Falling
identified, appropriate action by the multidisciplinary Temperature Vital capacity
team needs to be taken to relieve that cause where practi- Pulse rate Peak cough flow
cable (e.g. antibiotics for a respiratory infection, chest Anxiety
drain for pneumothorax). Symptom relief can be achieved Secretion quantity/viscosity
through physiotherapy management of the breathless Breathlessness
patient as described in Hough (2001). Techniques in

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abdominal/pelvic catheters. MCA should not be used in

b0025 Box 15.4 Techniques for managing sputum patients with Greenfield filters (filter in inferior vena cava
retention and/or atelectasis to prevent pulmonary emboli) (Boitano, 2006). Recent
research has reported that best cough improvement results
Abdominal binder Intrapulmonary percussive from a combination of breathstacking plus MCA and that
Active cycle of ventilation most benefit is derived by patients with VC >340 mL and
breathing techniques Manual hyperinflation and PEmax < 34 cmH2O, but that MCA seems to interfere
Assisted cough suction (intubated patients) with spontaneous cough in patients with stronger cough
Autogenic drainage Manual physiotherapy
and PEmax >34 cmH2O (Toussaint et al., 2009).
BiPAP/CPAP/IPPB* techniques
Bronchoscopy Nebulizers/humidifiers Mechanical cough assist (insufflation-exsufflation) s0105
ELTGOL** Physical exercise
Devices such as the CoughAssist (Figure 15.2) provide p0590
Glossopharyngeal Positioning/postural drainage
mechanical insufflation-exsufflation (MIE) via a face mask
breathing Positive pressure devices (e.g.
Incentive spirometry PEP mask) and promote maximum lung inflation during inspiration
In-exsufflator Respiratory muscle training with the use of positive pressure. A normal cough is
Suction simulated when inflation is followed by an abrupt switch
to negative pressure in the upper airway. The device can
*Bilevel positive airways pressure, continuous positive airways also be used in patients with tracheostomy or endotra-
pressure, intermittent positive pressure breathing
cheal tubes.
**Slow expiration with the glottis open in a lateral posture known
as ELTGOL (from the French: Expiration Lent Totale avec la Glotte MIE is indicated when inspiratory, expiratory and p0595
Ouverte in infraLateral) bulbar muscles are dysfunctional, but the latter are not
completely paralysed and glottic closure is still possible
(as is the case for most patients with neuromuscular dis-
eases). Potential contraindications include a history of
achieve glottis closure (Gauld, 2009). The aim is to increase bullous emphysema (abnormal increase in size of air
volume so that expiratory flow can be increased and a spaces arising from destruction of airway walls), suscepti-
cough is more effective. No barotrauma or complications bility to pneumothorax (air in the pleural space causing
have ever been reported from air stacking. collapse of lung tissue), or recent pulmonary barotrauma
(damage to the lung from rapid or excessive pressure
s0095 Augmenting expiration/cough changes). If bulbar function is intact, MIE is not needed
p0580 This can be achieved through forced expiratory techniques because cough flow can be greatly increased by abdomi-
in those who can perform them or through MCA, mechan- nal thrusts following air stacking. MIE has been in use
ical cough assist using an in-exsufflator (which augments for secretion clearance since its first description in 1954.
both inspiration and expiration), or expiratory muscle Despite increasing acceptance for airway clearance in
training. These are described below.

s0100 Manual cough assist

p0585 This involves using an abdominal thrust or a thoracic
compression to augment the patient’s own cough – usu-
ally after augmented inspiration. The abdominal thrust
is like a well-known manoeuvre to prevent choking, the
Heimlich manoeuvre (Heimlich, 1975), which involves
an upward thrust below the ribcage, so this technique
should not be performed if the patient has a full stomach.
Many patients prefer a thoracic squeeze, but its effective-
ness is limited if there is decreased chest wall compliance,
as is common in Duchenne muscular dystrophy (DMD;
see Ch. 10) and scoliosis. When performing an abdomi-
nal thrust it is important to stabilize the chest wall and
be careful not to injure abdominal organs or cause
gastric reflux (Finder et al., 2004). Various hand place-
ments can be used to provide costal lateral compression.
Evidence for benefits of MCA is not high level, but it has
consistently been found to increase peak cough flow. Its Figure 15.2 The CoughAssistW mechanical insufflator- f0015
use is limited by severe scoliosis, orthopaedic or abdomi- exsufflator. Photograph reproduced with kind permission from
nal abnormalities, abdominal surgery, or the presence of Philips Respironics.

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patients with neuromuscular disease, there remains a lack

of agreement on settings, with pressure settings ranging Box 15.5 Common signs and symptoms of b0030
from 15 cmH2O to 45 cmH2O (insufflation and exsuffla- respiratory muscle weakness/fatigue
tion pressures). Fauroux et al. (2008) demonstrated • Unexplained breathlessness – disproportionate on
greater efficacy at higher settings (up to peak pressures exercise, worse on immersion in water, worse/only in
of 45 cmH2O). During periods of acute illness the settings supine
may need to change as lung mechanics change (Finder • Ineffective cough – unable to clear secretions, repeated
et al., 2004). Bach (2003) believes that mechanical insuf- chest infections
flation/exsufflation is critical for avoiding hospitaliza-
• Poor chest expansion – may be bilateral or unilateral
tions, pneumonias, episodes of respiratory failure, and
• Abnormal breathing rate – may be fast or slow
tracheostomy for patients with DMD, spinal muscular
• Use of accessory muscles at rest
atrophy, and non-bulbar ALS.
• Abnormal movement of ribcage and abdomen – lack of
normal synchronicity
s0110 Expiratory muscle training (see Respiratory muscle
• Mental confusion or somnolence – due to arterial blood
training section) gas derangement.
s0115 Mobilizing/removing secretions
p0600 In patients with neurological disorders manual physio-
therapy techniques may be impossible due to chest wall alveolar hypoventilation include myasthenia gravis,
TS1 or spinal deformities, or osteoporosis (Haas, 2007). MND, Guillain-Barré syndrome, and muscular dystrophy.
Research in this group has focused on using mechanical Central respiratory drive is maintained in patients with
devices such as the intrapulmonary percussive ventilator neuromuscular disorders, so hypoventilation is secondary
(IPV) or high frequency chest wall oscillator/compressor to respiratory muscle weakness in these patients.
(HFCWO/C). HFCWO/C is administered via an external In the absence of significant respiratory muscle weak- p0630
device (a commercially available vest) that delivers rapid ness, it may be possible to correct hypoventilation
small compressions to the thorax and generates high through strategies such as positioning to improve dia-
flows in small airways, to mobilize secretions from smal- phragm mechanics, thoracic expansion exercises, respira-
ler airways to larger airways. Results for the use of tory muscle training or general physical exercise. In
HFCWO/C in neurological conditions have been incon- patients with significant respiratory muscle weakness,
sistent, so that although the technique is well tolerated some form of non-invasive ventilation is often recom-
and may be beneficial in some patients, it is not possible mended – see section on respiratory failure below.
to recommend its use at present. IPV vibrates the airways Box 15.5 provides the signs and symptoms of respiratory
internally, via the mouth, while the patient breathes spon- muscle weakness or fatigue. Paradoxical (inward) inspira-
taneously. Insufficient research has been conducted to tory movement of the abdominal wall signifies respiratory
judge its value in patients with neurological disorders. strength reduced to at least about 30% of normal (Polkey,
According to Haas (2007) when faced with a neurological 1999). TS2
patient with problems clearing secretions, and trying to
choose which therapy to apply, the physiotherapist Respiratory muscle training s0125
should ask four questions:
The respiratory muscles are physiologically, structurally p0635
u0355 • Is there a pathophysiological rationale for using this and biochemically similar to other skeletal muscles, and
therapy? it is therefore generally accepted that they will respond
u0360 • What is the potential for adverse effects? to appropriate strength and endurance training pro-
u0365 • What is the cost of the equipment needed? grammes in a similar manner (see Ch. 18). The contro-
u0370 • What are the patient’s preferences? versy surrounds the issue of whether an increase in
respiratory muscle strength or endurance confers any sig-
nificant health benefit. There are a number of commercial
s0120 Problem 3: Hypoventilation devices available, but as with skeletal muscle training,
p0625 Hypoventilation occurs when ventilation is reduced, so it there is a lack of consensus as to the optimal training
does not match the patient’s rate of oxygen consumption programme (i.e. load, repetitions, frequency).
and carbon dioxide production, resulting in hypercapnia. Although RMT has been studied extensively in some p0640
Hypoventilation may be secondary to several mechan- respiratory conditions, there is currently little evidence
isms, including central respiratory drive depression, neu- for use in patients with neurological conditions beyond
romuscular disorders, chest wall abnormalities, obesity spinal cord injury (SCI; see Ch. 4). According to a recent
hypoventilation and chronic obstructive pulmonary dis- systematic review by Sheel et al. (2008), there are insuffi-
ease (COPD). Neuromuscular diseases that can cause cient data to recommend the use of either exercise training

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or inspiratory muscle training for improved respiratory is essential to monitor patients regularly for signs and
function in people with SCI. From another systematic symptoms of impending failure (see Box 15.6).
review by Van Houtte et al. (2006) it was concluded that
respiratory muscle training in SCI tended to improve expi- Chronic respiratory failure s0140
ratory muscle strength, vital capacity and residual volume. Chronic respiratory failure associated with neuromuscular p0670
Insufficient data were available to make conclusions disease develops over several days or weeks and may initi-
concerning the effects on inspiratory muscle strength, ally have few symptoms. A history of fatigue, lethargy, dif-
respiratory muscle endurance, quality of life, exercise per- ficulty concentrating, poor sleep and daytime sleepiness,
formance or respiratory complications. and morning headache (indicating hypercapnia) suggest
p0645 There is some limited evidence of benefit from the use possible chronic ventilatory failure.Neuromuscular condi-
of RMT in multiple sclerosis (MS; see Ch. 5) and DMD tions in which this type of respiratory failure occurs in the
and currently a Cochrane review by Eagle and Chatwin late stages include muscular dystrophy, MND, MS, other
(2006) is underway (online protocol updated 14/01/ progressive neuropathies and myopathies, and spinal cord
2009), which aims to assess the benefit and risk of RMT injury (tetraplegia).
in children and adults with neuromuscular disease.
Management of respiratory failure s0145
The management of respiratory failure will primarily p0675
s0130 Problem 4: Respiratory failure be medical as invasive mechanical ventilation may be
s0135 Acute respiratory failure required and if the patient has impaired bulbar or upper
airway muscle function a tracheostomy is likely to be
p0650 Acute respiratory failure has many causes and develops
needed. See the section on care of the brain injured
over minutes to hours. It is characterized by changes in
patient for more information on physiotherapy during
ABGs and acid–base status and there are two types:
invasive ventilation.
u0375 • Type I or hypoxaemic respiratory failure – a PaO2 of
<8 kPa (60 mmHg) with normal or low PaCO2 Non-invasive ventilation s0150
u0380 • Type II or ventilatory/hypercapnic respiratory failure – In some institutions non-invasive ventilation (NIV) is p0680
a PaCO2 of >6.7 kPa (50 mmHg) usually managed by physiotherapists. NIV is effective in providing
accompanied by a fall in pH <7.3, in addition to intermittent, often nocturnal, support in various neuro-
hypoxaemia. muscular diseases and should be considered the standard
p0665 Guillain-Barré and myasthenia gravis account for the of care for patients with MND who develop respiratory
majority of cases of acute respiratory failure associated with muscle weakness with PImax of <60% predicted or hyper-
neuromuscular disease in the developed world (Mehta, capnia (Lechtzin, 2006). It is inappropriate for acute
2006). To avoid emergency intubation and ventilation it respiratory failure unless upper airway function is well

b0035 Box 15.6 Signs and symptoms of impending acute respiratory failure in neuromuscular disease
s0010 General warning signs Accessory muscle use
Increasing generalized weakness Abdominal paradox
Dysphagia Orthopnoea
Dysarthria Weakness of trapezius and neck muscles (inability to lift head)
Dyspnoea on exertion and at rest Single breath count* <15
Impaired gag reflex Cough after swallowing
Rapid progression of symptoms Objective assessment s0020
s0015 Subjective assessment VC<20 mL/kg or serial VC drop by 30%**
Rapid shallow breathing PImax <30 cmH2O
Tachycardia PEmax <40 cmH2O
Weak cough Nocturnal oxygen desaturation
Inability to talk in complete sentences Daytime hypercapnia (PaCO2 >6 kPa /45 mmHg)

(Adapted from Mehta, 2006.)

*Performed by asking the patient to count after a maximal inspiratory effort. Normal ¼ 50
**VC may be less reliable in myasthenia gravis due to fluctuating nature of disease

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preserved (Mehta, 2006) and therefore there is limited mmHg) and arterial oxygen saturation of greater than
evidence to support its use in Guillain-Barré or myasthe- 90%. However, use of high levels of oxygen is not recom-
nia gravis. mended and a SaO2 of 91–94% is considered optimal in
p0685 NIV can be delivered via volume limited or pressure neurosurgical patients. In patients with brain injury
limited ventilators. Volume limited units are used mainly PaO2 is believed to be less important than brain tissue
for long-term invasive ventilation. Pressure limited venti- partial pressure (PbtO2). Normal values for PbtO2 are
lators often allow the setting of both inspiratory and expi- 2.13 kPa (16 mmHg) þ/- 5.32 kPa (40 mmHg). A PbtO2
ratory pressures (i.e. bilevel). Pressures are set according <0.67 kPa (5 mmHg) is associated with severe brain
to patient tolerance, but Boitano (2006) suggests that injury and a low chance of brain survival.
‘wide-span’ bilevel airway pressure (BiPAP) support, in Hypocapnia (low CO2) is a potent cerebral vasocon- p0700
which the difference between inspiratory and expiratory strictor, effectively reducing intracranial pressure (ICP),
pressures is  10 cmH2O, most effectively augments ven- so short periods of hyperventilation to induce hypocap-
tilation. Typical pressures would, therefore, be approxi- nia to PaCO2 of 4.66 kPa (35 mmHg), and even of
mately 12–14 cmH2O for inspiration and 2–4 cmH2O 3.33 kPa (25 mmHg) may be used acutely in the treat-
for expiration. A minimal expiratory pressure is better tol- ment of increased ICP(Rozet & Domino, 2007). How-
erated by patients with neuromuscular disease provided ever, hypocapnia may exacerbate brain ischaemia in
upper airway patency remains good during sleep. A spon- patients with brain injury, although the degree of ischae-
taneous timed rate of 12–16 breaths per minute is neces- mia remains controversial. It is suggested that lowering
sary to provide back-up support during REM sleep when the PaCO2 produces vasoconstriction of the blood ves-
diaphragm weakness may preclude ability to trigger a sels, thus reducing blood flow and, ultimately, brain oxy-
breath. Interfaces vary, but nasal masks are the most com- gen delivery.
mon. Some patients with mouth weakness struggle to pre- The goals of respiratory management in brain injury p0705
vent air leakage around the mouth, in which case a chin patients are therefore to attain normocapnia and prevent
strap or full face mask may be needed. If a mask fails to hypoxia. The same physiotherapy techniques described
fit well or is too uncomfortable, a nose plug interface earlier may be used to achieve these goals in a spontane-
may be used, although this may not work as effectively. ously breathing patient, but invasive mechanical ventila-
Au4 Hess (2006) published a review of NIV equipment and tion will frequently be needed (see Box 15.7).
its application in neuromuscular disease.
p0690 A Cochrane review into the use of nocturnal ventila-
tion for hypoventilation in neuromuscular disorders
Management of brain injury patients s0160

has concluded that current evidence about any therapeu- requiring invasive ventilation
tic benefit is weak, but consistent, suggesting alleviation Care of the ventilated patient with brain injury is a com- p0710
of the symptoms of chronic hypoventilation in the short plex area, and respiratory physiotherapy will be aimed pri-
term. In three small studies survival was prolonged marily at minimizing secretion retention, maximizing
mainly in participants with MND. With the exception oxygenation, and re-expanding atelectatic lung segments.
of MND, they recommended that further larger rando- Techniques include those already described with the addi-
mized trials are needed to confirm long-term beneficial tion of more specialized techniques such as manual
effects of nocturnal mechanical ventilation on quality hyperinflation, suction and rotational therapy (see Stiller,
of life, morbidity and mortality, to assess its cost–benefit 2000 for a full description). Some patients will require a
ratio in neuromuscular and chest wall diseases and to
compare the different types and modes of ventilation
(Annane et al., 2007).
Box 15.7 Indicators of need for intubation/ b0040
ventilation in the neurosurgical patient
s0155 RESPIRATORY PHYSIOTHERAPY
• Inability to protect the airway or clear secretions
MANAGEMENT POST BRAIN INJURY • Need to reduce ICP by control of ventilation
• PaO2 <8 kPa (60 mmHg) in spite of supplemental
p0695 Respiratory dysfunction is the most frequent medical oxygen (by mask)
complication in patients with brain injury (see Ch. 3). • PaCO2 >6.67 kPa (50 mmHg), and /or pH <7.2
About 20–50% of neurosurgical patients develop pulmo- • Respiratory rate >40/minute or <10/minute
nary complications (such as aspiration of gastric contents
• Muscle fatigue
or pneumonia), which significantly worsen neurological
• Haemodynamic instability
outcome and increase mortality. In traumatic brain injury
the Brain Trauma Foundation (2000) recommends pre- (Adapted from Rozet & Domino, 2007.)
vention of hypoxia by maintaining PaO2 >8 kPa (60

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tracheostomy, the detailed management of which is physiotherapist in preventing respiratory complications

TS3 described in Jones and Moffat (2002). A tracheostomy is (rather than treating them), is less strong. The need to
a surgical procedure to create a direct airway through an avoid excessive stimulation of patients at risk of intracra-
opening in the trachea which facilitates secretion removal nial hypertension is often cited as a reason for avoiding
and protects the airway. It may be carried out for patients some techniques in these patients, but there is a lack of
requiring prolonged invasive ventilation or for patients conclusive evidence supporting the hypothesis that the
breathing spontaneously. It is therefore possible for a tra- techniques negatively impact ICP (Olson et al., 2007).
cheostomy to remain in situ after a patient has been Sogame et al. (2008) recommend daily respiratory physio-
weaned from invasive ventilation. Physiotherapists are fre- therapy and the use of a protocol to optimize early venti-
quently involved with decisions relating to timing of lator withdrawal for all ventilated neurosurgical patients.
weaning from mechanical ventilation and removal of tra- Recent guidelines for physiotherapy in the critically ill
cheostomy tubes. have been published (Gosselink et al., 2008), however
p0715 According to Olson et al. (2007) aggressive respiratory their recommendations are not specific to brain injury
care in brain injury patients who require ventilation is patients, for whom minimal handling may be best prac-
essential to promote recovery without respiratory compli- tice. When managing a brain-injured patient via mechani-
cations. However, although there is comparatively strong cal ventilation, the physiotherapist must make a clinical
evidence for physiotherapy as the treatment of choice in judgement based on the balance between potential posi-
acute lobar atelectasis, the evidence for the role of the tive and negative effects of interventions.

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