Principles of Physical Therapy Management

Physical therapists treat patients with hypertension as a primary or secondary diagnosis. If it is a secondary diagnosis, it is important that the diagnosis is not overlooked. What the physical therapist can do for the hypertension may be clinically more significant than management of the primary diagnosis for which the patient is referred. As with many other lifestyle-related conditions, antihypertensive medication may be perceived by the patient as addressing the problem, whereas in many instances, it only addresses the effect. Lifestyle changes are necessary to normalize blood pressure with the goal of eliminating the need for blood pressure medication.¹¹

Exercise therapy can be an effective intervention for the management of hypertension with the primary goal of eliminating the need for medication.¹² Secondarily, physical therapy with a focus on exercise and health education, including smoking cessation and basic nutritional counseling, is aimed at reducing the need for medication or its potency. The foundation of management in a patient with hypertension is a lifestyle review and recommendations in consultation with the patient. Recommendations include nutrition, weight control, exercise, smoking cessation, and stress management.¹³ Medical management may include beta blockers and diuretics to reduce plasma volume or other antihypertensive medication. A prescription of regular aerobic exercise may control hypertension.¹⁴ The prescription is based on a consideration of the patient’s coexistent problems and general health status. If obesity is a concurrent problem, an exercise program is prescribed to address both concerns.

More frequently, physical therapists treat patients whose hypertension is a secondary condition. Thus, whether the patient is being treated for osteoarthritis, stroke, or cardiovascular and pulmonary dysfunction, treatment is modified accordingly. An exercise prescription includes generalized aerobic exercise at an intensity that is optimally therapeutic and not associated with any excessive or untoward hemodynamic responses.

Patients with labile hypertension are the most difficult patients for whom to prescribe an exercise program because of the irregularity of their blood pressure responses. The intensity is modified at each session to accommodate these variations. Because beta blockers and other medications blunt heart rate responses to exercise, the exercise prescription parameters are defined on the basis of some other objective hemodynamic response or on subjective responses (e.g., the Borg scale of perceived exertion).

The benefits of a modified aerobic exercise prescription include elimination of medication, reduction of medication, and improved pharmacological control on the same dose of medication. In addition, the patient derives all the other multisystem health benefits of exercise. A program of aerobic exercise should be carried out in conjunction with other lifestyle changes associated with blood pressure control (e.g., nutrition, weight control, stress reduction, and smoking cessation program). Medications should be monitored by the physician during the training program. In addition to exercise having a direct effect on controlling hypertension, the effect of exercise on overall metabolism may alter the absorption and degradation of the medications, which in turn can reduce the prescriptive requirements of that medication. Those types of exercise that are associated with a disproportionate hemodynamic challenge (e.g., static movements and stabilizing postures) are not usually indicated. Rather, aerobic exercise that is rhythmic, involves the large muscles of the legs and possibly the arms, and is performed frequently is indicated. Physical therapy outcomes include reduction or elimination of antihypertensive medication with self-monitoring and optimal lifestyle management.

A patient who is being managed acutely with high blood pressure may benefit from relaxation strategies, breathing control, and stress management. Further, complementary therapies, as described in Chapter 27 may have an important role. For noninvasive physical therapy management of hypertension, see Chapter 31.

Angina refers to pain resulting from ischemia of the myocardium and often precedes myocardial infarction. Coronary artery disease is the primary cause of myocardial infarction and is among the leading causes of death in the Western world. Lifestyle factors, including high-fat diet, stress, and low activity levels, contribute to atherosclerosis and fat deposition within the coronary blood vessels. When these deposits narrow or totally occlude the vessel lumen, blood flow is restricted or totally obstructed. As the heart continues to demand oxygen and nutrients in order to work properly, blood supply must be increased. If one or more of the myocardial blood vessels is stenosed, insufficient blood reaches the working myocardial fibers, and ischemia and pain result. The classic description of anginal pain is retrosternal, vice-like, gripping pain radiating to the left side and down the arm and up into the neck; however, anginal pain may occur bilaterally anywhere above the umbilicus. Furthermore, patients vary considerably with respect to the degree to which the severity of the pain correlates with the degree of myocardial ischemia and infarction. Thus even apparently minimal chest pain may be associated with significant ischemia, and its clinical significance should not be minimized. Approximately 10% to 15% of individuals who have a myocardial infarction do not report chest pain. Chest pain can also be blunted in individuals with diabetes as a result of the autonomic neuropathy.

Principles of Physical Therapy Management

The management of patients with ischemic heart disease who are hemodynamically unstable and require intensive monitoring to assess and to monitor physical therapy treatment is described in Chapter 34. This section addresses management of the patient with a cardiac medical condition who is stable and uncomplicated. Physical therapists must be knowledgeable and proficient in management of the patient with cardiac conditions because these patients are referred with cardiac disease as a primary or secondary problem. With respect to heart disease being a secondary diagnosis, patients often come to the physical therapist for the management of an orthopedic complaint with a history of angina, frank myocardial infarction, or hypertension. The principles for physical therapy in management of patients with acute ischemic heart disease are presented within the principles of phase I cardiac rehabilitation (Table 29-1). Because physical therapy invariably involves physically stressing a patient either with therapeutic exercise or with the application of a therapeutic modality, the physical therapist must address the following questions when managing a patient with ischemic heart disease and its risk factors:

Table 29-1

Phase I of Cardiac and Pulmonary Rehabilitation (Inpatient, <7 to 10 days)*

Cardiac Rehabilitation	Pulmonary Rehabilitation
After anginal attack, myocardial infarction, operative procedures including bypass surgery and valve surgery	After acute exacerbation or thoracic surgery (e.g., admission lung resection)
Optimize oxygen transport by directing treatment to the underlying limitations of structure and function (impairments)	Optimize oxygen transport by directing treatment to the underlying limitations of structure and function (impairments)
Risk factors assessment	Risk factor assessment
Assessment of knowledge deficits and learning style	Assessment of knowledge deficits and learning style
Readiness to change assessment	Readiness to change assessment
Predischarge submaximal exercise test	Predischarge submaximal exercise test
Discharge lifestyle recommendations:	Discharge lifestyle recommendations:
Smoking cessation	Smoking cessation
Nutrition and weight control	Nutrition and weight control
Physical activity and exercise	Physical activity and exercise
Stress management	Stress management
Plan for follow-up	Plan for follow-up

^*Phases II, III, and IV are related to subacute and chronic care (see Chapter 31).

Modified from Piotrowicz R, Wolszakiewicz J: Cardiac rehabilitation following myocardial infarction. Cardiology Journal 15:481–487, 2008.

1. Does the patient’s cardiac status preclude treatment? Why?

2. Is additional information about the patient necessary before physical therapy assessment and treatment? What information?

3. How should treatment be modified? Why?

4. Is the patient using antianginal medication appropriately? Is the prescription current? Does the patient have the antianginal medication present at all times?

5. Are there other medications that may influence the patient’s cardiovascular and pulmonary status and response to treatment? What are they? How might the patient’s responses to treatment, particularly exercise, be affected?

6. What physiological parameters should be monitored before, during, and after treatment?

7. What is the patient’s knowledge about his or her condition? Can the patient clearly identify what triggers the angina and what makes it worse and better? What lifestyle changes have been made? What should be reinforced and what education is necessary?

A key consideration in the management of any person with cardiovascular dysfunction is minimizing myocardial strain. Thus mobilization and exercise prescription must incorporate appropriate warm-up, steady-rate, cool-down, and recovery phases, and the type of exercise should be rhythmic and involve the legs (i.e., areas of large muscle mass) and possibly the arms as well. Initially, low-intensity activity that restricts the heart rate to no more than 20 beats above resting heart rate may be indicated to minimize the work of the heart without immobilizing the patient completely. Ejection fraction is not necessarily a good indicator of exercise tolerance because these variables are not well correlated. Upper-extremity work alone is more hemodynamically demanding than lower extremity work and thus is prescribed cautiously, if at all, at least in the early stage. Exercise or physical activity involving sustained static postures and isometric muscle contraction are contraindicated. Breathing should be coordinated with activity such that breath holding and straining are avoided.

An individual with a history of angina, regardless of whether he or she is taking antianginal medications, must be hemodynamically monitored (i.e., heart rate, blood pressure, rate pressure product, and subjective responses; ECG monitoring may also be indicated).

Individuals prone to angina may exhibit symptoms in certain body positions.15,16 Usually, this reflects an increased workload and increased work of the heart. Recumbent positions increase the mechanical work of the heart by increasing central blood volume.¹⁷ These patients are not encouraged to lie flat. Instead, the head of bed is elevated 10 to 15 degrees. Side-lying positions, particularly left side-lying, increase the work of the heart by compressing the heart and impeding ventricular filling and ejection. Patients with impaired oxygen transport and without prior cardiac disease may exhibit myocardial stress and ischemia in these body positions. Thus patients with impaired or threatened oxygenation must be monitored closely, particularly during turning and activities in which oxygen demand is increased—at these times, oxygen delivery must be increased correspondingly.

The use of medication to minimize the risk for angina and ischemic heart disease warrants review. The need for statins, commonly prescribed lipid-lowering medications, can be reduced through optimal lifestyle choices in many patients. One inherent danger of such a drug, however, in addition to its well documented side effects, is that patients may become complacent, believing that the drug will offset the need to make necessary lifestyle changes. More important, lifestyle changes largely address the cause of the problem, whereas medication such as statins only address an effect. The principles of the physical therapy management of patients with stabilized angina include health education, risk factor reduction, and a long-term health program (see Chapters 24 and 31).

Myocardial infarction, commonly referred to as a heart attack, refers to insufficient myocardial perfusion resulting in a macroscopic area of damage and necrosis of the heart. Infarction results most frequently from narrowing and occlusion of the coronary blood vessels secondary to atherosclerosis. Other causes include occlusion secondary to a thrombus or embolus, reduced blood pressure, or coronary vasospasm. Angina, or ischemic chest pain, often precedes or accompanies a myocardial infarction. Infarctions vary in severity from being silent (i.e., having no characteristic signs and symptoms and thus going undetected) to being fatal. Most infarctions, when detected, require some hospitalization and monitoring to ensure that the infarction is not evolving further and that the patient is medically stable and in no danger. Chapter 34 describes the management of patients with complicated myocardial dysfunction who are admitted to a coronary care unit. This section focuses on the patient with mild heart disease, the patient with cardiac dysfunction who is discharged from hospital, the patient who has a history of ischemic heart disease, and the patient who is hospitalized for a condition other than heart disease but develops and is being managed for myocardial ischemia. Judicious movement and body positioning are essential elements in the management of the patient with myocardial infarction.¹⁸ Because these interventions can place significant demands on cardiovascular and pulmonary function and oxygen transport, they must be prescribed specifically by physical therapists with considerable knowledge and expertise in the area.

Routes of Infection

A patient who has impaired or ineffective defense mechanisms of the respiratory tract becomes susceptible to a variety of organisms. The major routes of infection include airborne organisms, circulation, contiguous infection, and aspiration. In the past 20 years, hospitalized patients whose immunity is compromised are susceptible to superbug infections, which necessitates aggressive medical management and isolation techniques.²⁶

Viral Pneumonias

Most respiratory viral infections are contracted by droplets from the respiratory tracts of infected persons. These viruses are responsible for interstitial pneumonias, tracheobronchitis, bronchiolitis, and the common cold. The ciliated cells of the respiratory tract are the most frequent site of infection. They become paralyzed and degenerate, with areas of necrosis and desquamation. The mucociliary blanket becomes interrupted because destruction of the cilia leaves a thin layer of nonciliated basal replacement cells. Inflammatory responses cause exudation of fluid and erythrocytes in both the alveolar septae and the airways. Congestion and edema become predominant with the formation of intraalveolar hyaline membranes. These changes in the normal mucosal structure and cilia increase the susceptibility of the involved lung to superimposed bacterial infections. This is the most common complication associated with viral infections and is usually responsible for the fatalities that occur.

The patient with viral pneumonia presents with fever, dyspnea, loss of appetite, and a persistent, nonproductive cough. On auscultation, normal breath sounds are heard throughout both lung fields with scattered inspiratory crackles. X-ray changes range from minor infiltrates to severe bilateral involvement. Consolidation and pleural effusions occur less frequently. Secondary bacterial infections occur frequently, causing patients to develop productive coughs.

Influenza may lead to viral pneumonia in 1% to 5% of cases. Influenza includes acute viral respiratory tract infection and is characterized by a sudden onset of headache, myalgia, and fever. The route of infection is by inhalation of airborne particles from an infected person. The incubation period is 24 to 72 hours.

Pulmonary lesions include edema of the respiratory epithelium with necrosis and hemorrhage. At the alveolar level, interstitial edema, proliferation of type I cells, hemorrhage, and an increased number of macrophages are seen. In patients with pneumonia, secondary bacterial infections are frequent and are the cause of most fatalities.

Medical management of viral infections is supportive and preventive. Patients should receive vaccines whenever possible to build up antibodies against specific viruses. Once the patient has contracted the organism, treatment becomes supportive, with rest, salicylates, and high fluid intake being the main treatment priorities. Patients who become more acutely ill with viral pneumonia should be on a vigorous preventative program to lessen the possibility of bacterial infection. Recovery also depends on good nutrition, hydration, sleep, rest, and reduced stress.

Bacterial Pneumonia

Bacterial pneumonia causes the largest number of deaths per year by an infective agent and is a major cause of death, particularly in young patients and older adults. The patient presents with an abrupt onset of a severe illness characterized by fever, tachypnea, dyspnea, hypoxemia, tachycardia, and a cough that produces bloody or purulent sputum. The clinical findings depend on the organism involved and the extent of the pneumonia in the lungs. The infective process may resolve with medications, aerosols, and physical therapy, or it may spread to contiguous areas, causing pleural effusion and empyema.

Bacterial pneumonia can occur as either primary or secondary infections. Primary pneumonias arise in otherwise healthy individuals and are usually pneumococcal in origin. Secondary pneumonias occur when the patient’s defense system becomes ineffective.

Pneumococcal pneumonia is caused by pneumococcal bacteria, a gram-positive organism. It occurs most frequently in the winter months in adults, often males, between 15 and 40 years of age. Patients present clinically with abrupt illness characterized by fever, cough, purulent or rust-colored sputum, and pleuritic chest pain over the affected lung field. Physical examination may reveal decreased expansion of the chest over the affected area and muscle splinting. On auscultation, there may be bronchial breath sounds (indicating consolidation), decreased or absent breath sounds, and wheezes or crackles over the affected lung. Chest x-rays may show atelectasis, infiltrates, and consolidation.

There are four stages associated with bacterial infection of lung tissue: engorgement, red hepatization, gray hepatization, and resolution. The engorgement stage occurs within the first few days of infection and is characterized by vascular engorgement, serous exudation, and evidence of bacteria colonization. Red hepatization occurs within 2 to 4 days as a result of diapedesis of the red blood cells. The alveoli are full of polymorphonuclear leukocytes, fibrin, and red blood cells. The organism continues to multiply within the fluid exudate. Areas of consolidation become evident. Gray hepatization occurs within 4 to 8 days and is characterized by evidence of abundant fibrin, decreased polymorphonuclear leukocytes, and dead bacteria. Consolidation continues to be a problem in this stage. Resolution occurs after 8 days as areas of consolidation begin to resolve. Many macrophages are seen, and evidence of enzymatic digestion of exudate is present. The affected tissue becomes softer with large amounts of grayish-red fluid present within the alveoli. This process continues for 2 to 3 weeks with the lung gradually assuming a more normal appearance.

Pleural involvement occurs frequently, with the pleural spaces filling with the same type of fluid seen within the alveoli. Resolution is slower because there are few surfaces available for phagocytosis. Complications that may occur in patients with pneumococcal involvement include empyema, superinfections (occur when large numbers of new organisms invade the lung), abscesses, atelectasis, and delayed resolution (defined as taking more than 4 weeks to resolve).

Treatment of pneumococcal pneumonia includes the use of antibiotics. Thoracentesis is performed when pleural fluid is present. The patient should also receive ultrasonic nebulization and physical therapy. If severe, supplemental oxygen therapy may be indicated.

Staphylococcal pneumonia is caused by a gram-positive organism. It rarely occurs in the healthy adult but is a frequent cause of pneumonia in children, infants, and patients with chronic lung diseases, especially carcinoma, tuberculosis, and cystic fibrosis. Clinically, the patient’s manifestations are similar to those seen in the patient with pneumococcal pneumonia. Some differences appear in the chest x-ray (e.g., patchy areas of infiltrate). Consolidation occurs infrequently in this type of pneumonia. Pleural effusions, empyema, abscesses, bronchopleural fistulas, and pneumatoceles (subpleural cyst-like structures) often occur. Treatment includes medication, rest, increased fluid intake, ultrasonic nebulization or medication nebulizers, and aggressive physical therapy.

Streptococcal pneumonia is caused by a gram-positive organism, Streptococcus pyogenes. It occurs most frequently in very young, very old, or debilitated patients. The clinical picture is very similar to that of staphylococcal pneumonia. Again, consolidation is rare and chest x-rays usually show one or more areas of patchy infiltrates. Complications are rare, but empyema does occasionally occur. Treatment for this organism is the same as that for pneumococcal pneumonia.

Haemophilus influenzae pneumonia is caused by a gram-negative organism and occurs primarily in children as bronchiolitis and in adults who have chronic bronchitis. The clinical picture is the same as for the other bacterial pneumonias, with numerous areas of infiltration evident on x-ray. On auscultation, breath sounds are generally good, with crackles heard at the end of inspiration. Treatment of this pneumonia includes antibiotics, oxygen, ultrasonic nebulization, and physical therapy.

Other gram-negative organisms causing pneumonia include Escherichia coli and Pseudomonas aeruginosa. These are seen most frequently in patients with underlying disease, especially pulmonary disease, and in those who are debilitated. These organisms are frequently the cause of superinfections in individuals who have received massive doses of broad-spectrum antibiotics. Clinically, these patients present with cough, fever, and dyspnea. On auscultation, crackles, bronchial breathing, and diminished or absent breath sounds can be noted. X-ray changes frequently show bibasilar infiltrates, with the amount of involvement being widely variable. As for other bacterial pneumonias, treatment includes medications, ultrasonic nebulization, and physical therapy.

Principles of Physical Therapy Management

The goals of management of bacterial pneumonia include reversing alveolar hypoventilation, increasing perfusion, reducing right-to-left shunt, increasing ventilation and perfusion matching, minimizing the effects of impaired mucociliary transport, minimizing the effects of increased mucous production, and optimizing lymphatic drainage of the lungs. Bacterial pneumonia is frequently associated with increased mucus production. With respect to airway clearance, management focuses on augmenting mucociliary clearance overall, reducing excess mucus accumulation, and reducing mucus stasis. The role of traditional manual physical therapy techniques remains equivocal in the management of adults with pneumonia.³² Patients are often mobile and should be encouraged to be so to promote lung expansion, augment flow rates, stimulate deep tidal volumes (breaths), and augment mucociliary transport and lymphatic drainage.^27,33,34 The oxygen demands of mobilization and exercise, however, must be within the patient’s capacity to delivery oxygen. These interventions are prescribed such that they avoid jeopardizing this balance and unduly fatiguing the patient. Deep breathing and effective coughing are important maneuvers for clearing airways with special attention to the avoidance of airway closure. Prescriptive body positioning can be used to optimize ventilation and perfusion matching,^29,35–37 which may be more uniform in the prone position³⁸ (see Chapter 20). A secondary goal is offsetting aerobic deconditioning from this episode of acute illness, particularly in older adults or patients who are debilitated with chronic conditions.

Principles of Physical Therapy Management

During an exacerbation requiring hospitalization, patients with chronic bronchitis are usually treated with intravenous fluids, antibiotics, bronchodilators, and low-flow supplemental oxygen. Diuretics and digitalis are often given to treat associated right heart failure. Airway clearance interventions are selected (i.e., mobilization, body positioning, and possibly postural drainage). These interventions are coordinated with breathing control and coughing maneuvers to facilitate secretion removal and optimize coughing and expectoration while minimizing dynamic airway compression and alveolar collapse. During recovery, exercise is increased with supplemental oxygen as needed. These patients need to avoid exposure to bronchial irritants (e.g., cigarette smoking, second-hand smoke, and air pollutants) and be adequately hydrated to thin secretions to facilitate mucociliary transport and expectoration.

Patients with chronic bronchitis can benefit from a comprehensive rehabilitation program designed for patients with chronic pulmonary disease, and such a program is best initiated within 1 month of an exacerbation.³⁹ Even modest exercise has long been known to improve walking capacity and subjective well-being.⁴⁰ Components of acute management are shown in Table 29-1 and are comparable to cardiac rehabilitation phase I. Specific details of exercise prescription in the management of chronic obstructive pulmonary disease and of a comprehensive pulmonary rehabilitation program are described in Chapters 24 and 31. Maximizing health and risk factor reduction are principal goals to minimize further pulmonary pathological changes and damage including irreversible emphysema. High-priority strategies include targeted education, smoking cessation, and nutritional and exercise counseling. Individuals who do not have access to such formal structured pulmonary programs (the majority of people), can be managed by the physical therapist, who applies the same principles of practice on an individual basis.

Principles of Physical Therapy Management

The principal pathophysiological deficits of bronchiolitis include ventilation and perfusion inequality and a diffusion defect. These deficits result from secretions produced by inflammation and increased mucus production and from atelectasis of adjacent alveoli. Physical therapy promotes mucociliary transport and the removal of secretions and mucus to central airways, promotes alveolar expansion and ventilation, optimizes ventilation and perfusion matching and gas exchange, and reduces the risk for infection.

Bronchiolitis is common in babies and young children. The effects of inflammation and obstruction in small children are always serious because the anatomical and physiological components of the cardiovascular and pulmonary systems are smaller, respiratory muscle tone is less well developed, the anatomical configuration of the chest wall is cylindrical, breathing is less efficient under 2 years of age, spontaneous movement and body positioning are more restricted (infants in particular spend more time in non-upright positions), and children are at greater risk for infection (see Chapter 37).

Principles of Physical Therapy Management

Standards of practice for chronic obstructive lung disease have been well documented globally.42,43 Priorities are minimizing exacerbations and reducing overuse of antibiotics.⁴⁴ Physical therapy has a primary role in helping to prevent this condition and its sequelae (including premature death), as well as in managing it without drugs and surgery as much as possible.

The patient with emphysema is prone to chronic pulmonary infections and respiratory insufficiency. The clinical picture is hallmarked by alveolar collapse and destruction, ventilation and perfusion mismatch, and diffusion defect. These defects result in impaired or threatened oxygen transport if the physiological compensations are unable to maintain adequate blood gases. Shortness of breath is exacerbated, and breathing is labored. Increased work of breathing reflects airway obstruction and inefficiency of respiratory mechanics and the respiratory muscles. Because of long-term airway disease, mucociliary transport is disrupted. Therefore in the presence of a pulmonary infection and increased production of pulmonary secretions, secretion removal can be a major problem for the patient.

Table 29-1 shows the primary components of care in the acute phase of management, which can be compared with acute cardiac care (phase I of cardiac rehabilitation). Specific treatments are prescribed for the patient based on the specific clinical findings (i.e., the type and severity of the cardiovascular and pulmonary dysfunction and the presence of infection). Therefore treatments include mobilization coordinated with breathing control and coughing maneuvers, which are effective in enhancing alveolar ventilation, mobilizing secretions, and facilitating ventilation and perfusion matching. Body positioning can be prescribed to alter the distribution of ventilation, to aid mucociliary transport, and to remove pulmonary secretions. Although “pure” emphysema is typically dry, postural drainage positions can facilitate the removal of pulmonary secretions from specific bronchopulmonary segments if indicated. In any given body position, alveolar volume is augmented in the uppermost lung fields and alveolar ventilation is augmented in the lowermost lung fields. The type and extent of pathology determine the degree of benefit these physiological effects will have on oxygen transport.

In addition, body positioning is essential to optimize respiratory mechanics and enhance pulmonary gas exchange, thereby reducing the work of breathing and the work of the heart. The assessment defines the parameters of the treatment prescription that will be effective in relieving the work of breathing and the work of the heart. This information is essential not only for prescribing beneficial positions but also for avoiding deleterious positions. A sitting, leaned-forward position will assist ventilation secondary to the gravitational effects of the upright position on cardiovascular and pulmonary function. If the arms are supported, this position stabilizes the upper chest wall and rib cage, thereby facilitating inspiration. Some patients, in respiratory distress and with horizontally positioned hemidiaphragms, benefit from recumbent positions in which the hemidiaphragms are elevated within the chest wall by the viscera falling against the underside of the hemidiaphragms in this position (i.e., viscerodiaphragmatic breathing).⁴⁵ The muscle fibers of the diaphragm are mechanically placed in a more favorable position with respect to their length-tension characteristics. This effect may further be augmented in the head-down position in some patients.⁴⁶ Other patients, however, cannot tolerate recumbent positions; in fact, respiratory distress may be increased. If optimal treatment outcome has not been achieved with mobilization and body positioning coordinated with breathing control and coughing maneuvers, conventional physical therapy procedures may offer additional benefit in some patients (e.g., postural drainage and manual techniques if a refractory purulent infective process is present).

Because of the tendency toward dynamic airway compression resulting from the highly compliant airways of individuals with emphysema, open-glottis coughing maneuvers are indicated. Specific outcome measures are recorded before, during, and after treatment to assess short- and long-term treatment effects. In addition, between-treatment maneuvers are central to maximizing overall treatment effectiveness. Conveying information effectively and specifically to the patient, nursing staff, and perhaps family members is therefore crucial to achieving a maximal treatment outcome.

As with the individual who has chronic bronchitis, people with chronic airflow limitation due to emphysema should be prescribed a lifelong health program that includes smoking cessation, basic nutritional counseling, and exercise counseling (see Chapters 24 and 31). Based on the assessment, the physical therapist makes a decision with respect to whether professional counseling may augment outcomes (e.g., smoking cessation counselor), whether the patient may benefit from pharmacological support for smoking cessation, and whether the general practitioner needs to be consulted. A decision is also made as to whether a professional nutritionist should be involved. Improved aerobic conditioning can reduce the frequency and severity of subsequent acute exacerbations.⁴⁷ Quality of life is associated with fewer clinical signs and symptoms.⁴⁸

Principles of Physical Therapy Management

The hallmark of an acute exacerbation of asthma is bronchospasm, an increased responsiveness of airway smooth muscle to various stimuli (i.e., reversible airway obstruction). Although bronchospasm can be a feature of chronic bronchitis and emphysema, the primary cause of airway obstruction in these conditions results from anatomical and physiological changes that are not usually reversible.

Table 29-1 shows the primary components of care in the acute phase of management, which are comparable to acute cardiac care (phase I of cardiac rehabilitation). Physical therapy is directed at improving gas exchange without aggravating bronchospasm and other symptoms and reversing these when possible. In one systematic review, the role of breathing exercises for people with acute asthma was not substantiated.⁴⁹ Thus relaxing the patient’s overbreathing by whatever method works best is recommended. Patients experiencing an acute asthmatic attack may reduce their respiratory rate with a CO₂ rebreathing bag; the benefits may be augmented by reducing a hyperventilatory response with optimal positioning.⁵⁰ Overall oxygen demand, including that associated with an increased work of breathing, needs to be reduced during an exacerbation of asthma. This may require reduced activity, body positioning that improves breathing efficiency, judicious rest and sleep periods, altered diet or restricted diet, adequate hydration, maintenance of a thermoneutral environment, rest, reduced arousal, reduced social interaction and excitement, and reduced environmental stimulation. Although general relaxation does not directly relax bronchial smooth muscle, it will assist breathing control, reduce arousal and metabolic demands, and promote more efficient breathing.

Airway narrowing and obstruction is a hallmark of this condition secondary to increased bronchial smooth muscle tone and airway edema. Even small amounts of pulmonary secretions can obstruct the lumen of narrowed airways, which leads to reabsorption atelectasis distal to the site of obstruction, impaired gas exchange, and reduced PaO₂. Thus mucociliary transport is a priority. Mucous clearance can be further impeded by the addition of serous fluid to pulmonary mucus, resulting from airway irritation and inflammation. Cilia are less effective at clearing mucoserous fluid compared with mucus alone. In addition, sheets of ciliated epithelium are shed into the bronchial lumen, further contributing to the stasis of secretions. Thus optimizing the mobilization of secretions and their removal is a priority even in the presence of scant secretions. Interventions that optimize mucociliary transport are selected to minimize exacerbating bronchospasm and further increases in airway resistance.

The primary goals in the management of asthma include reducing airway narrowing, improving alveolar ventilation, reducing the work and energy cost of breathing, reducing hypoxemia or minimizing its threat, and optimizing lung compliance.

Treatment outcome is assessed with indices of oxygen transport overall and of the function of the individual steps in the pathway.⁵¹ Bedside spirometry, including peak expiratory flow rate, is a sensitive indicator of ensuing compromise in oxygen transport. Some patients use a peak expiratory flow rate meter at home to detect such changes and as an early indicator of the need for medical attention.

Individuals with asthma can often learn to control their condition effectively with optimal health education and an overall lifelong health program (see Chapters 24 and 31).

Principles of Physical Therapy Management

Prophylactic cardiovascular and pulmonary physical therapy, including facilitation of mucociliary transport and maximizing alveolar ventilation, in conjunction with the judicious use of antibiotics, provides effective measures for controlling or slowing the effects of bronchial and bronchiolar obstruction. Involvement of the patient and caregivers in chronic care in the long term is particularly important. Understanding the pathology and course of CF is essential to modify treatment prescription during exacerbations and remissions of the disease.

Table 29-1 shows the primary components of care in the acute phase of management, which can be compared generally with acute cardiac care (phase I of cardiac rehabilitation). The clinical deficits related to oxygen transport include impaired mucociliary transport, increased mucus production, increased difficulty clearing mucus, impaired ventilation and perfusion matching, right-to-left shunt, a diffusion defect, respiratory muscle weakness or fatigue, and reduced cardiovascular and pulmonary conditioning. The increased production of mucus and the difficulty removing mucus increase the risk for bacterial colonization and chronic respiratory infections. These manifestations of CF are worsened with recumbency. Significant postural hypoxemia has been reported in patients with CF when moving from sitting to a supine position.⁵³ Thus the object of treatment is to optimize oxygen transport and pulmonary gas exchange. Given the pathophysiological deficits in an acute exacerbation of CF, the specific goals are to enhance mucociliary transport, promote airway clearance, optimize alveolar ventilation and therefore gas exchange, maximize the efficiency of oxygen transport overall, and prevent and minimize infection.

Although the degree to which patients with chronic lung conditions, and in particular CF, can respond to aerobic training may be limited, it is essential that their capacity to transport oxygen overall is optimized to compensate for deficits in specific steps of the oxygen transport pathway.⁵⁴ Deconditioning severely impairs oxygen transport. Improved aerobic capacity and cardiovascular and pulmonary conditioning are central in the management of patients with CF. Prescriptive aerobic exercise enhances the efficiency of oxygen transport overall by reducing airway resistance by mobilizing secretions, improving the homogeneity of ventilation in the lungs and therefore ventilation and perfusion matching, optimizing oxygen extraction at the tissue level, and increasing respiratory muscle endurance.⁵⁵ If optimal conditioning is maintained, oxygen transport is not as compromised during acute exacerbations given the improved efficiency of oxygen transport overall. These effects will be lost, however, as the patient deconditions secondary to restricted mobility and recumbency during the acute episode. Thus it is important that mobility is minimally restricted during an exacerbation (based on the clinical assessment and morbidity) and that exercise conditioning is a mainstay of management between exacerbations. An important additional effect of long-term exercise, which has particular importance for patients with CF, is improved immunity.⁵⁶ This may minimize the risk for infection and perhaps minimize the severity of an infection once acquired. Patients with CF can have an abnormal hemodynamic response to exercise and myocardial adaptation; thus appropriate cardiac assessment and monitoring is indicated.⁵⁷

In severe exacerbations the patient is extremely stressed physiologically and has significantly increased oxygen consumption because of the increased work of breathing and for the heart. In addition, the patient is prone to arterial desaturation. Thus minimizing undue oxygen demand and fatigue guides the selection of treatment interventions and their parameters in conjunction with stringent monitoring. These patients become hypoxemic and distressed readily. Treatment interventions are selected based on the assessment and the patient’s ability to tolerate the treatment and derive optimal benefit. Gradual, paced, low-intensity mobilization and frequent body positioning enhance mucociliary transport and airway clearance and maximize the efficiency of the steps in the oxygen transport pathway. Postural drainage can offer additional benefit in these patients if further clearance is required. The addition of manual techniques may be indicated; however, stringent monitoring must be carried out given their potential deleterious effects on gas exchange.⁵⁸

Forced coughing and expiratory techniques can contribute to airway closure, whereas huffing and other forms of modified coughing with an open glottis minimize airway closure and can be more effective in removing secretions that have accumulated centrally without compromising ventilation and gas exchange. Forceful coughing, in which the glottis closes, contributes to airway closure and thus should be avoided, particularly in patients with elevated pulmonary artery pressure, because of the concomitant increase in intrathoracic pressure and strain on the heart and lungs. Patients with CF have severe paroxysms of coughing. This significantly increases intrathoracic pressure, which in turn impedes venous return and cardiac output. Although coughing is an essential mechanism for mucociliary clearance in these patients, the untoward cardiac effects must be minimized.

Over the past decade, other interventions aimed at secretion clearance in the treatment of patients with CF have included autogenic drainage, the use of the positive expiratory pressure (PEP) mask, and the Flutter valve.2,59 One study of patients with CF hospitalized for acute exacerbations compared the short-term efficacy of three regimens: postural drainage (PD), positive expiratory pressure physiotherapy (PEP), and high-frequency chest compression (HFCC) physical therapy.⁶⁰ The authors reported no change in lung function or in sputum production when the number of coughs was considered.

Autogenic drainage is based on the theory that the equal pressure point is shifted along the airways by altering the lung volume at which the patient breathes. The patient initially breathes slowly and deliberately at low lung volumes, then at mid and high lung volumes. Breathing at low lung volumes is believed to loosen secretions from the walls of the airways. This is followed by breathing at mid lung volumes, which is believed to help localize and collect the secretions. Finally, breathing at high lung volumes is believed to centralize and facilitate the removal of the secretions with coughing. Thus autogenic drainage may enhance the effectiveness of the patient’s cough by manipulating lung volumes and flow rates and controlling coughing to avoid unproductive coughing and wasteful expenditure of energy. The patient is coached by the physical therapist to breathe slowly and deliberately at the volumes set by the therapist, who gauges the patient’s ventilatory effort and work by placing his or her hands around the patient’s chest. The patient is not encouraged to breathe below end-expiratory volume and is encouraged to suppress coughing until the expelling phase (i.e., the phase during which the patient is breathing at high lung volumes).

Autogenic drainage may be a useful adjunct for facilitating airway clearance in patients with CF. It is a procedure that patients may use independently and can be applied relatively unobtrusively. It helps optimize the patient’s coughing efforts and minimizes the potential for airway closure in these patients. This procedure is designed to minimize exhaustive, metabolically costly coughing and preserve energy to expectorate most effectively.⁶¹

The PEP mask and Flutter® valve device are believed to reduce airway closure in conjunction with exercise, thus optimizing alveolar ventilation and enhancing mucociliary clearance in patients with CF.⁶² Individuals with CF can often learn to control their condition effectively with optimal health education and overall lifelong health program (see Chapters 24 and 31).

Principles of Physical Therapy Management

The primary clinical manifestations of an acute exacerbation of interstitial pulmonary fibrosis reflect an acute or chronic problem, usually resulting from an inflammatory episode, pulmonary infection, or both. The mechanisms responsible include reduced alveolar ventilation, an inflammatory process and its manifestations, potential airway obstruction, increased work of breathing, and in severe cases, increased work of the heart. These patients are susceptible to desaturation during exercise and thus need to be monitored closely.

Table 29-1 shows the primary components of care in the acute phase of management, which are similar to those of acute cardiac care (phase I of cardiac rehabilitation). In mild cases mobilization increases the homogeneity of ventilation and ventilation and perfusion matching. Between treatments and in the management of the severely affected patient, body positioning is used to reduce the work of breathing and arousal, maximize alveolar ventilation, maximize ventilation and perfusion matching, and optimize coughing.

Patients with moderate-to-severe interstitial lung disease may desaturate during sleep and readily desaturate on physical exertion.⁶³ Thus they warrant close monitoring during and between treatments. Increased pulmonary vascular resistance secondary to hypoxic vasoconstriction contributes to increased work of the right heart and potential cardiac insufficiency.

General debility and deconditioning warrant an exercise program that can optimize the conditioning and function of all of the steps in the oxygen transport pathway.⁶⁴ Individuals with interstitial pulmonary fibrosis require health education and an overall health program to help manage their symptoms (see Chapters 24 and 31).

Principles of Physical Therapy Management

Although the acute presentation of tuberculosis is comparable with acute pneumonia (refer to pneumonia section), there are some important differences with respect to physical therapy management.⁶⁶ First, tuberculosis is particularly infectious; thus special precautions should be taken by the physical therapist to prevent its spread during its infectious stage. Second, patients may be prone to fatigue; treatments should be selected to promote improved oxygen transport without exceeding the patient’s capacity to deliver oxygen and without contributing to excessive fatigue. Stimulation of the oxygen transport system with exercise is necessary to avoid the deleterious effects of deconditioning and further compromise of oxygen transport. The patient warrants being monitored closely.

There are few evidence-based guidelines to inform physical therapy management of a patient with pulmonary tuberculosis. The effects of medication, however, are likely to be enhanced with a healthy diet, exercise, and rest. Based on extent and rate of recovery, regular, moderate-intensity exercise every other day for 30 minutes is the eventual goal. Initially, however, performing simple activities such as brisk walking outdoors can help eliminate the bacteria. For patients whose symptoms have largely subsided, stationary biking or resistance training can augment health. Maintaining a program of maximal health and regular exercise is essential.