Principles of Physical Therapy Management

Patients may be referred to physical therapy with a history of angina as a primary or secondary problem. Regardless, angina is managed with the same care and vigilance because it can be a life-threatening condition either way. A patient for whom antianginal medication is prescribed must have the medication present. The medication must not have expired and must be within visible access during treatment. The physical therapist should examine the medication before treatment to ensure that the expiratory date has not passed and to take responsibility for positioning the medication near the patient for access to it should the patient develop angina during treatment.

The goals of long-term management of the patient with angina include the following:

Patient monitoring includes hemodynamic monitoring (i.e., heart rate, blood pressure, rate-pressure product, and dyspnea). Subjective responses to treatment, particularly exercise, should also be recorded (e.g., Borg’s rating of perceived exertion). Signs of chest pain, dyspnea, anxiety, lightheadedness, dizziness, disorientation, discoordination, cyanosis, coughing, and chest sound changes (i.e., a gallop) must be monitored. Angina is not an acceptable symptom under any circumstance. Should it occur, treatment is immediately discontinued and emergency measures instituted as indicated. Treatments will be safer and more precisely prescribed with continuous ECG monitoring. Without ECG monitoring, treatments must be conservative. If there is any doubt at any time concerning the hemodynamic stability of a patient and his or her ability to tolerate treatment safely, the patient should be referred to a general practitioner or cardiologist for clearance before being treated.

Medication that is necessary to maximize treatment response is administered before treatment. Knowledge of the type of medication, its administration route, and time to as well as duration of peak efficacy is essential if treatment is to be maximally effective.

For the long-term management of patients with angina, interventions include some combination of education, aerobic exercises, strengthening exercises, chest wall mobility exercises, relaxation, activity pacing, and energy conservation. Education includes information about heart disease and risk factors (i.e., smoking, diet, stress, weight, alcohol, coffee, and being physically active in hot environments) and appropriate preventative strategies (i.e., smoking reduction and cessation, low-fat diet, reduced alcohol consumption, exercise, relaxation, activity pacing, and stress management).

Patients with angina are at risk of having an infarction; therefore vigilance and stringent monitoring are necessary to detect angina or frank myocardial infarction. These patients are potentially hemodynamically unstable; thus their hemodynamic responses before, during, and after treatment, particularly aerobic and strengthening exercises, should be monitored and recorded. Minimally, heart rate, blood pressure, and rate-pressure product should be recorded, along with the patient’s subjective responses to treatment. Heavy lifting, static exercise, straining, the Valsalva maneuver, and heavy, repetitive upper-extremity work are avoided during physical activity and exercise. These activities are associated with a disproportionate hemodynamic response. Physical activity and aerobic exercise are prescribed at a target heart rate or perceived exertion ranges that are below the anginal threshold based on a graded exercise tolerance test (see Chapters 19 and 24). Peak exercise tests in patients with cardiac dysfunction that may elicit angina or ST-segment changes are performed in a cardiac stress testing laboratory, usually under the supervision of a cardiologist unless in a specialized facility where physical therapists perform such testing.

The body position in which aerobic exercise is performed is important in patients with heart disease. Positions of recumbency increase the volume of fluid shifted from the periphery to the central circulation. This increases venous return and the work of the heart. Therefore upright body positions have long been known to minimize cardiac work during exercise in these patients and during rest after exercise.5,6

Sexual dysfunction is common in individuals with systemic atherosclerosis owing in part to underlying pathology (dyslipidemia, vascular insufficiency, and diabetes), medication, and the psychological impact of heart disease.⁷ In terms of energy demands, those of sexual activity are comparable to those of other daily activities (e.g., walking 1 mile on the level). Optimizing health in general with diet and exercise can contribute to regression of atherosclerosis and improved peripheral circulation. Breathing control, body positioning, and energy conservation strategies such as exercising at a high energy time of day may also help minimize symptoms. Also, patients should be advised to avoid sexual activity within an hour of eating, and even then not to consume a heavy meal.

Angina frequently precedes frank myocardial ischemia and infarction. Myocardial ischemia is reversible, whereas infarction denotes myocardial injury and cell death (i.e., necrosis). Injured myocardial cells either recover or die during the healing period. Thus minimizing further damage and maximizing the healing during this 6-week period is critical. Myocardial infarctions can range from being silent and unnoticed by the patient to being life-threatening. They can occur anywhere in the myocardium but occur primarily in the ventricles (in the left more frequently than in the right ventricle). The greater the severity, the greater the risk of ventricular insufficiency, acute pulmonary edema, and left ventricular failure. Because myocardial ischemia and infarction impair the pumping action of the heart and thus cardiac output, patients tend to be hypoxemic and in need of oxygen. Even after the oxygen has been discontinued and the myocardium has healed, the patient may continue to be vulnerable hemodynamically. The myocardium will have some scarring that will affect both the electrical excitability (producing dysrhythmias) and the mechanical function of the heart. In addition, the patient may continue to have low-normal arterial blood gases. Hypoxemia is lethal in that it triggers dysrhythmias and predisposes tissues to hypoxia. Thus hypoxemia must be avoided. After myocardial infarction, patients are usually discharged home on several medications (e.g., nitroglycerin, calcium antagonists, beta blockers, and diuretics). Depending on the severity of involvement, patients usually continue to require one or more of these medications over the long term. The need for oxygen is usually short term and restricted to the patient’s hospital stay.

The patient’s ECG will be important for determining the parameters of exercise, the level of monitoring required, and education. Dysrhythmias are described in Chapter 4, and basic ECG reading is presented in Chapter 12. Ventricular dysrhythmias can be lethal. Occasional premature ventricular contractions must be monitored to ensure that their frequency remains low and that coupling does not occur. Atrial fibrillation is considered a relatively serious dysrhythmia. It is associated with a high incidence of coronary disease, stroke, and overall mortality.⁸ Medication or a pacemaker may be necessary.

Central sleep-disordered breathing is highly prevalent in individuals with left ventricular dysfunction and is associated with abnormal cardiac autonomic control and increased dysrhythmias.⁹ Although sleep-disordered breathing may not be related to the severity of hemodynamic dysfunction, loss of recuperative sleep will affect functional capacity as well as capacity and motivation to participate in an exercise program and be physically active.

Health-related quality of life reported by individuals with chronic heart failure is associated with function and exercise capacity, not with ejection fraction.¹⁰ Health-related quality of life should be an outcome measure for all individuals managed for heart failure because it provides important supplemental information that is independent of physiological indices of cardiac function and the NYHA classification of function (see Table 31-2).

Nonpharmacological approaches to the management of individuals with heart failure are an essential component to the overall management of the condition.¹¹ These measures are incorporated into an individualized program of health behavior change, and include the following:

All patients with cardiovascular risk factors can benefit from cardiac rehabilitation. After a cardiac event, patients are typically discharged with drugs, the prospect of surgery, and rather infrequently with referral to an individual physical therapist or one who is a member of the cardiac rehabilitation team. There is a high incidence of recurrence and repeated surgery with further associated mortality and burden of disease. The physical therapist as a noninvasive practitioner has a primary responsibility to help avoid recurrence of symptoms and repeated surgeries. This is consistent with the physical therapist’s overriding objective of reducing the need for invasive care (i.e., drugs and surgery) and developing a sustainable, lifelong health plan with the patient.

Risk factor modification is a major goal. A marker of inflammation such as C-reactive protein along with appropriate lipid testing findings may be a more discriminating risk factor than lipid profiling alone.¹² Refining the risk factor definition on the basis of C-reactive protein level will help target management (e.g., indicate necessity for intensified exercise programs, weight loss, and smoking cessation).

Valve dysfunction is either congenital or acquired and may require treatment as a primary condition or be present as a secondary condition. Any of the heart and pulmonary valves may be affected. Rheumatic fever was a common cause of rheumatic heart disease and in particular mitral valve insufficiency. Interconnecting lymphatic vessels between the tonsils and the heart are thought to be responsible. Calcification of valves that impairs opening and closing is another example of an acquired valve dysfunction.

Clinically, patients with valve disease may demonstrate exertional dyspnea, excessive fatigue, palpitations, fluid retention, and orthopnea. These signs and symptoms are often relieved when exertion is discontinued. Aerobic exercise, however, has been shown to reduce the symptoms of prolapsed valve.¹⁶ Anxiety has been reported to decrease general well-being. If effectively managed, however, reduced anxiety can improve or reduce chest pain, fatigue, and dizziness.

Prophylactic antibiotics against endocarditis are administered to most patients with significant valvular involvement and in mild disease before procedures such as dental work.

Peripheral vascular disease refers to diseases of the arteries and the veins. Peripheral arterial disease results primarily from atherosclerosis and occlusion of the peripheral arteries (e.g., thoracic aorta, femoral artery, and popliteal artery).¹⁷ The diagnosis may be overlooked until serious limb ischemia is evident.¹⁸ Diabetes mellitus, which can result in microangiopathy and autonomic polyneuropathy, is another important cause of PVD in the lower extremities. Venous disease results in phlebitis, venous stasis, and thromboembolus and leads to valvular incompetence of the veins of the legs.

Arterial occlusion results in reduced blood flow to the extremities and hence reduced segmental blood pressure distal to the occlusion (i.e., lower ankle-brachial index). In mild cases of arterial stenosis the patient may be asymptomatic because considerable stenosis has to occur before there is significant reduction in peripheral blood flow. If atherosclerosis develops gradually, collateral circulation may develop sufficiently to offset progressive vessel narrowing. Clinically the patient reports limb pain on exercise, coldness in the affected leg, and possibly numbness. The characteristic limb pain results from ischemia and is referred to as intermittent claudication. Mild to moderately severe cases are managed conservatively. Pain at rest is suggestive of severe stenosis and significant reduction of blood flow to the limb. Significantly reduced blood flow leads to ischemic color changes, skin breakdown, ulceration, and eventually gangrene. Bypass surgery is performed to revascularize a threatened limb. In severe cases in which gangrene has developed, amputation of the limb is indicated. The severity of PVD is a significant predictor of cardiovascular mortality. Individuals with PVD show a systemic endothelial dysfunction and an increase in the serum concentration of white blood cells, endothelin, and C-reactive protein that may trigger acute coronary syndromes.

Individuals with intermittent claudication can have a marked decrease in exercise tolerance and thus can benefit from aerobic exercise, which may stimulate the development of collateral blood vessels around the stenosed vessel. This condition can severely restrict mobility, which reduces function in addition to aerobic capacity and efficient oxygen transport overall.

Individuals with PVD from diffuse systemic atherosclerosis can be expected to have stenosis of the coronary arteries even though they may be asymptomatic. These individuals are monitored as stringently as if they had overt ischemic heart disease.

Venous insufficiency can lead to thromboemboli, skin lesions, and poorly healing ulcers of the lower extremities. Furthermore, the risk of infection and slow healing is increased.

Individuals with PVD secondary to diabetes mellitus have accelerated atherosclerosis compared with age-matched individuals without diabetes. Diabetes affects the macrocirculation and microcirculation; thus wounds must be prevented, particularly in the lower legs and feet, and managed aggressively should they occur. These individuals may be at risk for lower extremity lesions because of autonomic neuropathy and angiopathy. To restore insulin sensitivity and promote weight loss, activity levels must be significantly increased, and a formal exercise program instituted. Weight-bearing activities are safe for individuals with poor sensation in the feet and do not increase the risk of reulceration.¹⁹

Systemic hypertension or high blood pressure is a serious condition. Most patients experience no symptoms; thus adherence to medication regimens is often poor. Approximately 90% of hypertension is termed essential hypertension (i.e., no known cause). Hypertension predisposes a patient to stroke, myocardial infarction, renal dysfunction and failure, hemorrhage, and infarction of other vital organs. Blood pressure tends to increase with age. With the aging of the population, the incidence of hypertension is increasing. Increased blood pressure results from increased peripheral vascular resistance; therefore medications are prescribed that reduce myocardial afterload and peripheral vascular resistance. Hypertension and antihypertensive medication are risk factors for type 2 diabetes mellitus.²³ Therefore avoiding a patient’s need for medication or at least reducing it is a singularly important physical therapy outcome.

There are other serious consequences of chronic high blood pressure. Patients with existing cardiovascular disease (i.e., hypertension) are at risk for multisystemic manifestations that must be assessed, e.g., signs and symptoms of cerebrovascular and renal impairments. In addition, this population tends to be older, and older populations are known to have a higher prevalence of cardiac dysrhythmias. Thus such patients’ cardiac status, including ECG history, should be obtained.

Pulmonary hypertension may occur in the absence of primary cardiac disease. So-called “primary pulmonary hypertension” is often associated with altered resting lung function. Abnormal lung mechanics and diffusing capacity are directly associated with disease severity and may contribute to the dyspnea and fatigue reported by individuals with primary pulmonary hypertension.²⁴

Type 2 diabetes mellitus is a condition associated with impaired insulin metabolism that can result in serious long-term multisystem consequences.²⁹ The disease is classified as either insulin-dependent or non–insulin-dependent diabetes mellitus. Insulin is the carrier responsible for transporting glucose into the cells to undergo oxidation. Juvenile-onset diabetes is frequently the insulin-dependent type, whereas adult-onset diabetes often is the non–insulin-dependent type. The underlying pathophysiology of juvenile- and adult-onset diabetes, however, is distinct. Juvenile-onset (type 1) diabetes results from an inadequate number of islets of Langerhans in the pancreas, which are responsible for insulin production. Adult-onset (type 2) diabetes, on the other hand, results from reduced insulin sensitivity. In Western industrialized countries, adult-onset diabetes is associated with obesity, inactivity, poor diet, and stress. In addition, medications can contribute to blood sugar disturbances. The sequelae of type 2 diabetes mellitus that frequently result from poor regulation and management of the disease include angiopathy, peripheral neuropathy, autonomic neuropathy, gastrointestinal paresis, visual disturbance, and renal dysfunction.³⁰

Individuals with type 2 diabetes mellitus have an accelerated rate of atherosclerotic changes in the vasculature compared with age- and sex-matched individuals without diabetes. These individuals are also prone to PVD secondary to microangiopathy, macroangiopathy, and autonomic neuropathy. People with type 2 diabetes mellitus constitute a significant proportion of patients with PVD who require surgical amputation of affected limbs as a consequence of peripheral ischemia. Muscle infarction is a less common but clinically important complication of longstanding diabetes.³¹ Muscle infarction manifests with pain and swelling over the affected area and at times a palpable mass and elevated creatine kinase levels. The symptoms resolve with conservative management including analgesics and relative immobility of the affected muscle.

Abnormalities of blood sugar metabolism can also be observed in individuals without diabetes. Diabetogenic factors, such as restricted mobility and stress, lead to glucose intolerance and insulin oversecretion.32,33 In the individual without diabetes, these effects can be tolerated over the short term. These factors, however, may result in a critical situation for the individual with diabetes.

Metabolic syndrome is increasingly common and includes central obesity, low high-density-lipoprotein cholesterol, hypertension, and often insulin resistance and hypertriglyceridemia.³⁴

Chronic bronchitis is usually associated with a history of smoking and is defined as mucous hypersecretion and cough producing sputum for 3 months or more over a 2-year period.³⁹ Over the first few years of smoking, reversible airway changes occur. Over 10 to 15 years of smoking, mucous hypersecretion and chronic bronchitis become apparent. After 25 to 35 years of smoking, irreversible airway damage and chronic disability occur. Smoking is the major cause of emphysema and lung cancer.

The patient with chronic bronchitis is prone to infection and repeated periods of morbidity. Deterioration of aerobic capacity and functional capacity is related to the severity of the condition. Nutrition and hydration may be impaired, particularly in severe cases, because of neglect and the excessive energy cost of activities of daily living. Sleep may be irregular; thus the patient’s symptoms are worsened (e.g., reduced endurance, fatigue, and lethargy) because of lack of normal physiological restoration from sleep.

The natural history of chronic bronchitis related to smoking includes mucous hypersecretion, reduction in forced expiratory volume in 1 second (FEV₁), and increased heterogeneity of the distributions of ventilation, perfusion, ventilation-perfusion matching, and diffusion.40,41 General debility and deconditioning ensue.

Smoking contributes to increased mucus production in the small airways, increased mucus in the large airways, respiratory bronchiolitis, reduced elastic recoil, increased airway reactivity, and vascular changes.³⁷ These changes lead to nonuniformity of time constants in the lung, with consequent inhomogeneous distribution of inspired gas and premature small airway closure, and to nonuniformity of ventilation, perfusion, and diffusion distributions. Although variable among smokers, pulmonary function changes generally correspond to the amount smoked and duration of smoking history. Over time the pulmonary function profile becomes increasingly consistent with chronic airflow limitation (i.e., reduced FEV₁ and reduced FEV₁/forced vital capacity); however, these are late indicators of pulmonary changes. Signs of uneven distribution of ventilation and increased closing volumes, indicative of small airway involvement, are early pulmonary function changes in smokers. Exercise diffusing capacity is reduced, which explains in part the reduced maximal volume of oxygen use of smokers. Dynamic compliance with breathing frequency is also reduced. Residual volume is increased as a percent of total lung capacity (TLC). Tracheal mucous velocity is reduced, and secretion clearance is impaired. Any patient with a smoking history, regardless of a diagnosis, has some degree of chronic airflow limitation, which must be considered when these patients receive medical or surgical care, as well as physical therapy.

The cardiac manifestations of chronic bronchitis stem from airway obstruction, secretion accumulation and reduced capacity to expectorate effectively, polycythemia, low arterial oxygen tension, and cardiovascular and pulmonary deconditioning. Increased airway resistance secondary to obstruction increases oxygen demand and hence the work of breathing. This increased demand is superimposed on an oxygen transport system that is already compromised. The cardiovascular system attempts to compensate for chronically reduced arterial oxygen tension by increasing cardiac output (i.e., stroke volume and heart rate). As blood gases deteriorate, the production of red blood cells increases (i.e., polycythemia) to enhance the oxygen-carrying capacity of the blood. Polycythemia increases the viscosity of the blood, however, and in turn, the work of the heart to pump blood to the pulmonary and systemic circulations. Furthermore, viscous blood is prone to circulatory stasis and clotting.

Low arterial oxygen tension leads to hypoxic pulmonary vasoconstriction and increased pulmonary vascular resistance (i.e., pulmonary hypertension). This also increases the work of the right side of the heart in terms of ejecting blood to the lungs. Chronic overwork of the right ventricle leads to hypertrophy, insufficiency, and eventual failure of the right heart (cor pulmonale). Chronically reduced arterial oxygen can increase the demand on the left side of the heart to maintain cardiac output. Similar to right-sided failure, the left side of the heart may become hypertrophied and over time may fail.

The increased intrathoracic pressures generated during chronic coughing reduce venous return, cardiac output, and coronary perfusion and increase blood pressure. These effects exert additional myocardial strain, lead to arterial desaturation, and increase the potential for cardiac dysrhythmias.

The complications of chronic bronchitis are exacerbated by cardiovascular and pulmonary deconditioning. Despite the pathology, the efficiency of oxygen transport along the steps in the pathway is suboptimal. This reduced efficiency results in an overall increase in the oxygen demands of the patient, who is unable to adequately supply oxygen.

Pharmacological support in the long-term management of chronic bronchitis includes bronchodilators (e.g., oral, metered-dose inhalant, inhaled powdered, or aerosol), corticosteroids (e.g., oral or inhaled), expectorants, antibiotics, inotropic agents (e.g., digitalis), beta blockers, antidysrhythmic agents, and diuretics. Patients with chronic lung disease must be monitored closely during exercise because of the potential cardiac effects of disease and medications (e.g., beta-blocker agents attenuate the normal hemodynamic responses to exercise; bronchodilators, such as albuterol (Ventolin), elicit tachycardia).

Emphysema is associated with a prolonged history of smoking and chronic bronchitis and indicates significant irreversible lung damage. A less common type of emphysema not associated with smoking is alpha₁-antitrypsin deficiency. Antitrypsin is essential in balancing elastin production and degradation and in preserving optimal lung compliance. A deficiency of antitrypsin reduces lung elasticity and contributes to the characteristic increase in lung compliance that is the hallmark of emphysema. The pathophysiology of emphysema is detailed in Chapter 5. The principal pathophysiological deficits include irreversible alveolar damage resulting from loss of elastic recoil and the normal tethering of the alveoli, which renders the lung parenchyma excessively compliant and floppy. Excessive distension and dilatation of the terminal bronchioles and destruction of alveoli reduce the surface area for gas exchange. Hence diffusing capacity is correspondingly reduced. The dead space in the lungs and TLC increase significantly. Breathing at normal tidal volume, the patient’s airways close beyond the degree normally occurring with aging, and this contributes to ventilation and perfusion mismatch and hypoxemia. Time constants are altered such that alveolar units are not evenly ventilated. In the nonacute, chronic stages the primary problems include inadequate and inefficient gas exchange resulting from the structural damage to the lungs and altered respiratory mechanics of the lungs and chest wall and their interaction. The lungs are hyperinflated, the chest wall becomes rigidly fixed in a hyperinflated position, the normal bucket handle and pump handle motions of the chest wall are impaired, the hemidiaphragms are flattened, the mediastinal structures are shifted, and the heart is displaced and rotated, making it mechanically inefficient.⁴⁰ The normal mucociliary transport system is ineffective because years of smoking destroy the cilia, reduce their number, and alter their configuration and orientation; thus their function is correspondingly obliterated or impaired. In addition, these patients are unable to generate high transpulmonary pressures and forced expiratory flow rates because of altered respiratory mechanics. Consequently, coughing is weak and ineffective. The administration of supplemental oxygen is limited because these patients rely on their hypoxic drive to breathe. This life-preserving drive can be attenuated with even moderate levels of oxygen. Thus oxygen administration is limited to low flows. The respiratory muscles are often weak, if not fatigued from being in a flattened position, and hence suboptimal on the length-tension curve.⁴³ The clinical consequences of hyperinflation include abnormal chest wall movement, impaired inspiratory muscle function, increased oxygen cost of breathing, impaired exercise capacity, hypoxemia and hypercapnia, and breathlessness. Overall, patients with emphysema, particularly severe emphysema, tend to be inactive and deconditioned, which further compromises the efficiency of the oxygen transport system and the capacity of other steps in the pathway to compensate.

Several physiological compensations occur in response to chronic hypoxemia. Stroke volume and cardiac output are increased. The red blood cell count increases (polycythemia); however, the blood becomes more viscous and requires more work to eject and distribute throughout the body. Thus the stroke work of the heart is further increased. This load on the heart occurs in addition to the increased afterload of the right ventricle because of an increase in pulmonary vascular resistance secondary to hypoxic vasoconstriction in the lungs. Over time the heart becomes enlarged and pumps even less efficiently. In the long-term management of the patient with emphysema, the primary pathophysiological problems are impaired alveolar ventilation, impaired gas exchange, reduced oxygen transport efficiency, and the work of breathing and of the heart. Unlike in chronic bronchitis, secretion accumulation may be less problematic in patients with emphysema during nonacute periods. Nonetheless, optimizing mucociliary transport is an ongoing goal of prevention in that the consequences of mucous retention and infection can be life-threatening.

Noninvasive positive pressure mechanical ventilation (NPPV) has been an important advance in the management of individuals with chronic lung disease.⁴⁴ Those with daytime hypercapnia with nocturnal hypoventilation may benefit most.⁴⁵ The efficacy of NPPV, however, is jeopardized by poor adherence to its use. Predictors of successful use include ability to protect the airway, acuteness of illness, and a good initial response within the first couple of hours. Barriers include discomfort of the nose piece or face mask, patient-ventilator asynchrony, excess sternocleidomastoid activity, unstable vital signs, prolonged hours of ventilator use, problems with adaptation, symptoms, and poor gas exchange. In addition to immediate clinical benefits, NPPV may help avoid or postpone respiratory failure and invasive mechanical ventilation and weaning in this population. Other benefits that may be associated with NPPV include improved sleep and quality of life and reduced hospitalization. The physical therapist needs to identify potential barriers and address these to maximize adaptation and adherence to NPPV. Patient subgroups of those who will benefit from NPPV must be identified. Technology research must improve comfort and adherence to NPPV.

Long-term outcome of lung volume reduction surgery for people with severe emphysema has been positive. Six months after surgery, right ventricular performance increases, particularly during exercise.⁴⁶

Asthma is a common respiratory condition that is characterized by hypersensitivity of the airways to various triggers resulting in reversible airway obstruction (i.e., bronchospasm and bronchial edema) (see Chapter 5).³⁹ In mild cases, no treatment other than prophylaxis may be needed. In severe cases, asthma can be life-threatening. Once affected by the trigger, the airways narrow, increasing the resistance to airflow and reducing oxygen delivery. Breathing through narrowed airways contributes to wheezing, reduced alveolar ventilation, rapid shallow breathing, shortness of breath, increased work of breathing, desaturation, and cyanosis. Increased inhomogeneity of the distribution of ventilation is present in some patients with nonacute asthma.⁵⁸ Expiratory flow-volume loops remain the cornerstone of monitoring asthma.⁵⁹ Although some triggers may produce mucous hypersecretion, even normal amounts of pulmonary secretions can obstruct narrowed airways and lead to atelectasis. Asthma that has well-defined triggers is easier to manage than cases in which the triggers are less specific.

Principles of Physical Therapy Management

The goals of long-term management of the patient with asthma include the following:

Patients are monitored for dyspnea, respiratory distress, inappropriate breathing pattern (depth and frequency), arterial desaturation, and cyanosis (delayed sign of desaturation); heart rate, blood pressure, and rate-pressure product are monitored. Patients with cardiac dysfunction or low arterial oxygen tension require ECG monitoring, particularly during exercise. Subjectively, breathlessness is assessed using a modified version of the Borg scale of perceived exertion.

Medication that is needed to maximize treatment response (e.g., bronchodilators and antiinflammatories) is administered before treatment. Knowledge of the type of medication, its administration route, and time to and duration of peak efficacy is essential if treatment is to be maximally efficacious. When patients are taking multiple medications, their interactions and the implications for management must be known.

The primary interventions for maximizing cardiovascular and pulmonary function and oxygen transport in patients with asthma include education, aerobic exercise, strengthening exercise, chest wall mobility exercises, range-of-motion exercises, relaxation, activity pacing, and stress management.

Education is central to self-management of asthma. The patient is taught the basic pathophysiology of the disease and its triggers. Other central topics, including preventive health practices, are also taught (e.g., cold and flu prevention; flu shots; medication types, administration, and effects; aerobic exercise; nutrition; weight control; hydration; air quality control including smoking reduction and cessation; relaxation and stress management; and the benefits of an integrative, lifelong, self-management rehabilitation program).

Special mention must be made regarding the use of medications and inhalers. These are frequently used unknowledgeably (i.e., the patient is unfamiliar with the basic pharmacokinetics of the medications being used and thus is not deriving optimal effects). Inhalers are often used improperly; therefore the patient does not derive the full benefit of the medication. The instructions provided by the supplier of the inhalers should be strictly followed. There are numerous types of inhalers, all with different applications. In not adhering to the instructions, the patient’s time and effort are wasted by using the inhaler ineffectively, the patient does not derive the full benefit of the medication, an excessive amount of inhaler may be used to compensate for ineffective application, there may be increased exposure of the patient to the side effects of the medication, and there is considerable economic waste.

Knowledge of the triggers of increased airway sensitivity enables the patient to exert control over bronchospastic attacks. The patient is taught to record the frequency of bronchospastic attacks and identify what triggers and relieves them. In this way the patient learns to avoid or minimize their frequency, severity, and duration and minimizes the amount of medication required. In turn, doctor and hospital visits may be minimized. These are significant benefits.

The exercise prescription parameters are set below the bronchospasm threshold, which is established based on an exercise test (see Chapters 19 and 24). Specialized challenge tests are performed in a pulmonary function laboratory. Exercise training enables the patient to determine the balance between optimal aerobic capacity and medication and the optimal physical environment for exercise. Temperature and humidity can have significant effects on work output in patients with asthma.

Bronchiectasis is characterized by dilatation and anatomical distortion of the airways and obliteration of the peripheral bronchial tree.⁴¹ Bronchiectasis is often the sequela of prolonged chronic lung infection. The associated inflammation leads to occlusion of the airways, which results in atelectasis of the parenchyma and consequent dilatation of central airways by increased traction on the peribronchial sheath. In addition, chronic inflammation weakens the walls of the airways, leading to further dilatation. Fibrotic connective tissue changes in the wall contribute further to dilatation and airway distortion. These anatomical changes adversely affect normal respiratory mechanics and hence pressure volume characteristics of the lung. The chest wall becomes hyperinflated and assumes the barrel shape associated with chronic airflow limitation. The overall severity of bronchiectasis depends on the number of lung segments involved. There is often some reversible airflow limitation associated with bronchiectasis.

The patient with bronchiectasis has copious tenacious secretions, lung hyperinflation and impaired respiratory mechanics, an inefficient breathing pattern, reduced ability to clear secretions, and reduced aerobic capacity and is generally debilitated.

The increased intrathoracic pressures generated during bouts of chronic coughing limit venous return, cardiac output, and coronary perfusion. Blood pressure is also increased. These effects exert additional myocardial strain, lead to arterial desaturation, and increase the potential for cardiac dysrhythmias and dysfunction.

Cystic fibrosis is a complex exocrine disease that has significant systemic effects.³⁹ The disease is congenital and is hallmarked by nutritional deficits contributing to impaired growth and development. Pulmonary function shows progressive decline with commensurate reductions in homogeneity of ventilation and inspiratory pressures.⁵⁸ Cardiovascular and pulmonary involvement can be classified into three groups: no physical signs in the chest; occasional cough and sputum; and constant cough, sputum, and other signs. Patients in each classification can benefit from physical therapy with respect to enhancing oxygen transport. Moderate and severe disease is characterized by significant airflow obstruction secondary to copious, tenacious secretions. In addition, pulmonary hypertension and right heart insufficiency may be manifested and eventual failure may ensue. Left ventricular diastolic failure may also be a feature of advanced disease.⁶⁰

Between exacerbations, the medical priorities are to reduce the risk of infection and morbidity and promote optimal health, growth, and development.

Principles of Physical Therapy Management

The goals of long-term management of the patient with ILD include the following:

Patients are monitored for dyspnea, respiratory distress, and inappropriate breathing pattern (depth and frequency); arterial desaturation; in addition heart rate, blood pressure, and rate-pressure product are monitored. Patients with cardiac dysfunction or low arterial oxygen tension require ECG monitoring, particularly during exercise. Subjectively, breathlessness is assessed using a modified version of the Borg scale of perceived exertion.

Medication that is needed to maximize treatment response is administered before treatment. Knowledge of the type of medication, its administration route, and time to and duration of peak efficacy is essential if treatment is to be maximally effective.

The primary interventions for maximizing cardiovascular and pulmonary function and oxygen transport in patients with ILD include some combination of education, aerobic exercises, strengthening exercises, chest wall mobility exercises, range-of-motion exercises, body positioning, breathing control and coughing maneuvers, relaxation, pacing, and energy conservation. An ergonomic assessment of the patient’s work and home environments may be indicated to maximize function in these settings.

Education is a central component of a comprehensive rehabilitation program for the management of ILD. Education includes information on preventative health practices (e.g., removal from the causative environment, cold and influenza prevention shots, triggers of disease exacerbations and their prevention, smoking reduction and cessation, nutrition, weight control, hydration, relaxation, activity pacing, and energy conservation).

During aerobic exercise, patients with ILD are prone to arterial desaturation.⁶⁶ Patients who desaturate during sleep require supplemental oxygen during exercise. The intensity of the exercise prescribed is based on arterial saturation, breathlessness, and work of the heart, in conjunction with other objective responses.

Lung cancer is a leading cause of death for men and the incidence is increasing for women. Once diagnosed, 80% of patients survive 1 year. Lung cancer is highly correlated with a history of smoking and exposure to coal tars, asbestos, and radioactive dusts. The majority of primary malignant tumors are bronchogenic carcinomas. They are centrally located and thus contribute to bronchial obstruction, atelectasis, and pneumonia. Pathophysiologically, lung cancer has features of both obstructive and restrictive lung disease. Presenting signs include airway obstruction, dyspnea, cough, and hemoptysis.³⁹ Treatment is limited to surgery, if metastasis has been ruled out, or conservative management with radiation and chemotherapy.

Bronchogenic carcinomas metastasize readily through the circulation and lymphatic channels to other organs including the brain, bone, liver, kidneys, and adrenal glands.

If detected early, thoracic surgery may be performed to excise the cancerous tumor (see Chapter 29). If inoperable, or in the case of metastases, a patient may be managed at home or in a hospice. Patients are debilitated, often undernourished, fatigued, short of breath, lethargic, depressed, and in pain. Although these patients are often extremely ill, there is a growing trend to manage these patients in the community whenever possible. As the disease progresses, maintaining function and reducing the rate of deterioration become primary goals.

End-of-life issues and palliative care must be discussed. If the patient is managed at home, these principles of care can be practiced in this setting, and they are common to other conditions as well.