Mary Massery & Lawrence P. Cahalin
INTRODUCTION
The physical therapy examinations and interventions presented in this chapter focus on the patient with cardiopulmonary dysfunction fitting the model of preferred Practice Pattern 6E: Impaired Ventilation and Respiration/Gas Exchange Associated with Ventilatory Pump Dysfunction or Failure.1 In the first edition of the Guide to Physical Therapy Practice in 1997,2 this pattern was separated into two different practice patterns to distinguish ventilatory pump dysfunction (PPP 6F) from ventilatory pump failure (PPP 6H). However, the main difference between the dysfunction and the failure is the severity and/or acuity of the dysfunction; thus, it is more appropriate that they be grouped into one practice pattern. In this way, particular levels of impairment or function may be used to specifically distinguish ventilatory pump dysfunction from ventilatory pump failure using identifiable characteristics within a continuum of ventilatory pump function. As we shall see, several specific patient characteristics can be used to distinguish ventilatory pump dysfunction from failure that will enable more specific and appropriate physical therapy interventions.
VENTILATORY PUMP DYSFUNCTION
Ventilatory pump dysfunction can be caused by a wide variety of pathologies and impairments. Identifying the primary pathology or impairments is critical to the physical therapist for planning and implementing an effective intervention plan. In the Guide, four broad categories of pathologies and impairments were identified to help the physical therapist categorize their patient’s primary impairment pattern.1 These pathology and impairment categories are (1) musculoskeletal, (2) neuromuscular, (3) cardiopulmonary, and (4) integumentary. Practice Pattern 6E would include patients who frequently come from the cardiopulmonary impairment category and may include patients with a number of different primary pulmonary disorders such as asthma, emphysema, chronic bronchitis, and restrictive lung disease, among others. In other words, if the lung disorder causes a patient to work harder than a normal person for their next breath, then the ventilatory pump will be impaired secondary to the lung disorder.1 The primary goal of the physical therapist should be to identify the degree of impairment and functional capacity, regardless of the pathology.
Ventilatory pump dysfunction can originate from any of the other pathology and impairment categories (musculoskeletal, neuromuscular, cardiopulmonary, or integumentary). These pathologies and impairments are listed under the “Patient/Clients Diagnostic Classification” section of each practice pattern.1 For example, “severe kyphoscoliosis” is listed under Pattern 6E as a cause for ventilatory pump dysfunction. Why? Because, pump dysfunction will occur where there is a restriction to the mobility of the chest wall and/or spine (ie, with arthritis, scoliosis, kyphosis, traumas). The resultant restriction will decrease the efficiency and/or the potential for optimal function of the ventilatory muscle pump.
Likewise, patients with “neuromuscular disorders” are also listed as patients with potential ventilatory pump dysfunction. Neurologic disease or trauma can affect the strength and motor control of the trunk as well as the respiratory muscles, which may cause ventilatory pump dysfunction (ie, spinal cord injury, brain injuries, cerebral palsy, multiple sclerosis, or Parkinson disease).
Last, patients with integumentary disorders, in whom the movement of skin or other connective tissue over the spine, rib cage, and proximal extremity joints (such as the upper extremities, lower extremities, or neck) is limited, may also present with ventilatory pump dysfunction. Patients with burns and connective tissue disorders may have such a ventilatory pump dysfunction. Thus, simply because the practice pattern states that the problem is “ventilatory pump dysfunction,” the cause of that dysfunction may not initially stem from the cardiopulmonary system (Table 20-1).
TABLE 20-1 Impairment Categories from the Guide to PT Practice: A Sampling of Diagnoses Associated with Ventilatory Pump Dysfunction or Failure Originating from That Category
VENTILATORY PUMP FAILURE
Ventilatory pump failure occurs when the demands placed on the ventilatory muscles prevents adequate ventilation and respiration. Ventilatory pump failure is commonly diagnosed by an elevation in partial pressure of carbon dioxide (PCO2) and reduction in partial pressure of oxygen, arterial (PaO2). Ventilation is also reduced.
Ventilatory pump failure can result from abnormal lung tissue or poor ventilatory muscle performance. Abnormal lung tissue from a variety of lung disorders may impose a significant workload on the ventilatory muscles that along with poor ventilation and respiration may eventually cause them to fail. It has been suggested that ventilatory pump failure can be recognized by a paradoxical breathing pattern. There are several different paradoxical breathing patterns, and the paradoxical breathing pattern most often associated with ventilatory pump failure (and likely most often observed) is an abdominal paradoxical breathing pattern that is seen in patients with severe chronic obstructive pulmonary disease (COPD). The patient with neuromuscular pathology will often show a different paradoxical pattern where the belly rises and the chest falls (upper chest paradoxical breathing).
The effects of severe COPD and hyperinflated lungs as well as limited diaphragmatic excursion appear to produce a less efficient diaphragmatic descent during breathing. The inefficient diaphragmatic descent and subsequent ineffective ventilation of the lungs stimulate the accessory muscles of breathing to play a more active role in breathing. As such, patients often exhibit a breathing pattern that is characterized by an inward movement of the abdomen and outward movement of the upper chest during inspiration rather than by the normal breathing pattern of simultaneous outward movements of the abdomen and upper chest during inspiration.
FACTORS ASSOCIATED WITH NORMAL AND PARADOXICAL BREATHING
Two factors that appear to be associated with development of an abdominal paradoxical breathing are hyperinflation of the lungs and the subsequent flattening of the diaphragm. The flattening of the diaphragm is likely to produce two specific changes including (1) a greater use of accessory muscles for inspiration and (2) an inward pull on the lower ribs when the flattened and shortened costal diaphragmatic muscle fibers contract with a different angle of inclination. The greater use of the accessory muscles generates a negative pressure in the upper chest area rather than the normal generation of negative pressure in the abdominal area from the downward descent of the diaphragm. If the diaphragm is unable to generate adequate negative intrathoracic pressure, the abdominal area may actually be sucked in from the negative pressure generated in the upper chest area (producing an abdominal paradox) from the increased activity of the accessory muscles.
Under normal conditions, the muscles of the diaphragm contract and pull the central tendon and the dome of the diaphragm caudally. The descending diaphragm increases the volume of the thorax. According to Boyle’s law, the increased volume in the thorax decreases the intrathoracic pressure, which facilitates inspiration. These particular changes are shown in Fig. 20-1. It is important to note that the biomechanical changes occurring as a result of increased intra-abdominal pressure (letters a and b in Fig. 20-1) are due to specific changes in the costal diaphragmatic fibers upon the inner aspect of the lower rib cage (the zone of apposition). The costal diaphragmatic fibers at the lower rib cage within this zone of apposition produce (1) a cranially oriented force on the lower ribs, (2) outward motion of the lower ribs, and (3) separation of the lower ribs, as the abdominal viscera (with adequate abdominal muscle support) opposes the descent of the diaphragmatic dome.
FIGURE 20-1 Biomechanics of breathing.
Hyperinflation of the lungs and flattening of the diaphragm shorten the muscle fibers of the diaphragm providing it (1) little to no room to descend downward, (2) an inadequate length–tension relationship, and (3) less activity at the zone of apposition. The aforementioned changes may result in the development of inadequate intrathoracic pressure in the abdominal area and inadequate ventilation of the lungs. As a result, the accessory muscles become more active and generate the needed negative pressure to ventilate the lungs. Therefore, the pump handle motion of the upper chest referred to in Fig. 19-1 may become greater than the bucket handle motion of the lower ribs, resulting in a paradoxical breathing pattern.
In the same manner, excessive bucket handle motion with accompanying lack of structural support in the upper chest may produce an upper chest paradoxical breathing pattern that is characterized by an inward motion of the upper chest and profound outward motion of the abdominal area. Such a breathing pattern is occasionally seen in patients with spinal cord injury or other neurological disorders. It appears to be less often associated with ventilatory pump failure, but may contribute to ventilatory pump failure if the inward upper chest motion is excessive and contributes to an increased work of breathing and decreased degree of lung ventilation.
It is hopefully apparent from these examples that the topic of ventilatory pump dysfunction and failure is so extensive that it would be impossible to discuss every possible patient scenario. Hence, this chapter will focus on one case at length to illustrate cardiopulmonary preferred Practice Pattern 6E. The case presented is the result of a neuromuscular disorder, an SCI, and is the patient case presented in Chapter 18. Why is a spinal cord injury a good example for Pattern 6E? Following an SCI, the mechanics of breathing are compromised because of the weakness and paralysis of the chest wall muscles, thus impairing the ventilatory pump. In fact, these impairments can be so significant that respiratory problems have consistently been identified as the major cause of death in America for this population.3–5 Therefore, a patient with an SCI shows both ventilatory pump dysfunction and the potential for pump failure. This chapter will follow a patient with a cervical SCI who was first described in the acute phase of injury in Chapter 19 (Practice Pattern 6F). He will be used to illustrate the cardiopulmonary risks, examinations, and interventions associated with patients who have ventilatory pump dysfunction.
MICROANATOMY AND PHYSIOLOGY
The biomechanics of breathing were described in detail in Chapters 4, 5, and 9 and will now be reviewed in respect to the musculoskeletal support that is necessary to prevent ventilatory pump dysfunction. Following this review of both inhalation and exhalation, the case study introduced in Chapter 19 will be presented with emphasis on the biomechanics of breathing following an SCI.
Normal Skeletal Support for Breathing
The rib cage is an inherently mobile structure designed to move three-dimensionally, freely, and efficiently via skeletal support from the thoracic spine and muscle support from the respiratory and postural muscles.6–10 Without muscle support, the skeletal structure of the rib cage would collapse anteriorly, particularly in an upright posture. This would occur because the only significant stabilization of the thoracic cage is derived from its posterior attachment to the thoracic spine through the costotransverse ligaments. This leaves the anterior chest wall particularly vulnerable to external forces. The costotransverse ligaments, 3 per spinal segment, are aligned in three different planes of movements and overlap the thoracic segment above and below them (see Chapter 4). This provides a very stable posterior junction, limiting chest wall movements and making dislocations or subluxations of the costotransverse joints a rare event (rib shaft fractures are far more common than rib shaft dislocations). On the other hand, the anterior chest wall is attached only to the sternum, which has no inferior bony attachment and superiorly is only attached to the clavicle. This provides little structural support, but maximizes mobility potential. In fact, the lowest rib segments, ribs 8 to 12, are often called “false ribs” because they do not insert into the sternum at all (ribs 10–12), or they insert into the sternum via the seventh rib’s cartilage (ribs 8–10), giving these rib segments even greater potential for mobility than ribs 1 to 7.
Clinically, we see these skeletal facts played out when a therapist examines a patient’s breathing pattern. The therapist will find greater anterior chest movement and less posterior chest movement during inhalation. Hence, the rib cage’s structural support significantly influences breathing in the anterior and posterior chest (see Chapter 9).
Normal Muscle Support for Breathing: A “Triad” of Support for Inhalation
How do the muscles of the trunk allow optimal mechanical alignment of the thoracic cage and thoracic spine in stationary, static postures while still allowing the active movements of breathing and dynamic trunk movements? Here we will discuss the most significant muscle groups involved in the dual role of providing trunk stability and trunk/respiratory movement.
Recall that the diaphragm is the major muscle of inspiration. Add to that, the importance of two other muscles, the intercostals and the abdominal, which provide the proper pressure support necessary for the diaphragm to move optimally and efficiently, creating a “triad of muscles” for optimal quiet breathing (Table 20-2). The diaphragm provides the greatest volume displacement, whereas the intercostal muscles stabilize the chest wall, and the abdominal muscles provide visceral support for the descending fibers of the diaphragm’s central tendon.11 This results in an increase in circumferential expansion of the chest which is noted as a “positive” chest wall expansion measurement when assessed with a tape measure during inspiration (see Chapter 9).12,13
TABLE 20-2 Muscle Support Necessary for Optimal Inspiratory Function: A “Triad” of Support
The contraction of the diaphragm initiates the inhalation phase by essentially creating a vacuum, a negative inspiratory force (NIF), within the chest cavity. The NIF facilitates the movement of air from the atmosphere (positive pressure) into the lungs (now a negative pressure system). Air in the atmosphere rushes into the lungs because of the development of this area of negative pressure during inspiration (movement from a high-pressure to low-pressure area is common in this and many other similar pressure systems). This creates positive pressure within the lungs and chest cavity and therefore forces air out during exhalation. Without the active participation of the intercostal muscles to lift the upper chest upward and outward, the anterior chest wall would collapse inward during inhalation, toward the negative pressure.14–16 This abnormal type of breathing pattern is called an upper chest paradoxical breathing pattern and is characterized by the excessive rising of the abdomen and the simultaneous collapse of the anterior rib cage. Frequently this collapse is seen near the junction of the xiphoid process and the corresponding ribs because without the intercostal muscle’s support, this area of the chest wall has the greatest potential mobility and the least anatomical stability. Clinically, this is seen in patients with spinal cord injury and may result in the development of a pectus excavatum, otherwise known as a concave deformity along the lower sternum.
The importance of the stabilizing function of the intercostal and abdominal muscles was noted while taking chest wall expansion measurements of patients with complete cervical SCIs.13 While measuring inspiratory expansion at the xiphoid process in supine, every patient in the study demonstrated paradoxical or inward movements of the upper chest. Measurements with a tape measure revealed negative upper chest wall movements of one-fourth in or more of upper chest wall depression during inspiration. The expected positive upper chest wall expansion of resting (or quiet) inspiration did not occur and was replaced with an inward paradoxical motion of the upper chest. The reason that this was observed was likely due to a lack of intercostal muscle contraction that left the upper chest unsupported during inspiration. As the descending diaphragm created greater negative pressure, the upper chest simply fell into the vacuum created by the descending diaphragm.
Worse yet, when the patients were asked to take a deep breath (or vital capacity breathing), creating an even greater negative inspiratory pressure, the inward paradoxical movement of the upper chest wall became more severe with as much as two in of depression in many of the patients. Can patients with SCI generate the kind of negative pressure gradients that would cause a collapse of the rib cage? Yes. As long as their diaphragm remains functional, patients with SCI can still generate significant negative inspiratory mouth pressures (PImax). A study by Gounden17 found that patients with cervical SCI could generate a mean PImax of −65 cmH2O (see Chapter 9 for normal values and methods of measuring PImax; normal PImax for this patient population was between −75 and −100 cm H2O). Thus, patients must have adequate function of the intercostal muscles to support the negative inspiratory pressures necessary for effective breathing strategies.
The last muscle group in the normal triad of breathing is the abdominal muscles. These muscles provide positive-pressure support on the viscera in order to maintain their placement up and under the dome of the diaphragm in upright postures. The abdominal muscles also provide positive-pressure support for the diaphragm to help stabilize the central tendon during the initial phase of inhalation. Without functional abdominal muscles, the abdominal contents will rest too low in the abdominal cavity in upright positions and produce a classic “beer belly” appearance which is frequently seen in patients with spinal cord injury (Fig. 20-2A). The lack of abdominal muscle support and lower resting position of the abdominal contents places the diaphragm’s resting position very low in the thoracic cavity which reduces its length–tension relationship and mechanical efficiency. In addition, without abdominal muscle support (as in spinal cord injury), the central tendon of a descending diaphragm moves excessively in an inferior plane because of the absence of positive abdominal pressure. This excessive movement in the inferior plane produces paradoxical breathing characterized by greater lower abdominal protrusion and simultaneous flattening of the upper abdominal wall.16,18 This paradoxical breathing pattern is also referred to as “belly breathing” (see Chapter 9). This paradoxical breathing can be reversed, or at least minimized by the use of an abdominal binder in upright.19 Finally, a classic study by McCool20 showed that providing a “substitute” abdominal muscle support through the use of an abdominal binder for patients with tetraplegia resulted in greater total lung capacity and greater chest wall excursion than that without the binding.
FIGURE 20-2 (A) Typical posture of a patient with cervical spinal cord injury in sitting. Lee demonstrates inadequate muscle strength to mechanically hold the trunk and vertebrae in proper alignment. Note the appearance of a “beer belly,” protracted scapulae, internally rotated shoulders, and a mid-trunk fold between the ribs and abdomen. (B) Use of a towel roll as a temporary seating position adjunct: placed vertically along thoracic and lumbar spine to provide posterior mechanical stabilization. (C) Note the improvement in trunk alignment compared to “A”: expansion of anterior chest wall, shoulder external rotation, scapular retraction towards neutral, and a reduced mid-trunk fold between ribs and viscera. Lee would also benefit from an abdominal binder to support the viscera.
Abdominal muscle support also appears necessary to provide the stimulation to activate the intercostal muscles during normal chest wall development in the first 12 months of life.21 If the child is hypotonic, that is, congenital hypotonia, Down Syndrome, and so forth, the diaphragm will continue to move primarily in an inferior plane as a newborn does, rather than recruiting its peripheral fibers and the intercostals at around 6 months of age. This results in a similar muscle imbalance as seen in adult patients with weak or paralyzed intercostals, but the resultant chest wall deformities (usually a pectus excavatum, rib flares, and concave anterior ribs around ribs 6–8) tend to be more extreme in the child. The irony is that the child may actually have innervation to the intercostal musculature but was never given the correct environmental cues to stimulate his or her development.
For all of the previously cited reasons, the primary muscles of inspiration appear to exist as a “triad” of coordinated muscle contractions among the diaphragm, intercostals, and abdominals, rather than as a sole diaphragmatic contraction.22–24 Together, these muscles support the function and efficiency of the inspiratory effort in both normal quiet breathing and vital capacity maneuvers.25 Other muscles assist in ventilation and are referred to as “accessory muscles of ventilation.” A summary of the most significant accessory muscles is listed on Table 20-3.
TABLE 20-3 Significant Accessory Muscles of Ventilation
Examples of Inspiratory Pump Dysfunction
What happens to the ventilatory pump when the muscles of the trunk can no longer support an ideal skeletal alignment to facilitate proper biomechanics of breathing? Does it only pertain to patients with neuromuscular weakness? No. Ventilatory biomechanical dysfunction can stem from any impairment category. An example from each of the Guide’s four major impairment groups will demonstrate this dysfunction.
Neuromuscular—When a patient with weak or paralyzed trunk muscles attempts to assume an independent sitting posture, the patient’s spine collapses into a kyphotic posture, the chest collapses forward, and the abdominal contents protrude anteriorly and inferiorly (“beer belly” impression).26 Mechanically, the rib cage is then “blocked” from expanding in the anterior and lateral plane, thus markedly restricting inspiratory potential. In addition, this same patient also loses expiratory potential because of paralyzed intercostal and abdominal muscles. Consequently, 1-single injury can cause the patient to lose both inspiratory and expiratory lung function, creating ventilatory pump dysfunction or failure. To give the reader even more detailed examples, Table 20-4 presents specific respiratory muscle impairments as it relates to patients with spinal cord injuries.
TABLE 20-4 Functional Limitations to Breathing Secondary to Spinal Cord Injury
Cardiopulmonary—Consider the child with significant asthma. From a young age, the child learns to excessively recruit his accessory muscles to meet the increased workload associated with “pulling air” into the lungs. This will result in abnormal development of the respiratory muscles and an abnormal appreciation of what “normal breathing” should be. The child may present to the clinician with elevated shoulders, an elevated sternal angle, a pectus excavatum, a thoracic kyphosis, excessive inferior descent of the diaphragm, and excessive recruitment of the trapezius and sternocleidomastoid muscles. Thus, although asthma caused the initial muscle pump dysfunction, poor neuromuscular recruitment of respiratory muscles, and the resultant imbalance in the strength and length–tension relationships of these muscles, exacerbates the pump dysfunction.27,28
Musculoskeletal—Consider the teenager with idiopathic scoliosis or the geriatric patient with spontaneous collapsed vertebrae.29 These musculoskeletal pathologies will likely produce mild to moderate pulmonary impairments due to pain and poor spinal alignment which will limit breathing and subsequent chest wall movement. Patients with such pathologies and impairments are frequently treated with a thoracic brace, such as a total contact thoracic-lumbar-sacral-orthosis (TLSO), to stabilize the spine and thoracic cavity. However, most TLSOs are provided to patients without an abdominal cutout that may have adverse pulmonary effects. In fact, patients may begin to complain of shortness of breath almost immediately after the TLSO is applied. Patients may be told that “it is in their head” because they have a skeletal problem not a cardiopulmonary problem. However, the only ventilatory muscle really capable of assisting with breathing for a person in a TLSO without an abdominal cutout is the trapezius muscle (which has limited respiratory muscle function because it only expands the chest in the superior plane). The trapezius is the only muscle capable of assisting with breathing, because the diaphragm’s inspiratory descent is limited by the TLSO that does not allow for adequate forward displacement of the viscera. Therefore, the diaphragm is essentially locked into a very limited “range of motion.” Likewise, the TLSO also limits the ability of the intercostals, sternocleidomastoid, and scalene muscles from expanding the upper chest. The limited upper chest motion and diaphragmatic descent will result in less generation of negative pressure necessary for ventilation and will ultimately produce increased dyspnea, work of breathing, and oxygen consumption.30
Therefore, a TLSO with an abdominal cutout will allow for optimal visceral displacement during the diaphragm’s inspiratory descent. Thus, the initial musculoskeletal problem that produced a mild to moderate pulmonary impairment was exacerbated from the application of a TLSO without an abdominal cutout that restricted diaphragmatic descent and optimal biomechanics of breathing.
Integumentary—Consider the patient with chest and upper extremity burns.31 Initially, pain would limit chest wall excursion, but as the scars heal and the resultant skin tissue and grafts become more fibrotic, the connective tissue itself may limit chest wall excursion and cause muscle imbalances from disuse atrophy or poor length–tension relationships for the anterior chest wall musculature. If this patient develops a significant kyphotic posture as a result of an extensive burn, it is possible that a posterior chest wall breathing pattern will emerge. As presented earlier, there is limited natural excursion posteriorly because of the stability provided by the rib cage with the thoracic spine, so each posterior inspiration would require a much greater effort for the patient, thus adding to his ventilatory pump dysfunction.
Normal Muscle Support for Breathing: Exhalation
Not only is inspiration compromised from a variety of different disease/trauma situations, but also exhalation and its many functions can become compromised. Classically, exhalation is described as a passive activity caused by the release of the diaphragmatic contraction and by the natural elastic recoil properties of the lungs.32 This makes exhalation very energy efficient, consuming very little if any oxygen in the process. However, exhalation can also be active for normal activities, such as in coughing or talking. The change in the expiratory process is described here first for normal function and then for those patients with ventilatory pump dysfunction resulting in poor expiratory maneuvers. Active exhalation is achieved by either an eccentric or a concentric contraction of the respiratory muscles. The process is distinctly different and will be discussed in the following section.
Eccentric Exhalation
In eccentric exhalation, the expiratory phase is prolonged by slowly releasing (eccentric contractions) the inspiratory muscles until the chest wall and lungs are near functional residual capacity (FRC), at which time the expiratory muscles become active.33–35 Prolonged controlled exhalation is necessary for speech production or for gentle pursed-lip breathing.36 For speech, the use of eccentric expiration allows for precisely controlled volume and flow rates through the vocal folds for the optimal production of vocal sounds. For normal adults, a typical vocalization of a vowel sound can be sustained for 15 seconds,34 but it is not uncommon for the trained individual (ie, singers, wind-instrument players, long-distance athletes) to sustain a vowel sound for 30 to 60 seconds.
If, instead of eccentrically releasing the air, the air is allowed to passively escape during exhalation, the speech pattern will sound very breathy, the vocalization will be sustained for only a brief period of time (often only 1–3 seconds), and there will be markedly fewer syllables per breath (often only 1–3 rather than the normal of 8–10). There will also be a notable “falling” of the chest wall during exhalation, as the patient cannot slow down the expiratory maneuver. This undesired passive exhalation may be a result of (1) poor motor control, (2) weakness or paralysis of the respiratory muscles, (3) pain, (4) vocal fold dysfunction, or (5) the presence of a tracheostomy tube which prevents the patient from using his or her glottis to aid in the eccentric maneuver. This results in the patient inhaling larger inspiratory volumes prior to talking in order to sustain their expiratory effort, or in the patient learning to talk by forcefully (concentrically) contracting the expiratory muscles.37 Both compensations lead to greater energy expenditure.38
Consequently, many patients who present with poor eccentric control of their respiratory muscles will complain of fatigue when talking, especially on the phone. To compensate, they may withdraw socially or respond to questions with short answers. Inevitably, if respiratory muscle dysfunction limits a patient’s social interactions, it may contribute to the development of depression.39
Concentric Exhalation
The other type of active exhalation pattern is a concentric exhalation pattern. This occurs when the air is forcibly expelled (ie, coughing or yelling), calling into action a concentric contraction of the expiratory muscles. The intercostals and abdominal are the primary muscles recruited for this activity, although the pectoralis and latisimus dorsi muscles can also be recruited. When these muscles contract, they apply significant positive pressure on the thoracic cavity to assist in fast and forceful expirations. These expiratory flow rates, which are termed peak expiratory flow rates (PEFR), are generally between 6 and 12 L/s as determined by the individual’s sex, height and age.40,41However, in patients who are unable to adequately contract the above expiratory muscles beneath a functional glottis (because of paralysis, weakness, pain, or a tracheostomy tube), the PEFR may be so low that forceful, concentric exhalation becomes ineffective for expelling particles from the airway.41–43 This would obviously impair the patient’s ability to cough or clear their airways, as well as impair their ability to talk loudly.
Examples of Inspiratory/Expiratory Pump Dysfunction and Failure Stemming from Primary Lung Disease
Primary lung diseases can also result in secondary dysfunction of the inspiratory and expiratory muscles. The muscles themselves may be functional and capable of demonstrating passive, concentric, and eccentric patterns, but the disease process demands that the expiratory muscles are activated with every expiratory effort, causing the patient significant fatigue. For example, the patient with a COPD, such as emphysema, may report of greater difficulty with expiratory maneuvers than with inspiratory maneuvers. An extended example of how obstructive and restrictive lung disease can adversely affect the normal biomechanics of breathing is presented in the following paragraphs.
Emphysema causes destruction to the alveolar sacs, resulting in the creation of large bulbous distal air sacs which in turn creates (1) excessive compression forces on the conducting airways, especially during exhalation, and (2) abnormal increases in the overall inspiratory lung volumes. Over time, this change in lung structure pushes outward on the chest wall, changing the length–tension relationship of the respiratory muscles and changing the alignment of the ribs to the spine. The resultant changes produce the characteristic “barrel chest” appearance of COPD, which adds a significant musculoskeletal impairment to an often-profound lung pathology.44
Early in COPD, patients have minimal impairments to the inspiratory muscles in spite of the underlying lung changes. In fact, the pulmonary function test results of patients with early COPD may be 100% of their predicted vital capacity values. However, as COPD advances, many pulmonary function test values become less of a percentage of the predicted value. Forced vital capacity [FVC] and forced expiratory volume in 1 second [FEV1] in advanced COPD will often be 30% to 60% of the predicted value. Such values demonstrate that the ability to exhale air from the lungs is markedly diminished (only 30%—60% of the expected volume is expelled; see Chapter 9). The diminished ability to exhale air from the lungs is due to the alveolar damage, which traps air within the lungs. During exhalation, the pressure within the thorax, lungs, and airways becomes less negative (possibly even positive), which further increases the already positive pressure within the lungs of a patient with advanced COPD. As the pressures continue to increase within the lungs during exhalation, the distal and proximal airways may become compressed and narrowed which will limit the amount of air moving out of them. This makes patients with advanced COPD forcefully exhale, rather than passively exhale during quiet breathing, to get rid of excessive CO2. Thus, even though the muscles and skeletal structures are technically intact, the biomechanics of their breathing is now altered, resulting in an increase in their work of breathing and ventilatory pump impairment. As their disease progresses, the chest wall itself is pushed outward by air trapped in destroyed alveoli and compressed airways, decreasing the efficiency of the diaphragm and accessory muscles of inspiration. Eventually, the resting position of the diaphragm itself will be pushed down by the ever-enlarging lung tissue, which will decrease the dome shape of this muscle and render the length–tension relationship of diaphragm less efficient. At the end stage of the disease, the diaphragm’s dome may become completely flattened, which would render it ineffective in its ability to increase the chest wall dimensions for inspiration. At this point, the mechanics of both inspiration and exhalation are significantly impaired.
A different presentation is noted in the patient presenting with a restrictive lung disorder such as pulmonary fibrosis or pulmonary hypertension.45 In this case, the lung tissue resists expansion, hence the term restrictive lung disease. The patient must generate a larger than normal NIF to ventilate the lungs. Thus, even though the muscles are neurologically intact, they must use greater force to generate the same inspiratory lung volumes as patients without restrictive lung disease. Unlike the patient with COPD, these patients will show a significant decrease in vital capacity and inspiratory capacity volumes. However, the patient with a restrictive lung disorder can exhale relatively more comfortably than patients with COPD. Patients with obstructive and restrictive lung disease will show an increase in the overall mechanical work of breathing. However, patients with restrictive lung disease will demonstrate more biomechanical impairments to inspiration, and the patients with obstructive lung disease will demonstrate more impairments to the expiratory mechanics until obstructive lung disease becomes more severe.32,46Patients with severe end-stage COPD experience marked biomechanical impairments to inspiration and expiration.
The remainder of this chapter will focus on a lengthy illustration of ventilatory pump dysfunction and potential for failure as it pertains to a patient with SCI. Applying these concepts extensively to a single case study will allow a more detailed depiction of how ventilatory pump dysfunction and the potential for failure occurs and what clinicians can do to minimize their impact on patient function. However, it is important to keep in mind that the examinations and interventions presented in the following case study of a patient with SCI can and should be applied to a patient with ventilatory pump dysfunction or failure from any etiology. Therefore, these same examinations and interventions will likely apply to a patient with COPD, pulmonary fibrosis, or even CVA.
CASE STUDY
This case study was introduced in Chapter 18 in the ICU setting, where the patient’s case was applied to Practice Pattern 6F. It will now be continued into a new setting: the rehabilitation hospital. The patient, Lee, is a 38-year-old male Caucasian postal worker who sustained a motor-complete C5-SCI secondary to a motor vehicle accident (see Chapter 18 for a full detailed description of his ICU experience). The summary report sent to the rehabilitation hospital from his physical therapy (PT) in the ICU states the following:
On day 20 (in the ICU setting), the patient had increased the periods of spontaneous ventilation to 18 hours per day, using the mechanical ventilator for 6 hours during sleep. The physicians decided to monitor the patient during the night while spontaneously breathing on a continuous positive airway pressure (CPAP) of 8 cm H2O pressure. The patient tolerated this final step in weaning for the next 48 hours, no longer requiring mechanical ventilation. [See Table, Respiratory Parameters, Day 16, in Chapter 19.] When the patient was weaned from the ventilator, he was tolerating sitting out of bed in a wheelchair with his legs dependent twice daily for 90-minute sessions with the abdominal binder and ace wraps. The nursing and physical therapy staff assisted the patient with pressure relief every 15 to 30 minutes while sitting. He was participating in active and active-assistive ROM [range of motion] exercises to the upper extremities and able to sit on the edge of the bed supported by both upper extremities for 10 minutes. He was able to assist the nurses and therapists with applying abdominal pressure to cough. Although he remained dependent in bed mobility, he could roll side to side and transfer supine to sitting with moderate assistance from a caregiver. The patient was discontinued from this practice pattern due to successful separation from the mechanical ventilator.
This chapter begins with the patient 3 weeks after his SCI accident, as he is transferred to the acute rehabilitation hospital. He was weaned from a mechanical ventilator and was just discontinued from CPAP and O2 support. He is still paralyzed secondary to the C5–SCI and consequently demonstrates neuromuscular impairments to the ventilatory pump. Upon review of his admitting paperwork, the doctors determine that he is currently medically stable. For these reasons, as he begins his rehabilitation phase, he clearly falls into Practice Pattern 6E: Impaired Ventilation and Respiration/Gas Exchange Associated with Ventilatory Pump Dysfunction or Failure.
What will be the overriding cardiopulmonary concerns and risks for this young man as he begins the rehabilitation phase? Will they be different from those in the ICU? One major concern does not change following a patient with SCI regardless of whether he is in the ICU or at home: impaired respiratory mechanics leading to potential respiratory complications/failure.3,4 Therefore, from the initial admission onward, the entire team will be closely monitoring the patient’s respiratory status and determining the degree of ventilatory pump dysfunction or failure.
CARDIOPULMONARY RISKS FOLLOWING A SCI
Table 20-5 lists a summary of many cardiovascular and cardiopulmonary risks for patients with an SCI.47–49 These risks are then explored specifically as they apply to our patient as he enters the rehabilitation phase of his recovery.
TABLE 20-5 Cardiopulmonary Risk Factors Following an SCI
Impaired Respiratory Mechanics
Lee was found to have paralysis of the intercostal and abdominal muscles, which means that, of the core “triad” respiratory muscle groups, only the diaphragm is spared. However, without the muscle support above and below the diaphragm from the intercostals and abdominal muscles, the diaphragm will not be capable of contracting at its highest level of function. In addition to paralysis, his spinal shock is now resolving and spasticity is beginning to develop in his trunk musculature.50,51 Lee is finding that when he takes in a quick deep breath, it causes spasms and spasticity, which limits his ability to perform a maximal inspiratory effort. He says this shortness of breath is particularly evident when he is telling a story, laughing, or any other “breathing activity” that causes him to spontaneously take quicker inspiratory efforts. He also says that his Halo fixation device (cervical fixation device attached to a trunk vest that restricts cervical motion) restricts his chest causing him to feel confined when he tries to inhale. In fact, between his Halo device and the tracheostomy tube, Lee states that he is finding it impossible to bend forward and tuck his chin to cough, making him sense that he “cannot get the secretions out of his lungs.” He also states that his cough is “wimpy.”52 To complicate the matter, he says that he is now experiencing right shoulder pain. When he recruits his trapezius to take a deep breath, it exacerbates his shoulder pain.
Sleep Dysfunction
Because of impaired respiratory mechanics and the inability to counteract gravity due to weak or paralyzed respiratory muscles, patients with SCI will often develop secondary sleep dysfunction, especially chronic nighttime hypoxemia. If the patient is using a compensatory breathing pattern during the day to maintain his or her lung volumes, but does not spontaneously use this pattern at night, the patient may retain CO2 during sleep. This may cause the patient’s respiratory centers in the brainstem to “wake them up” in order to get the patient to take a deep breath to blow off CO2, or else the patient will wake up “groggy and disoriented” from inadequate gas exchange all night (hypoventilation). This may go undetected unless the clinician is aware of its symptoms: nocturnal desaturation (O2 saturation below 90%), morning headaches, insomnia or frequent “wakeups” during the night, nocturnal restlessness, nightmares of suffocation, difficulty concentrating during the day, falling asleep during the day. This can be serious and even fatal if not diagnosed and treated.53,54
Patients with SCI are often reported to have obstructive sleep apnea secondary to supine positioning.53 Lee reports that he always slept prone or three-fourth prone before his injury, but that now nurses position him supine. He hates sleeping on his back and has increasingly complained of headaches first thing in the morning.
Autonomic Dysfunction and Cardiovascular Dysfunction
Because of the disruption of the autonomic nervous system after a C5–SCI, numerous dysfunctions may occur.48 During his stay in the ICU, Lee was complaining about being cold (normal hypothermic response immediately following SCI due to excessive peripheral vasodilation), but now he says he is more likely to feel too warm (after a few weeks, reflexive tone returns to peripheral vasculature, and the hypothermia usually resolves, but because the ability to sweat is lost below the level of lesion causing patients with SCI to overheat more easily in the chronic phase). He also stated that other “weird things happened in the ICU”: His heart rate ran really low (typical bradycardic response in the acute phase) and he became easily dizzy when they sat him upright (orthostatic hypotension secondary to excessive peripheral vasodilation); but now all that seems better (these abnormal cardiovascular response effects generally resolve approximately 2 to 3 weeks after an SCI).
However, the most frightening incident that he described was his first bout of autonomic dysreflexia which was short lived, but very disturbing. Autonomic dysreflexia is caused by the disruption of the autonomic nervous system below the level of the SCI causing unbalanced sympathetic input. A noxious stimulus below the level of lesion, such as a full bladder, a urinary tract infection, constipation, or even an ingrown toenail, to name a few, starts a whole chain of cardiovascular responses.48,55 These responses present quickly and often include marked increase in blood pressure (hypertension), marked decrease in heart rate (bradycardia), profuse sweating (above the level of lesion), intense headaches (secondary to the hypertension), flushing (vasodilation above the level of lesion), and anxiety (Table 20-6). This can be life-threatening because of the extreme hypertension. Autonomic dysreflexia, sometimes called hyperreflexia, does not occur until after spinal shock has resolved; thus, it is more commonly seen in the rehabilitation setting or later.47,48,56
TABLE 20-6 Autonomic Dysreflexia
The last cardiovascular abnormality that may affect our patient is the risk of developing deep vein thrombosis (DVT). During spinal shock, the patient experiences peripheral vasodilation, poor reflexive vascular tone, general immobility, a transient hypercoagulable state, and flaccid paralysis of the lower extremity musculature, all which lead to venous stasis and the potential development of a blood clot (DVT).48,57 If the blood clot is released into the circulatory system, the patient may develop a pulmonary embolus (PE), which can be fatal. The risk for DVTs and PEs is highest for the first few months following their SCI; hence, thromboprophylaxic measures are aggressively pursued in this population starting in the ICU. Lee reports that his doctors in the ICU put him on a thromoboprophylactic program to minimize this risk, the physical therapists ace-wrapped his legs, and luckily he has not had any problems.56,58
Increased Risk of Infections
In the ICU, our patient had a right lung atelectasis with possible pneumonia, both of which resolved prior to his discharge. However, lately he has not been drinking adequate fluids due to pain, vocal fold irritation (from being intubated initially after the accident), and depression. He is currently slightly dehydrated which dramatically increases his risk for respiratory, urinary, and blood infections, as well as an increased risk for DVTs and poorer overall healing capabilities. It is important to note that respiratory, urinary, and blood infections are some of the most common causes of morbidity in this population.3,4 This means that an intervention as simple as maintaining adequate hydration levels can have a tremendously positive impact on the patient’s successful recovery. It can improve pulmonary secretion mobility, decrease toxic concentrations in the blood, flush bacteria out of the urinary system, and decrease potential noxious stimuli that may trigger autonomic dysreflexia. Hearing this information, Lee declares that he will definitely drink more water now.
Heterotopic Bone Formation
For reasons not yet clear, ectopic bone is often laid in the muscles or other soft tissue beneath the level of lesion of injury following an SCI.48,59 So far, our patient has not had any signs of heterotopic bone formation, but the staff will be watching for it. If it forms around the spine, shoulder, or pelvis and causes our patient to assume a more kyphotic posture, he will compromise the mechanics of his ventilatory pump, which would cause a decrease in inspiratory lung capacity.
Decubiti (Bed Sores)
Immobility, skin collagen degradation, circulatory changes, dehydration, and decreased sensation all contribute to an increase potential for skin breakdown, especially around bony prominences.60 Lee preferred to lie on his left side in the ICU, and the nurses’ discharge report indicated that he had increased redness around his left greater trochanter. This will have to be watched carefully to make sure the connective tissue does not break down completely and cause an open sore. This opening would invite infections and the potential development of septicemia, as well as limit his available options for positioning.
Poor Nutrition/Hydration
A secondary complication that has only more recently been recognized is poor nutrition and underhydration. Many patients are initially intubated following their SCI, and may develop transient vocal fold dysfunction after they are extubated. In addition, patients may find swallowing difficult due to cervical bracing, or other traumas that occurred with their injury. These oral-motor deficits will increase the risk of aspiration and aspiration pneumonia, as well as decrease the patient’s willingness to eat and drink. Furthermore, gastrointestinal (GI) ulcers, bleeds, gastroesophygeal reflux (GER), or other GI disorders are not uncommon following SCI.61,62 Consequently, many SCI acute care facilities are now taking a prophylactic approach and surgically inserting a gastrostomy tube (G-tube) early in the acute phase to ward off these problems and guarantee the delivery of adequate nutrition and hydration. According to his family, our patient’s appetite has recently been returning and he has even asked for “Chicago-Style Pizza,” so adequate caloric intake no longer appears to be a problem. He has already pledged to increase his hydration level following our discussion noted previously.
Other Inherent Risks
Numerous other cardiopulmonary risks exist, such as advanced age, obesity, other medical problems accrued during the accident, past medical problems, previous lifestyles, etc. These additional factors all play a role in the patient’s potential for a successful rehabilitation. In particular, the patients’ outlook following the injury and their outlook on life prior to the injury will influence their outcome. It is not surprising that the most well-adjusted, healthy persons, prior to the SCI, report the highest satisfaction level long after the SCI.63–65 Our patient comes from a well-grounded family with strong support within both the family and the postal service communities. He was healthy prior to the accident, and had no other medical “risks” to potentially complicate his recovery from the SCI.
SUMMARY OF CARDIOPULMONARY RISKS FOLLOWING A SCI
In light of the preceding information, is our patient at risk for developing secondary cardiopulmonary complications? Yes. Even though he survived the acute phase of his injury and was successfully weaned from the ventilator, he still carries a risk for developing cardiopulmonary problems as long as his paralyzed state remains (Table 20-7). Because the research shows that this risk is higher with a complete SCI injury, and even higher with a cervical rather than a thoracic lesion, our patient and the medical team will need to monitor and reevaluate his cardiopulmonary status on an ongoing basis.49,66 Also, the often fluctuating status of this patient’s and many other patients’ ventilatory pump (moving from ventilatory pump dysfunction to the potential for failure and back to dysfunction or even failure) requires frequent examination to determine the degree of dysfunction, potential for failure, or failure.
TABLE 20-7 Lee’s SCI Cardiopulmonary Risk Factors
Examination and Evaluation
What tests and measures are important to consider for this patient or for other patients with ventilatory pump dysfunction, and how do you prioritize your examination to ensure that the most important tests are completed? In a perfect world, every single possible test would be performed for every single patient. However, this is not realistic. Priorities must be made because of time, money, available resources, patient’s fatigue factor, etc. In this section, numerous different assessment tests will be presented with their relative value of information given our particular patient and 6E Practice Pattern. A review of the literature suggests that the following tests and measures are the most important evaluative tools to assess ventilatory pump dysfunction.32,41,61,62,67,68 They are summarized in Table 20-8 and will be discussed in detail in the following section.
TABLE 20-8 Appropriate Tests and Measures: Assessing the Cardiopulmonary Status and Function of a Patient with SCI
Medical History
A complete medical history is especially important when assessing the complex medical patient. The medical history for this patient can be found in Chapter 19. Our patient was healthy prior to his injury; thus, his medical history does not add complicating factors. However, other patients may have serious extenuating circumstances such as congestive heart failure, emphysema, asthma, hypertension, etc, which will significantly impact the patient’s potential progress and functional outcomes relating to their current crisis. For example, let us say that instead of a young, healthy, college student sustaining an SCI, our patient was a 75-year-old sedentary gentleman with a history of emphysema (adding more respiratory compromise) and diabetes (adding more cardiovascular compromise). This past medical/social information would have a significant impact on which test procedures the clinician chose for that patient, what medical/social concerns the clinician would have for that patient, what interventions would be appropriate and effective, and what outcome would be realistic to project. With our young relatively healthy patient from the case study in mind, we review possible tests and measures to be performed by the physical therapist and/or the entire medical team.
A pharmacological history is also noted during the history. There are a wide range of medications that may be appropriate for our patient or other patients with ventilatory pump dysfunction, potential for failure, or failure. Our patient is currently on antireflux medications, vitamins, a muscle tone relaxant for his spasticity, and a stool softener.
Medical Tests and Measures
Vital Signs—Heart Rate, Blood Pressure, Respiratory Rate, and Temperature
Heart rate (HR), blood pressure (BP), respiratory rate (RR), and temperature are meant to give the clinician a quick, inexpensive look into the patient’s current medical status, and is seen as the “first line of attack” in performing a cardiopulmonary assessment. For example, if our patient showed a significant drop in HR accompanied by a significant elevation of his BP and an increase in RR, it could be indicative of the onset of autonomic dysreflexia. An increase in RR and temperature could be signaling the onset of pneumonia or other respiratory infection. A drop in BP with a change in posture, particularly a change from a recumbent to an upright posture, could indicate that our patient was experiencing orthostatic hypotension. Thus, vital signs are helpful for assessing stability at rest and with activity. Because of its ease of application, low cost, and valuable information, all patients should have ongoing assessments of their vital signs. Vital signs are assessed by any and all of the medical staff. Our patient’s vital signs were stable, but BP tended to be on the low side (see Table 20-9).
TABLE 20-9 Lee’s Vital Signs in Two Different Postures
Arterial Blood Gases (ABGs)
Patients who fall into Practice Pattern 6E are already identified as having ventilatory pump dysfunction. This means that they will have trouble providing the exterior support (optimal respiratory biomechanical support) for optimal gas exchange. They may have problems efficiently removing CO2 and subsequently ABGs would be observed to have an elevated PCO2 (normal is 35–45 mmHg) and a resultant drop in pH (normal pH 7.35–7.45).32 Each patient and each facility may have a slightly different threshold that indicates acute ventilatory pump failure, but the generally accepted threshold value for a patient with ventilatory pump dysfunction (without lung disease) is a PCO2 of greater than 50 mmHg and a pH of less than 7.30.67,69 However, observation of a paradoxical breathing pattern should alert the clinician that (1) the ventilatory pump has the potential to fail and (2) judicious administration of a variety of interventions may correct the paradoxical breathing pattern and prevent the aforementioned changes in ABGs.
Patients with SCI generally do not have a problem with their PaO2 level except when developing an acute respiratory infection. This value is then particularly important when the patient is acutely ill and the doctor needs to decide if the patient’s gas-exchange efficiency is so compromised that mechanical ventilation and/or oxygen support is needed. Generally a PO2 less than 60 mm Hg would indicate the need for supplemental oxygen.67,69 Consequently, ABGs are an essential evaluative tool during the acute phase and during changes in the patient’s medical status, but are not necessary on a daily basis for the patient who is medically stable. Our patient, who is clearly in Practice Pattern 6E, is entering the rehabilitation center in stable condition with relatively normal ABGs; thus, there would be no reason to repeat the test unless his condition changed for the worse or if a paradoxical breathing pattern were observed. The nursing staff or physicians generally perform this test in the United States.
Oximetry (O2 sat/SaO2)
A normal oxygen saturation (O2 sat) level is between 96% and 100%. A level of 90% or less is often used as a threshold value to indicate inadequate oxygenation and the need for supplemental oxygen. Clinicians can also use this test to determine how well the patient is tolerating a particular activity and examine the O2 sat in contrast to the breathing pattern and RR. For example, a clinician may choose to monitor the O2 sat, RR, BP, and breathing pattern when our patient moves from a reclining chair to a fully upright chair. A drop in O2 sat and BP accompanied by an increase in RR and paradoxical breathing pattern indicates that the patient is presently unable to tolerate movement from a reclining position to a fully upright position. In view of the results of these tests and measures, the clinician knows that his physiologic state is not quite ready for a fully upright position without the use of some other intervention such as an abdominal binder or elevated footrests or simply less of an upright position (45-degree upright position using the reclining chair or a specialized bed).
Because oximeters are noninvasive, easy to apply, and easy to transport, and can give immediate feedback to the clinician, it can be a valuable ongoing evaluation tool. Like ABGs, once the patient is medically stable and the clinician knows that the patient’s saturation level is stable in a variety of physical activities, then his oximetry level no longer needs to be monitored. Oximetry can be assessed by any and all of the medical staff. Our patient’s O2 sat values were stable at rest, but dropped to 86% to 88% when sitting fully erect and when transferring without his abdominal binder. Thus, his O2 sat should continue to be monitored until no sign of desaturation is observed.
Pulmonary Function Tests (PFT)
Pulmonary function tests inform the clinician about lung volumes and flow rates for both inhalation and exhalation maneuvers. A few pertinent tests will be discussed here, and Chapter 9 can be reviewed for further material on PFTs.
Vital Capacity
One of the simplest and most readily available tests is the VC maneuver. It can tell the clinician about the patient’s voluntary ability to move maximal volumes of air in and out of the lungs. The patient inhales and then blows out as hard and as long as he can. The expired volume is called VC. In general, when a patient’s VC is less than 60% of the predicted value, it is generally indicative of inadequate lung volume. If VC falls to less than 25% of the predicted value, it is generally indicative of the patient’s inability to support adequate gas exchange (ventilatory failure) and the need for mechanical ventilation.32
Tidal Volume
TV is a normal quiet breath and should be approximately 10% to 20% of the predicted VC.32,70 This shows that the person has adequate respiratory reserves to meet the oxygen demands of activities that demand a greater inspiratory or expiratory effort, or both. When TV becomes a higher percentage of VC (because VC is shrinking or TV is increasing), it tells the clinician that the patient’s respiratory reserves are lower, thus potentially limiting the patient’s physical potential. If the patient cannot transport oxygen to the muscles because of limited reserves, he or she will not have the “energy” to perform physical tasks.
Flow Rate Measurements
Flow rates are also important to determine cough effectiveness as well as to detect any obstructive lung impairments. Two different methods of assessing flow rates will be presented. According to Bach,41,71 normal peak cough flow rates (PCFR) are between 6 and 12 L/s, and that any rate less than 2.7 L/s will clearly result in a nonproductive expectoration.
Another way of measuring ineffective rates necessary for cough would be to test FEV1. Normal FEV1 is 80% of the actual VC. Like a PCFR of less than 2.7 L/s, a FEV1/actual VC below 60% indicates inadequate flow rates for cough.
During acute episodes, PFTs may need to be taken daily or even more frequently to detect an improving or worsening situation. This is particularly true of the patient with neuromuscular impairments such as Guillian–Barré syndrome, amyotrophic lateral sclerosis, muscular dystrophy, or other progressive disorders. For a stable patient, PFTs may be rechecked periodically to make sure that the patient’s functional lung capability has not changed. Portable models are available that are simple, relatively inexpensive, and usually available in the hospital setting. They are often not available in the home or community setting. The downside to PFTs is that they require the full cooperation of the patient; thus, their value is determined by the patient’s ability to consistently give their maximal effort to the test. PFTs cannot be performed with the patient who is cognitively impaired, or with the patient with oral motor dysfunction who cannot make and maintain a good lip seal over the mouthpiece. PFTs can be performed by any and all of the medical staff.
Our patient’s PFT results are summarized in Table 20-10. The results show a significant decrease in VC and PCFR, which indicates an impaired cough. Other PFT results show a higher TV/VC ratio than normal, indicating that he may not be capable of meeting the ventilatory demands of activities that require greater levels of oxygen consumption due to decreased ventilatory reserves. Obviously, these test results are important to the physical therapist whose activities often demand the greatest amount of oxygen consumption of any of the medical disciplines. These tests should be repeated periodically during his rehabilitation stay in order to see if they are improving or worsening with time.
TABLE 20-10 Lee’s Pulmonary Function Tests with Tracheostomy Tube Capped
Sputum—Sputum is cultured if an infection is detected or suspected in the lungs, or it can be done prophylactically for patients with a history of repeat infections. Our patient did not have an infection upon discharge from the acute care; thus, no sputum culture was ordered. Nursing, respiratory therapy, or PT performs this test.
Chest radiographs (X-rays)—Chest X-rays can tell a clinician about the current condition of the lung such as the presence of a pneumonia, atelectasis, or disease processes such as emphysema (see Chapter 9 for a more detailed review of radiographic techniques). Past X-rays may show a pattern of problems that would influence the clinician’s future interventions. Our patient had an atelectasis in the acute care hospital so that X-ray would be compared to the admitting X-ray at the rehabilitation hospital to make sure that there was no residual deficit or new problem. Acute lung problems, such as atelectasis, can quickly occur so it is important to “treat the patient,” not “the X-ray report.” Contact the physician about any suspected changes. Only X-ray technicians perform X-rays. Our patient’s admitting X-ray showed no residual atelectasis.
Cardiac/circulation tests—Patients with ventilatory pump dysfunction or failure may also have a history of cardiac dysfunction, or may be at risk for developing problems. An ECG may be performed to rule out any cardiac problems. Our patient’s doctor decided that an ECG was not necessary. His HR was normal and his distal pulses were present. All cardiovascular tests were within normal limits (WNL) for our patient.
Renal/urinary tests—Because urinary tract infections (UTIs) are common complications following a spinal cord injury, periodic urine tests will be performed to monitor this possibility. Our patient’s test returned negative, but all disciplines need to be trained to watch for signs of UTIs because of their quick onset and their potential trigger for autonomic dysreflexia and possibly death. Nursing typically performs this test in the United States.
Nutrition/hydration/reflux/swallowing dysfunction—The patient with ventilatory pump dysfunction may be expending a significant amount of their energy on breathing and may decide that eating “takes too much effort,” as our patient did in the acute care setting. Nutrition can be assessed by weight loss/gain, gastrointestinal status, and the patient’s report. Likewise, hydration is critical to his health and can be monitored by fluid intake/urine output, the color of the urine, the thinness of lung secretions, complaints of dry mouth and sore throat, to name a few. Our patient was determined to be slightly dehydrated upon admission. He also recently started taking in adequate calories to maintain his weight.
Occasionally, patients will develop reflux or other gastric dysfunctions secondary to SCI.61,62 Reflux can be dangerous because of its potential for aspiration pneumonia as well as poor nutrition. Upon pH test, our patient was determined to have a slight case of reflux. This may have contributed to his poor appetite in the acute care. The patient will be started on antireflux medication to control the reflux. If our patient were also suspected of aspirating his food, fluids, or saliva, then a swallow study would be performed by a speech pathologist to determine if the patient’s swallowing mechanism was impaired. Our patient showed no sign of aspiration; therefore, the test was not ordered.
Physical Tests and Measures
Tests and measures that are more specific to physical therapy will now be presented, as it would pertain to our patient Lee.
Range of Motion
Relatively good ROM with mild limitations only in shoulder flexion (right more than left), finger flexion, and ankle dorsiflexion were observed.
Manual Muscle Tests/Muscle Tone
Motor complete C5-SCI with no voluntary motion below C5 was observed. His key C5 muscles are 3/5 bilaterally (deltoids, biceps, brachioradialis). Above his lesion, his muscles are 4/5. Lee has mild spasticity in the trunk extensors, leg extensors, and biceps, and he complained to the physical therapist that his spasticity was making it hard for him to use his biceps functionally.
Sensation
Sensation was observed to be intact above C5 dermatome, somewhat spotty within C5–C6, and absent below C6.
Skin
Lee’s skin was observed to be intact but shows an increased redness over the left greater trochanter. Surgical scar from liver laceration repair on right upper abdomen is healing well, but therapist suspects tightening onto underlying connective tissue. Restrictions to scar tissue movements noted superiorly and inferiorly. Chest tube scars healing well with no noted restrictions.
Gross Motor Skills/ADLs
Lee was just beginning to relearn gross motor skills when he was discharged from the acute care setting. Upon admission to rehabilitation he needed:
•Moderate assistance to roll to both sides, with the therapist noting poor coordination of breathing and movement.
•Maximal assistance to assume supine to sitting, demonstrating a “breath-holding” pattern when he assisted the therapist with elbow flexion maneuvers.
•Maximal assistance with sliding board transfers. Has not been instructed yet in how he can assist and direct the transfer.
•Moderate assistance for balance short-sitting on a mat table with right foot on the ground for 10 minutes. Left leg elevated due to long leg cast.
•Tolerating fully upright posture in wheelchair up to 30 to 60 minutes before complaining of fatigue. In addition, notes: pressure hose on his right lower extremity, long leg cast on left lower extremity, abdominal binder.
Postural Assessment
Lee is of moderate stature (5 ft 8 in. tall, 150 lb) with a flat anterior chest wall (normal for him) and no noted spinal abnormalities (other than surgical site). No abnormality noted over right rib fracture sites. Surgical scar on right upper abdomen is taut, pulling abdomen into a slightly “flexed” posture even in supine. Sitting with therapist’s support in short-sitting posture without an abdominal binder, the therapist notes a midchest fold line between the chest and abdominal area, an excessive anterior and inferior displacement of the abdominal viscera (a “beer-belly” look in spite of his moderate frame), internal rotation of the shoulders, an excessive kyphotic posture in the lower thoracic/lumber spine area (just below the base of support for the Halo vest), and an increase in posterior tilting of the pelvis (see Fig. 20-2). When the therapist reapplied the abdominal binder, (1) the midchest fold and the poor visceral alignment were corrected, (2) the upper extremities assumed a less internally rotated posture, (3) the pelvis was less posteriorly tilted, (4) and the functional kyphotic posture improved but was not eliminated. These observations will be considered in relationship to Lee’s positioning and support in a wheelchair. BP was taken in upright when he first went upright and 30 minutes later to test his cardiovascular tolerance of the posture. Supine: BP 110/75. Upright initial: BP 90/60. Upright 30 minutes: BP 100/65. No signs of dysreflexia.
Breathing Pattern Assessment
Lee was observed to be spontaneously breathing, but complains that with talking or eating, he becomes more easily short of breath. He reports a perceived exertion rating of 8 out of 10 (8/10) during these activities. Other activities: quiet breathing in bed 4/10, sitting in wheelchair with a binder 5/10, without binder 7/10. His breathing pattern in supine with the Halo vest opened reveals an excessive rise of the abdomen, and a slight collapsing of the anterior chest (paradoxical or “inward” breathing). In the wheelchair with the Halo vest tightened and the abdominal binder applied, his breathing pattern demonstrates less abdominal excursion and a significant increase in superior or trapezius breathing. Patient is primarily a diaphragmatic breather with little upper chest support in any posture. See Table 20-11 for circumferential chest wall excursion measurements in supine and wheelchair sitting.12 Note the increase in paradoxical breathing while Lee was in supine.13 The RR was 16 in supine with vest opened, 20 in upright with vest and binder, 28 in upright without the binder. Auscultation revealed decreased breath sounds in basal segments, but no adventitious sounds, indicating hypoventilation, but not secretion retention.
TABLE 20-11 Lee’s Circumferential Chest Wall Excursion Measurements
Cough Assessment
There are four phases to a normal cough which are described in Table 20-12.41,71,72 Phase 1 is the inspiratory phase, phase 2 is considered a hold phase, and phases 3 and 4 are the force and expulsion phases, respectively. Lee stated that he has trouble coughing. Examination of the patient’s cough and pulmonary function revealed inadequate inspiratory volume for phase 1 and an inability to use phases 2 and 4 effectively due to his tracheostomy. Phase 3 was also markedly impaired because of abdominal and intercostal paralysis. The cough was quiet and high pitched, and the patient was only able to produce two “weak and breathy” coughs per breath. In summary, Lee demonstrated significant impairments at every phase of cough and the PFTs confirmed these suspicions (Table 20-12).
TABLE 20-12 Lee’s Cough Assessment
In addition, during these coughs, Lee did not show any spontaneous incorporation of natural ventilatory strategies with the maneuver (ie, trunk/head extension with the inspiratory phase 1, and trunk/head flexion with the expiratory phases 3 and 4). For all of these reasons, our patient is classified as “at risk” for developing respiratory complications secondary to secretion retention unless his neurologic condition improves or an adequate intervention program is implemented. At this moment, he does not have a secretion problem, but his airway clearance assessment shows that he will be unable to effectively clear secretions when he needs to, such as when he develops a cold. Obviously, resolution of this problem is paramount to his successful rehabilitation outcomes, because pulmonary infections are the primary cause of death in patients with SCI and are likely the result of suboptimal secretion clearance due to a poor cough.
Breath Support for Phonation
Lee can sustain a vowel sound (ah) for 4.5 seconds (normal 15 seconds),34 and uses 4 to 5 syllables per breath (normal 8–10) in upright with an abdominal binder on and a cap over his tracheostomy site. Without the binder, he sustains a vowel sound for 3.1 seconds and uses 2 to 3 syllables/breath (see Table 20-13). Patient states that he prefers to have the binder on in upright.37 He tries to use an eccentric pattern for voicing (normal breath support pattern for quiet breathing), but he will move into a residual volume (RV) speech pattern, which uses a concentric pattern (utilizing his pectoralis, bicep, and neck flexors) when he wants to finish a sentence before taking another inspiratory effort. This is most likely a significant contributing factor to his complaint of dyspnea with conversations. The patient is a good candidate for a speaking valve or a tracheostomy button to facilitate speech prior to decannulation.
TABLE 20-13 Lee’s Phonation: Sustained Vowel Sound Production
Sleep Assessment
Because of the patient’s compliant of headaches in the morning, and a “poor night’s sleep” in general, Lee had a sleep study screening test performed with nursing and PT during a day-time nap session. While the patient was supine, his O2 sat level dropped to 89% and his RR increased to 24. The patient was then turned one-fourth off of supine with his uppermost upper extremity positioned in extension against a pillow to maximize the upper chest opening. His O2 sat and RR improved. The patient was also evaluated on his side and three-fourth prone with similar positive results73 (Table 20-14).
TABLE 20-14 Lee’s Screening Test for Sleep Dysfunction
Equipment
The Halo vest was observed to be restricting head, neck, and upper chest movements, and consequently impairing inspiratory maneuvers. However, the Halo vest provides much-needed spinal support and will remain in place until spinal precautions are removed (anticipated date: 3 months postinjury). Several studies show that the Halo vest has the potential to decrease VC.74 A fenestrated tracheostomy, right lower extremity cast, and an abdominal binder were provided to the patient. Bilateral hand splints were provided to maintain ROM and bilateral nighttime ankle splints were applied to maintain ankle ROM.
PHYSICAL THERAPY DIAGNOSIS AND IMPRESSION
Diagnosis
The patient was a previously healthy young male who is now stable and recovering from an SCI 3 weeks ago. Lee is spontaneously breathing, but not as efficiently as he can or needs to be in order to maximize his function and minimize his long-term respiratory risk. (Common respiratory complications associated with SCI are chronic hypoventilation leading to atelectasis and/or pneumonia, chronic nighttime hypoxemia, and increased risk of infection.) He demonstrates a paradoxical breathing pattern at rest that worsens with increased effort and his O2 sat decreases with upright body positions. He has poor respiratory endurance and resulting poor functional endurance. His cough is weak and ineffective, rendering secretion management ineffective. His breath support for speech is poor, hampering his communication efforts. Lee’s nocturnal ventilation is inadequate in supine, contributing to his daytime fatigue level and poor concentration. His musculoskeletal alignment in upright is faulty and could have long-term effects on the continued development of his spine, chest, shoulders, and pelvis. His nutritional and hydration state is improving from the acute care, but not yet adequate.
Impression
Lee’s impairments demonstrate ventilatory pump dysfunction with the potential for ventilatory pump failure due to the presence of a paradoxical breathing pattern and desaturation with upright body positions. It is important for the physical therapist to identify specific signs and symptoms to distinguish among ventilatory pump dysfunction, the potential for ventilatory pump failure, or true ventilatory pump failure. This information can then be used to maximize ventilatory pump function and prevent ventilatory pump failure.
Figure 20-3 highlights the importance of distinguishing between ventilatory pump dysfunction and failure. Identifying the absence or presence of a paradoxical breathing pattern can be used to direct the interventions most appropriate for a particular patient. This hypothesis-oriented algorithm can be applied to patients with ventilatory pump dysfunction and the potential for failure due to a variety of etiologies.
For example, the upper chest paradoxical breathing pattern observed in the patient in this case is due to inadequate biomechanics of breathing. The inward movement of the upper chest during inspiration is because the upper chest wall structural support system (the muscles) is paralyzed and the contracting and descending diaphragm creates a sufficient negative pressure to pull (or actually suck) the upper chest inward (see Chapter 9). Continued upper chest paradoxical breathing may place other patients at risk of developing ventilatory pump failure. The upper or middle chest paradoxical breathing pattern that is common in patients with SCI is more often an indication of significant ventilatory pump dysfunction, rather than ventilatory pump failure.
Nonetheless, sitting the patient with an upper or middle chest paradoxical breathing pattern upright and leaning them forward (or giving them an abdominal binder) may provide them with greater abdominal support and decrease the effects of gravity on the upper or middle chest which should decrease the upper chest paradoxical breathing pattern (Fig. 20-3).
FIGURE 20-3 A hypothesis-oriented algorithm for patients with ventilatory pump dysfunction and the potential for ventilatory pump failure.
An abdominal paradoxical breathing pattern, as seen in patients with severe COPD, appears to be much more strongly associated with the potential for ventilatory pump failure. The abnormal biomechanics of breathing in COPD are characterized by excessive accessory muscle activity and diminished diaphragmatic activity because of hyperinflation of the lungs and subsequent flattening of the diaphragm. Flattening of the diaphragm places the muscle fibers of the diaphragm in a shortened and suboptimal position for contraction and relaxation. This suboptimal position decreases the diaphragm’s ability to produce the much-needed bucket-handle motion of the lower ribs and subsequent generation of negative pressure to ventilate the lungs.
CLINICAL CORRELATE
In COPD, ineffective diaphragmatic contraction and relaxation force the accessory muscles of inspiration to become more active in producing the negative pressures necessary to ventilate the lungs. The forceful contraction of the accessory muscles in the upper chest area produces the negative pressures to ventilate the lungs, but without opposition from the diaphragm, the abdominal area is pulled inward during inspiration. This inward motion of the abdominal area associated with upward and outward upper chest motion is referred to as an abdominal paradoxical breathing pattern. Prolonged abdominal paradoxical breathing in a COPD patient with worsening ABGs and PFTs is associated with ventilatory pump failure.
Leaning such a patient forward may improve this paradoxical breathing pattern and subsequently ventilatory pump failure. However, many patients will likely require mechanical ventilation to rest the muscles of breathing and ventilate the lungs (Figure 20-3).
Returning to the chapter case study, Lee’s evaluation indicates that he is capable of making tremendous improvement in the rehabilitation setting to offset these initial ventilatory deficits. However, the inherent risk of secondary respiratory complications will always be present as long as the impairments from his SCI are present; thus, a comprehensive multi-disciplined respiratory management program is critical to the success of his rehabilitation. With this in mind, specific goals are outlined in the following section.
LONG-TERM CARDIOPULMONARY GOALS
These goals are expected to be achieved within the next 30 to 60 days and then maintained throughout Lee’s lifetime (see Box 20-1).
BOX 20-1
Lee’s Long-Term Cardiopulmonary Goals
•Optimize the biomechanics of breathing
•Educate the patient and family about potential respiratory complications
•Maximize potential for ADL function and endurance by optimizing oxygen transport
1.Optimize the biomechanics of breathing to promote optimal respiratory function and oxygen transport.
a.Optimize musculoskeletal alignment of all joints in order to continue optimal development and function of respiratory mechanics.
b.Optimize strength and functional use of all remaining respiratory/trunk musculature to achieve maximal pulmonary functional status with the lowest oxygen energy cost, being careful to monitor for long-term overuse complications.
2.Educate the patient and family to know all the signs and symptoms of possible respiratory complications and to develop ongoing programs to help the patient successfully and independently manage his respiratory system after discharge from the hospital.
3.Maximize potential ADL function and endurance. All of the aforementioned will maximize potential ADL function and endurance because of improved oxygen transport.
SHORT-TERM GOALS AND INTERVENTIONS
The expectation is that these goals could be achieved within the next 1 to 3 weeks. Possible interventions and strategies are listed under each goal (see Box 20-2).
BOX 20-2
Lee’s Short-Term Cardiopulmonary Goals
•Increase hydration/improve nutrition level
•Improve cough effectiveness/secretion clearance
•Coordinate decannulation program with the entire team
•Improve postural alignment in reclining and upright postures
•Improve sleep
•Increase tolerance to multiple postures
•Coordinate breathing with movement to improve overall motor performance (ventilatory strategies)
•Improve the patient’s breathing pattern
•Improve breath support for speech
•Increase strength, function, and endurance of remaining respiratory musculature (power and endurance training)
Increase Hydration and Improve Nutrition Levels
Immediate attention to improve the hydration level will likely thin and improve the mobilization of airway secretions and promote clear and odorless urine. The result of improved hydration is a decreased risk of respiratory and urinary tract infections. It is important to coordinate a patient’s hydration and nutrition program with the entire medical staff to determine the optimal level of hydration and means of attainment. For example, Lee may need a water bottle holder attached to his arm rest, or a “camel pack” system (used by bicyclists for long-distance rides) attached to the back of his wheelchair, etc, so he can readily and independently maintain adequate hydration levels. This is important for both short-term and long-term respiratory management strategies. The patient must be educated about the respiratory and renal risks associated with dehydration to promote long-term carryover into his home life after discharge.
Improve Cough Effectiveness/Secretion Clearance
It is important to place a high priority on determining the best method of secretion mobilization and of airway clearance to prevent hypoventilation and atelectasis, thus reducing his chance of developing an acute respiratory infection. This section will focus on describing options for Lee’s immediate airway clearance needs, but we will keep in mind that his needs may change with time and with the environmental setting (acute care, rehab hospital, home, work, etc).
Secretion Mobilization
In order to get secretions to the level where they can be expectorated, they must first be mobilized, or moved, from the periphery of the lungs to the proximal airways. Thus, an effective airway clearance program focuses initially at mobilizing secretions. Box 20-3 lists various strategies that can be used to accomplish this goal. Many studies have been done to evaluate the efficacy of mobilizing secretions with each of these techniques.75–79 In particular, Hardy’s 1994 article78 details a comparison of approximately 40 different studies evaluating the effectiveness of airway clearance interventions. The conclusion drawn from this and other articles is that no single mobilizing or expectorating technique is “the most effective.” All the methods demonstrate advantages and disadvantages. A clinician must decide which intervention works best for each particular patient based on the availability of an intervention, therapist’s skill, time factors, finances, patient comfort, patient fatigue, and independent airway clearance effectiveness. With all things considered, the best combination for the patient in our case would probably be (1) an adequate humidification program, (2) the implementation of postural drainage positions in his recumbent positioning program, (3) the purposeful timing of his medications to coincide with therapy sessions, (4) improving his overall hydration level, and (5) possibly the use of a PEP device if needed. Percussion and vibration can be added if this initial treatment was ineffective. Finally, the costly Vest could be used if it was available and the other methods failed.
BOX 20-3
Possible Secretion Mobilization Strategies
•Using a humidification system at the level of the tracheostomy to thin the secretions and keep them mobile
•Increasing systemic hydration level to thin secretions
•Incorporating postural drainage positions into recumbent positioning
•Adding percussion and vibration if necessary to loosen tough secretions
•Changing the timing of medications such as nebulizing medications (secretion thinning) or tone reduction medications (spasticity management) to occur 30 to 60 minutes prior to physical therapy to maximize secretion mobilization
•Implementing the use of PEP (positive expiratory pressure) devices such as the Ther-a-PEP, Flutter, or Acapella to mobilize secretions
•May not be capable of generating the expiratory pressure necessary to benefit from a PEP device
•Using the pneumatic vibrating vest (the Vest) which mechanically vibrates the entire chest wall while the patient is sitting
(Effective, but very expensive. Currently about $16,000.)
Expectoration
Now Lee is ready for us to help him expectorate his secretions more effectively. He showed impairments at all four phases of cough (expectoration). He cannot inhale deep enough to have an adequate inspiratory volume for coughing (impaired phase 1), he cannot close his glottis due to the tracheostomy (impaired phase 2), he cannot build up intra-abdominal or intrathoracic pressures due to intercostal and abdominal paralysis (impaired phase 3), and he cannot forcefully open his glottis and cough due to the tracheostomy (impaired phase 4). Thus, Lee needs assistance at all four levels.53
Start simply (Box 20-4). Begin with educating the patient on the importance of avoiding a secondary respiratory complication and about the lifelong risk he has for acquiring a respiratory complication secondary to paralysis. After his tracheostomy tube is removed, Lee will regain normal control of his glottis (phases 2 and 4), but he will always have significant impairments with phases 1 and 3 if his paralysis remains.
BOX 20-4
Possible Secretion Expectoration Strategies
Education
Educate the patient about secondary respiratory complications due to inadequate airway clearance.
Instruction
Instruct the patient to utilize ventilatory strategies with coughing to improve phase 1 (inspiration) and phase 3 (building up intrathoracic pressure).
Instruct the patient in active cycles of breathing (ACB) with or without forced expiratory technique (FET).
Manual Assistive Cough Techniques
Use assistive cough techniques, such as costophrenic assist, anterior chest compression, Heimlich-type assist (aka quad cough or abdominal thrust), counterrotation assist (see CD-ROM), etc.
Mechanical Devices
Use mechanical assistive devices such as suction machines or the cough assist (aka Cof-flator, mechanical in-exsufflator) to physically remove secretions.
At this point of his rehabilitation, part of the patient’s education involves teaching him to use independent ventilatory strategies (see the section on coordinating breathing with movements later) to augment the phases of cough. For example, teaching him to use trunk extension (or at least shoulder/scapular movements); eye gaze up, and a quick, long inspiratory effort before coughing should augment phase 1. Then, instruct him to look down, bring his shoulders/trunk forward into flexion (as far as he can safely control the motion), while he coughs or huffs through his tracheostomy, to augment phases 3 and 4. The one phase that he cannot assist at this point is phase 2 (closing the glottis) because the tracheostomy tube allows the air to escape below the level of the glottis. Patients with cervical SCIs appear to be able to increase their PCFR by using these ventilatory strategies during independent coughing. This early, simple education assists the patient in developing lifelong skills that will be necessary for effective management of pulmonary secretions.
Another type of independent airway clearance strategy was developed for patients with cystic fibrosis, but can sometimes be adapted for some patients with neuromuscular impairments or other diseases. This independent airway clearance strategy is called the active cycle of breathing (ACB) with forced expiratory technique (FET or “chicken wings”).80 ACB involves varying inspiratory lung volumes in an attempt to mobilize secretions from peripheral to proximal airways (secretion mobilization). It is then followed up by FET, which uses ventilatory strategies and chest wall compression to aid in expectoration.80,81 Theoretically, the patient with SCI can follow the instructions necessary for ACB and FET, but they may not have the potential to sufficiently increase inspiratory lung volumes adequately to effectively mobilize their secretions. Additionally, if SCI patients lack adequate trunk support, they may be unable to raise both upper extremities at the same time to perform the FET technique. Therefore, the compressive force on their chest wall may not be adequate to aid in expectoration. At this point in his rehabilitation, ACB is probably not a realistic intervention for our patient. However, as his lung volume potential increases, and his sitting balance gets better, it may become a viable option.
If independent strategies do not work well enough, the therapist can try manually assisted cough techniques. Many different assistive cough techniques are available and the majority of them appear to quite effective.41,53,82,83Several are demonstrated on the accompanying CD-ROM.84 Each of these assistive cough techniques addresses all four components of effective coughing, so how do you decide which assistive cough technique is the most effective for our patient? Several assessment methods are available, such as production of secretions, changes in breath sounds, improvement in ABGs or PFTs, or PCFR during an independent cough effort and during a cough while assisting the patient (see Chapter 9). The intervention that produces the greatest PCFR is the most effective and should be used with that particular patient. The minimal threshold PCFR for an effective cough appears to be 2.7 L/s.70
Thus, any intervention that produces a PCFR of at least 2.7 L/s can be considered a viable choice of interventions. The peak flow meter can measure the PCFR and is an inexpensive, readily available device.85 In addition to objective data, the therapist also needs to consider which technique is (1) the most comfortable to the patient, (2) the most effective from the patient’s perspective, (3) the one the patient is willing to have performed on him, and (4) the easiest and safest one to use by different staff or family members.
If secretion mobilization, independent strategies, or manually assisted cough techniques cannot adequately clear secretions, then mechanical assistance can be added or substituted for the less effective intervention. The most common mechanical device is a suction machine (tracheal suctioning). A sterile catheter is introduced into the patient’s airway through the tracheostomy down to or near the level of the carina (second rib). The secretions in the mainstem bronchus and trachea can then be suctioned out through this catheter (see Chapter 19). The advantage of this technique is that it is completely passive for the patient (however, it can also be seen as a disadvantage in terms of learning independent strategies to clear secretions). It is an extremely effective intervention for clearing secretions in the large airway.86 However, it is an invasive procedure and complications can arise, such as (1) transient oxygen desaturation, (2) soft tissue damage to the airway from the catheter, and (3) secondary increase in secretion production, in response to the introduction of a foreign object in the airway.86
Another mechanical device that has been reintroduced as an airway clearance device is the Cough Assist (or the Cofflator or Mechanical In-Exsufflation by JH Emerson, Cambridge, MA). This device delivers a positive-pressure cycle (inspiration) to the patient through an upper airway mask, or in our patient’s case, through his tracheostomy, tube, to augment phase 1. It is followed by a negative-pressure cycle (exhalation) to pull the secretions out. This device was originally developed in the 1950s for patients with polio and was almost completely abandoned in the 1960s when tracheotomies became commonplace.87 It was modified and reintroduced as a noninvasive means to mechanically assist expectoration in the 1990s. Thus far, the literature has shown it to be as viable as suctioning in expectorating secretions from patients with neuromuscular impairments.53,88–90 In addition, the Cough Assist has been successfully used to combat chronic hypoventilation (micro- and macroatelectasis) that often occurs secondarily to a decreased inspiratory lung capacity following a neuromuscular impairment such as a SCI. Complications of the Cough Assist noted in literature include (1) complaints of musculoskeletal pain along the chest wall due to the passive expansion of the chest during the inspiratory cycle, (2) dry mouth, and (3) nose bleeds.
No single intervention will work for every patient, and often several can be incorporated during physical therapy. It is important to note that finding and implementing an effective strategy to prevent secondary pulmonary complications is not the sole responsibility of any one medical discipline; rather it is the responsibility of the entire team, including the patient and his family. If the patient needs assistance with clearing his secretions, every team member shares a part of the responsibility in helping the patient. Thus, once an effective program has been developed, every team member, perhaps most significantly the family members and caretakers, needs to be educated about the best interventions. They also need to show competence in performing these interventions. Methods of evaluating competence should be based on the desired goals and the methods of examination that family members and caregivers feel most comfortable in using.
Coordination of the Decannulation Program with the Entire Team
It is imperative to work with the entire team to assist in a speedy and effective decannulation program (see Chapter 19 for further information on decannulation). Regardless of the method of decannulation, the patient will demonstrate a readiness for decannulation by demonstrating (1) his ability to breathe adequately through his upper airway; (2) his ability to clear his airways independently, or with assist, through his upper airway; and (3) his ability to safely swallow and protect his lower airway from aspiration. Closing off the tracheostomy site will allow the patient to use his upper airway to assist in cleansing, heating, and humidifying the inspired air before it reaches the lungs, thus helping to reduce the risk of further respiratory complications. In addition, removal of the tracheostomy tube allows the patient to use his glottis for functional tasks such as (1) coughing, (2) talking, (3) valsalva maneuvers for bowel and bladder management, and (4) the generation of subglottal pressures utilized for fine gradations of trunk movement necessary for upright posture control and balance.
Decannulation programs may include the use of one-way tracheostomy valves that allow for unrestricted inhalation through the tracheostomy site, but prevents exhalation through the site, thus forcing exhalation through the upper airway. These are also called “speaking valves” (ie, Passy Muir valves) because the exhalation volume passes through the vocal folds.
Another option to foster decannulation would be to place a “trach-cap” or a “trach-button” in the tracheostomy tube. The tracheostomy cap literally prevents any air from entering or exiting the tracheostomy tube, thus forcing inspiration and expiration through the upper airway. Because the resultant blocked tracheostomy tube is simply taking up space in the trachea, creating an obstruction and not assisting with ventilation, the trach-cap inadvertently makes it harder for the patient to breathe. Additionally, the patient cannot have an inflated cuffed tracheostomy tube with any of these valves because the cuffed tube prevents air from entering the upper airway; thus, the patient would have no method of exhaling.
Perhaps a better method to progress the patient with a tracheostomy toward decannulation is to use a “trach-button.” The tracheostomy button also forces upper airway breathing for both inhalation and exhalation, but the tracheostomy tube is removed and is replaced with a button at the level of the tracheostomy stoma. The patient still relearns to breathe through his upper airway, but the obstruction in the trachea from a tracheostomy tube is no longer present.
There are multiple methods to decannulate a patient. The type of decannulation program that Lee would utilize depends on the type of institution, as well as on personnel and equipment resources. The physical therapist generally plays a supportive rather than a leading role in this process.
Improve Postural Alignment in Reclining and Upright Postures
It appears to be critically important to develop and implement a program for the whole team that maintains an optimal alignment of the chest wall and spine to facilitate efficient and effective ventilation.91 In order to maximize the biomechanical properties of the diaphragm and other accessory muscles, passive alignment of our patient should include (1) opening his anterior chest wall to facilitate use of the pectoralis muscle as a substitute for the paralyzed intercostal muscles and to maximize the recruitment of the upper accessory muscles to counteract the paradoxical forces on his chest caused by gravity and an unopposed diaphragmatic contraction, (2) positioning his shoulders in relative external rotation, again to facilitate pectoralis activation, to improve the length–tension relationship of the long neck flexors and to promote scapular adduction which supports more thoracic spine extension, and (3) positioning his pelvis in a relative anterior tilt to take advantage of the mechanical stacking of the vertebral spine to minimize the potential for a secondary scoliosis and/or kyphosis. Obviously, maintaining ROM of all joints will aid in his positioning options. The physical therapist will also need to focus on reducing the adhesions from the scar tissue around his liver laceration, which is preventing his trunk from being positioned in a full-extension posture. If the scar is allowed to heal with limited mobility, it may secondarily contribute to the development of a spinal deformity (pulling him into kyphosis), thus limiting his respiratory mechanics.
In the short term, Lee still has a Halo vest on for cervical spine fixation; therefore, his spine will stay in a more optimal alignment during his acute rehabilitation. However, he needs to be educated about the need for continued optimal spinal positioning once the Halo is removed in order to prevent the development of adverse spinal curves over the long term.92
These concepts can and should be applied in both the upright and the reclining postures and can often be accomplished through the use of simple supports such as towel rolls or pillows (Figs. 20-2B and 20-2C). Of course, as with any assistive device used for positioning, the patient’s skin tolerance must be closely monitored to watch for any breakdown areas. However, because of his abdominal paralysis, Lee will always need an abdominal binder to help maintain visceral alignment under the dome of the diaphragm in upright posturing.37,53,93,94 This “need” for an abdominal binder will continue as long as his abdominal muscles are paralyzed. He will not “outgrow” it simply because he had his SCI a long time ago or because he has achieved cardiovascular stability.
Consideration for the mechanics of breathing, and the maintenance of the spine, pelvis, and chest wall alignment, can and should be adapted into a patient’s personal seating system. The seating system is normally designed and ordered along with a personal wheelchair during the patient’s rehabilitation phase. Long-term positioning management may also include a medication regimen (coordinated with the doctor) to help regulate our patient’s spasticity levels if they become so significant as to limit ROM and positioning options.
Improve Sleep
It also appears important to develop and implement a positioning plan with nursing to optimize our patient’s ability to get a good night’s sleep in order to function more effectively during the day. In addition to making sure that the patient can breathe effectively in a particular sleep posture, several other aspects need to be considered for nighttime positioning including (1) airway protection—Can he safely swallow or spit his saliva/secretions in a particular posture; (2) joint alignment—Are his joints positioned safely and effectively considering his long-term ROM maintenance; and (3) skin tolerance—Does his skin tolerate weight bearing without breakdown in that position? His sleep evaluation showed several possible alternative postures to supine to improve his respiratory support (see Table 20-14).
If these simple positioning changes are unable to adequately support nocturnal ventilation, then he could be evaluated for use of a positive pressure device, most commonly a CPAP or a BiPAP (bilevel positive airway pressure) system (see Chapter 19). Through the use of continuous positive pressure during exhalation, these devices help to prevent hypoventilation during sleep that results from shallow breathing. Both systems can be used with a tracheostomy attachment, or with a nasal or face mask attachment, and can be used if needed during the day as well. A modification of nocturnal nasal CPAP that automatically fine-tunes the level of positive pressure support while the patient is sleeping is currently being evaluated clinically and shows an improvement in patient comfort. One recent study showed that breathing could be well supported by both CPAP and the autoadjusting model (APAP), but that the APAP could accomplish this task with significantly less positive pressure and greater report of patient comfort.95
Increase Tolerance to Multiple Postures
It also appears to be very important to monitor patient’s cardiovascular response to different postures and activities and implement changes where necessary to increase the patient’s tolerance to postures that improve cardiopulmonary function and functional activities. Lee’s BP tends to be low, especially in upright postures (orthostatic hypotension); thus, the team will continue with periodic BP checks, especially if the patient complains of lightheadedness. The patient’s BP improved following the application of his abdominal binder and should therefore continue to be used. The patient also needs to be educated about the importance of the abdominal binder for both cardiovascular and pulmonary reasons. If the binder alone did not work, “pressure support hose” on his lower extremities could be continued to help increase the BP. Within a few weeks our patient should be able to tolerate sitting in a wheelchair for most of the day without the support hose, but the binder should always be worn for favorable cardiovascular, pulmonary, and postural adaptations.
A significant rise in BP will often accompany autonomic dysreflexia, which Lee has experienced. The patient must be educated about the signs and causes of dysreflexia and what to do during an episode. He should be told to instruct those around him to elevate his head, drop his legs down, open his binder (anything to decrease the hypertensive response caused by the dysreflexia), and to immediately check for a full bladder or impacted bowel which are often the precipitating causes.48,56
Tolerance to postures may also be determined by noncardiovascular responses, such as skin tolerance, painful joints, scar tissue adhesions, abnormal tone (spasms/spasticity), and restricted ROM. The entire team should be checking for signs of skin breakdown along weight-bearing points in both upright and reclining postures. Our patient has had signs of skin intolerance along the left greater trochanter, so left side-lying should be closely monitored. The patient’s position should be modified (such as upper extremity positioning) within each posture in response to pain or joint limitations.
Coordinate Breathing with Movement to Improve Overall Motor Performance (Ventilatory Strategies)
Teaching a patient to breathe in coordination (using ventilatory strategies) with all motor tasks appears to be important for all patients with ventilatory pump dysfunction and failure. Our patient has limited muscular resources due to paralysis, thus learning to purposely coordinate his breathing with these movements can help to augment his functional motor skills.93 The common theme of ventilatory strategies is to match the type of thoracic spine movement inherent in a particular motor task (extension vs flexion), and the type of muscular contraction needed to perform that task (concentric, eccentric, or isometric contractions), to the same type of movement associated within a specific breathing pattern (inhalation, exhalation, slow-, or fast-breathing patterns) and specific sensory cues (visual, auditory, manual, or others). By doing so, Lee can take advantage of well-established motor plans to assist in maximizing his motor response. Breaking this concept down into four component parts is helpful to understanding its global application.96
Thoracic Spine/Cage
Similar musculoskeletal movements can be paired with similar respiratory movements for efficiency of movement. Trunk extension is associated with inspiration (thoracic spine/thoracic cage complex expands), whereas trunk flexion is associated with exhalation (thoracic spine/thoracic cage complex compresses).
Muscle Contractions
Pair similar types of muscle contractions: concentric trunk/limb movements with concentric respiratory movements, eccentric with eccentric.
Breathing Patterns
Inspiration is always a concentric muscle contraction regardless of which muscles are used to inhale, whereas exhalation can be (1) passive, (2) eccentric (speech or controlled slow exhalation maneuvers), or (3) concentric (yelling, coughing, sneezing).
Sensory Patterns
Loud, fast commands tend to recruit the fast-twitched, power-oriented, accessory muscles (upper chest breathing). Slow, softer commands tend to recruit the slow-twitched, endurance-oriented diaphragm. Thus, audible cues can be used to encourage a specific type of breathing pattern. Likewise, the eyes tend to follow respiratory patterns. Eye-gaze-up is associated with inspiration (learned synergistic pattern through normal development), whereas eye gaze down is associated with exhalation. Last, manual cues make use of the muscle spindle and joint receptor responses to facilitate specific muscle (breathing pattern) responses.
By combining all four components, the therapist can teach any patient to move more efficiently combining the musculoskeletal, neuromuscular, cardiopulmonary, and sensory systems as an integrated, dynamic system, rather than looking at these systems as isolated, independent systems.96 For example, early in the rehabilitation program, Lee will begin to learn bed mobility skills to increase his independence. Rolling from supine to side-lying can be achieved with either trunk flexion (the most common method) or with trunk extension (a less common method). Because our patient has a Halo cervical fixation device restricting his neck motion, and because of the weight of this device, he will likely find it easier to attempt rolling with a trunk extension pattern.
How should he breathe when rolling in this scenario? Analyzing this movement, the therapist would note that his rolling required trunk extension and concentric muscle contractions. Thus, according to the principles of ventilatory strategies stated earlier, our patient should pair rolling with (1) inhalation, (2) upward eye gaze, and (3) a loud command to roll. If, 3 months later, when the Halo is removed, he finds trunk flexion to be a more natural trunk pattern to use for rolling, he would switch to another strategy. Rolling for him would then utilize a trunk flexion/concentric pattern, and as a result, he would then pair rolling with (1) exhalation, (2) downward eye gaze, and (3) a loud command (because he still needs to recruit accessory neck flexors). Using the concepts of ventilatory strategies, each movement is separately analyzed according to how a patient actually moves, not according to what is supposed to happen. This individualized approach encourages the most optimal pairing of breathing and movement for each individual patient based on their own motor planning and performance. Examples of ventilatory strategies are illustrated on Table 20-15.
TABLE 20-15 Examples of Pairing Ventilatory and Sensory Strategies with Movement
Ventilatory strategies are based on normal anatomic alignments, the normal biomechanics of movement and breathing, and the normal development of motor plans. If a particular pattern does not work for your patient, do not force the issue. Rather, find a pattern that does work to maximize that patient’s motor response. Once a patient learns the basics of applying ventilatory strategies to movement, they appear to spontaneously carry it over to new motor activities because they find it more efficient.
Improve the Patient’s Breathing Pattern
Teaching a patient to recruit accessory muscles to compensate for paralyzed intercostal muscles, thereby preventing or minimizing paradoxical chest wall movements, should improve breathing, ventilation, and functional abilities. The goal of this intervention is to create an efficient balance of the utilization of the respiratory muscles to maximize inspiratory volumes with a minimal “energy cost” of breathing and to simultaneously minimize the muscle imbalance (paradoxical breathing) that leads to the development of a pectus excavatum (or other musculoskeletal deformities) and smaller inspiratory volumes. The goal is not to prevent the diaphragm from participating in inspiratory maneuvers. The goal is to balance the diaphragm’s role with the other remaining respiratory muscles.19
It is important for the reader to realize that for this particular patient learning to activate the upper accessory muscles of ventilation is exactly what he needs to create a balanced inspiratory force with a minimum of unwanted side effects. However, for many patients with ventilatory pump dysfunction, the exact opposite may be true. For a wide variety of diagnoses stemming from primary pulmonary disorders such as COPD or asthma to secondary ventilatory dysfunction resulting from neuromuscular or musculoskeletal limitations, many patients overly recruit the upper accessory muscles and underutilize the diaphragm. For those patients, the goals of facilitation techniques would be to promote greater participation of the diaphragm and lessen the excessive activation of the upper accessory muscles. Lee needs a relatively greater amount of upper accessory muscle activity to counter the predominant diaphragmatic contraction. Thus, the techniques described here are appropriate only for the patient who needs to learn to recruit the accessory muscles. In this case study, our patient does not have functional abdominal or intercostal muscles and must therefore substitute the task of stabilizing the anterior chest wall with the utilization of his remaining respiratory musculature.
How quickly and effectively a patient with SCI learns to modify his breathing pattern depends on the individual patient. Breathing is a motor activity with a certain degree of volitional control that will require an active learning process. The patient in our case could learn it as quickly as 1 session or as slowly as 20 sessions or longer. Breathing retraining appears to be possible and beneficial.97,98 It is up to the therapist to find the most effective training method for their patient based on the disease process, patient and physical therapist skill level, costs, time availability, and available equipment. Examples of manual techniques that can be utilized successfully to facilitate upper chest expansion are demonstrated in the accompanying CD.84,99 They primarily utilize the principles and practice of PNF (proprioceptive neuromuscular facilitation) techniques.100 In order to take full advantage of the therapist’s manual input, the therapist must be sure to position the patient successfully first (optimize the length–tension relationship of the muscles to be facilitated) and to utilize appropriate ventilatory strategies during the technique.97 This will facilitate quicker success and carryover into function.
Success of these techniques is easily assessed by (1) repeating PFTs taken pre- and posttraining sessions, (2) measuring chest wall excursion pre- and posttraining, (3) timing phonation length or noting a change in number of syllables/breath, and/or (4) noting the patient’s report of shortness of breath using a dyspnea scale,100 Borg scale,101 or fatigue level (see Chapter 9).
Immediately following successful activation of the desired breathing pattern, activities must be used that promote a direct incorporation of this new breathing pattern into functional tasks in order to promote a functional carryover. In other words, breathing retraining cannot take place in a vacuum, or the patient will learn that proper breathing is only done in “therapy sessions,” but not in “real life.” For example, for our patient, a progression of the manual intervention could include, initially using manual, visual, and audible cues. This could be progressed to giving less audible, visual, or manual input to the patient’s chest wall and observing whether the patient could maintain the proper activation of the accessory muscles. Once positive results are observed, a therapist could use different postures and body positions to examine whether the desired pattern of breathing is maintained. Finally, the therapist could demand more functional use of the breathing pattern by incorporating it into tasks such as bed mobility, dressing, ROM exercises, and strengthening exercises. By this point, the pattern should become so well ingrained into the patient’s daily movement patterns (a result of active motor learning) that it would become his “preferred breathing pattern” and not just a therapeutic intervention.
Other training methods can be utilized in addition to manual facilitation techniques such as air stacking, biofeedback, and visualization.94 The important factor is to find an intervention that hastens the patient’s learning curve to achieve competency with upper chest muscle recruitment for both quiet breathing and deep breathing to achieve ventilatory efficiency. See Box 20-5 for a summary of possible breathing retraining methods.
BOX 20-5
Strategies to Facilitate Breathing Retraining
“Positioning for success”—to facilitate the likely activation of a particular breathing pattern
Ventilatory strategies—to maximize a desired breathing pattern response via the purposeful coordination of trunk movements, breathing, and sensory input
Manual facilitation techniques—to facilitate specific muscle spindle and joint receptor responses of the desired respiratory muscle
Air stacking—to add the effort of numerous smaller inspiratory efforts into 1 larger inspiratory volume
Biofeedback—to provide visual and/or audible feedback
Visualization—to provide internal feedback training
Training in tai chi or other Eastern modalities—to improve breath control
Glossopharyngeal breathing—to maximize voluntary inspiratory efforts in spite of devastating respiratory muscle impairments
If our patient had a higher cervical SCI, it may have been necessary to teach him glossopharyngeal breathing (GPB).102 This technique was developed during the polio epidemics, by patients themselves, to develop spontaneous breathing independent of a ventilator (iron lung), in spite of diaphragmatic, intercostal, and abdominal muscle paralysis. Using the innervation of the upper accessory muscles via the cranial nerves, the patient learns to draw air into his or her mouth and then “push” it down into his or her lungs. They do not actually push the air down, but that is a common description of the technique. The patient actually increases the size of his or her oral cavity, which creates a negative inspiratory pressure, thus facilitating inspiration. Second, they pull their chin and tongue back toward their neck causing positive pressure in the mouth, which forces the air down the trachea into the lung.99 This sequence, or stroke as it is called, is repeated numerous times per breath (~3–12 strokes per inspiratory effort) and can result in dramatic increases in vital capacity.103 Learning this technique can result in successful time off the ventilator for patients who would otherwise be completely ventilator dependent.104,105 In some cases, the learner has been so successful as to be off the ventilator during all wakeful hours. For other patients, it may simply represent a life-saving technique that would help them ventilate independent of a ventilator for a few minutes. A patient with a C4-SCI demonstrates the GPB technique on the accompanying CD.106
Improve Breath Support for Speech
Teaching the patient to utilize expiratory breath support for speech with a more controlled pattern will likely improve the disablement of cardiopulmonary disorders. This would require our patient to learn to use his inspiratory muscles eccentrically during phonation in order to elongate the expiratory phase for phonation. Refining breath support for phonation is a natural continuation of the patient’s breathing retraining program. Here our patient is asked to refine his breath control at a fine motor skill level, which is the production of speech. This does not require strength, but rather control. It will be much easier to accomplish once Lee is decannulated or at least once he is using a speaking valve, trach cap, or trach button. Decannulation or one of the aforementioned devices provides a closed system in which the glottis is able to alter (open and close) the entrance into the lungs. A tracheostomy tube without a speaking valve, trach cap, or trach button does not allow the glottis to control air leaving the lungs. Consequently, the air just “falls out” of the open airway, making one unable to use the slow expiratory volumes and flow rates generated during eccentric exhalation patterns that are necessary for speech.33,34
Because breathing retraining at any level requires the development of a new motor plan, success may be accomplished very quickly or slowly depending on the patient’s ability to learn motor tasks. It appears that patients who are relatively athletic tend to learn these maneuvers quickly (~1–4 sessions, with independent follow-up practice), whereas people who are less athletic and relatively clumsy tend to be slower in learning new breathing techniques (>6 sessions and follow-up practice). It appears to be related to their general ability to plan and learn new motor tasks.
Several approaches to phonation breathing retraining can be taken. All of the approaches focus on refining the length and control of expiratory maneuvers. Common recreational activities such as singing, humming, choral readings, blow toys that require prolonged exhalation, and/or wind and brass instrument playing demand refinement of expiratory control in order to be successful, thus directly improving breath support for phonation. Using these types of activities also provide the repetition that is necessary for the development of a new motor plan.
If the patient needs more sensory or motor input to develop adequate breath support for speech, then manual techniques can be employed. These techniques are demonstrated on the accompanying CD and all focus on developing better kinesthetic awareness of the chest wall movements during exhalation in order to assist the patient in better eccentric motor planning.99,107
A final suggestion for assisting the patient in developing a more refined breathing pattern comes from the incorporation of ventilatory strategies with movement. Because quiet everyday speech is primarily an eccentric contraction, the patient can be taught to purposely combine eccentric movements with speech. Thus, if the patient’s trunk or limb muscles have better eccentric control than his breath support, he can use his limb or trunk musculature to facilitate the ventilatory muscles. The reverse is also true. If the patient has better phonation breath support than eccentric control of the limb or trunk muscles, he can be taught to use his phonation to augment other motor responses. Let us say, for example, that our patient wants to reach up to the top of his dresser from his wheelchair to pick up a comb and bring it down to his lap. According to ventilatory strategies described earlier in this section, the patient uses trunk extension and shoulder flexion (both concentric contractions) to reach the comb; thus, an upper chest inspiratory pattern and upward eye gaze would be the natural corresponding ventilatory pattern. On the way back down, he must use eccentric contractions of his shoulder flexors and trunk to slowly lower (not drop) the comb in his lap; thus, the natural corresponding ventilatory pattern would be eccentric exhalation, or speech. Lee could easily be instructed to inhale and look up while reaching for the comb to augment his reach through the chest and spine position associated with inhalation, and then to count outloud or hum and watch the comb (downward glance) while he lowers the comb to his lap. If his phonation skills are better developed than his shoulder muscle skill, then his voice can be used to facilitate better shoulder control. However, if his shoulder skill is better developed than his phonation skills, then his shoulder movements can be used to facilitate better breath control.
Like the interventions described in the previous section on improving breathing patterns, effectiveness of any particular technique or activity can be immediately assessed by pre- and posttesting such as (1) length of a vocalization, (2) number of syllables per breath, (3) loudness of vocalization, and (4) report of fatigue. It is not unusual for a patient to double or even triple their length of phonation following specific retraining programs because it appears to improve control, not strength. Thus, the effort it takes to implement a program for improved phonation is well worth the investment in terms of potential benefit in functional abilities.
Increase Strength, Function, and Endurance of Remaining Respiratory Musculature (Power and Endurance Training)
Development and implementation of a program to strengthen remaining respiratory muscles and develop the necessary endurance of those muscles to support maximal gross motor activity are of great importance for patients with ventilatory pump dysfunction and the potential for failure. In other words, even though our patient may now be capable of breathing properly (a good motor plan), he may still have weakness within that pattern. Second, once he develops some strength or power with this breathing pattern, he may not have the necessary endurance to use the power functionally. Consequently, even though our patient can now properly activate his ventilatory musculature, he still needs a basic strengthening/endurance program.
Endurance
Respiratory muscles normally become stronger in response to a physiologic demand. For example, running a marathon is a high-oxygen-consuming task, which requires higher TVs and RRs over a prolonged period of time, to meet the physiologic need. As a result, the body secondarily builds strength and endurance of the respiratory muscles to be able to consistently supply the inspiratory volume needed. However, how do you get patients with SCI to strengthen their respiratory muscles if they cannot sustain a gross motor activity, like pushing the wheelchair, long enough to demand a greater physiologic response from the respiratory system? How will they ever build endurance? For patients like Lee, the therapist will need to bypass the large muscle groups and go straight to the respiratory muscles themselves. Creating an artificial demand for greater inspiratory and/or expiratory muscle contraction like that demanded when running, the respiratory muscles can be specifically targeted for strengthening and endurance training. Ventilatory muscle trainers (VMTs) were designed to accomplish such a goal.
VMTs can be either inspiratory muscle trainers (IMT) or expiratory muscle trainers (EMT). Both work by creating resistance to inspiration or expiration, thereby forcing the patient to create a stronger muscle contraction to exchange their ventilatory volumes. It is similar to breathing in or out through your mouth with a straw, while wearing a nose clip to prevent cheating via nasal breathing. VMTs focus on improving the strength and endurance of the ventilatory muscles because they offer resistance to muscular contraction. There are several devices to choose from such as the P-flex or Threshold devices (Respironics/Healthscan Products in Cedar Grove, NJ). Numerous recent studies have shown the efficacy of such programs with both primary and secondary lung dysfunction populations108–111; hence, every patient with respiratory muscle weakness or poor endurance, who has the capability to use a VMT, should be started on a program. Most programs last 4 to 6 weeks for 15 to 20 minutes per session, 5 to 7 days/wk. The instructions are to breathe in or out against resistance, not at a maximal level, but at a level the patient can sustain. The patient progresses to greater levels of resistance as he can tolerate it during the 4- to 6-week period. In the most recent studies, all groups show improvement in inspiratory muscle strength (PImax) and endurance (minute ventilation) regardless of whether their condition was acute, chronic, primary lung dysfunction, or ventilatory pump dysfunction.108–111 More specific methods to perform IMT and EMT are provided in Box 20-6, and methods to measure ventilatory muscle endurance are presented in Chapter 9.
BOX 20-6
Methods to Perform Inspiratory and Expiratory Muscle Training
Measurement
Measurement device: Several different types of devices are used to measure ventilatory muscle strength. The methods to measure the positive and negative pressure (in centimeters of water) generated by the patient during such testing is by using a manometer or pressure transducer. When using a manometer, a needle is deflected to the point of maximal generated pressure after which the needle may fall back to the resting level of 0. Such devices typically have poorer resolution and reliability. Newer devices have an internal pressure transducer that provides a digital display, which remains illuminated and as a result has desirable resolution and reliability.
Body position: During the measurement of ventilatory muscle strength the patient should wear a noseclip and be seated with the trunk at a 90-degree angle to the hips.
1.Maximal inspiratory pressure (MIP):
a.Have patient expire fully (near residual volume).
b.Motivate patient to inspire as forcefully as possible.
c.Document the MIP and repeat the aforementioned until a stable baseline is observed.
2.Maximal expiratory pressure (MEP):
a.Have patient inspire fully (total lung capacity).
b.Motivate patient to exhale as forcefully as possible.
c.Document the MEP and repeat the aforementioned until a stable baseline is observed.
Administration of ventilatory muscle training
Ventilatory muscle training should be administered by using the aforementioned results.
Inspiratory muscle training: Begin breathing with one of several available devices at 20% to 40% of MIP for 5 to 15 minutes, 2 to 3 X/day. Increase resistance to 40% to 60% of MIP based on patient tolerance.
Expiratory muscle training: Begin breathing with one of several available devices at 5% to 10% of MEP for 5 to 15 minutes, 2 to 3 X/day. Increase resistance to 10% to 15% of MEP based on patient tolerance.
Strength and Power
Similarly, our patient should start a power (strengthening) program. In order to focus on strength and power, Lee needs to work at higher resistance levels with shorter repetitions, generally 3 sets of 10 repetitions (or modified per patient). The patient can use the same IMTs with the resistance increased and the time decreased. Inspiration strengthening can also be achieved through the use of incentive spirometers with specific target ranges. The patient is asked to give a maximal effort and sustain the inspiration for a few seconds (if possible) before releasing the breath. Expiratory muscles can be strengthened using a peak flow meter or an EMT with target ranges. The patient is instructed to take a deep breath first and then to blow hard and fast. Lee should show significant gains in both respiratory strength and endurance, as measured by ventilatory muscle strength and PFTs following completion of this program (see Chapter 9 for methods to measure ventilatory muscle strength).
Endurance and strengthening programs overlap in their application and choice of assistive devices. The main objective, regardless of the chosen intervention, is to improve the respiratory muscle “strength and endurance” enough to provide the maximal benefit to the patient in terms of oxygen delivery for functional ADL use and reducing the work of breathing and the “risk” for acute pulmonary complications.
MEDICAL INTERVENTIONS FOR VENTILATORY PUMP DYSFUNCTION AND POTENTIAL FOR FAILURE
Medical Interventions for Ventilatory Pump Dysfunction
The medical interventions for ventilatory pump dysfunction include many of the interventions presented in Chapters 7 (Pulmonary Pathophysiology) and 8 (Medications). These interventions are summarized in Table 20-16 with focus on the correction of ventilatory pump dysfunction and failure. The primary methods to correct ventilatory pump dysfunction or failure appear to be risk factor reduction and pharmacologic, mechanical, surgical, and pulmonary rehabilitation. All of the interventions listed in Table 20-16 have the potential to (1) decrease the amount of bronchospasm in the bronchials, (2) decrease the work of the breathing, or (3) improve the length–tension relationships of ventilatory muscles. It is important to note that pharmacologic agents combined with optimal pulmonary rehabilitation services have the potential to decrease the amount of bronchospasm and work of breathing and possibly improve the length-tension relations of the ventilatory muscles.112–114
The primary goals of medical treatment for persons with ventilatory pump dysfunction are to decrease bronchospasm and the work of breathing. Pharmacologic agents such as bronchodilators and glucocorticoids are the primary methods to achieve the aforementioned goals. Mechanical interventions such as CPAP or BiPAP may be used either in conjunction with pharmacologic agents or alone to also achieve the aforementioned goals. The provision of these noninvasive positive-pressure mechanical ventilators often decrease bronchospasm, the work of breathing, and may provide the ventilatory muscles an improved length–tension relationship.110–113 Brief to prolonged use of CPCP or BiPAP may improve the breathing of patients with ventilatory pump dysfunction or the potential for ventilatory pump failure and improve exercise and functional abilities.115–118 If the previous methods of treatment are ineffective at improving ventilatory pump dysfunction or failure, surgical techniques may be employed. Several surgical techniques that appear to be beneficial for select patients include volume-reduction surgery and lung transplantation. Administration of supplemental oxygen appears to improve most of the previous goals of medical treatment and often improves the dyspnea associated with ventilatory pump dysfunction or failure. Finally, optimal pharmacologic therapy in conjunction with a comprehensive pulmonary rehabilitation program appears to improve the disablement of ventilatory pump dysfunction and failure.112–118
MEDICAL INTERVENTIONS FOR VENTILATORY PUMP FAILURE OR THE POTENTIAL FOR VENTILATORY PUMP FAILURE
The medical interventions for patients with ventilatory pump, failure, or the potential for ventilatory pump failure are also listed in Table 20-16. The methods to attain these goals are similar to the medical interventions for ventilatory pump dysfunction. Furthermore, the goals of treatments for ventilatory pump failure are similar to those presented in Chapter 18 (Physical Therapy Associated with Cardiovascular Pump Dysfunction or Failure) for cardiovascular pump failure but are directed at the ventilatory pump. For example, the goals of most interventions for ventilatory pump failure or the potential for failure are to decrease the work of breathing and improve the work performed by the ventilatory muscles, whereas the goals of most medical treatments for cardiac pump failure are to decrease the work of the heart and improve the work of the heart.112–118
TABLE 20-16 Medical Interventions for Ventilatory Pump Dysfunction and Failure
OUTCOMES—UTILIZATION OF THRESHOLD BEHAVIORS FOR IMPROVEMENTS IN EXERCISE AND FUNCTIONAL ABILITIES FROM AEROBIC EXERCISE TRAINING: IDENTIFICATION OF RESPONDERS VERSUS NONRESPONDERS TO PULMONARY REHABILITATION
The identification of patients with ventilatory pump dysfunction or the potential for failure who are likely to respond to pulmonary rehabilitation is critical to allocate optimal pulmonary physical therapy.119–123 A recent study by Troosters, Gosselink, and Decramer found that patients with reduced exercise capacity, maximal inspiratory strength, and peripheral muscle strength (handgrip and quadriceps strength) who experience less ventilatory limitation to exercise are most likely to improve from exercise training.121 Table 20-17 lists these and several other threshold behaviors associated with improvements in disablement from pulmonary rehabilitation for patients with a variety of pulmonary disorders.119–123
TABLE 20-17 Possible Predictors of Success or Failure of Patients With Ventilatory Pump Dysfunction or the Potential for Ventilatory Pump Failure in Pulmonary Rehabilitationa
Tables 20-18 through 20-20 provide an overview of the literature by providing select studies of aerobic and strengthening exercise studies (Table 20-18),124,125 IMT studies (Table 20-19),126–134 and diaphragmatic breathing studies (Table 20-20) for patients with ventilatory pump dysfunction and potential for failure.134 The information provided in these Tables appears to support the clinical utility of the threshold behaviors provided in Table 20-17 and reveals the beneficial effects of these interventions in the majority of patients enrolled in aerobic/strengthening exercise and breathing exercise programs. Identification of optimal patients for specific interventions should enable even greater improvements in the disablement of patients with ventilatory pump dysfunction, potential for ventilatory pump failure, or even ventilatory pump failure.
TABLE 20-18 Aerobic Exercise Training of Patients With Ventilatory Pump Dysfunction due to Asthma or COPD–Results of Meta-Analytic Studies
TABLE 20-19 Select Studies of Inspiratory Muscle Training in Patients With Ventilatory Pump Dysfunction
TABLE 20-20 Studies of Diaphragmatic Breathing in COPD
Boxes 20-7 and 20-8 provide specific methods to perform aerobic or strength training and Box 20-9 provides important methods to administer diaphragmatic breathing exercises to patients with ventilatory pump dysfunction or the potential for failure. The methods to perform aerobic and strength training in patients with ventilatory pump dysfunction and the potential for failure are similar to the methods of training patients with cardiac pump failure, except that patients with ventilatory pump dysfunction or the potential for failure often have more of a ventilatory limitation to exercise. In view of this, more emphasis should be placed on attempting to decrease the ventilatory limitation to exercise via medications, body positions, ventilatory muscle training, and airway clearance techniques when needed. Patients who are unable to decrease ventilatory constraints to exercise training likely require noninvasive mechanical ventilation like CPAP and BiPAP.
BOX 20-7
Exercise Training Methods for Patients with Ventilatory Pump Dysfunction and the Potential for Failure
1.Perform an exercise test or utilize recent exercise test results—6- or 12-minute walk tests may be substituted for a structured exercise test (see Chapter 9)*
2.Determine whether the cardiovascular and pulmonary response during the exercise test is adaptive
3.If exercise test results are adaptive without signs or symptoms of myocardial ischemia or cardiac arrhythmias, the exercise prescription should be developed via one of several methods including:
a.Karvonen method
b.60% to 85% of peak heart rate or peak oxygen consumption
c.Rate of perceived exertion corresponding to optimal training heart rate or level of oxygen consumption
d.Heart rate or rate of perceived exertion just below the ventilatory threshold/anaerobic threshold
e.Level of dyspnea
4.If exercise test results are not adaptive and show signs of signs or symptoms of myocardial ischemia, cardiac arrhythmias, desaturation, excessive accessory muscle with or without a paradoxical breathing pattern, or a marked ventilatory limit to exercise (see Chapters 9 and 10), the exercise prescription should be developed via one of several methods including:
a.Ischemic threshold via heart rate
b.Ischemic threshold via rate pressure product (double product)
c.Ischemic threshold via electrocardiographic evidence of myocardial ischemia or cardiac arrhythmias
d.Heart rate or rate of perceived exertion/dyspnea just below the threshold for maladaptive cardiovascular or pulmonary exercise test results
5.Perform physical exercise using the most appropriate mode, duration, frequency, and duration based on exercise test results, the level of dyspnea and resting and exercise breathing pattern, and patient goals/enjoyment.
6.Begin with gentle stretching and aerobic exercise and progress to a greater exercise duration and intensity as exercise training continues.
7.Set realistic goals for exercise with a range of 20 to 45 minutes exercise duration, 3 to 5 X/wk frequency, and at an appropriate training intensity based on numbers 3 and 4 above.
8.Monitor patient during exercise using the methods described in Chapters 9 and 10 and determine the frequency of monitoring during an exercise training session based on the exercise test results, level of dyspnea, resting and exercise breathing patterns, and other patient signs/symptoms.
9.Reexamine the patient during each exercise session using the methods described in Chapters 9 and 10.
10.Perform a second exercise test after 1 to 3 months of exercise training to establish safety of progressive exercise training and develop a new exercise prescription.
*Bolded sections identify key concerns for patients with ventilatory pump dysfunction or the potential for failure.
BOX 20-8
Criteria for the Initiation and Progression of Exercise Training in Patients with Ventilatory Pump Dysfunction or the Potential for Ventilatory Pump Failure (Compensated Ventilatory Pump Failure)
I.Relative criteria necessary for the initiation of an aerobic exercise training program—Compensated ventilatory pump failure
1.Ability to speak relatively comfortably without signs or symptoms of marked dyspnea (able to (1) vocalize and sustain vowel sounds like “ah” for ≥5 seconds before taking a breath, (2) ≥5 syllables per breath, or (3) loudly with a RR < 40 breaths/min)
2.≤Moderate fatigue
3.Breath sounds present in one-half of the lungs
4.No paradoxical breathing pattern or a paradoxical breathing pattern is resolved with forward leaning.
5.Ability to increase tidal volume above a reliable (repeatedly stable) baseline value via change in body position, breathing pattern, or other perturbation/intervention
6.Oxygen saturation level >90%
II.Relative criteria indicating a need to modify or terminate exercise training
a.Marked dyspnea or fatigue (eg, Borg rating >4–5/10)
b.Oxygen saturation <88%
c.Respiratory rate >50 breaths/min during exercise
d.Development of S3 or pulmonary crackles
e.Increase in pulmonary crackles
f.Significant increase in the intensity of the second component of the second heart sound (P2)
g.Poor pulse pressure (<10 mm Hg difference between the systolic and diastolic blood pressures)
h.Decrease in heart rate or blood pressure of >10 bpm or mm Hg, respectively, during continuous (steady-state) or progressive (increasing workloads) exercise
i.Increased supraventricular or ventricular ectopy
j.Increase of >10 mm Hg in the mean pulmonary artery pressure (for invasively monitored patients)
k.Increase or decrease of >6 mm Hg in the central venous pressure (for invasively monitored patients)
l.Diaphoresis, pallor, or confusion
Adapted with permission from Cahalin LP. Heart failure. Phys Ther. 1996;76:529.
BOX 20-9
Specific Methods to Instruct and Perform Diaphragmatic Breathing—A Literature and Research Synthesis130
1.Comfortable body position—sitting, semi-Fowler’s position (sitting at a 45-degree angle), side-lying, or sitting with trunk flexion if marked hyperinflation of the lungs and a paradoxical breathing pattern are present at rest or during diaphragmatic breathing. Measure tidal volume before beginning instruction in DB.
2.Appropriate position of the pelvis, neck, eyes, and upper and lower extremities—posterior pelvic tilt, neck extension, upward position of the eyes, upper extremities in external rotation and flexion, and lower extremities in external rotation and flexion may improve diaphragmatic breathing.
3.Tactile stimulation—placement of patients hand and therapists hand on the abdomen (level of the umbilicus) and the upper chest (level of the manubrium) with a quick stretch inward and upward at end exhalation at the abdominal area.
4.Auditory stimulation—Therapist loudly inspires with the inspiratory maneuver of the patient and loudly exhales with the expiratory maneuver of the patient.
5.Visual stimulation—Patient instructed to observe increased motion of hand over the abdomen and decreased motion of hand over the upper chest; biofeedback of respiratory maneuvers via electromyography of respiratory muscles, oxygen saturation, or a mirror may be useful.
6.Breathing instruction—Request patient to “breathe into my hand” during inspiration while instructing the patient to inspire through the nose and exhale orally with pursed lips.
7.Provide supplemental oxygen, bronchodilator therapy, and secretion removal if needed.
8.Breathing instruction—Request patient to “sniff” to promote a diaphragmatic contraction and then to “breathe into my hand” during inspiration.
9.Evaluate competency in diaphragmatic breathing—Doubling of abdominal tidal excursion with reduced upper chest excursion. Measure tidal volume during DB.
10.Possibly use an abdominal–diaphragmatic breathing pattern which incorporates an abdominal contraction at end-expiration followed by DB.
One potential method to train the ventilatory muscles is diaphragmatic breathing. Diaphragmatic breathing may be beneficial for select patients, and an extensive review of diaphragmatic breathing in COPD revealed that patients who have elevated respiratory rates, low tidal volumes that increase during DB, and abnormal arterial blood gases with adequate diaphragmatic movement are most likely to benefit from diaphragmatic breathing.135 Administering diaphragmatic breathing to such patients while using the methods described in Box 20-9 should optimize efforts to administer diaphragmatic breathing. Furthermore, administering inspiratory and expiratory muscle training as described in Box 20-6 with the methods of diaphragmatic breathing presented in Box 19-9 should enable patients with ventilatory pump dysfunction and the potential for failure to develop improved ventilatory pump function.
SUMMARY AND APPLICATION TO THE DISABLEMENT MODEL
The Disablement Model by Nagi (pathology, impairments, functional limitations, disability) was described in Chapter 2 and has been applied to a patient with SCI throughout the chapter. In this chapter, the focus has been on identifying the long-term impairments and risk factors associated with cardiopulmonary dysfunction following an SCI (ventilatory pump dysfunction/failure, preferred Practice Pattern 6E) and the potential for decreasing the resulting functional limitations based on successful cardiopulmonary management of these impairments and risks.
The management of the patient with ventilatory pump dysfunction, and the ongoing risk for ventilatory pump failure, is complicated and unending. All team members need to be part of the evaluation process, the development and implementation of a successful cardiopulmonary program, and the continuing reassessment of its effectiveness. Perhaps the most important component of the program in the rehabilitation setting versus the acute ICU setting is the education of the patient and his family. Although our patient, Lee, was in the ICU, the emphasis of his medical intervention was to “save his life.” In the rehabilitation setting, the emphasis switches to helping the patient regain and maintain a “quality to his life,” thus focusing on minimizing his long-term disability. The patient and his family must know how to continue these programs after discharge from the hospital setting in order to foster a lifelong successful management of his cardiopulmonary risks. If well managed, this patient should encounter fewer respiratory complications.4,63,136,137 This will result in minimizing his long-term functional limitations and resultant disability level. However, if he fails to be vigilant about managing his impairments, they can result in acute pulmonary problems and secondary functional limitations with potential for greater physical disability.
Close examination of the case study presented in this chapter should make it clear that the proposed examinations and interventions can be applied to a patient with ventilatory pump dysfunction or failure from any etiology. These same examinations and interventions likely apply to a patient with COPD, pulmonary fibrosis, or CVA and should enable optimal physical therapy to patients with ventilatory pump dysfunction or failure. One important behavior that appears to be capable of differentiating between ventilatory pump dysfunction and the potential for failure is a paradoxical breathing pattern.138–144 Identification of the absence or presence of a paradoxical breathing pattern may be helpful in allocating physical therapy interventions.138–144
The primary domains of disablement most affected in patients with ventilatory pump dysfunction or failure are similar to those of patients with cardiac pump failure which are listed in Table 18-20. Subtle differences exist, but the methods to manage these domains of disablement are very similar for patients with cardiac pump failure and for patients with ventilatory pump dysfunction and failure.
LIMITS OF OUR KNOWLEDGE
Significant research on SCI and resultant ventilatory pump dysfunction and on secondary respiratory complications has already been conducted, but more research is needed on the effectiveness of current physical therapy interventions in minimizing these risks. Which interventions, or combination of interventions, are the most effective and efficient? Airway clearance interventions are probably the best studied area of intervention within the physical therapy realm, with good evidence-based data to assist the therapist in planning a plausible intervention. More clinical research is needed in evaluating the effectiveness of interventions such as using ventilatory strategies with movement, improved breath control for speech, and the best methods for successful breathing retraining and carryover into function. Furthermore, further investigation of the clinical utility of paradoxical breathing patterns in physical therapy examinations and allocation of specific interventions is needed.138–144 Other areas worthy of further investigation include patient motivation, family support, and financial issues which should assist the physical therapist’s clinical decision-making skills and optimal allocation of physical therapy interventions.
Heads Up!
This chapter includes a CD-ROM activity.
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CHAPTER 20
An International Perspective: Japan
Yoshimi Matsuo
Physical therapy (PT) enjoys widespread utilization within the Japanese health care system. There are currently about 31,000 practicing physical therapists who are members of our professional organization, the Japanese Physical Therapy Association (JPTA). Japanese physical therapists practice in a wide variety of practice settings, including hospitals, outpatient facilities, rehabilitation centers, and many long-term care facilities. We practice in many other areas, including home care, acute care, orthopedics, neurology, and sports. Japanese physical therapists can obtain board certification as clinical specialists in one of seven specialty areas of practice, of which cardiopulmonary physical therapy is one. To date there are around 38 cardiopulmonary clinical specialists. In Japan, physical therapists must practice with a doctor’s prescription. There are no licensed PT assistants.
Cardiopulmonary physical therapy is an important, though relatively small, specialty area of practice in Japan. Nonetheless, cardiopulmonary physical therapists may be found in intensive care units, outpatient facilities, wellness programs, and acute care hospitals. They are an integral part of cardiac and pulmonary transplant teams and open heart surgical teams, among others. Currently there is a measure of competition and overlap of service provision to patients with cardiovascular and pulmonary disease. Nursing may provide “chest physical therapy” in some hospitals; exercise physiologists may provide exercise programs; and nursing may oversee cardiac rehabilitation programs and monitor the patient during exercise. Currently, cardiopulmonary physical therapists are actively engaged in reducing hospital stay through the prevention of pulmonary complications. Also, cardiopulmonary physical therapists in Japan are developing evidence-based models of practice in order to improve PT outcomes in all practice settings.
Development of evidence-based practice in physical therapy is much needed in Japan. The American Association of Cardiovascular and Pulmonary Rehabilitation (AACVPR) guidelines have the potential to promote change in Japanese clinical settings.1 Japanese physical therapists need evidence in order to select the most effective methods to examine and treat patients. The Japanese Respiratory Society and Japan Society for Respiratory Care have both produced statements for respiratory rehabilitation in 2001.2 The latter published “A Manual for Respiratory Rehabilitation—Therapeutic Exercise” in 2003.3
The medical payment system in Japan is presently changing, with the Japanese government adopting a DPC (diagnostic procedure combination) system, which is somewhat different from the DRG-PPS methods employed in the United States. As a result, the number of days that patients are in-hospital after an acute event is rapidly decreasing. Japanese physical therapists treat a wide variety of patients during the hospitalization period including patients with acute myocardial infarction or those with angina, those with thoracic and abdominal surgery including transplantation, those with chronic obstructive pulmonary disease (COPD) or other type of restrictive lung disease, those with neuromuscular disease or spinal cord surgery, and those in the intensive care unit. Although only a moderate number of Japanese physical therapists currently practice in the cardiopulmonary environment, more are showing interest. This greater interest in cardiovascular and pulmonary physical therapy in Japan may be due to recent advances in treatment techniques developed by Japanese physical therapists. However, the language barrier between Japan and other countries limits what Japanese therapists can learn about cardiovascular and pulmonary physical therapy in the United States, and what American therapists or physical therapists from other countries can learn about Japanese cardiovascular and pulmonary physical therapy. The role of respiratory physical therapy in Japan will be described in the following sections.
PULMONARY REHABILITATION PROGRAM CHARACTERISTICS: AN INTERNATIONAL SURVEY
Kida et al. surveyed pulmonary rehabilitation programs in Tokyo, Japan, and compared them to similar programs in North America and Europe.4 The survey instrument was a 13-item questionnaire sent in December 1994 to institutions in North America (n = 178), Europe (n = 179), and Tokyo (n = 399). Response rates were 51%, 40%, and 51%, respectively. Survey results showed that pulmonary rehabilitation programs (PRP) were available at 56% of hospitals in North America and at 74% of hospitals in Europe, but at only 20% of hospitals in Tokyo. Most pulmonary rehabilitation programs existed as outpatient clinics in North America (98%), whereas both outpatient (55%) and inpatient programs (65%) were found in Europe. Although COPD was the predominant type of lung disease for which patients in both North America and Europe were referred, this accounted for only 34% of referrals in Tokyo. Referrals for primary tuberculosis sequelae (p = 0.028) and bronchiectasis (p = 0.021) were more common in Tokyo, as well as in Europe. Table 1 shows that many of the program components available in North America were less available in Europe; most were unavailable in Tokyo. These included family education, psychological support, nutritional instruction, treadmill and bicycle ergometry, gait training, and activity of daily living sessions. The survey showed that pulmonary rehabilitation programs in North America are more multidimensional. However, target diseases differ between North America, Europe, and Tokyo. Problems common to all three regions included a lack of staff and insufficient reimbursement. In summary, these findings demonstrate a need for Japanese physical therapists to have a greater role in the care provided to patients enrolled in Japanese respiratory programs.
TABLE 1 Comparison of Pulmonary Rehabilitation Program Content in North America, Europe, and Tokyo
DIFFERENCES IN INTERVENTION EFFECT IN PATIENTS WITH COPD BETWEEN JAPAN AND OTHER COUNTRIES
Many investigations in the United States and Europe have reported that respiratory rehabilitation does not improve pulmonary function. However, Gimenz et al. reported that endurance training in patients with COPD improved maximum inspiratory and expiratory pressures.5 Furthermore, some Japanese investigators emphasize that physical therapy and respiratory rehabilitation do improve pulmonary function.6,7 Taniguchi et al.8 found that the percentages of vital capacity (VC), forced expiratory volume (FEV), residual volume (RV), functional residual capacity (FRC), and the ratio of residual volume (RV) to total lung capacity increased with pulmonary physical therapy. The authors hypothesized that physical therapy decreased FRC and improved ventilatory efficacy.8
Watanabe et al.9 evaluated the effects of pulmonary rehabilitation on pulmonary function in 15 patients with chronic emphysema who underwent pulmonary rehabilitation for 6 weeks as inpatients. Pulmonary rehabilitation consisted of relaxation techniques, breathing retraining, thoracic massage, therapeutic exercise, and walking. In 8 of the 15 patients, vital capacity increased by more than 200 mL (over 10%; Table 2), and in 7 of the 15 patients maximum exercise capacity increased by more than 5 watts (over 10%). Increases in vital capacity were not associated with increases in maximum exercise capacity. The percentage of change in vital capacity associated with pulmonary rehabilitation correlated significantly with the percentage of change in tidal volume and the percentage of change in expiratory minute ventilation at the maximum workload. The percentage of change in tidal volume at maximum workload correlated significantly with the percentage of change in maximum oxygen uptake. The increase in vital capacity was attributed to an improvement in thoracic cage movement. These findings suggest that pulmonary rehabilitation can increase vital capacity in some patients with chronic pulmonary emphysema, and that such an increase is not directly connected to increases in exercise capacity.
TABLE 2 Outcomes of a Pulmonary Rehabilitation Program
An important goal of Japanese physical therapist interventions is to mobilize the chest wall of patients with COPD. The techniques used to mobilize the chest include relaxation and stretching of the respiratory muscles and arthrokinematic intervention for the synovial joints. For example, Japanese physical therapists have started to mobilize the costovertebral and costosternal joints, meeting with apparent success. This type of arthrokinematic intervention appears to reduce chest wall size on forced expiration and may be useful in improving the elasticity of the chest wall. These mobilization techniques, however, require further investigation in treating various pulmonary disorders.
CHANGES IN PULMONARY FUNCTION FOLLOWING SURGERY
Postoperative pulmonary complications are still a major cause of postoperative mortality in Japan, especially in elderly patients. Toyota and his colleagues reported on the change in pulmonary function after surgery and an adequate period of intervention for chest physical therapy.10 They performed pulmonary rehabilitation in 98 patients who had undergone surgery using general anesthesia. Lung function (%VC and %FEV1) was measured via spirometry preoperatively and weekly for 3 weeks following surgery. Patients were divided into four groups: thoracotomy incision with lung lobectomy, thoracotomy incision without lung lobectomy, upper abdominal incision, and lower abdominal incision. The changes in %VC relative to preoperative values were significantly reduced within 7 days after surgery in all groups (Figs. 1 and 2). This finding was most remarkable in the lung lobectomy group. The second most remarkable response was in thoracotomy; the third was in upper abdominal incision, the fourth was in lower abdominal incision. The incidence of postoperative pulmonary complication was 13.8% in lobectomy, 4.0% in thoracotomy, 3.0% in upper abdomen, 0% in lower abdomen. These data identify areas of need for physical therapy services in patients who undergo thoracoabdominal surgery.
FIGURE 1 Changes of %VC following surgery. (Reprinted with permission from Toyota A. Pulmonary rehabilitation and the changes of pulmonary function after surgery. Jpn J Rehabili Med. 2001;38:771.)
FIGURE 2 Changes of % VC recovery rate following surgery. (Used with permission from Toyota A. Pulmonary rehabilitation and the changes of pulmonary function after surgery. Jpn J Rehabil Med. 2001;38:771.)
SOME INTERESTING PHYSICAL THERAPY THERAPEUTIC INTERVENTIONS IN JAPAN
Most Japanese physical therapists believe percussion is not an effective manual technique for bronchial hygiene. They prefer squeezing with postural drainage and breathing-assist techniques.
Squeezing
In Japan, squeezing is performed by the physical therapist in order to facilitate inspiration and exhalation and consists of manually compressing different areas on the thorax during expiration. The therapist pushes into areas of the thorax which have limited motion or under which retained secretions lie. Squeezing appears to increase both expiratory flow and expiratory pressures. As a result, passive inspiration and sputum clearance is facilitated. Miyagawa and Kaneko11 showed bronchoscopic evidence of improved sputum clearance from squeezing compared to percussion.
Okumura and Sakata12 reported on the efficacy of squeezing and postural drainage for children with asthma. A total of 21 chest physiotherapy treatments were performed on 10 children hospitalized for acute asthma attacks between June and November 1999. Ages of the patients ranged from 1 to 4 years. All patients received standardized basic treatment with administration of bronchodilators as a continuous infusion of aminophylline and inhalation of disodium cromoglycate and salbutamol 3 times a day. In 13 out of 21 treatments O2 saturation by pulse oximetry was significantly elevated from 0.8 to 3.8% after chest physiotherapy. However, O2 saturation by pulse oximetry decreased in two cases. Overall, chest physiotherapy was generally well tolerated by these infants based on their cardiovascular response and O2 saturation. The authors state that chest physiotherapy may be a useful adjunctive treatment for children with asthma attack.
Miyagawa13 analyzed several research reports published from 1966 to 1997 related to respiratory physical therapy. His meta-analysis revealed that squeezing was often used in Canada, but not in the United States. He compared squeezing and percussion for pulmonary complications. Table 3 shows the odds ratios for acute respiratory failure in emergency rooms and intensive care units, revealing that pulmonary complications were similar among patients who received squeezing or percussion in both emergency rooms and intensive care units. Additionally, Uzawa and Yamaguchi14 described beneficial changes in lung mechanics during application of chest physical therapy techniques, which included squeezing, percussion, and vibration. See Table 4. In summary, it appears that squeezing may be an important adjunctive treatment for a variety of patients with respiratory disorders.
TABLE 3 Differences of Pulmonary Complication Between Squeezing and Percussion
TABLE 4 The Change in Lung Mechanics During Application of Chest Physical Therapy Techniques
Breathing-Assist Technique
The breathing-assist technique (BAT) is often used in Japan for patients with respiratory disorders. The BAT assists the patients’ ventilation by passive or active-assist maneuvers performed by the physical therapist (Fig. 3).15 This technique facilitates air entry into the thoracic cavity. Improved air entry promotes airway hygiene by mobilizing sputum from peripheral to central airways. This technique may improve ventilation and possibly reeducate breathing control. We often use BAT during the extubation process while patients are still in the intensive care unit. Patients appear to more easily shift to natural breathing after being extubated and receiving BAT. Furthermore, Ihashi and his colleagues16 found that BAT improved arterial blood oxygenation and assisted with general conditioning exercises in 12 patients with dyspnea.
FIGURE 3 Breathing-assist technique.
Mechanical external chest compression (MECC) has been used in Australia and is similar to BAT, but is mechanical rather than manual.17,18 Both MECC and BAT have been used to suppress asthmatic attacks. The technique of external chest compression to assist expiration has been used in asthmatic patients for some years. Fisher et al.18 described a method similar to MECC and BAT that assisted expiration and reported on its apparent value in the emergency treatment of asthma. These techniques require further evaluation to determine their role in the resuscitation of patients with asthma. Although the MECC or BAT techniques are not discussed in the Resuscitation Guideline 2000, the need for it within the intensive care unit may be less than it is outside of specialized units where acute respiratory disorders require immediate attention. MECC or BAT will likely have its greatest impact when initiated in the prehospital setting for patients suffering from severe, sudden-onset, asphyxic anthma. Fukada and co-workers19 reported MECC improved hypoxemia due to asthma when administered in the ambulance and prevented deaths in Japan. BAT has been used in emergency vehicles and on transport carts for patients with acute asthmatic attacks. Shigemoto and colleagues20 have educated paramedics in the use of BAT with patients on emergency transport carts and suggest that physicians, physical therapists, and emergency medical technicians should initiate BAT immediately to improve outcomes of acute asthmatic attacks (Fig. 4). However, It is controversial whether we can actually control chest wall motion and subsequent ventilation during asthmatic attacks; therefore, further investigation on the use of these techniques is needed.21,22
FIGURE 4 BAT in an emergency car. (Modified with permission from Nakano T. Breathing assist technique. Emerg Nurs. 2003;16:63.)
Respiratory Muscle Stretch Gymnastics
Respiratory muscle stretch gymnastics (RMSG) have been designed to stretch and condition the respiratory muscles, mainly the chest wall muscles, and to decrease chest wall elasticity. Several Japanese researchers have studied the use of RMSG.23–26 Kakizaki and colleagues26 reported the effects of RMSG on chest wall mobility, pulmonary function, and dyspnea during activities of daily living in 22 patients with COPD who were regularly treated in an outpatient clinic of a university hospital. The patients did not have severe limitations in shoulder range of motion and were unfamiliar with RMSG. Chest wall mobility (difference of chest circumference during deep expiration and that during deep inspiration), pulmonary function tests (forced expiratory volume in 1 second (FEV1) and VC), and dyspnea in daily living (Fletcher’s rating) were measured before and after 4 weeks of RMSG. Four RMSG patterns were demonstrated to each patient to ensure that they could perform the gymnastics without assistance. The patients were instructed to perform each pattern four times during each session (3 sessions per day) for 4 weeks, at which time the patients were asked to return for reevaluation. Chest wall expansion and reduction increased at both the upper (0.8 ± 0.2 and 1.3 ± 0.2 cm, respectively) and the lower (0.4 ± 0.2 and 0.7 ± 0.2 cm, respectively) chest walls (Figs. 5 and 6). Vital capacity increased 1019 6 43 mL, whereas FEV1 remained unchanged (Fig. 7). Fletcher’s rating improved in 12 patients and remained unchanged in 10; it did not worsen in any of the 22 patients. RMSG, therefore, appeared to increase chest wall mobility by improving chest wall elasticity in patients with COPD.
FIGURE 5 (A) Mean 6 SE of upper chest circumference during deep expiration (E1), deep inspiration (I), and subsequent expiration (E2) before and after respiratory muscle stretch gymnastics (RMSG) in 22 patients with chronic obstructive pulmonary disease. (B) Upper-chest expansion and reduction. (Used with permission from Kakizaki F. Preliminary report on the effects of respiratory muscle stretch gymnastics on chest wall mobility in patients with chronic obstructive pulmonary disease. Respir Care. 1999; 44:412-413.)
FIGURE 6 (A) Mean 6 SE of lower-chest circumference during deep expiration (E1), deep inspiration (I), and subsequent expiration (E2) before and after respiratory muscle stretch gymnastics (RMSG) in 22 patients with chronic obstructive pulmonary disease. (B) Lower-chest expansion and reduction. (Used with permission from Kakizaki F. Preliminary report on the effects of respiratory muscle stretch gymnastics on chest wall mobility in patients with chronic obstructive pulmonary disease. Respir Care. 1999;44:412-413.)
FIGURE 7 Vital capacity (VC) and forced expiratory volume in 1 second (FEV1) before and after 4 weeks of respiratory muscle stretch gymnastics (RMSG) in 22 patients with chronic obstructive pulmonary disease. Lines indicate individual results; boxes indicate group mean 6 SE. NS, not significant. (Used with permission from Kakizaki F. Preliminary report on the effects of respiratory muscle stretch gymnastics on chest wall mobility in patients with chronic obstructive pulmonary disease. Respir Care. 1999;44:412-413.)
Muscle Relaxation Technique—The Designed Plate Method
It has been suggested that respiratory muscle dysfunction plays a major role in the development of acute respiratory failure in patients with COPD. Because of this, Fujimoto et al.27 created a specially designed plate method to treat spasm of the respiratory muscles and other muscles (Fig. 8). This tool is curious in appearance and the therapist uses it like a carpenter, with the anticipated goal of decreasing muscle spasm or muscle tone. Fujimoto et al. devised this method, which combines respiratory muscle relaxation exercises and the use of wedge-shaped wooden plates with which pressure is applied to the intercostal and accessory respiratory muscles. The specific techniques of the designed plate method includes placing a wooden plate on a hypertonic muscle and applying pressure either by hand or by tapping the wooden plate with a light hammer for 15 to 20 minutes twice a day. The effects of this muscle relaxation maneuver with designed plates on pulmonary function was examined in five patients with moderate-to-severe pulmonary emphysema for 4 weeks and in seven patients with mild to moderate emphysema for 6 weeks. After the specially designed plate therapy, inspiratory capacity (IC) and vital capacity (VC) increased in both the 4-week and the 6-week-treated groups, and the (FEV1) increased in the 6-week-treated group. Furthermore, CO2retention was also improved and daily peak expiratory flow (PEF) showed significant increases from 2 weeks until the end of therapy. These results suggest that the respiratory muscle relaxation maneuver with specially designed plates is an effective method to improve pulmonary function of patients with pulmonary emphysema.
FIGURE 8 Schema for procedure of the respiratory muscle relaxation maneuver. A wedge-shaped wooden plate of appropriate size was placed on each bilateral intercostal, trapezius, scalenes, and antigravity muscles, and pressure was exerted by hand or by tapping the plate with a wooden hammer. (Used with permission from Fujimoto K. Effect of muscle relaxation therapy using specially designed plates in patients with pulmonary emphysema. Intern Med. 1996;35:756-763.)
Upper Limb Exercise Test
Patients with emphysema frequently have dyspnea during upper limb exercise alone or combined with lower limb exercise. Several investigators have explored the role of upper limb exercise tests, which appear to be helpful in identifying dyspnea and determining treatment effects from pulmonary rehabilitation programs.28–31 Several upper-limb exercise tests have been described including a supported test, an arm ergometry test, an unsupported test, and a test of simulated activities of daily living. Each of these tests has advantages and disadvantages. Takahashi et al. have described an unsupported and dynamic progressive exercise test for upper-limb performance in patients with emphysema, during which a patient sits against a wall and elevates 200 g of weight to a low target and then repeats the lift to a progressively higher target.32 This progressive lifting protocol is performed 30 times per minute and has been found to be more strongly correlated with (
O2peak) and maximum voluntary ventilation than static-upper-limb exercise testing. Therefore, dynamic upper-limb exercise testing appears to be an important test to include in the examination of patients with emphysema and with possibly other respiratory disorders.
ORGAN TRANSPLANTATION
In March of 1999 the Boston Globe ran a headline stating, “Heart transplantation ends old taboo in Japan.” Organ transplantation from brain-dead donors began in 1999 under a new law of organ transplantation in Japan. Some physical therapists in Japan are now treating patients before and after transplantation. The Japanese government has approved lung transplantation in four Japanese medical institutions and cardiac transplantation has been approved in three institutions. To date, there have been 17 cardiac and 14 lung transplantations from brain-dead donors from 1999 to October, 2003. As of October 2003, 32 living-donor lung transplants have been performed.
Living-Donor Lobar Lung Transplantation
Lung transplantation has not been reported in Japan until recently when Shimizu and his colleagues performed the 1st successful bilateral living-donor lobar lung transplantation.33,34 A 24-year-old woman with primary ciliary dyskinesia began experiencing severe respiratory insufficiency and required mechanical ventilation. On October 28, 1998, she underwent bilateral living-donor lobar transplantation, receiving her sister’s right lower lobe and her mother’s left lower lobe under cardiopulmonary bypass. The patient was discharged from the hospital 61 days after transplantation. Six months postoperatively, she has returned to a normal life and is able to perform daily activities comfortably. She is currently in good physical condition and has a vital capacity of 1770 mL. One year after transplantation, her forced vital capacity was 2160 mL (73.2% of her predicted forced vital capacity). The recipient’s sister was observed to have a decrease in forced vital capacity of 410 mL, and her mother had a decrease in forced vital capacity of 440 mL. Both donors have since returned to normal, unrestricted lives.
In Japan and internationally, patients undergo lung transplantation when a recipient’s chest size and donor lung size do not match. We have found that patients who have undergone lung transplantation often demonstrate excessive work of breathing which we attempt to manage using many of the techniques described within this Chapter 20, “Physical Therapy Associated with Ventilatory Pump Dysfunction and Failure.” We also focus on maintaining and improving the functional status and cardiorespiratory capacity of patients before and after transplantation.35
Lung Transplantation from Brain-Dead Donor
Miyoshi et al. reported on the results of two single-lung transplants from a single cadaveric donor that were successfully conducted at two different institutions on March 29, 2000. This was the 1st such procedure in Japan under newly introduced legislation.36 One of the patients was a 48-year-old woman with idiopathic pulmonary fibrosis who underwent left single-lung transplantation under cardiopulmonary support at Osaka University Hospital. The postoperative course was uneventful. The patient was discharged on postoperative day 62 with satisfactory respiratory function. Several physical therapists have been engaged in the patients preoperative and postoperative care. The other patient suffered from end-stage emphysema and expired shortly after the transplantation.
Cardiac Transplantation
Cardiac transplantation began in 1968 and has been established as a therapeutic strategy for patients with end-stage heart failure throughout most of the world. In Japan, however, cardiac transplantation has been performed only occasionally. Although legislation for its approval was passed in 1997, it was not until February of 1999 that Japan experienced its first cardiac transplantation.37 This was the result of long and steady efforts to enlighten Japanese society about the concept of brain death and the importance of organ transplantation. The patient was 47-year-old male with a dilated hypertrophic cardiomyopathy who had been supported with an implantable left ventricular assist device (LVAD). At present, several physical therapists work with cardiac surgeons and a transplantation coordinator to allocate care to patients before and after heart transplantation. We have successfully treated many patients awaiting cardiac transplantation (with and without LVADs) and one additional patient after cardiac transplantation. The fifth cardiac transplant patient was a 24-year-old patient who was in Osaka University Hospital with LVAD over 500 days and subsequently received a donor heart. She has returned to her home and is independent and preparing to return to her job.
SUMMARY
This International Perspective has presented the strengths and weaknesses of “Physical Therapy Associated With Ventilatory Pump Dysfunction and Failure” and has highlighted several Japanese issues that demonstrate the similarities and differences of physical therapy in Japan and around the globe. Many similarities exist between the physical therapy examination and management techniques of Japan and those of other countries, but differences also exist. The major differences between the physical therapy practiced in Japan and that practiced in other countries may be the primary focus on manual techniques to treat patients with ventilatory pump dysfunction and failure and on the relationship of medical practices to society at large in Japan. The key similarities between physical therapy in Japan and that in other countries is the continued search for evidence to support physical therapy care and the increasing role of physical therapy in many novel areas.
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