INSPIRATORY MUSCLE TRAINING

Individuals with chronic respiratory disease, for example COPD, experience inspiratory muscle dysfunction due to a combination of problems, which include hyperinflation, increased work of breathing, hypoxaemia, and hypercapnia (Laghi & Tobin 2003). Other problems that may reduce inspiratory muscle strength and endurance include corticosteroid-induced myopathy, chronic inflammation and chronic gas exchange abnormalities (Maltais et al 2000). Factors that lead to inspiratory muscle dysfunction contribute to the development of dyspnoea and to limitation of exercise tolerance (Solcher & Dechman 1998). Optimizing function through a reduction in dyspnoea is a key aim of therapy and there is now unequivocal evidence that pulmonary rehabilitation is the only treatment shown convincingly to reduce dyspnoea in chronic respiratory disease. A contributory factor in this is through training-induced improvements in aerobic capacity of the skeletal muscles, achieved through increasing mechanical efficiency and lowering blood lactate concentrations (Casaburi et al 1991, O’Donnell et al 1995). However, it is also established that whole-body exercise conditioning fails to improve respiratory muscle strength and endurance (Weiner et al 1992). As inspiratory muscle dysfunction contributes to dyspnoea in COPD, it is evident that specifically targeting the inspiratory muscles may lead to further reductions in dyspnoea (Hill et al 2004).

The inspiratory muscles, like other skeletal muscles, undergo physiological adaptations in response to training. Despite this being evident, the early literature on the use of inspiratory muscle training (IMT) in patients with COPD presented a rather mixed picture. In part this was due to the paucity of controlled clinical trials, but more importantly due to the nature of the training adopted. In general the trials were confounded by the methodology of the training in which the frequency, duration and intensity of training were less than that required to achieve a true training response, as highlighted in an early meta-analysis (Smith et al 1992). Ten years later Lotters et al (2002) published a second meta-analysis, which included only studies in which IMT was controlled in terms of fixing the intensity of IMT in order to achieve a training response. This review concluded that IMT improved respiratory muscle strength and endurance although the effects of IMT on exercise capacity remained to be determined. More recently Geddes et al (2005) published a systematic review in which IMT was shown to be effective, not only in terms of increasing inspiratory muscle strength and endurance but also in improving exercise capacity in adults with COPD. However, this review emphasized that the method of IMT employed is important if clinical benefits are to be obtained and that training of the ventilatory muscles must follow the basic principles of training for any striated muscle with regard to the intensity and duration of the stimulus, the specificity of training and the reversibility of training.

The principle of specificity of training states that the effects of training are very specific to the neural and muscular elements of overload. The overload principle states that overload must be applied to a muscle for a training response to occur (Kennedy 1995). Overload may be applied by increasing the frequency or duration of training or the intensity of the loading, or a combination of these factors. Generally, training theory suggests that inspiratory muscle strength gains can be achieved at intensities of 80–90% of maximal inspiratory pressure. Strength-endurance gains (maximal effective force that can be maintained) can be achieved at 60–80%, and endurance (the ability to continue a dynamic task for a prolonged period) at approximately 60% of peak, which equates with high-intensity training regimens used in systemic exercise (Kraemer et al 2002).

Overload may also include the concept of incremental loading. This involves decreasing the rest periods between muscle contractions (Komi & Hakkinen 1991), which has been shown to recruit a larger proportion of muscle fibres and, hence, a larger pool of fibres are trained for subsequent lower but potentially fatiguing loads (Reid & Samrai 1995, Reid et al 1994). In studies that have used the principle of high-intensity incremental IMT improvements in lung volumes, diaphragm thickness and exercise capacity have been obtained in healthy subjects and in patients with cystic fibrosis (Enright et al 2004, 2006).

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In many previous investigations training methodologies have varied to include loads imposed on the respiratory muscles which can be characterized as flow, pressure and volume loads (McCool 1992). A low-pressure high-flow load was first described in 1976 by Leith & Bradley which involves training the respiratory muscles by voluntarily ventilating at high levels for a prolonged period (usually 15 minutes). It is therefore analogous to the high ventilatory demands imposed on the inspiratory muscles during high-intensity exercise (Belman 1993). The load imposed on the inspiratory muscles requires a high flow rate at low pressure, although it is generally impractical, as it requires the assembly of complex breathing circuits in order to ensure that the individual remains normocapnic. In addition, breathless patients find this method of IMT uncomfortable to maintain and hence this method of IMT tends to be reserved for laboratory-based investigations rather than being used in a clinical setting (Scherer et al 2000). In contrast to a flow load, a high-pressure low-flow load occurs with any process that increases the transpulmonary pressure required to breathe in. These loads can be experimentally imposed by inhaling from a rigid chamber or by breathing through an external resistance. Such loads can be achieved by either resistive or threshold devices. Resistive training devices incorporate a range of apertures, which vary in size in order to apply the prescribed resistive load. Threshold devices impose a threshold or a critical inspiratory opening pressure that the subject is required to overcome before the start of an inspiratory flow. The efficacy of both these modes of IMT have been the subject of some debate, although recently it has been shown that targeted resistive IMT is as effective as threshold IMT for adults with COPD (Hsiao et al 2003). On a practical level some issues require consideration, for example targeted resistive devices provide visual feedback which enhances motivation, although ensuring that the patient is maintaining the required training intensity can be problematic. Conversely, threshold trainers provide a more constant resistance although the loss of visual feedback may result in loss of motivation.

In addition to the mode of training adopted, the frequency of training in IMT interventions, the duration of the training intervention and the issue of reversibility of training requires consideration. Standard guidelines of the American College of Sports Medicine (Kennedy 1995) suggest a training frequency of one to two times per day for a total duration of 20–30 minutes, three to five times per week for 6 weeks. However, functional improvements and adaptive cellular changes in the inspiratory muscles have been shown to occur following 5 weeks of training (Ramirez-Sarmiento et al 2002) although training must be maintained for the cellular training effects to be sustained (McArdle et al 2001). In summary, the optimal frequency of training is thought to be three times weekly, to continue beyond 4 weeks and with maintenance achieved by continuing training at one or two times weekly (Fleck 1994).

In conclusion, although there is much conflicting evidence in the literature, which has cast doubt on the place of IMT in patients with respiratory muscle dysfunction, more recent data that have incorporated the appropriate physiological training principles during IMT look promising (Geddes et al 2005). The use of targeted inspiratory resistive or threshold modes of IMT as opposed to non-targeted inspiratory resistive modes ensures that the training intensity is achieved and maintained. Thus with effective IMT regimens, exercise intolerance, dyspnoea and hypercapnic ventilatory failure may be prevented or alleviated. In addition, another indication for IMT is that weakness of the inspiratory muscles may lead to an inability to generate an adequate flow to assure lung deposition when using dry powder inhalers. Hence strengthening the inspiratory muscles may improve the efficacy of inhaled drug therapy (Weiner & Weiner 2006). These considerations are vital if IMT is to find a proven place in pulmonary rehabilitation programmes (Hill & Eastwood 2005).

INTERMITTENT POSITIVE PRESSURE BREATHING

Intermittent positive pressure breathing (IPPB) is the maintenance of a positive airway pressure throughout inspiration, with airway pressure returning to atmospheric pressure during expiration. The American Association for Respiratory Care (AARC) has developed clinical practice guidelines for the use of IPPB as a hyperinflation and aerosol delivery technique (American Association for Respiratory Care 2003). The literature on IPPB has been reviewed by Bott et al (1992) and Denehy & Berney (2001). Denehy & Berney concluded that although the use of IPPB has declined, it may still have a place in the management of patients with re-duced lung volumes. They also state that the rationale for using IPPB should be based on its known physiological effects, the availability of other treatment modalities, the condition of the patient and the current research knowledge base. The Bird ventilator (Fig. 5.56) is a pressure-cycled device convenient to use for providing IPPB as an adjunct to physiotherapy in the spontaneously breathing patient.

image

Figure 5.56 The Bird Mark 7 ventilator.

IPPB has been shown to augment tidal volume (Stiller et al 1992, Sukumalchantra et al 1965) and using an IPPB device in the completely relaxed subject, the work of breathing during inspiration approaches zero (Ayres et al 1963). These two effects support the use of IPPB to help in the clearance of bronchial secretions when more simple airway clearance techniques alone are not maximally effective, for example in the semi-comatosed patient with chronic bronchitis and sputum retention (Pavia et al 1988), the postoperative patient or in a patient with neuromuscular disease and a chest infection. The reduction in the work of breathing can be used with effect in the exhausted patient with acute severe asthma, but there is no evidence that the effect of bronchodilators delivered by IPPB is greater than from a nebulizer alone (Webber et al 1974).

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An ideal IPPB device for use with physiotherapy should be portable and have simple controls. Other important features are as follows:

Positive pressure.

The range of pressures is likely to be from 0 to 35 cmH2O.

Sensitivity.

The patient should be able to ‘trigger’ the inspiratory phase with minimal effort. Fully automatic control is unpleasant for most patients and unnecessary for physiotherapy. A hand triggering device is useful to test the ventilator and nebulizer.

Flow control.

With ventilators such as the Bird Mark 7, the inspiratory gas is delivered at a flow rate that can be preset by means of a control dial. Optimal distribution of gas to the more peripheral airways is achieved at relatively slow flow rates, but if the patient is very short of breath and has a fast respiratory rate, a slow inspiratory phase may be unacceptable. It is often useful to alter the flow control several times during a single treatment session, providing slow breaths during the periods attempting to mobilize peripheral secretions and a faster flow rate when a patient is recovering his breath after expectoration. Some Bennett positive pressure ventilators do not require flow rate adjustment because automatic variable flow is provided with each breath. This feature is known as ‘flow sensitivity’ and means that the flow of the inspired gas adapts to the resistance of the individual’s airways.

Nebulizer.

An efficient nebulizer in the circuit is necessary to humidify the driving gas and, when appropriate, to deliver bronchodilator drugs.

Air-mix control.

When driven by oxygen, air must be entrained by the apparatus to provide an air/oxygen mixture for the patient. Some Bird ventilator devices have a control that should be set to give a mixture, while others have no control but automatically entrain air. The use of 100% oxygen for a patient is very rare and when it is indicated, an IPPB device with an air-mix control will be needed. When air is not entrained through the apparatus, the flow rate control must be regulated to provide an adequate flow to the patient.

When IPPB (a Bird ventilator) is driven by oxygen and the air-mix control is in use, the percentage of oxygen delivered to the patient is approximately 45% (Starke et al 1979). This percentage will be considerably higher than the controlled percentage delivered by an appropriate Venturi mask, for example to a patient with chronic bronchitis. This higher percentage is rarely dangerous during treatment because the patient’s ventilation is assisted and the removal of secretions as a result of treatment is likely to lead subsequently to an improvement in arterial blood gas tensions (Gormezano & Branthwaite 1972).

It has been suggested that a few patients become more drowsy during or after IPPB as a result of the high percentage of oxygen received. Starke et al (1979) showed that increased drowsiness caused by hypercapnia occurred whether oxygen or air was the driving gas for IPPB and that the deterioration was dependent on inappropriate settings of the ventilator. The pressure and flow controls must be set to provide an adequate tidal volume, this being particularly important when treating patients with a rigid thoracic cage (Starke et al 1979).

Occasionally, IPPB may be powered by Entonox and in this case the air-mix control would need to be in the position to provide 100% of the driving gas with no additional air entrained.

Breathing circuit.

To prevent cross-infection it is essential for each patient to have his own breathing circuit, which consists of tubing, nebulizer, exhalation valve and a mouthpiece or mask. The majority of patients prefer to use a mouthpiece, but a facemask is required when treating confused patients. A flange mouthpiece (Fig. 5.57) is useful for patients who have difficulty making an airtight seal around the mouthpiece.

image

Figure 5.57 Flange mouthpiece for use with IPPB.

The type of breathing circuit used will depend on local infection control guidelines. The circuits can be autoclavable, non-disposable but non-autoclavable, or disposable. Many countries use single patient disposable circuits.

Preparation of the apparatus

1. Normal saline solution or the drug to be nebulized (3–4 ml in total) is inserted into the nebulizer chamber.
2. The breathing circuit is connected to the IPPB ventilator and the ventilator connected to the driving gas source. It can be used from an oxygen or air cylinder if piped compressed gas is unavailable.
3. If there is an air-mix control, this should be in the position for entrainment of air.
4. If there is an automatic control (expiratory timer) this should be turned off to allow the patient to ‘trigger’ the machine at his desired rate.
5. The sensitivity, flow and pressure controls are set appropriately for the individual. With the Bird Mark 7 the sensitivity control is usually adjusted to a low number (5–7) where minimal inspiratory effort is required. The pressure and flow controls are adjusted to provide regular assisted ventilation without discomfort. A patient with a rigid rib cage will require a higher pressure setting to obtain an adequate tidal volume than someone with a more mobile rib cage. When adjusting the settings for a new patient, it may be easiest to start with a pressure at approximately 12 cmH2O and the flow at about ‘10’, then gradually increase the pressure and reduce the flow until the pattern of breathing is the most appropriate for the individual. Some IPPB devices do not have numbered markings, but after finding the most effective settings for a patient during one treatment, it is useful to note the positions of the controls in order to use these as a starting point at the next treatment. The controls to be set on the Bennett PR-1 are the nebulizer, sensitivity and pressure.
6. Before starting a treatment, the hand triggering device is operated to check that there are no leaks in the breathing circuit and that the nebulizer is functioning well.
Treatment of the patient

The position in which IPPB is used depends on the indication for treatment. It may be used in side lying, high side lying or in the sitting position. The patient should be positioned comfortably and encouraged to relax the upper chest and shoulder girdle.

After the purpose of the IPPB treatment has been explained, the patient is asked to close his lips firmly around the mouthpiece and then to make a slight inspiratory effort, which will trigger the device into inspiratory flow. The patient should then relax throughout inspiration, allowing his lungs to be inflated. When the preset pressure is reached at the mouth the ventilator cycles into expiration; the patient should remain relaxed and let the air out quietly.

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If the patient attempts to assist inspiration there will be a delay in reaching the cycling pressure. A delay will also occur if there is a leak around the mouthpiece, at any of the circuit connections or from the patient’s nose. A nose clip may be required until the patient becomes familiar with the technique.

Observation of the manometer on the ventilator should allow detection of any faults in the patient’s technique. At the start of inspiration the needle should swing minimally to a negative pressure and then swing smoothly up to the positive pressure set, before cutting out into expiration and returning to zero. A larger negative swing at the beginning of inspiration shows that the patient is making an unnecessary effort in triggering the device. If the patient makes an active effort throughout inspiration, the needle will rise very slowly to the inspiratory set pressure and if they attempt to start expiration before the preset pressure is reached, the needle will rise sharply above the set pressure and then cut out into expiration.

When IPPB is taught correctly the work of breathing is relieved, but if the patient is allowed to assist either inspiration or expiration there may be an increase in the work of breathing.

A short pause between completion of expiration and the next inspiration avoids hyperventilation and possible dizziness. Occasionally children using IPPB tend to swallow air during treatment. It is important to observe the size of the abdomen before and during IPPB to rec-ognize signs of abdominal distension and discontinue treatment if this occurs.

When IPPB is used to relieve the work of breathing while delivering bronchodilator therapy, for example in the acute severe asthmatic patient, it is often helpful for the physiotherapist to hold the breathing circuit to allow the patient to relax the shoulders and arms as much as possible (Fig. 5.58).

image

Figure 5.58 to reduce the work of breathing during inhalation of nebulized bronchodilator.

A facemask for IPPB is used in the drowsy or confused patient and in those with facial weakness unable to make an airtight seal at the mouth. When using IPPB to assist in mobilizing secretions, the patient should be appropriately positioned to assist loosening and mobilization of secretions, for example in side lying. The patient’s jaw should be elevated and the mask held firmly over the face, ensuring an airtight fit. Chest shaking during the expiratory phase may be used to assist in mobilizing secretions. In a drowsy patient it may be necessary to stimulate coughing using nasotracheal suction if spontaneous coughing is not stimulated by IPPB and chest shaking.

In medical patients with retained secretions and poor respiratory reserve, IPPB may be useful both to mobilize secretions and to relieve the effort of breathing following expectoration. The flow control on a Bird ventilator should be adjusted to give a slow, comfortable breath to mobilize secretions, but following the exertion of expectoration there may be an increase in respiratory requirements, which may necessitate increasing the flow and possibly reducing the pressure until the breathing effort and pattern return to normal or baseline.

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IPPB may be used in patients with chest wall deformity, for example kyphoscoliosis (Sinha & Bergofsky 1972), when there is difficulty with clearing secretions during an infective episode. To achieve an adequate increase in ventilation in patients with a rigid rib cage, the pressure setting needs to be higher than for a more mobile rib cage.

Occasionally, in postoperative patients, IPPB is the adjunct of choice when the patient is unable to augment tidal volume adequately during treatment. In these patients, in contrast to the relaxed technique normally used with IPPB, thoracic expansion may be actively encouraged during the inspiratory phase.

Contraindications for IPPB

image Pneumothorax.
image Large bullae.
image Lung abscess, as the size of the air space may increase.
image Severe haemoptysis, as treatment is inappropriate until the bleeding has lessened.
image Postoperative air leak, unless the advantages of IPPB would outweigh the possibility of increasing the air leak during treatment.
image Bronchial tumour in the proximal airways. Air may flow past the tumour during inspiration and may be trapped on expiration as the airways narrow. There would be no contraindication if the tumour were situated peripherally.

MANUAL HYPERINFLATION

The technique of manual hyperinflation may be indicated to mobilize and assist clearance of excess bronchial secretions and to reinflate areas of lung collapse in the intubated patient. It is described in Chapter 8.

MANUAL THERAPY TECHNIQUES

Musculoskeletal dysfunction is common in people with respiratory disease. People with chronic cardiorespiratory disease may often demonstrate skeletal, musculoskeletal and nervous systems adaptations over time, related to the severity and management of their disease. As age increases the incidence of musculoskeletal deterioration will also increase (Parasa & Maffulli 1999). Any postural or degenerative changes are likely to have implications for physical function and quality of life as well as influencing the cardiorespiratory system.

Postural and skeletal changes occurring over time relate to the overuse of upper chest breathing patterns, lack of lower rib expansion and reduction in the more efficient pattern of diaphragmatic breathing. Chronic hyperinflation typically leads to the development of a barrel-shaped chest with an increase in the anteroposterior diameter of the chest. Pain may limit rib expansion and abdominal breathing, particularly in patients following abdominal surgery.

Secondary malalignment of the scapulae is associated with prolonged coughing using trunk flexion and the increased outward pressure on the chest wall. More sputum may mean more pain and less efficient airway clearance (Massery 2005).

In a study of 143 young adults with cystic fibrosis, Henderson and Specter (1994) found 77% of females and 36% of males over 15 years of age had a kyphosis of more than 40° (the upper limit of normal). Kyphosis tends to worsen with age and disease severity (Massie et al 1998).

The neck and shoulder girdle structures adapt to counterbalance the flexed trunk sitting position. Neutral neck and head position is compromised as the neck and head are drawn forwards by the large superficial muscle groups and hyperactivity of the suboccipital extensors. The greater the thoracic kyphosis, the more likely it is that the middle and upper cervical regions will become lordotic, as the upper cervical spine hyperextends and tilts the head upward to maintain a vertical orientation of the face.

This upper cervical spine hyperextension and forward head posture combine, with a loss of endurance of the deep cervical flexor muscles, to increase the likelihood of cervicogenic headache (Jull et al 2002, Watson & Trott 1993). Chronic headaches may also be associated with medical causes in patients with cardiorespiratory disease (Festini et al 2004, Ravilly et al 1996).

The incidence of musculoskeletal chest pain in people with cystic fibrosis tends to increase as the disease progresses. Painful stiffness in the chest may inhibit airway clearance and increase the work of breathing (Massery 2005). A decrease in muscle strength and mobility in the trunk, chest and shoulders has been demonstrated in people with cystic fibrosis (Ross et al 1987).

In the presence of an inefficient, upper chest breathing pattern, the overactive scalene muscles elevate the first and second ribs while the levator scapulae depress and rotate the lateral shoulder girdle (Fig. 5.59). Shortening of upper trapezius and tightness of pectoralis minor and major elevate and anteriorly tilt the scapulae, respectively. At the same time the antagonist and stabilizing muscles, serratus anterior and the middle and lower fibres of trapezius, lengthen and weaken, causing winging and inferior rotation of the scapulae (Sahrmann 2005). Over time the long thoracic extensors and multifidus lose their segmental stabilizing capacity and endurance, and become less able to sustain the upright sitting neutral posture.

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Figure 5.59 CJ, aged 16, cystic fibrosis. (A) Relaxed sitting posture (posterior view). Note: forward head position, tight suboccipital and mid-cervical extensors, tight upper and middle fibres of trapezius, asymmetry and abducted and protracted position of the scapulae, increased thoracic kyphosis, reduced upper lumbar lordosis, posterior rotation of pelvis. (B) Relaxed sitting posture (side view). Note: forward head position, increased sternocleidomastoid activity, increased low cervical lordosis and thoracic kyphosis, abducted and protracted scapulae, anterior position of humerus in glenoid fossa, internal rotation of humerus, lax abdominal muscles.

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The sternocleidomastoids are used excessively during coughing. Muscle fatigue related to the excess work of breathing may further accentuate poor posture in people with moderate to severe chronic lung disease. The existing kyphosis of the thoracic spine is increased due to prolonged bed rest and reductions in general exercise tolerance. Habitual slouching due to dyspnoea and feeling unwell will place more kyphotic strain on the thoracic and lumbar spines, and the lumbopelvic angle will be flexed instead of lordotic.

Vertebral intersegmental motion will be gradually lost as the chest becomes fixed in elevation and flexion. Reduced range of thoracic extension will contribute to loss of the final 30 degrees of shoulder flexion and abduction; while tightness in anterior deltoid, teres major and latissimus dorsi muscles and disturbance of normal scapulothoracic rhythm will decrease the free range of external rotation and flexion available at the glenohumeral joint. As a consequence the overstretching of infraspinatus and teres minor, associated with the internally rotated position of the humerus, may lead to poor stability of the humerus in the glenoid fossa (Fig. 5.60).

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Figure 5.60 (A) Sitting posture (posterior view) following active assisted anterior rotation of pelvis. Note: decreased mid-cervical lordosis, improved position of scapulae, reduced thoracic kyphosis, neutral rotation of pelvis and improved lumbar lordosis. (B) Sitting posture (side view) following active assisted anterior rotation of pelvis. Note: less forward head position, activation of deep cervical flexors, reduced sternocleidomastoid activity, improved scapulae and humeral position and thoracic kyphosis.

These muscular and skeletal aberrations are likely to have consequences on the range and quality of pelvic position in sitting, neck and shoulder motion, and both general and specific trunk and shoulder movement and function. In particular they cause a physical limit to the end range of shoulder elevation and an alteration in muscle recruitment likely to increase the risk of shoulder tendon impingement and wear.

Individuals with respiratory disease may complain of acute or chronic cervical, thoracic or rib joint pain, which may decrease chest expansion as measured by a reduction in vital capacity. Joint manifestations (mainly hypertrophic osteoarthropathy) are common in children with cystic fibrosis, affecting 2–8.5% of patients (Botton et al 2003, Parasa & Maffulli 1999). Back pain may be due to cystic fibrosis-related arthropy, arthritis due to coexistent conditions or drug reactions as well as the more obvious mechanical reasons. Mechanical back pain in people with cystic fibrosis has been described in the literature, but the incidence and prevalence have not been reliably established for the different age groups.

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With increasing longevity in people with cystic fibrosis, musculoskeletal changes will become more important. Decreased bone mineral density is common at all ages but further reduction tends to occur with time, increasing illness and adverse effects of medication. With an increased emphasis on encouraging general exercise to improve respiratory and general health and bone density, musculoskeletal problems may become more prevalent, requiring careful monitoring (Buntain et al 2004).

With chronic respiratory disease, fracture rates are reported to be approximately twice as high in women aged 16 to 32 years and the same increase is observed at a slightly later stage in men (Parasa & Maffulli 1999). Low bone mineral density is related to poor nutrition, reduced weight bearing, resistive muscle activity and the use of corticosteroids (Aris et al 1998, Bachrach et al 1994, Henderson & Madsen 1996). The combination of vertebral wedging, soft tissue contractures, poor posture and coughing may also cause persistent back pain in these patients (Fok et al 2002).

There is a high prevalence of acute episodes of pain in adults with cystic fibrosis (Festini et al 2004). As children with chest pain and cystic fibrosis are more likely to have a lower FEV1 per cent predicted and poorer quality of life, the assessment of musculoskeletal pain in this client group should be routine (Koh et al 2005).

Pain may restrict the ability to attain an upright posture and to use an efficient muscle pattern. Tensioning or compression of the neural tissues, as they exit from the cervical spine and proceed through the axilla, may also occur in some individuals (Butler 1991) associated with chronic overuse of the accessory muscles of respiration, elevated first rib and a depressed lateral shoulder girdle.

Subjective assessment

Assessment of those with chronic respiratory disease, or following heart or chest surgery, should include questioning regarding headache, neck, thoracic or lumbar pain and any upper limb pain or distal arm paraesthesia. The use of valid and reliable outcome measures improves evaluation of the effect of treatment. The area of pain can be recorded on a body chart and the intensity quantified using an absolute visual analogue scale (AVAS). The impact of any pain or movement restriction on activities of daily living may be assessed using a functional disability scale (e.g. Neck Disability Index (Vernon & Mior 1991), Shoulder, Arm and Hand Disability Index (Institute for Work & Health 1996) or headache questionnaire (Niere & Jerak 2004)). Individual involvement in the identification of treatment goals and expectations will enable clearer planning and prioritization. In those with dyspnoea, it will be helpful to quantify dyspnoea intensity using an AVAS or Borg scale (Pfeiffer et al 2002) before any postural correction or treatment. Questioning about the behaviour of musculoskeletal pain, during the night and in the morning, will help to clarify the degree of inflammation involved. Headache may be multifactorial in origin and may be related to upper cervical spine dysfunction or to various other physiological and biochemical changes.

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Activities that aggravate the problem may include sustained end-range postures of the neck or thoracic spine, trunk movements which require a reversal of the thoracic kyphosis or activities involving shoulder elevation. Repetitive coughing will load the costotransverse joints and may result in localized pain. Additionally, the increased abdominal pressure related to persistent cough may result in increased lumbar disc pressure and rupture, while the repetitive flexion and extension of the spine during coughing may aggravate existing cervical pathology or dysfunction.

Physical assessment: posture

Musculoskeletal assessment should proceed in a systematic manner from evaluation of posture to assessment of joint mobility, muscle recruitment patterns, muscle length, strength and endurance, keeping in mind the specific function loss or pain area and type reported. Any change in symptoms during assessment should be noted. In particular any improvement in pain when posture is modified may assist motivation to change.

In the presence of chronic respiratory disease, the physiotherapist will need to keep in mind the possibility of reduced bone density and fragile skin tissue related to age or the long-term use of systemic steroids. Pain, dyspnoea and fatigue will also need to be monitored concurrently and the assessment adjusted as necessary. The presence of wound and drain sites in the postsurgical patient may require modified assessment positions. While the assessment is ideally performed in sitting, supine and prone, examination of those with dyspnoea may need to be conducted in semi-supine, sitting or high side lying.

With the individual in relaxed sitting, the following should be noted:

1. The relaxed posture of the pelvis, lumbar, thoracic and cervical spines
2. The point of maximal curve of each of these segments
3. Whether the spinal posture is fixed or able to be corrected
4. The position of the scapulae and the location of the humeral head within the glenoid
5. The posture of the neck and head and alignment with the trunk and pelvis.

If it is possible to assist the pelvis to roll anteriorly to move the body weight on to the ischial tuberosities, note whether the thoracic kyphosis, cervical lordosis and head forward position all automatically improve (Fig. 5.60). Is the lumbosacral flexed position able to be reversed as the pelvis is assisted to roll forward? The cervical spine and the head may need to be guided to move the centre of gravity of the body over the pelvis and the head placed in a less protracted position to assess the reversibility of the resting posture. The inability to maintain this corrected position will indicate the extent of loss of endurance of the postural muscles.

Observe where the scapulae are resting and how the arms are hanging in standing and then in sitting. Usually if the position of the pelvis and spine is faulty, the scapulae will be elevated or dropped, protracted and winging with either upward or downward rotation. This ‘weak’ position of the scapulae means that stress will be transferred to the shoulder and neck joint structures during overhead activities. Arm elevation will also be weak. If the arms rest in an internally rotated position, this will interfere with smooth coordinated arm elevation and increase the risk of shoulder tendon impingement.

Physical assessment: range of motion

Total range of thoracic motion is dependent on the mobility of the apophyseal, costovertebral, costotransverse joints and ribs and in particular the extensibility of the intercostal, pectoralis and latissimus dorsi muscles. Stiffness in the upper thoracic spine may be indicated by an inability to reverse the kyphosis on request or during cervical extension and shoulder abduction. A flattened or lordotic area in the mid-thoracic region usually indicates hypomobility (Boyling & Palastanga 1994). People with chronic respiratory disease and breathlessness are often unable to lie flat during the night, due to difficulty breathing and/or persistent coughing, and the spine is not rested in extension.

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The major portion of thoracic rotation is expected to be in the middle thoracic spine (T6 to T8) (Gregersen & Lucas 1967) with lateral flexion occurring as a conjunct movement (White & Panjabi 1990). During lateral flexion the ribs should flare and spread on the contralateral side and approximate on the ipsilateral side (Boyling & Palastanga 1994).

The end-feel of normal thoracic rotation is springy due to limitation by ligamentous tissue and joint capsules. Age or postural changes at the costovertebral joints may restrict rib motion and lead to a harder end-feel (Nathan 1962). Gentle overpressure applied at end-range will assist determination of the quality of restriction, but overpressure should be used with caution if the risk of osteoporosis or existing fracture is suspected.

During spinal flexion, the inferior facets of the apophyseal joint of the superior vertebra normally glide superoanteriorly on the facets of the inferior vertebra. In extension the reverse movement occurs. Although the initial limitation to extension is from the anterior ligaments, the anterior annulus and the posterior longitudinal ligament, the normal end-feel is one of bony impingement as the inferior articular facets contact the lamina of the caudad vertebrae (White & Panjabi 1990). The mobility of the upper and middle ribs may be assessed by palpating bilaterally anteriorly and posteriorly during a deep inspiration; the lower ribs are assessed by palpating laterally during a full cycle of inspiration and expiration (Lee 2003).

The range of glenohumeral rotation will depend on the resting position of the humerus and tightness of the anterior and posterior shoulder capsule and muscles. During normal bilateral shoulder flexion and abduction the thoracic spine extends (particularly in the younger age group). Any restriction in the range of thoracic lateral flexion and rotation will limit the range of unilateral shoulder elevation (Boyling & Palastanga 1994). Shortened or overactive latissimus dorsi and teres major will add further limitation.

Observing posteriorly during shoulder elevation should enable assessment of any abnormal patterns of muscle recruitment. The upper trapezius and levator scapulae muscles, sternocleidomastoid and the scalenes tend to be overactive in people with respiratory disease while the deep upper cervical and scapular stabilizers will be underactive (Fig. 5.61). Abnormal scapulohumeral rhythm is usually most obvious as shoulder movement is initiated and then again towards the end of range. Assessing passive shoulder motion in supine (or half sitting in those with dyspnoea) will enable better differentiation between scapulohumeral and scapulo-thoracic motions. The excursion, strength and endurance of specific muscle groups identified as overactive or underactive need to be examined individually, in order to determine the relationship of movement impairment to pain and disability. Neural tissue provocation tests (Butler 1991) and tests for reflexes, power and sensation should be performed if any arm or hand pain or paraesthesia is reported. Thoracic outlet disorder may develop in the chronic respiratory disease due to the fixed and limited posture of the neck and upper body structures.

image

Figure 5.61 Shoulder abduction. Note: overactivity of upper trapezius, poor reversal of thoracic kyphosis, abducted, protracted and rotated scapulae, shortened teres major and latissimus dorsi and absence of lower trapezius activity.

Physiotherapy management

Prioritization of the main problems needs to be identified before treatment is started; the severity of musculoskeletal and cardiorespiratory dysfunction and the chronicity of the pain and disability need to be assessed. The time available and ability to perform home treatment techniques need to be considered in the choice of technique and in estimated prognosis.

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Postural correction and motor control training

Postural correction may change the breathing pattern and the intensity of dyspnoea. These factors need to be monitored carefully during treatment. As the individual becomes familiar with the gentle effort required to activate the correct muscles, oxygen consumption may be reduced. Adherence to a home exercise programme will be improved if a direct link can be demonstrated between improvement in posture and relief of pain or shortness of breath.

The ‘ideal’ posture is one where the body is positioned so that the spine, pelvic and shoulder girdle are in their neutral zone allowing the muscles to work in the most efficient manner. In the ideal posture the deep neck flexors, lower trapezius, transversus abdominus, gluteus medius and the pelvic floor will be softly activated milliseconds before the movement is begun.

Posture may be improved by educating awareness of positioning of the pelvis in sitting and the use of more efficient movement patterns using visual, auditory and sensory feedback. Postural correction utilizes motor learning with training of the holding ability of the postural stabilizers, while avoiding substitution by the stronger prime movers (White & Sahrmann 1994). The principles of motor control require frequent gentle repetition of the corrected movement or position. The initial focus should be on correcting any posterior pelvic rotation in sitting and on reducing the lumbar and thoracic kyphosis to bring the head back over the trunk. A small pillow or lumbar roll may then be used to maintain this position. If necessary, postural correction can be started in semi-supine or high side lying and then incorporated into maintenance of corrected posture during specific activities. The use of the diaphragm, abdominal and neck shoulder muscles will need to be monitored and changed if inappropriate.

Mobilization techniques

Physiotherapy management of joint restriction and pain may include passive mobilizations of cervical and thoracic apophyseal, costotransverse, costochondral and sternochondral joints and the glenohumeral joint (Bray 1994, Vibekk 1991). Manipulation is usually contraindicated. The focus of treatment will most commonly be on improving the range and quality of thoracic extension and rotation and on increasing the mobility of the ribs. Positioning during treatment will need to be carefully selected to minimize dyspnoea or pain. Specific joint restrictions may be treated with passive mobilization techniques in static positions or functional movements, and then optimally followed by active assisted or active exercises. General techniques to the upper, mid or lower regions of the spine or localized techniques to a specific vertebral level or rib can be performed in sitting, forward lean sitting or in high side lying (Lee 2003) (Figs 5.62, 5.63). Mobilization of the ribs may be performed in side lying, with the upper arm elevated to stretch the intercostal muscles or in sitting, using active shoulder abduction combined with lateral flexion. In forward lean sitting with the head and arms supported on pillows, the rib cage will be free to move during mobilization techniques.

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Figure 5.62 Mobilization of thoracic extension. Passive or active assisted, with fulcrum at T8.

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Figure 5.63 Mobilization of thoracic rotation. Passive or active assisted, with posteroanterior pressure on ribs 7 and 8.

Active or passive bilateral arm flexion and spine extension may be combined with deep inspiration and expiration to improve rib mobility. In sitting, the active extension or rotation can be performed while the therapist assists the movement to encourage an increase in range. Self-mobilizations can be performed over the back of a chair, in four-point kneel or leaning against a wall using a rolled towel for localization (Fig. 5.64). Home mobilization exercises will be necessary if the respiratory condition is chronic and the musculoskeletal dysfunction long term. A mirror, or training a family member, will assist self-treatment and provide helpful feedback.

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Figure 5.64 (A) Assisted active exercise for rotation of cervical and thoracic spine. (B) Active assisted exercise for thoracic spine extension. (C) Active exercise for thoracic spine lateral flexion and stretching of the intercostal muscles. (D) Active mobilization exercise for mid-thoracic extension. (E) Passive stretch of anterior shoulder muscles and mobilization of thoracic extension.

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Following surgery via sternotomy or thoracotomy, specific gentle passive mobilizations of the sternocostal joints or costotransverse joints may be required, if localized painful limitation of shoulder or thoracic movement or pain on breathing are present. Following thoracotomy, patients may tend to immobilize the arm on the side of the incision and need to be encouraged to move within pain limits as early as possible to reduce the risk of frozen shoulder. The scapula may be taken through its range of protraction, retraction, elevation and depression while the patient is in side lying. Bilateral arm movements are preferred in the early stage following surgery, initially avoiding abduction and external rotation to reduce stress on the scar.

The long-term ventilated patient may also develop musculoskeletal problems. Routine passive mobilization of the shoulder through its full range of flexion, external rotation and abduction should be mandatory. Lateral flexion and extension of the thoracic spine can be performed via arm elevation when in side lying. Gentle passive rotation of the thoracic spine can also be performed in this position with the upper arm resting on the lateral chest wall.

Muscle-lengthening techniques

Stretching of tight muscle groups may precede or accompany endurance training of the lengthened muscle groups (Janda 1994). Stretching of the anterior deltoid and pectoralis major muscles, using a proprioceptive neuromuscular facilitation hold–relax technique, has been shown to increase vital capacity and shoulder range of movement (Putt & Paratz 1996). Other muscles that may require careful stretching are: sternocleidomastoid, the scalenes, upper and middle fibres of trapezius, levator scapulae, pectoralis minor, teres major, latissimus dorsi, subscapularis and the suboccipital extensors (Table 5.2). Sustained stretches may be facilitated by conscious or reflex relaxation of the muscle during exhalation. Hold–relax techniques using the agonist or contract-relax techniques using the antagonist of the shortened muscle (White & Sahrmann 1994) may augment sustained stretches and myofascial release massage along the line of the muscle fibres. Where possible, individuals should be taught to perform their own stretches and mobilizations as part of long-term maintenance.

Table 5.2 Assessment of muscle length

Muscle Observation if muscle tight Length testing position
Pectoralis major Internal rotation and anterior translation of the humerus Horizontal extension and abduction to 140°
Pectoralis minor Anterior and inferior position of coracoid process and elevation of ribs 3–5 Retraction and depression of scapula
Upper cervical extensors Forward position of head on neck, increased upper cervical lordosis Flexion of the head on the upper cervical spine
Upper trapezius Elevation of scapula, palpable anterior border of trapezius (occiput to distal clavicle) Cervical flexion with contralateral lateral flexion and ipsilateral rotation
Levator scapula Increased muscle bulk anterior to upper trapezius and posterior to sternocleidomastoid from C2–4 to superior angle of scapula Cervical flexion, contralateral lateral flexion and contralateral rotation, keeping the medial superior scapula border depressed
Sternocleidomastoid Forward position of head on neck, elevated 1st rib and prominence at the clavicular insertion of sternocleidomastoid Upper cervical flexion with lower cervical extension
Anterior scalenes Elevation of ribs 1–3, ipsilateral lateral flexion of head on neck Exhalation with depression of ribs 1–3 and upper cervical flexion
Latissimus dorsi Internal rotation of humerus Elevation of shoulder in external rotation with posterior pelvic tilt
Teres major Medial rotation of humerus, protracted and upward rotation of scapula Flex shoulder while sustaining scapular retraction and depression
Diaphragm Flexed thorax and localized lordosis at the thoracolumbar junction Relaxed diaphragmatic breathing
Taping

Taping of the scapula in a more neutral position, or of the thoracic spine in a reduced kyphosis, may temporarily unload the affected tissue to gain pain relief and facilitate healing. It will also provide a feeling as to which posture will assist pain reduction of the thoracic kyphosis and what may need to be assisted until the holding capacity of the thoracic extensors and lower fibres of trapezius has been improved. Strapping tape (over anti-allergy tape), applied in the corrected sitting, may give proprioceptive feedback in the early stages of retraining. It is important to ensure comfort and that cervical motion is freer following taping. Appropriate warnings and instructions regarding removal of the tape should be given.

There are many different approaches to taping. A long piece of tape starting anteriorly above the clavicle and crossing the mid-fibres of trapezius may inhibit overactivity of this muscle. The tape is then crossed over at the peak of the thoracic kyphosis and extended down to the lumbar spine if necessary. It should not be so firm that pain is produced or neural symptoms provoked. A horizontal tape to lift the lateral edge of the acromion and a tape around the inferior border of the scapula to facilitate serratus anterior action may both help. Tape under the axilla to lift the scapula and relieve neural tension may also assist pain reduction, but care needs to be taken with the sensitive skin of the axilla. All taping should be designed and applied related to the individual’s specific and individual needs. Retesting range of motion and pain on aggravating movements will allow direct appraisal of the effectiveness of taping. Warnings regarding possible skin reaction and pain provocation should be given.

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Muscle retraining (strength and endurance)

Training of scapular retraction and depression using middle and lower fibres of trapezius is important to complement any gain in range of thoracic extension and to improve scapular stability (Fig. 5.65). The holding capacity of the deep upper cervical flexors and cervicothoracic extensors will need to be trained to reduce the degree of forward head posture and to assist relaxation of sternocleidomastoid and the scalene muscles (Table 5.3). The longus colli and rectus capitus anterior major may be trained initially in high sitting, then progressed to supine if shortness of breath allows (Fig. 5.66). Alternatively, gentle nodding of the head on neck against slight self-applied resistance using the thumb can be taught in sitting. The serratus anterior action of holding the scapula against the chest wall will be improved with training using a half push-up action against a wall (taking care that upper trapezius is not overactive) (O’Leary et al 2007).

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Figure 5.65 (A) Active scapulae retraction/depression (rhomboids, middle and lower trapezius). (B) Active scapulae retraction/depression in shoulder elevation. (C) Active scapulae retraction/depression in shoulder extension.

Table 5.3 Assessment of holding capacity of lengthened muscles

Muscle Test position
Deep upper cervical flexors Half supine, nodding of head on neck. Test holding ability
Middle and lower trapezius With patient prone (or sitting if short of breath), test holding ability by placing scapula in retraction and depression and asking patient to hold
Serratus anterior Note ability to maintain scapula against chest wall during a partial push-up against a wall
Infraspinatus Test strength of external rotation
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Figure 5.66 Position for training activation of deep upper cervical flexors and lower trapezius and for stretching of upper cervical extensors and pectoralis minor and major.

A gym ball may be useful for encouraging a more upright sitting posture in younger clients. Prone positions over the ball may be used to stimulate the antigravity muscles. Side lying over the ball will assist with rib mobility and stretching of the intercostal muscles if mobility and shortness of breath allow. Thera-Band® can be used to apply resistance to weak motion and to give more specific directional feedback.

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Neural tissue techniques

When neural tissue provocation tests reveal irritation or restriction, the primary aim of treatment will be to mobilize the tight adjacent structures and improve posture to reduce load on the sensitive tissues. The effect on the neural system should be monitored during and after treatment. If progress is inadequate, gentle mobilization (not stretching) of the neural tissues at the site of restriction may be required.

Summary

People with chronic respiratory disease may have postural dysfunction and musculoskeletal pathology in addition to their cardiothoracic disease. Early identification of disability and musculoskeletal limitations will provide the physiotherapist with the opportunity to teach preventative strategies and enable early, more effective intervention. Postural awareness and education with a home mobilizing and strengthening programme may be usefully included in a holistic home programme.

Clinical research is required to evaluate whether the musculoskeletal complications described in this section can be prevented or minimized by an early intervention programme, and whether improving the function of the musculoskeletal system has a positive effect on respiratory function.

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NEUROPHYSIOLOGICAL FACILITATION OF RESPIRATION

The respiration of mammals involves a ventilatory system in which the essential part, the lung, effects exchange between the surrounding air and the blood. Even though this organ is richly supplied with nerves, it does not have an autonomous function. It undertakes this task by the conjoint action of two elements, the rib cage and the diaphragm, which form the chamber enclosing it (Duron & Rose 1997).

Breathing is a complex behaviour. It is governed by a variety of regulating mechanisms under the control of large parts of the central nervous system. Ongoing research into the respiratory ventilatory system (rib cage and diaphragm) has dramatically altered traditional understanding of the respiratory muscles and their neural control. The motor synergy of respiration includes the major and accessory respiratory muscles and motoneuron pools from the level of the fifth cranial nerve down to the upper lumbar segments (Euler 1986).

Respiratory rhythmicity, as with other rhythmical repetitive motor actions (i.e. locomotion and mastication), is supported in the central nervous system by a central pattern generator (CPG). CPGs are neuronal networks capable of generating the characteristic rhythmic patterns in the complete absence of extrinsic reflexes and feedback loops (Atwood & MacKay 1989, Euler 1986, Gordon 1991). However, in order to adapt the ventilatory system to prevailing and anticipated needs and to achieve coordination with the cardiovascular system, breathing is regulated by a multitude of reflexes, negative feedback circuits and feedforward mechanisms (Ainsworth l997, Euler 1986, Koepchen et al 1986).

The purpose of this discussion is to assist the integration of evidence from biological research with clinical practice and to consider the implications of models of respiratory neural control for clinical work. Much biological research now validates empirical practices of earlier years. For example, research into the function of the abdominal muscles now supports empirical practices of the 1940s and 1950s, when abdominal supports were used to assist those with emphysema (Alvarez et al 1981, De Troyer 1997, Grassino 1974). The present models of the neural control of respiration, with their emphasis on the roles of spinal neurons and on the importance of afferent (sensory) input, provide further biological support for neurophysiological facilitation procedures, i.e. clinical use of selective afferent input in respiratory care.

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Neurophysiological facilitation of respiration is the use of selective external proprioceptive and tactile stimuli that produce reflexive movement responses in the ventilatory apparatus to assist respiration. The responses they elicit appear to alter the rate and depth of breathing and can be demonstrated to occur in other mammals (dogs) as well as in humans (Bethune 1975, 1976). These procedures are particularly useful in the chest care of the unconscious patient and of the conscious postsurgical patient who frequently find that the reflexive nature of the respiratory movements reduces the perception of pain (Bethune 1991).

Neural control

Research on ventilatory muscle control presently places considerable emphasis on spinal respiratory motoneurons and their controlling or modifying influence on central respiratory programmes. One of the newer theoretical models of the functional organization of the neural control of breathing identifies three major central nervous system levels: suprabulbar mechanisms, bulbar mechanisms and spinal motoneuron pools and integrating mechanisms (Euler 1986) (Fig. 5.67).

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Figure 5.67 Functional organization of neural control of breathing.

(Modified from Euler 1986)

Based on a similar model, Miller et al (1997) have considered the many neural structures that can potentially modify the final output of the ventilatory muscles. Input from peripheral sensory structures (proprioceptive, cutaneous, vagal and chemoceptive) and from a variety of brain regions (cerebral cortex, pons, cerebellum and others) is all integrated in the premotor bulbospinal respiratory neurons. Adjustments to the respiratory control of these multifunctional muscles occurs in order to support their many non-respiratory behaviours including speech, swallowing, coughing, vomiting. The motoneuron pools that drive these multifunctional ventilatory muscles are subjected to changes in activity pattern due to their control by the neuronal networks, recruited on the basis of the different incoming stimuli. The spinal respiratory motoneurons are the final common pathway. They determine the output of the major respiratory muscles including their ‘rhythmic breath-by-breath respiratory drive’. The actions of the ventilatory apparatus only during eupneic respiration (normal easy breathing) will be discussed.

Breathing in all mammalian species depends on a bilateral neuronal respiratory network within the lower brainstem, which generates three neural phases: inspiration, post-inspiration and expiration. Inspiration involves augmenting activity in the inspiratory nerves and muscles. The post-inspiratory phase represents declining activity in the inspiratory nerves (early expiration). During late or active expiration the expiratory nerves and muscles exhibit augmenting activity which ends abruptly at the next inspiration. All phase activities are generated without the need for peripheral feedback. Although classical studies proposed a hierarchical organization of various ‘centres’ in the pons and medulla, studies have revealed that supramedullary structures are not essential for the maintenance of respiratory rhythm. Respiratory neurons in the rostral pons, previously known as the ‘pneumotaxic center’ controlling respiratory rhythm, are not necessary for rhythm generation. These pontine neurons are now thought to stabilize the respiratory pattern, slow the rhythm and influence timing. Efferent axons from the medullary neurons project to the inspiratory neurons in the spinal cord (Atwood & MacKay 1989, Bianchi & Pasaro 1997, Richler et al 1997).

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The origin of the respiratory rhythm remains unclear as precise knowledge of all possible interactions among neurons in the respiratory network is incomplete.

‘Respiratory drive is regulated by information from sensory receptors within the airway, lungs and respiratory muscles, as well as central and peripheral chemoceptors’

(Frazier et al 1997)

Proprioceptive information arising from respiratory muscles may regulate the motor activity through long loop reflexes that include the medullary respiratory centres. Proprioceptive information through segmental and intersegmental loops at the spinal level may also influence the motor activity. Although complex spinal circuitry exists for modulating diaphragmatic activity through large and small phrenic afferents, proprioceptive regulation of phrenic motoneurons seems weak or absent. Afferent information from the lower intercostals and the abdominal muscles (T9–10) may facilitate phrenic motoneurons by a spinal reflex. Emerging evidence suggests that phrenic afferents are more involved in respiratory regulation during stressed breathing (Frazier et al 1997, Hilaire & Monteau 1997). There are apparent differences between the neural mechanisms controlling the diaphragm and those controlling the thoracic muscles. While phrenic motoneurons appear mainly under medullary control and seem insensitive to proprioception, thoracic respiratory neurons seem to receive respiratory drive mainly via a network of thoracic interneurons.

Respiratory muscles

The diaphragm

The diaphragm is the major inspiratory muscle in humans. Current understanding of its action suggests that it does not expand the entire chest wall, as previously proposed. Actions of the diaphragm are being investigated with more attention being paid to the direction of the muscle fibres that compose it and the insertional and ‘appositional’ forces that are generated. The insertional forces are the result of muscular attachments. The appositional force is that pleural pressure that develops on the inner aspect of the lower ribs between the ribs and the diaphragm where the diaphragmatic fibres, that are directed cranially, are in direct contact with the rib cage (De Troyer 1997).

Diaphragmatic muscle fibres originate from three major sites: the xiphisternal junction, the costal margin of the lower rib cage and the transverse processes of the lumbar vertebrae. All fibres insert into the central tendon. Thus, the orientation of these fibres differs. For example, midcostal diaphragmatic muscle fibres are perpendicular to midsternal and midcrural fibres. In humans, diaphragmatic muscle fibres have tendinous insertions within the muscle and do not traverse the full length of the muscle from origin to insertion, as in some smaller animals. Therefore, the mechanical action of these fibres is complex, depending on relationships imposed by the specific attachments and the loads imposed by the rib cage and abdominal wall.

Older literature raised the possibility that there might be motor innervation of some parts of the diaphragm from intercostal nerves. It is now clear that the only innervation is the phrenic nerve via the phrenic motoneurons originating in the third, fourth and fifth segments of the cervical cord in humans. Animal studies have demonstrated that the diaphragm is somatotopically innervated. In the cat, C5 innervates the ventral portions of both costal and crural diaphragmatic fibres, while their dorsal portions are innervated by C6. Studies in other animals have produced similar data. The compartmentalization related to these innervation patterns and the further sub-compartmentalization of motor unit territories within these areas ‘provide the potential for differential control’ of different regions of diaphragmatic muscle. The differences between the diaphragmatic fibres from the three sites of origin have prompted some investigators to suggest that the crural portion is a separate muscle, under separate neuromotor control (Sieck & Prakash 1997). The crural portion has no costal attachment. Crural fibres surrounding the oesophagus may be under separate neural control in order to act as a sphincter. Detailed histochemical studies have demonstrated other differences between fibres from the three originating sites. A recognized uniqueness of the diaphragm is that it has few muscle spindles. When they are present, they are found primarily in the crural portion (Agostoni & Sant’ Ambrogio 1970, Sieck & Prakash 1997).

Studies of isolated diaphragmatic contractions, examined by electrical stimulation of the phrenic nerve in dogs, demonstrated that while the lower ribs moved cranially and the cross-sectional area of the lower rib cage increased, the upper ribs moved caudally and the cross-sectional area of the upper rib cage decreased. Similar results have been obtained in human subjects with phrenic nerve pacing following traumatic transaction of the upper cord and during spontaneous breathing in subjects with transaction of the lower cord, who use the diaphragm exclusively. In seated humans (as in the dog) the diaphragm has both an expiratory action on the upper rib cage and an inspiratory action on the lower rib cage, which increases in its transverse diameter.

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It has been established that the inspiratory action of the diaphragm on the rib cage is due in part to the insertional force of its attachment to the lower ribs. During inspiration the muscle fibres of the diaphragm shorten and the dome descends relative to the costal insertions of the muscle. The descent of the dome, which remains relatively constant in size and shape during breathing, expands the thorax vertically, resulting in a fall in pleural pressure. The descent also displaces abdominal viscera caudally, increasing abdominal pressure, which pushes the abdominal wall outwards. The diaphragmatic fibres inserting on the upper borders of the lower six ribs also apply a force on these ribs when they contract. This force equals the force exerted on the central tendon. If the abdominal viscera effectively oppose the diaphragmatic descent, the lower ribs are lifted and rotated outwards.

The inspiratory force of the diaphragm is also related to its apposition to the rib cage. This is best explained in the words of De Troyer (1997):

‘The zone of apposition makes the lower rib cage in effect part of the abdominal container and measurements in dogs have established that during breathing the changes in pressure in the pleural recess between the apposed diaphragm and the rib cage are almost equal to the changes in abdominal pressure. Pressure in the pleural recess rises, rather than falls during inspiration, thus indicating that the rise in abdominal pressure is truly transmitted through the apposed diaphragm to expand the lower rib cage’

The inspiratory efficiency of the insertional and appositional forces is largely dependent on the resistance the abdominal viscera provide to diaphragmatic descent. If the resistance of the abdominal contents was eliminated, the zone of apposition would disappear during inspiration and the contracting diaphragmatic muscle would become oriented transversely at their attachments onto the ribs. In this case, the insertional force would have an expiratory action on the lower ribs. These studies reinforce the view of Goldman (1974) that abdominal muscle contraction, commonly associated only with an expiratory action, appears to have an important role in defending diaphragmatic length during inspiration.

The intercostal muscles

The place of the intercostal muscles has been more difficult to establish. Conventional wisdom regards the external intercostals as inspiratory in function, elevating the ribs, and the internal intercostals as expiratory in function, depressing the ribs. This theory was based on geometric considerations proposed in 1848 (the Hamberger theory) and it has been challenged since 1867, when electrical stimulation of the intercostal muscles was undertaken for the first time. These latter studies suggested that the external and internal intercostal muscles were synergistic in action. The Hamberger theory is regarded as being incomplete. Its theoretical model is planar but real ribs are curved. Therefore, the changes in length of the intercostal muscles (i.e. their mechanical advantage) vary with respect to the position of the muscle fibres along the rib. Also, the Hamberger theory assumed that all ribs rotate by equal amounts around parallel axes. The radii of curvature of the different ribs are different (Duron & Rose 1997).

Histological and electrophysiological studies have disclosed that the rib cage is non-homogeneous. It has motor components that vary with their location in the upper or lower thorax. In addition, each intercostal can be functionally different depending on its position in the same intercostal space (Gray 1973). It is now generally accepted that most of the external intercostal muscles do not participate in the ventilatory process during quiet breathing (De Troyer 1997, Duron & Rose 1997). Unlike the diaphragm, the intercostal muscles also have a postural function. Detailed studies of the respiratory and postural actions of the intercostal muscles have revealed functional differences from segment to segment and between external and internal intercostal muscles within the same segment. The major place of each intercostal muscle in postural activity and/or respiratory cycles has yet to be established. Nevertheless, Duron & Rose (1997) reviewed extensive studies in animal and human subjects and report precise distributions of inspiratory and expiratory activity. A summary of their findings follows:

1. In addition to the diaphragm, the inspiratory muscles active during normal breathing are the ventral intercartilaginous part of the intercostal muscles and the dorsal levator costae muscle.
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2. The lateral part of the external and internal intercostal muscles of the upper rib spaces are synergistic muscles. They often have a postural type of activity. Their motoneurons may be activated by the central inspiratory drive; thus they may participate in respiration.
3. In the four lowest intercostal spaces, the lateral parts of the external and internal intercostal muscles are also synergistic. The lateral part of the internal intercostal is active in expiration during quiet breathing. The lateral part of the external intercostal is also expiratory but only during dyspnoea, similar to abdominal expiratory action.
4. The lateral part of the intercostal muscles are antagonistic in the 5th–8th intercostal spaces. The external intercostals are inspiratory and the internal intercostals are expiratory.
5. In every intercostal space the dorsal part of the external (inspiratory) and the dorsal part of the internal (expiratory) muscles are antagonistic during quiet breathing.
6. All intercostal muscles of the lateral part of the rib cage participate in posture. There appears to be a clear distinction between the dorsal and ventral part of each intercostal space from which phasic respiratory activities are always recorded and the lateral part of each intercostal space where tonic postural activities are observed.

The insertions of both the external and internal intercostal muscles suggest that their orientation would assist rotation of the thorax. Indeed, electromyographical (EMG) studies on normal human subjects have demonstrated that external intercostals on the right were activated when the torso was rotated to the left, but silent when the torso was rotated to the right. On the other hand, the internal intercostals on the right were only active when the torso was rotated to the right. The abundance of muscle spindles and the preponderance of type I (slow) muscle fibres in intercostal muscles are consistent with postural activity. Eighty-five percent of external intercostal muscle fibres in dogs are type 1, a percentage that is higher than that of antigravity limb muscles.

Accessory muscles of inspiration

The scalene muscles in humans have traditionally been considered as accessory inspiratory muscles. However, EMG studies have established that scalene muscles invariably contract with the diaphragm and parasternal intercostals during inspiration. No clinical situation exists in which paralysis of all inspiratory muscles occurs without also affecting the scalene muscles, so it is impossible to accurately define the isolated action of these muscles on the human rib cage. Observations on quadriplegic patients have demonstrated that persistent inspiratory action in scalene muscles is observed in those subjects with a spinal transection at C7 or lower that preserves scalene innervation. In these situations the anteroposterior diameter of the rib cage remains constant or increases, as opposed to the inward displacement of the upper rib cage when the level of transection interferes with scalene innervation (De Troyer 1997). Accessory muscles of the neck assist thoracic respiration by stabilizing the upper rib cage. This is a minor function in normal persons at rest. These muscles become more active during exercise and in the presence of diseases such as asthma and chronic obstructive pulmonary disease. Generally, neck and upper airway muscles have a higher proportion of fast muscle fibres, faster isometric contraction times and lower fatigue resistance than the diaphragm (Lunteren & Dick 1997).

Many other muscles can elevate the ribs when they contract and are therefore truly ‘accessory’ muscles of inspiration. These are muscles running between the head and the rib cage, shoulder girdle and rib cage, spine and shoulder girdle. Such muscles as the sternocleidomastoid, pectoralis minor, trapezius, serrati and erector spinae are primarily postural in function. They are active in respiration in healthy humans only during increased respiratory effort. Of these accessory muscles, only the sternocleidomastoids have been extensively studied. In patients with transection of the upper cord causing paralysis of the diaphragm, intercostals, scalene and abdominal muscles, the sternocleidomastoids (innervation cranial nerve 11) contract forcefully during unassisted inspiration, causing a large increase in the expansion of the upper rib cage but an inspiratory decrease in the transverse diameter of the lower rib cage (De Troyer 1997).

The abdominal muscles

The four muscles of the ventrolateral wall of the abdomen, the rectus abdominis, the external oblique, the internal oblique and the transversus abdominis, have significant respiratory function in humans. The fibres in each of these muscles assume a direction different from each other; consequently, the mechanical action of an abdominal muscle contraction depends on fibre direction and the concurrent action of the other abdominal muscles. Added to this complexity is the fact that the force generated by the abdominal wall is applied to a load that is determined by viscous and non-linear elastic resistances. The capacity of the abdominal wall to function adequately varies markedly among individuals and correlates well with an individual’s activity level, gender, corpulence and age.

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Abdominal muscle fibres are similar to those of other skeletal muscle. Differences in fibre composition between them are minor. Generally speaking, type 1 (slow) muscle fibres predominate. Bishop (1997) reports that although details of the morphology of abdominal motor units are not known and information on the number and distribution of muscle proprioceptors (muscle spindles and tendon organs) in abdominal muscle is scarce, proprioceptive feedback is recognized as an important modulator of abdominal motoneuron excitability. Electrically evoked reflexes studied in cats under the conditions of bilateral rhizotomy of the lumbar segments or C6 spinal cord transection, demonstrated that both segmental feedback and supraspinal signals control abdominal motoneurons. Furthermore, studies on the phasic and tonic abdominal stretch reflexes suggest a special functional significance for the gamma-spindle loop. Normal individuals, when standing, develop tonic abdominal muscle activity unrelated to respiratory phases.

Many brain regions can modify abdominal motoneuron output via multiple descending pathways. Spinal abdominal motoneurons receive strong projections from the brainstem. However, brainstem and spinal abdominal motoneurons receive direct and indirect projections from the premotor cortex, the motor cortex, the cerebellum, the hypothalamus, the pons and many other regions of the brain. The voluntary control over the abdominal muscles via the motor cortex is very similar to control by the cortex over muscles of the limbs and digits.

The respiratory action of the abdominal muscles is first to contract and pull the abdominal wall inward and so increase abdominal pressure. This pressure causes the diaphragm to move upwards into the thoracic cavity, which in turn results in an increase in pleural pressure and a decrease in lung volume. The abdominal muscles also displace the rib cage. By virtue of their insertions on the ribs, it would appear that the action of the abdominal muscles is to pull the lower ribs caudally and thus deflate the rib cage in another expiratory action. However, experiments in dogs have shown that these muscles also have an inspiratory action. Because of the large zone where the diaphragm is directly apposed to the rib cage, the rise in abdominal pressure due to abdominal muscle contraction is transmitted to the lower rib cage. In addition, the rise in abdominal pressure forcing the diaphragm cranially and the consecutive increase in passive diaphragmatic tension also tend to raise the lower ribs and expand the lower rib cage (insertional force of the diaphragm). Regardless of their actions on the ribs, the abdominal muscles are primarily expiratory muscles through their actions on the diaphragm and the lung.

Neurophysiological facilitatory stimuli

The proprioceptive and tactile stimuli selected produce remarkably consistent reflexive responses in the ventilatory muscles. Inspiratory expansion of the ribs, increased epigastric excursion, visibly increased and often palpably increased tone in the abdominal muscles and change in the respiratory rate (usually slower) are among the responses observed. In the clinical setting these res-ponses are often accompanied by involuntary coughing, changes in breath sounds on auscultation, rapid return of mechanical chest wall stability, less necessity for suctioning, a more normal respiratory pattern and retention of the improved breathing pattern for some time after the treatment period. In some unconscious patients there is an apparent increase in the level of consciousness (more reaction to other stimuli). These effects appear to be cumulative. Successive application of the stimuli elicits faster responses and longer retention of the altered pattern. The changes noted during treatment application are frequently dramatic. The responses are most pronounced in the most deeply unconscious. The facilitatory stimuli are:

image intercostal stretch
image vertebral pressure to the upper thoracic spine
image vertebral pressure to the lower thoracic spine
image anterior-stretch lift of the posterior basal area
image moderate manual pressure
image perioral pressure
image abdominal co-contraction.

The foregoing discussion of neural control models, with the emphasis on the importance of afferent input and the place of spinal motoneurons, indicates that the majority of the responses to these stimuli are mediated by muscle stretch receptors via dorsal roots and intersegmental reflexes (Table 5.4).

Table 5.4 Neurophysiological facilitation for the chest

image
Intercostal stretch (Fig. 5.68A)

Intercostal stretch is provided by applying pressure to the upper border of a rib in a direction that will widen the intercostal space above it. The pressure should be applied in a downward direction, not pushing inward into the patient. The application of the stretch is timed with an exhalation and the stretched position is then maintained as the patient continues to breathe in his usual manner. As the stretch is maintained, a gradual increase in inspiratory movements in and around the area being stretched occurs. This may be done as a uni- lateral or bilateral procedure. It should not be performed on fractured or floating ribs. Care must be exercised around sensitive mammary tissue in females. When performed over areas of instability, as in the presence of paradoxical movement of the upper rib cage or over areas of decreased mobility, this procedure is effective in restoring normal breathing patterns. Epigastric excursions can be observed if intercostal stretch is performed over the lower ribs, but above the floating ribs. This may represent the reflexive activation of the diaphragm by the intercostal afferents that innervate its margins.

image

Figure 5.68 (A) Intercostal stretch: pressure down towards the next rib, not ‘in’ towards the patient’s back. (B) Vertebral pressure (i) over T2, 3, 4, (ii) T9, 10, 11. (C) Lifting posterior basal area. (D) Perioral stimulation: moderate pressure on top lip (the airway should not be occluded). (E) Co-contraction of abdominal muscles: pressure over lower ribs and pelvic bone.

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Vertebral pressure (Fig. 5.68B)

Firm pressure applied directly over the vertebrae of the upper and lower thoracic cage activates the dorsal intercostal muscles. Pressure should be applied with an open hand for comfort and must be firm enough to provide some (intrafusal) stretch. For this reason it is easier to apply when the patient is supine, as in the supine position it is not necessary to stabilize the body and one may also observe the patient’s reactions. Afferent input that activates the dorsal intercostal muscles is consistent with the observations of Duron & Rose (1997) that in every intercostal space the dorsal part of the external (inspiratory) and the dorsal part of the internal (expiratory) intercostal muscles are antagonistic during quiet breathing.

Firm pressure over the uppermost thoracic vertebrae results in increased epigastric excursions in the presence of a relaxed abdominal wall. Pressure over the lower thoracic vertebrae results in increased inspiratory movements of the apical thorax. These responses correlate with the observations of Helen Coombs (1918) who demonstrated that section of the thoracic roots diminished costal respiration. She stated:

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‘If the spinal roots are cut in the thoracic region alone there is diminution of costal respiration although abdominal respiration remains unaltered and the rate is very little changed: if the cervical dorsal roots are also involved, independent costal respiration disappears ‘

In 1930, in research with kittens, Coombs and Pike said:

‘… when dorsal roots of spinal nerves are divided in the thoracic region, costal respiration in kittens from birth to ten days old almost ceases … when dorsal roots of cervical nerves are sectioned, the thoracic nerves being intact, the movements of the diaphragm are much cut down and the respiratory rate is slower at no matter what age’

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There is little to be found in the literature defining intersegmental respiratory reflexes. Sieck & Prakash (1997) noted that phrenic motoneurons do not receive a major excitatory input from muscle spindle afferents. However, they recognize that there are extrasegmental reflexes that affect phrenic motoneuron activation. Group I and II afferents from intercostal nerves have been shown to exert both inhibitory and facilitatory influences on phrenic nerve activity.

Anterior-stretch basal lift (Fig. 5.68C)

This procedure is performed by placing the hands under the ribs of the supine patient and lifting gently upwards. The lift is maintained and provides a maintained stretch and pressure posteriorly and an anterior stretch as well. This may be done bilaterally if the patient is small enough. If this is not possible or necessary, it should also be effective when performed unilaterally. As the lift is sustained, stretch is maintained and increasing movement of the ribs in a lateral and posterior direction can be seen and felt. Increased epigastric movements also often become obvious. The lift to the back places some stretch on the dorsal intercostal area and should also stretch the spaces between some of the mid-thoracic ribs (5–8). These are both areas where the intercostal muscles are considered to be antagonistic in action. The epigastric movements suggest that the diaphragm is being activated by intercostal afferents.

Maintained manual pressure

When firm contact of the open hand(s) is maintained over an area in which expansion is desired, gradual increasing excursion of the ribs under the contact will be felt. This is a useful procedure to obtain expansion in any situation where pain is present; for instance, when there are chest tubes or after cardiac surgery which may have required splitting of the sternum. Manual contact over the posterior chest wall is also useful and comfortable for persons with chronic obstructive pulmonary disease. The inspiratory response is thought to be due to cutaneous tactile receptors. The contact should be firm so that it does not tickle.

In 1963 Sumi studied hair, tactile and pressure receptors in the cat and reported thoracic cutaneous fields for both inspiratory and expiratory motoneurons. He proposed that since the excitatory skin fields for inspiratory motoneurons were more extensive than those for expiratory motoneurons, more inspiratory motoneurons could be excited by a single skin stimulus. Local cutaneous stimulation of the thoracic region would then tend to reflexly produce an inspiratory position of the rib cage. Duron & Bars (1986) also studied thoracic cutaneous stimulation in the cat. They directly electrically stimulated desheathed lateral cutaneous nerves in anaesthetized decerebrate cats and cats that were both decerebrate and spinal. Among their findings was widespread inhibition on both inspiratory and expiratory activity after stimulation of the cutaneous nerve. Their observations also suggested that responses from the upper and lower thoracic areas were different. They acknowledge that the place of each of the different cutaneous afferent components needs to be identified.

Perioral pressure (Fig. 5.68D)

Perioral stimulation is provided by applying firm maintained pressure to the patient’s top lip, being careful not to occlude the nasal passage. (The use of surgical gloves is advised to avoid contamination.) The response to this stimulus is a brief (approximately 5 second) period of apnoea followed by increased epigastric excursions. The initial response may frequently be observed as a large maintained epigastric swell. Pressure is maintained for the length of time the therapist wishes the patient to breathe in the activated pattern. As the stimulus is maintained the epigastric excursions may increase so that movement is transmitted to the upper chest and the patient appears to be deep breathing. Respiratory rate is usually slower. The patient may sigh on initiation of the procedure or some time after the response has become established.

The paucity of muscle spindles in the diaphragm determines that phrenic motoneurons which provide its motor activation do not receive any significant excitatory input from muscle spindle afferents and there are few, if any, gamma motoneurons in the phrenic motor nucleus (Sieck & Prakash 1997). Information regarding afferent facilitation of phrenic motoneurons and/or other reflex interactions influencing their excitability is sparse. The responses that are observed on application of this stimulus correlate very well with the work of Peiper (1963).

When this perioral stimulus is applied to the unconscious patient if the mouth is open, it will close. Swallowing is noted and sucking movements are often evident even in the presence of oral airways. Swallowing and sucking may not be evident initially, but may appear in the more deeply unconscious after re-peated stimulation. Occasionally such a patient has been observed to push pursed lips forward in a ‘mouth phenomenon’ or ‘lip phenomenon’ or ‘snout phenomenon’. These observations are similar to observations made by Peiper (1963) while studying the neurology of respiration and the neurology of food intake and the relationship between sucking, swallowing and breathing in infants. The ‘mouth’ or ‘lip’ or ‘snout phenomenon’ has been reported by Peiper and other investigators, as a reflex response to gentle tapping on the upper lip noted in young normal infants and in adults with severe cerebral disorders. Movement of the lips, sucking, swallowing and chewing motions have been reported on stroking the lips of comatose adults and are thought to be related to infantile rooting reflexes.

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Peiper observed that three centrally directed rhythmic movements arise during an infant’s food intake: sucking, breathing and swallowing. Earlier experiments on young animals had established that there was a sucking centre located bilaterally in the medulla. Peiper established the dominance of the sucking centre over respiration. Infants can breathe while they nurse, partly due to the high position of the larynx. The initiation of sucking was observed to immediately disturb respiration. There was initial lowering of the diaphragm for 5 seconds or more before respirations began at a new rhythm led by the sucking centre. When the sucking movements ceased, the respiratory movements continued in the new pattern for a period (in this instance, faster rhythm). The similarity between the observations recorded by Peiper and those observed in response to the perioral stimulus suggests that these phenomena are related. The stimulus on the top lip is thought to imitate, in part, the pressure of the mother’s breast against the lips of a nursing infant. The lack of recent recorded material would seem to indicate that the investigation into sucking centres per se has not been pursued much further. The related activity of swallowing has been investigated, especially with respect to its interactions with respiration.

Swallowing is a complex behaviour. Although it is one of the most elaborate of motor functions in humans, swallowing is a primitive reflex with implications of a stereotyped and fixed behaviour (Jean et al 1997). In most mammals, including humans, all the muscles concerned with swallowing are striated. Similar to respiration, swallowing is considered an autonomic function, but is governed by the same neural principles as those serving some somatic functions, such as locomotion. Great differences among species are observed concerning swallowing during the respiratory cycle. Most of the significant data were obtained from sheep. The oropharynx serves both deglutition and respiration. Several muscles in the mouth, pharynx and larynx are active to ensure the patency of the upper airways and to regulate the airflow during the respiratory cycle. In humans, swallows occur mainly during expiration. When the swallowing rhythm is regular, one swallow occurs for every one or few breaths. A brief minor inspiration called a ‘swallow breath’ (‘Schluckatmung’ by pioneer investigators) occurs at the onset of swallowing. The functional significance of this brief inspiration is not known.

The central pattern generator (CPG) for swallowing is located in the medulla in two main groups of neurons in two regions that also contain respiratory neurons. The mechanisms that generate its rhythms are not understood. The factors regulating the functional interactions between swallowing and respiration have yet to be determined. Margaret Rood (1973) taught the use of perioral stimulation to reduce spastic muscle tone. She believed that it induced a parasympathetic bias (as opposed to a sympathetic bias) and that it promoted general relaxation. It was a prerequisite for her light, moving touch facilitation procedure to activate limb muscles. Rood’s treatment focus and patient population probably accounts for her lack of awareness of the respiratory responses to this stimulus.

Co-contraction of the abdomen (Fig. 5.68E)

Rood (1973) taught co-contraction of the abdomen as a procedure to facilitate respiration. Pressure is applied simultaneously over the patient’s lower lateral ribs and over the ilium in a direction at right angles to the patient. Moderate force is applied and maintained. Rood believed that this procedure increased tone in the abdominal muscles and also activated the diaphragm. She proposed that the pressure directed across the abdomen produced intrafusal stretch, thus activating the muscle spindles (mainly in the rectus). She thought that the side contralateral to the pressure reacted first. As those muscles responded to the stretch and shortened, they would stretch the intrafusal fibres of the opposite muscles, which in turn would activate their homonymous extrafusal muscles, which would contract, shorten and stretch the first set again and so the cycle would be repeated. A series of alternating contractions was thought to occur as long as the pressure was maintained. Co-contraction of the abdomen should be performed bilaterally with pressure applied alternately and maintained for some seconds on either side. The maintained pressure is repeated as necessary to obtain and maintain the response for the desired period.

In practice, activation of the abdominal muscles does not always occur in the contralateral side first. There can be considerable variation in individual responses. Pre-existing muscle tone, corpulence, postoperative status and the integrity of the abdominal wall are some of the influencing factors. Lax abdominal muscles (for any reason) appear to respond more slowly. If activation is slow, it is often helpful to observe the umbilicus, which may exhibit changes in its movement pattern, becoming more depressed on exhalations before changes in the muscles can be detected.

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This is an effective procedure. As pressure is maintained, increasing abdominal tone can be both seen and palpated. In the presence of retained secretions abdominal co-contractions may produce coughing more readily than the other procedures. As ventilation increases with any procedure, coughing may occur. In obese patients abdominal co-contraction has frequently resulted in decreased abdominal girth.

Clinical application

In the clinical setting auscultation and standard chest assessment should be undertaken before, during and after treatment. Ventilatory movement patterns should be noted. Is chest expansion simultaneous and equal? Are there paradoxical movements or any areas of indrawing on inspiration? The therapist must be aware of the patterns of ventilation and how they are changing. Since the patient’s response determines the duration of treatment, assessment is critical. The procedure of choice is continued until the desired treatment effect has been achieved, whether increased breath sounds, cough or stabilized respiratory pattern. Many patients raise secretions and cough. (Advice given to therapists was frequently ‘co-contract and duck’.) Unconscious patients need assistance to get rid of their secretions, but suctioning may not be required as often or as deeply. Some unconscious patients appear to become less obtunded. Eyelids may flutter, eyes may open or there may be spontaneous movements. Sometimes, such a patient will initially turn the head away or push the therapist’s hand away. These are positive signs as these patients are often thought to be unresponsive.

Responses to the facilitatory procedures are individual reactions and therefore every patient will not demonstrate the same level of responsiveness to each procedure. It is not necessary to do each procedure with every patient, but it is imperative to observe the individual response and modify treatment accordingly. Treatment should not be continued in the presence of an undesirable response. Anecdotally a dramatic example of an undesirable response was observed in a decerebrate patient who was so hypertonic that abdominal co-contractions applied in the supine position began to elevate him into a sitting position. Such a res-ponse necessitates the use of other procedures. Conscious medical patients often appreciate the sense of relaxation and the lack of a sense of effort when facilitation procedures are used in their care. Many perform their own perioral stimulation. Acute and chronic neurological conditions such as amyotrophic lateral sclerosis, Guillain–Barré, cerebral vascular accidents and others may also be treated with these procedures and derive benefit.

OXYGEN THERAPY

Oxygen therapy is indicated for many patients with hypoxaemia. The physiotherapist frequently treats patients requiring added inspired oxygen and may be involved with the setting up of oxygen therapy equipment. Oxygen is a drug and should be prescribed. The delivery device, flow rate, concentration, frequency and duration should be documented on the patient’s drug chart (Dodd et al 2000, Thiagamoorthy et al 2000). It should be monitored using arterial blood gas analysis or oxygen saturation (SpO2) recordings. When measuring SpO2 recordings only, it must be remembered that an increase in PaO2 may be associated with an increase in PaCO2, but any rise in PaCO2 will be difficult to detect. If a patient is dependent on continuous oxygen therapy the mask should be removed only briefly for expectoration, eating and drinking and sometimes during these periods it may be appropriate to continue oxygen therapy using nasal cannulae.

Devices for administering oxygen therapy may be divided into fixed and variable performance devices (Hinds & Watson 1996):

A variable performance device supplies a flow of oxy-gen that is less than the patient’s minute volume. The inspired oxygen concentration (FiO2) will vary with the rate and volume of breath and considerable variations between and within subjects have been demonstrated (Bazuaye et al 1992). Commonly used variable performance devices are the simple facemask (Fig. 5.69A) and nasal cannulae (Fig. 5.69B). Nasal cannulae are often preferred as the patient can eat, drink and speak more comfortably and may find them less claustrophobic than a mask. Although high flows of oxygen can be delivered via nasal cannulae, 1–4 l/min (approximately 24–36%) is optimal in terms of patient comfort. Higher flows, up to 6 l/min, tend to irritate and dry the nasal mucosa, but this may be alleviated by including a bubble-through humidifier in the circuit. However, humidification via narrow-bore tubing is not the most effective means of humidifying dry inspired gas (Campbell et al 1988). Nasal cannulae should be used with caution with very breathless hypoxic patients, as they are likely to be breathing through the mouth and not benefiting from nasal oxygen. Wide variations in inspired oxygen concentration have been shown to be produced by variable performance devices, even with the recommended flows (Jeffrey & Warren 1992).

image

Figure 5.69 Oxygen delivery devices: (A) Variable performance mask. (B) Nasal cannulae. (C) Fixed performance Venturi mask. (Intersurgical)

A fixed performance device should be used when accurate delivery of oxygen concentrations is required, especially at low concentrations. This will deliver a known inspired oxygen concentration (FiO2) by providing a sufficiently high flow of premixed gas that should exceed the patient’s peak inspiratory flow rate. A Venturi system allows a relatively low flow of oxygen to entrain a large volume of air and the mixed gas is conveyed to the facemask (Fig. 5.69C). With a 24% Venturi mask the usual setting of 2 l/min flow of oxygen will entrain approximately 50 l/min of air, giving a total flow of approximately 52 l/min. An extremely breathless patient, with a greatly increased work of breathing and high peak inspiratory flow rate, may find this flow too low and then it is necessary to increase the flow to exceed the inspiratory flow of the patient (Hill et al 1984). The manufacturer should provide information for each mask (e.g. a 24% mask run at 3 l/min may augment the total flow to 78 l/min without changing the oxygen concentration). It is not easy to measure the critically ill patient’s peak inspiratory flow, but by careful observation the physiotherapist should be able to tell if the total flow is sufficient. If gas can be felt flowing out through the holes and around the edges of the mask during inspiration, the flow will be exceeding the patient’s requirements.

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For most patients using a Venturi mask, the entrained room air provides sufficient humidification, but occasionally additional humidification is indicated. A bubble-through humidifier attached to the narrow-bore tubing of a Venturi mask is inappropriate as the flow of oxygen is likely to be reduced by the back pressure from the humidifier device and by condensation blocking the narrow-bore tubing.

When high concentrations of oxygen, at high flows, are required, a high-flow variable FiO2 generator can be used. The gas flows along wide-bore tubing from the generator across an appropriate heated humidifier to the facemask. It is essential to have an oxygen analyser in the circuit. Oxygen concentrations between 35% and 100% can be delivered at flows of up to 130 l/min. High-flow oxygen should be considered when patients requiring oxygen concentrations greater than or equal to 40% are not responding to a fixed-performance device.

Nebulizers for the delivery of drugs in hospital are frequently powered by piped oxygen but in the patient dependent on his hypoxic drive to breathe, air should be used as the driving gas. Occasionally in the severely hypoxic patient, who is also hypercapnic and dependent on a controlled 24% oxygen mask, it is important not to deprive the patient of this added oxygen while using a nebulizer. The level of oxygen entrained to maintain the baseline oxygen saturation can be monitored using an oximeter.

For most patients an intermittent positive pressure breathing device (IPPB) should be driven by compressed oxygen. Starke et al (1979) demonstrated that in hypercapnic patients oxygen can be used as the driving gas. In hypoxic patients without hypercapnia, for example in acute asthma, oxygen is required and it may be dangerous to use air alone as the driving gas for IPPB.

Long-term oxygen therapy

Long-term oxygen therapy (LTOT) has been shown to improve the length and quality of life in selected patients with severe chronic airflow limitation (Medical Research Council Working Party 1981, Nocturnal Oxygen Therapy Trial Group 1980). Clinical guidelines for the prescribing of domiciliary oxygen have been established (Royal College of Physicians 1999) and three main forms of home oxygen services have developed (Wedzicha & Calverley 2006):

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1. LTOT for patients with chronic hypoxaemia (PaO2 = 7.3 kPa (55 mmHg) for continuous use at home.
2. Ambulatory oxygen therapy for oxygen therapy using a portable device during exercise and daily activities.
3. Short-burst oxygen therapy for the intermittent use of oxygen at home for periods of 10–20 minutes at a time, to relieve the symptom of breathlessness. There is little evidence for the benefit of short-burst oxygen therapy.

A Cochrane Review (Ram & Wedzicha 2002) looked at the effectiveness of long-term ambulatory oxygen therapy and concluded that it was not possible to determine whether patients on long-term oxygen therapy should be provided with ambulatory oxygen during exercise and for activities of daily living. Bradley & O’Neill (2005) looked at the effects of short-term ambulatory oxygen. They concluded that there was strong evidence that short-term ambulatory oxygen improves exercise capacity.

Ambulatory and training oxygen have been discussed in the review by Young (2005) and ambulatory oxygen, assessment and practical considerations for physiotherapists have been outlined by O’Neill & Dodd (2006).

Oxygen supply

For domiciliary provision, patients should be assessed to determine the flow rate and concentration for short- burst, ambulatory or long-term oxygen therapy use. There are three sources of oxygen: compressed gas cylinders, oxygen concentrators and liquid reservoirs.

Compressed gas cylinder (Weg & Haas 1998). Large cylinders can provide oxygen for up to 57 hours at a flow of 2 l/min and flows up to 15 l/min can be attained. Small, portable oxygen cylinders can be used for short trips outside the home and either carried or transported on a lightweight trolley.

Oxygen concentrator. This is a convenient and efficient means of providing oxygen therapy in the home, in the presence of a reliable supply of electricity. The concentrator filters and concentrates oxygen molecules from ambient air, generating flows of 3 to 8 l/min, but the fraction of oxygen in the inspired gas (FiO2) will decrease as the flow increases (Weg & Haas 1998). Oxygen tubing can be fitted in areas of the home to allow for mobility, but a maximum length of 50 feet (15.25 metres) has been recommended (DeVilbiss Oxygen Services 2000). A back-up compressed gas cylinder is necessary for emergency use. Humidifiers are sometimes fitted to oxygen concentrators, but care must be taken as these are a potential source of infection (Pendleton et al 1991).

Liquid oxygen reservoir. This will provide oxygen for 5 to 7 days at 2 l/min and can be used to fill small portable units (Weg & Haas 1998). The portable units are lightweight, convenient and may improve compliance with treatment (Lock et al 1992, Wurtemberger & Hutter 2000).

In an attempt to give patients, dependent on oxygen, greater mobility and the opportunity to participate in activities outside the home, an inspiratory phased delivery system or oxygen by transtracheal catheter may be considered (Shneerson 1992). A microcatheter inserted into the trachea will reduce the dead space and decrease the requirement for oxygen. Some patients find this more cosmetically acceptable than nasal cannulae, but there is the increased possibility of infection.

Acknowledgement

For many of the figures in this chapter, we are indebted to the Photographic Department of the Royal Marsden Hospital, Ella Thorpe-Beeston, Matthew Thorpe-Beeston, Daniel Wallis, Catherine Sandsund, Barbara Webber and the Intensive Care Unit, Royal Brompton Hospital. We are also grateful to Catherine Sandsund for her help with the section on incentive spirometry.

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