Medical rehabilitation medicine needs to encompass the needs of patients with cardiopulmonary disorders as well as patients with debility and renal dysfunction. There are ever greater numbers of patients who are now presenting with these issues, especially as the population ages. Cardiac disease is still the number one cause of mortality and disability in the United States, with chronic obstructive pulmonary disease now being the third leading cause of mortality. Even if it is not primary rehabilitation for patients with these diseases, many patients with other disabilities will have cardiac, pulmonary, and renal disabilities, and a common theme among all of these conditions is a degree of frailty.
This issue of frailty underlies a great number of the common features of disability in these underlying conditions and will be discussed in the section on frailty . Key areas that will be addressed include sarcopenia, acute and chronic deconditioning, and the role of exercise as medicine to improve patients with all of these conditions.
Important contributors to the prevalence of all of these conditions are the aging of the population as well as the effects of combinations of these conditions on the ability to rehabilitate patients. The overall approaches to exercise treatment in these patients will be discussed and also how to approach these conditions in the acute, rehabilitation, and outpatient settings.
Cardiopulmonary Rehabilitation
It must be remembered that there are two types of cardiopulmonary patients, those with primary cardiac and pulmonary disease who need cardiac/pulmonary rehabilitation and those patients with other disabilities who have a cardiac or pulmonary secondary disability. Patients with respiratory failure and patients who have need for ventilatory support are also in this group but are beyond the scope of this chapter. Dual disability patients are more prevalent than ever in rehabilitation because more patients are now older and have multiple comorbidities. Many patients with stroke, vascular disease, or other conditions can be included in active cardiac and pulmonary rehabilitation programs or benefit from the application of cardiopulmonary rehabilitation principles to their rehabilitation. Remember also that cardiopulmonary rehabilitation is one of the most underused yet most effective treatments for patients with cardiopulmonary disease. Because we work with frail older adults and other compromised populations, it is important for rehabilitation specialists to know how to provide cardiopulmonary rehabilitation in patients with either primary or secondary cardiopulmonary disability.
To use cardiac and pulmonary rehabilitation principles for patients with cardiopulmonary disease, whether it is a primary or secondary disability, it is necessary to review some of the basic principles of cardiac and pulmonary physiology and learn how to apply these principles to improve the exercise capacity of these patients. It is also essential to have an understanding of normal exercise physiology to appreciate the issues of patients with abnormal cardiopulmonary physiology.
Assessment of Cardiopulmonary Function
History and Physical Examination
A complete cardiopulmonary history and physical examination is an essential part of the evaluation of patients with cardiopulmonary disease who participate in rehabilitation. Key parts of the history include both verbal and nonverbal cues and will allow the establishment of goals and improve patient compliance with the treatment program.
History
The history should include emotional state, concurrent illnesses, other disabilities, functional history, occupational history, social history, personal habits, family dynamics, and the effect of disability and cardiopulmonary illness on the patient in the community. Both rest and activity symptoms are reviewed with particular emphasis on the following.
Dyspnea.
Shortness of breath is usually the prime complaint for patients with cardiopulmonary disease. The history of dyspnea helps to differentiate the role of cardiac or pulmonary disease in the patient’s symptoms. Cardiac dyspnea can be from ischemic heart disease, congestive heart failure, valvular heart disease, and arrhythmias. Pulmonary dyspnea can come from pulmonary vascular disease, restrictive lung disease, and obstructive lung disease. In some patients both cardiac and pulmonary issues may be present, and in all cases physical conditioning needs to be assessed. Because psychological factors are also important, patients should also be screened for anxiety and depression. Finally, an assessment for hypoxemia should be done. See Table 27-1 for a list of common causes of dyspnea.
| Site of Pathology | Pathophysiology | |
|---|---|---|
| Pulmonary Causes | ||
| Airflow limitation | Airways | Limitation to ventilation through flow through airways |
| Restriction (intrinsic) | Lung parenchyma | Poor lung compliance |
| Restriction (extrinsic) | Chest wall | Poor chest wall compliance with or without poor chest wall strength |
| Acute pulmonary disease | Lungs | Increased ventilation/perfusion (V/Q) mismatch |
| Cardiac Causes | ||
| Valvular disease | Heart valve stenosis or incompetence | Limited cardiac output |
| Coronary disease | Heart muscle ischemia | Coronary insufficiency leads to myocardial ischemia |
| Heart failure | Ventricular failure | Limited cardiac output from decreased stroke volume |
| Circulatory | ||
| Anemia | Low hemoglobin can be from blood loss or from hemoglobinopathies | Limited oxygen-carrying capacity |
| Peripheral circulation | Peripheral arterial disease | Inadequate oxygen supply to metabolically active tissues, leading to early anaerobic threshold |
| Whole Body | ||
| Obesity | Excess adipose tissue with associated physiologic changes | Increased work of movement, decreased efficiency May have respiratory restriction if severe—both extrinsic chest wall restriction and upper airway obstruction |
| Psychogenic | Emotional | Hyperventilation, anxiety |
| Deconditioning | Multiple organ systems, muscle weakness, cardiac deconditioning | Loss of ability to effectively distribute systemic blood flow, inefficient aerobic metabolism |
| Malingering | Emotional | Inconsistent results |
Chest Pain.
Chest pain and tightness is not only a mark of coronary insufficiency but can also be seen with valvular heart disease or arrhythmia. Assessing the duration, quality, provocation, location of the pain, and any ameliorating factors can help assess functional limitations and help design the appropriate therapy program. In addition, Lung conditions can cause chest pressure in both obstructive and restrictive lung disease, and is very common in pulmonary vascular disease.
Palpitations.
Symptoms of palpitations can be indicative of serious arrhythmias.
Syncope.
Cardiac syncope is usually abrupt with no warning or only a brief warning (with the patient feeling as if he or she were about to pass out) and can be caused by aortic stenosis, idiopathic hypertrophic subaortic stenosis, primary pulmonary hypertension, hypercarbia, hypoxemia, ventricular arrhythmias, reentrant arrhythmias, high-degree atrioventricular block, or sick sinus syndrome. Pulmonary syncope is often gradual in onset and can be caused by hypercarbia, hypoxemia, or pulmonary vascular disease. Orthostatic syncope can be caused by autonomic dysfunction, neurologic disease, vagal stimuli, or psychological stimuli.
Edema.
Peripheral edema may be an indication of heart failure and may indicate the onset of right ventricular failure in pulmonary vascular disease.
Fatigue.
Fatigue is likely to be the most common complaint in cardiopulmonary disease and may be worsened by the presence of depression, physical exhaustion, medication side effects, and deconditioning.
Cough.
Cough can be from both cardiac and pulmonary diseases. “Cardiac” cough is often nocturnal and postural, with little to no sputum production, relieved by assuming an upright position. Cough is common in both restrictive and interstitial lung disease, with or without sputum production.
Physical Examination
A description of the complete and detailed physical examination of the patient with cardiopulmonary disease is beyond the scope of this chapter. Still, some important elements of the examination include a general survey of the patient for exophthalmos (possible thyrotoxicosis), xanthelasma (hypercholesterolemia), acrocyanosis (chronic hypoxemia), clubbing (chronic hypoxemia), ankylosis (aortic valve disease and conduction defects), Down syndrome (cardiac abnormalities), myasthenia gravis, or neuromuscular disease (cardiomyopathy, conduction disease, and ventilatory failure). A good cardiopulmonary examination and history can help to prevent complications in a cardiopulmonary rehabilitation program and should be done as a part of the physiatrist’s initial history and physical examination.
A few key cardiopulmonary examination findings are highlighted here.
Cardiac auscultation can indicate an atrial septal defect, a midsystolic click may indicate mitral valve prolapse, and a murmur may indicate valvular heart disease. Pulmonary hypertension typically produces a heightened second heart sound, a noncompliant ventricle can be detected via an atrial gallop at the cardiac apex, and a left ventricular gallop may reveal heart failure. The pulse contour, split heart sounds, and the quality of the murmur can help differentiate aortic sclerosis from aortic stenosis. In younger patients, pulmonary stenosis or valvular heart disease needs to be differentiated from idiopathic hypertrophic subaortic stenosis. Diastolic murmurs may be mitral stenosis or pulmonary hypertension with pulmonary valve regurgitation, and continuous murmurs may be from ventricular septal or atrial septal defects. New findings or changes in findings are important as they may indicate the need for further evaluation or alterations in the program of cardiopulmonary rehabilitation.
Lung physical examination may have decreased breath sounds and/or barrel chest in obstructive disease, whereas interstitial lung disease may have diffuse or basilar crackles. Inspiratory stridor may indicate upper airway obstruction, whereas expiratory wheezing and rhonchi can be seen with obstruction or secretions. It is also important to assess symmetry of breathing, accessory muscle use, and possible compromise to diaphragmatic function.
Cardiac Anatomy and Physiology
Cardiac Anatomy
To supervise cardiac rehabilitation, it is essential to be familiar with the normal distribution of the major arteries of the heart, the anatomy of the heart valves, and the distribution of ischemia or infarction from the coronary arteries.
The heart has paired atria and ventricles, with deoxygenated venous blood entering the right atrium, traversing the right ventricle through the tricuspid valve, and entering the pulmonary artery through the pulmonic valve. Oxygenated blood enters the left atrium, goes to the left ventricle through the mitral valve, and is ejected into the aorta through the aortic valve. The cardiac valves ensure unidirectional unobstructed flow of blood, with atrial contraction adding up to 15% to 20% to the total cardiac output (CO). Atrial contribution to blood flow is greater with increased heart rate and in conditions with decreased ventricular compliance. Atrial fibrillation can cause a loss of this atrial “kick” and may contribute to cardiac dysfunction.
The cardiac conduction system allows coordinated contraction of the atria and ventricles at a controlled rate. The normal heartbeat is initiated at the sinoatrial node and then travels through three atrial internodal pathways to the atrioventricular node where conduction is delayed to cause sequential atrial and ventricular contraction. Below the atrioventricular node, the signal passes into the bundle of His and divides into left and right bundles. All cardiac fibers then end in terminal branches, which excite the myocytes and cause contraction. The conduction system can be injured by myocardial infarction (MI), aging, and other conditions, and can cause heart block or sick sinus syndrome. Accessory pathways that bypass the atrioventricular node can be seen in Wolff-Parkinson-White syndrome.
Variation of Arteries
There are three main distributions of coronary circulation. Normally the left main coronary artery divides into the left anterior descending and the circumflex arteries, whereas the right coronary artery continues on as a single vessel. Right dominant circulation is seen in 60% of individuals, whereas left dominant circulation with the posterior descending artery arising from the left circumflex is seen in 10% to 15% of individuals. The remaining 30% of individuals have balanced circulation with the posterior descending artery coming from the left circumflex and right coronary arteries.
Cardiac Physiology
Cardiac myocytes extract nearly 65% of oxygen from the blood at all levels of activity (compared with 36% for brain and 26% for the rest of the body). Cardiac myocytes prefer carbohydrates as an energy source (40%), with fatty acids making up most of the remaining 60%. With high oxygen extraction and coronary blood flow only during diastole, the heart is at high risk of ischemic injury, especially in the endocardium. Coronary vasodilation with exercise is normally done via nitric oxide–mediated pathways and increases blood flow with exertion. The goal of most medical and surgical therapies for ischemia is to restore or preserve myocardial perfusion, through vasodilation, bypass, or endovascular procedures. Exercise can increase cardiac collateral circulation and also improve arteriolar vasodilation, and has long been known to be a primary therapy for cardiac ischemia.
Another important issue to manage with patients with cardiac disease is fluid volume. Appropriate venous return can maintain appropriate cardiac “preload,” whereas fluid overload can lead to too much venous return and exacerbate heart failure. In cases of mechanical cardiac constriction surgery can restore CO, and in dilated heart failure medical treatment aims to decrease the size of the ventricles to increase CO. In refractory or end-stage disease, left ventricular assist devices (LVADs) and cardiac transplantation are options.
Pulmonary Anatomy and Physiology
Pulmonary Anatomy
Important pulmonary anatomy includes the upper and lower airways (the oropharynx, larynx, trachea, main stem bronchi, and smaller bronchi), the lung parenchyma, the chest wall, and musculature (diaphragm, accessory muscles of breathing, rib cage, and pleura). Pulmonary limitations can come from abnormalities in any of these structures. The lungs also have a dual circulation with pulmonary arteries and veins, which deliver deoxygenated blood to the lungs and deliver oxygenated blood to the left atrium and intrinsic pulmonary artery circulation delivering oxygenated blood to the respiratory tree.
Stridor can result from upper airway obstruction from vocal cord paralysis or tumor, whereas asthma, bronchitis, or reactive airway disease may cause dyspnea from lower airway obstruction. Emphysema is a result of parenchymal lung disease with a loss of alveoli leading to decreased intrinsic recoil of the lung and subsequent hyperinflation and dyspnea. In interstitial lung disease and pulmonary fibrosis, there is interstitial scarring with increased recoil and decreased ability to diffuse oxygen through the lung tissues. In some patients, both restrictive and obstructive diseases can be present with one predominant over another (cystic fibrosis and sarcoidosis). In these cases, it is important to evaluate the lung parenchyma with imaging or physiologic testing (pulmonary function tests) to assess which condition may predominate.
Pulmonary Physiology
Normal breathing is regulated in the medulla oblongata by the respiratory center. Respiratory signals are carried by the phrenic and other somatic nerves to the diaphragm and secondary inspiratory muscles (intercostals, sternocleidomastoids, and pectorals) and cause rhythmic breathing by generating negative pressure in the chest wall. Normal exhalation is passive, resulting from the elastic recoil of the chest wall and the lung parenchyma. Chronic obstructive lung disease (COPD) and emphysema can create the need for active exhalation, markedly increasing the work of breathing. Interstitial lung disease with scarring decreases compliance of lung tissue so severely that lung volumes decrease and hypoventilation can result. Any disease affecting the brain, spine, phrenic nerves, respiratory muscles, or changing the mechanical properties of the chest wall or diaphragm can affect normal respiration.
Pulmonary vascular disease can result in either primary or secondary pulmonary hypertension. Primary pulmonary hypertension can be idiopathic or can result from vasculitis, thromboembolic disease, or from intrinsic parenchymal disease. Secondary pulmonary hypertension is from vascular congestion, often a result of left heart failure. Secondary pulmonary hypertension can lead to intrinsic vascular compromise if the condition is chronic. Chronic hypoxemia may also create pulmonary hypertension in individuals with obesity, obstructive sleep apnea, or high-altitude exposure through a mechanism of pulmonary vascular constriction. Chronic hypoxemia can lead to vascular intimal hypertrophy with resultant fixed pulmonary vascular resistance and pulmonary hypertension.
Basic Terminology for Exercise
Aerobic Capacity
Aerobic capacity (V o 2 max) is the measure of the work capacity of an individual and is expressed as the oxygen consumed by the individual (liters of oxygen per minute or milliliters of oxygen per kilogram per minute). Oxygen consumption (V o 2 ) increases linearly with workload, up to the V o 2 max where it reaches a plateau. Maximal exercise capacity assessment can assist in rating disability and planning exercise and recovery programs.
Heart Rate
Heart rate is a useful guide for exercise as a result of having a linear relationship to V o 2 . Maximum heart rate is best determined by testing and decreases with age. It can be estimated either by the Karvonen equation or by the equation heart rate = 220 − age. Physical conditioning can alter the slope of the relationship of heart rate and V o 2 with improved conditioning lowering the slope (less heart rate increase for a given V o 2 ). A limitation to using heart rate can be the alteration of heart rate response in the setting of medications that alter vagal and sympathetic tone.
Stroke Volume
Stroke volume (SV) is the volume of blood ejected with a left ventricular contraction. Maximal SV can be increased with exercise, is sensitive to postural changes (least increases in supine), with the greatest increase during early exercise. Normally SV increases in a curvilinear manner, achieving maximum at approximately 40% of V o 2 max. SV declines with advancing age, with decreased cardiac compliance, after MI, and in heart failure.
Cardiac Output
CO is the product of the heart rate and SV. It has a linear relationship with work and is the primary determinant of V o 2 max. CO is greater in the upright position compared with the supine position.
Myocardial Oxygen Consumption
Myocardial oxygen consumption (M vo 2 ) is the oxygen consumption of the heart muscle increasing in proportion to workload. When the M vo 2 exceeds the maximum coronary artery oxygen delivery, an individual will have myocardial ischemia and angina. The rate pressure product (RPP) = [heart rate × systolic blood pressure (SBP)]/100, and has a direct relationship to the M vo 2 . Another consideration is that arm exercise, isometric exercise, and exertion in the cold, extreme heat, after eating, and after smoking all have a higher M vo 2 for a given M vo 2 . Supine exercises have a higher M vo 2 at low intensity and a lower M vo 2 at high intensity compared with erect exercises.
Basic static lung volumes and dynamic responses to exercise are helpful in the assessment of exercise capacity in individuals with lung disease. Although complete pulmonary function evaluation is beyond the scope of this chapter, some important values include:
Total lung capacity (TLC): Volume of air in the lungs at full inspiration.
Vital capacity (VC): Volume of air between full inspiration and full expiration.
Forced expired vital capacity (FVC): Maximum volume expired after a maximal forced expiration.
Forced expiratory volume in 1 second (FEV 1 ): The maximum volume exhaled in 1 second.
Maximal voluntary ventilation (MVV): Measurement of the maximal ventilation over 15 seconds.
Residual volume (RV): Volume of the chest wall after a full expiration.
Tidal volume (TV): The volume of regular resting breath.
Diffusion of the lung for carbon monoxide (D lco ): Diffusion of carbon monoxide (oxygen analog) across the alveolar membrane.
The best evaluation of the capacity to exercise in cardiac and pulmonary conditions is with a cardiopulmonary exercise test (CPET). The CPET yields diagnostic, prognostic, and exercise prescription guidance in patients with cardiopulmonary disease. The interpretation of pulmonary exercise testing in a number of conditions is shown in Table 27-2 .
| Abnormality | Physiologic Abnormality | Gas Exchange |
|---|---|---|
| Obesity |
|
|
| Peripheral vascular disease |
|
|
| Pulmonary vascular disease |
|
|
| Anemia |
|
|
| Chronic obstructive pulmonary disease |
|
|
| Restrictive lung disease (intrinsic) |
|
|
| Restrictive lung disease (extrinsic) |
|
|
| Asthma |
|
|
| Ventricular failure |
|
|
| Ischemic heart disease |
|
|
| Metabolic acidosis |
|
|
Interventions for Cardiopulmonary Disease
Aerobic Training
Physical exercise that increases the cardiopulmonary capacity (V o 2 max) allows for aerobic training. All aerobic training prescriptions must include four components: intensity, duration, frequency, and specificity.
Intensity.
How hard an exercise is. Can be prescribed by a target heart rate, metabolic level (MET level), or intensity (wattage). Usual intensity target for cardiac primary prevention is a heart rate of 80% to 85% of the predicted maximum heart rate/peak heart rate from the exercise tolerance test (ETT). For secondary prevention in patients with known cardiopulmonary disease, exercise should be at a safe level at 60% or more of the maximum heart rate to achieve a training effect.
Duration.
How long a given bout of exercise is. Usual cardiopulmonary conditioning requires 20- to 30-minute sessions, and should have a 5- to 10-minute warm-up and cool-down period. The lower the intensity of an exercise, the longer the duration will need to be to achieve a similar training effect.
Frequency.
How often exercise is performed over a fixed time period (usually a week). Moderate-intensity training programs should be done at least three times per week, and low-intensity programs should be five times per week.
Specificity.
The activity to be done in exercise. Training benefits specifically related to the activities performed. Thus, elliptical exercise is not as beneficial for walking as treadmill training. Specificity in prescription should be altered to adapt to the needs of each patient. For a patient with spinal cord injury, upper arm ergometry would be more functional, and cycle ergometry would be better for a patient with severe leg arthritis than a treadmill. The law of specificity of conditioning should be remembered when designing a cardiopulmonary conditioning program.
The benefits of aerobic training include the following:
Aerobic capacity: Maximum capacity increases with training. Resting V o 2 is stable as is the V o 2 at a given workload. The changes are specific to the trained muscles.
Cardiac output: Maximum CO increases, whereas resting CO is stable. Resting SV increases with a corresponding decrease in resting heart rate.
Heart rate: Heart rate is lower at rest and at any given workload, whereas maximum heart rate is unchanged. The lower heart rate at rest and submaximal exercise causes a lower M vo 2 with normal activity.
Stroke volume: SV increases at rest and at all levels of exercise. CO is thus maintained at a lower heart rate and causes a lower RPP for a given level of exertion.
Myocardial oxygen capacity: After training, maximum M vo 2 does not usually change, but is less at a given workload. This reduces episodes of angina and increases safety for moderate activity. M vo 2 can also increase after pharmacologic treatments or revascularization procedures.
Peripheral resistance: Exercise training decreases peripheral vascular resistance (PVR) by reducing “afterload” through lowering arterial and arteriolar tone. The reduction in PVR results in a lower RPP and a lower M vo 2 at a given workload and at rest.
Minute ventilation: With improved conditioning, individuals will require a lower V o 2 and thus a lower minute ventilation for a given activity. For patients with pulmonary and cardiac disease, this can lead to a large reduction in dyspnea.
Tidal volume: Exercise can lead to a higher tidal volume on exertion, with a subsequent decrease in respiratory rate and decreased dyspnea.
Respiratory rate: As tidal volume is improved, respiratory rate will be lower for a given minute ventilation, decreasing dyspnea.
The application of basic physiologic principles to the design of cardiopulmonary rehabilitation programs can improve function, decrease symptoms, and improve outcomes for patients with cardiopulmonary disease. The prime effect of cardiac conditioning is in reduction of cardiac risk and improved cardiac conditioning. Reduction of cardiac risk has been well established since 1989, when pooled data from 22 randomized studies of exercise in 4554 patients following acute MI demonstrated a 20% to 25% reduction in all-cause mortality, fatal MI, and cardiac mortality in a 3-year follow-up study. These benefits of cardiac rehabilitation apply across populations, including older adults, women, and patients after bypass. Similar benefits have also been shown for pulmonary rehabilitation in COPD with decreased hospitalizations, improved function, and improved quality of life, and new studies are showing that interstitial disease and pulmonary vascular disease can also benefit from exercise.
Pulmonary Rehabilitation
Abnormal Physiology: Lung
Patients with pulmonary disease demonstrate three main impairments: (1) obstructive lung disease, (2) restrictive lung disease, and (3) pulmonary vascular disease. Often more than one type of limitation may be present in a given patient and will increase the complexity of their condition. Understanding the underlying physiology can assist in the design of a specific exercise program for an individual patient.
For primary pulmonary disease, it is essential to know if the patient has primarily an obstructive or restrictive condition. Obstructive lung disease is marked by an inability to exhale resulting from either upper airway or large airway disease (sleep apnea, tracheomalacia, vocal cord disease, asthma, and bronchitis) or as a result of lower airway disease from either secretions or lung parenchymal disease (emphysema and bronchiectasis). Obstruction can also be exacerbated by a component of acute obstruction (asthma) combined with a chronic condition (COPD). The hallmark of severe COPD is carbon dioxide retention and active exhalation. Medical treatments are limited for COPD, with steroids and bronchodilators offering incomplete relief. Lung reduction surgery is only appropriate in selected individuals and transplant is only for end-stage disease. For all levels of obstructive disease, pulmonary rehabilitation is appropriate and in the “GOLD” recommendations for treatment of COPD, pulmonary rehabilitation is recommended for all patients with moderate to severe disease.
In restrictive lung disease, the primary limitations are low tidal volumes from an inability to expand the chest wall (extrinsic restriction) or from very noncompliant lung tissue (intrinsic restriction). In extrinsic restrictive disease (neuromuscular disease, paralysis, and kyphoscoliosis), the parenchyma of the lung is normal and gas exchange is preserved, meaning that treatment is usually respiratory muscle training and mechanical ventilatory support as needed. With intrinsic restrictive lung diseases (pulmonary fibrosis, sarcoidosis, etc.), there may be a profound associated hypoxemia from severely decreased diffusion capacity of scarred lung tissue. Patients with parenchymal restrictive disease classically have severe hypoxemia and may need high-flow supplemental oxygen. Patients with end-stage intrinsic restrictive disease can have ventilatory failure with hypercarbia and hypoxemia and may be refractory to ventilatory support, and lung transplantation is then often the only remaining treatment option. Table 27-3 shows some of the lung pathologies and effects on inspiratory reserve and residual volume (obstructive diseases), and the effects of various conditions on lung compliance (restrictive diseases).
| Restrictive Diseases | Obstructive Diseases |
|---|---|
|
|
Finally, patients with pulmonary vascular disease have a similar presentation in many ways to patients with heart failure. And in the end stages of the disease, right ventricular heart failure is a major part of the condition and leads to excess mortality and morbidity. Rehabilitation is focused on a program that resembles exercise for patients with heart failure, with the addition of close monitoring of oxygen saturation and the use of appropriate levels of supplemental oxygen to prevent hypoxemia.
For patients with either intrinsic restrictive or obstructive disease, pulmonary rehabilitation is an important treatment to consider and should be offered for patients whether or not they have their pulmonary condition as a primary or a secondary disability. A brief overview of pulmonary rehabilitation programs for primary pulmonary disease is shown in Table 27-4 .
| Goals | Methods |
|---|---|
| Primary and Secondary Prevention | |
| Smoking cessation |
|
| Immunization |
|
| Prevent exacerbations |
|
| Appropriate medication use |
|
| Pulmonary toilet |
|
| Appropriate use of oxygen therapy |
|
| Nutritional counseling |
|
| Family training |
|
| Dyspnea Relief: Exercise Training | |
| Exercise |
|
|
|
|
|
|
|
|
|
|
|
| Dyspnea Relief: Lifestyle Modifications | |
| Breathing retraining |
|
| Anxiety reduction |
|
| Improve confidence |
|
| Disease Management | |
| Disease acceptance |
|
| Coping skills |
|
| Quality of life improvement |
|
| Advance directives review |
|
| Encouragement |
|
| Continuing exercise and disease management compliance |
|
Cardiac Rehabilitation
Abnormal Physiology: Heart
An understanding of abnormal cardiac physiology in disease is necessary for appropriate cardiac rehabilitation. In general, cardiac limitation is caused by either decreased CO, or ischemic disease, or a combination of these. Ischemia causes the myocardium to have lower contractility and lower compliance reducing SV. Valvular heart disease lowers maximum CO through stenotic valves (e.g., aortic or mitral stenosis) or valvular regurgitation (e.g., aortic or mitral insufficiency). Finally, heart failure is a state of low CO, often as a result of low SV, and is associated with a reduction of V o 2 max, increased resting heart rate, and often a greater M vo 2 for a given V o 2 .
Arrhythmias decrease CO by lowering SV and increase heart rates. For atrial arrhythmias, the mechanism can be by a loss of atrial ventricular filling (atrial “kick”) during atrial fibrillation or supraventricular tachycardias, or from high heart rates without atrial coordination as in ventricular tachycardias and ventricular bigeminy.
Surgical treatments for heart disease either restore coronary circulation (e.g., bypass and intravascular procedures) or restore normal anatomy (e.g., valve replacement). Surgical treatment for heart failure can include LVADs or transplantation. Medical treatment for heart disease either aims to improve coronary circulation for ischemia or works to improve blood flow and restore CO for heart failure by lowering afterload, reducing fluid overload, and increasing inotropy. Although medical treatment of ventricular arrhythmias has been limited, implantable defibrillators and pacemakers have been very successful. Severe end-stage heart disease of all types may require cardiac transplantation or an LVAD. In all of these conditions and treatments, cardiac rehabilitation has an important role to play. Some basic concepts to remember include that patients before transplantation are similar to patients with heart failure, whereas patients after transplantation have several physiologic changes that are unique, including high resting heart rate, limited increase in SV, and peak heart rate with exercise. The basic principles of cardiac rehabilitation are discussed as follows.
Cardiac rehabilitation is either primary prevention, which includes risk factor modification and education before a cardiac event, or secondary prevention, which is cardiac rehabilitation after the onset of cardiac disease including both exercise and risk factor modification.
Primary prevention is usually performed in primary care settings rather than a rehabilitation setting. The focus is on the reduction of cardiac risk factors with a combination of education and exercise for patients in the community. Primary prevention can have a profound effect on the rate of cardiac disease with a decrease in obesity, blood pressure, and lipid profiles. Ideally, behavior modification should begin in childhood with the establishment of healthy behavior and then maintained throughout life. Because populations who are disabled are generally sedentary and may have other risk factors, primary prevention should be an important component of the care of the disabled, and should include management of hypertension and lipids, along with encouraging exercise and consideration of antiplatelet agents. These are all cost-effective approaches and can decrease mortality and morbidity on a population-based scale, in addition to the individual benefits.
After an episode of cardiac disease, it is essential to have secondary risk factor modification, which includes all of the features of primary prevention programs discussed earlier. In addition, disease-specific education and formal exercise is a part of the secondary prevention program. In both cardiac and pulmonary disease, smoking cessation is crucial as part of both primary and secondary prevention programs.
Pulmonary Rehabilitation Programs
Rehabilitation programs for patients with pulmonary disease are similar to cardiac rehabilitation programs. After severe acute exacerbations, some patients can benefit from a short acute inpatient rehabilitation, but the majority of pulmonary rehabilitation is done in an outpatient setting. For patients who are in an intensive care setting, early mobilization programs are now being used to limit debility in these vulnerable patients. Outpatient pulmonary rehabilitation programs also have primary prevention for pulmonary disease with smoking prevention and cessation, occupational safety, and prevention of exposure to environmental and infectious agents. Secondary pulmonary prevention involves medication adherence and education, smoking cessation, supplemental oxygen use and education, and environmental modification for known environmental triggers.
For patients with ventilatory failure that cannot be supported with noninvasive ventilation, lung transplant may become necessary. Rehabilitation before transplantation is focused on both the underlying condition and transplant-specific education, whereas rehabilitation after transplantation includes education and restoration of muscle strength, which is impaired from the medical regimen for patients after transplantation.
Cardiac Rehabilitation of the Patient After Myocardial Infarction
The standard model for cardiac rehabilitation after MI was first described by Wenger and Skoropa in 1971. Because revascularization is now common and infarcts are smaller than in the past, there have been modifications to the classical program with a reduction to three phases, eliminating the classical stage 2 recovery phase. A modern acute phase mobilization program is illustrated in Table 27-5 .
| Day | Activity |
|---|---|
| Day 1 | Passive range of motion (ROM), ankle pumps, introduction to the program, self-feeding |
| Progress to dangle at side of bed, initiate patient education | |
| Progress to active assisted ROM, sitting upright in a chair, light recreation and use of bedside commode | |
| Increased sitting time by the end of the day, light activities with minimum resistance, continue patient education | |
| Progress to light activities with moderate resistance, unlimited sitting, seated activities of daily living (ADLs) by end of first day | |
| Day 2 | Increased resistance, walking to bathroom, standing ADL, up to 1 hour long group meetings |
| Progress walking up to 100 feet, standing warm-up exercises | |
| Begin walking down stairs (not up), continued education | |
| Progress exercise program with a review of energy conservation and pacing techniques | |
| Day 3 | Advance exercise to include light weights and progressive ambulation |
| Increase the duration of activities | |
| Progress stair activity to climbing two flights of stairs, continue to increase resistance in exercises | |
| Consolidate home exercise program teaching | |
| Aim to safely walk up and down two flights of stairs (assures safety for normal activities), complete instruction in home exercise program and in energy conservation and pacing techniques | |
| Discharge planning and education |
The exception to bypassing the recovery phase for cardiac rehabilitation comes for surgical patients with sternotomy who may require recovery from their surgery before starting the training phase of rehabilitation. In summary, phase 1 rehabilitation is the acute phase in hospital immediately following a cardiac event and ends at discharge. Phase 2 is an outpatient training phase, with secondary prevention, intense education, and aerobic conditioning. Phase 3 is the most difficult, the maintenance phase where patients seek to achieve continued aerobic exercise and maintenance of lifestyle modifications. Risk factor modification is performed at all phases. This model is similar for patients with pulmonary disease. For patients with cardiopulmonary disease who are not hospitalized, the goal is essentially phase 2 and phase 3 for all patients at the time of diagnosis. A more detailed description of each of the phases follows.
Acute Phase (Phase 1)
The basics of the phase 1 program are illustrated in Table 27-5 . Education about cardiopulmonary risk factor modification is introduced at the time of acute hospitalization. For patients with cardiac disease, all acute mobilizations should be done with cardiac monitoring with appropriate supervision of trained therapists or nurses. Post-MI heart rate increase with activity should be kept to within 20 beats per minute of baseline, and SBP kept within 20 mm Hg of baseline. A decrease of 10 mm Hg or more is indicative of further medical issues and exercise should be halted. The target intensity at the end of the phase I program exercise is to a level of four METs, covering most of the daily activities patients may perform at home after discharge.
For patients with pulmonary disease, similar phase 1 goals exist and there is new emphasis on early mobilization in the intensive care unit (ICU) to prevent frailty and deconditioning. Patients are aggressively mobilized, some while still on the ventilator. Innovations, including extracorporeal membrane oxygenation, are also now allowing more aggressive mobilization of patients because sedation is less, and patients may maintain better nutritional status. These patients with pulmonary disease should be enrolled in outpatient pulmonary programs to maintain their early gains and complete a full program of education and exercise.
Inpatient Rehabilitation Phase (Phase 1B)
To distinguish between patients who have a rapid recovery after their cardiopulmonary event (pure phase 1) and those patients who require either acute or subacute rehabilitation treatment before discharge home, the designation of phase 1B rehabilitation has been established. With advanced age or substantial comorbidities or other disabilities that make mobilization more difficult, many rehabilitation specialists will care for these patients in phase 1B. The guidelines for exercise are the same as they are for patients in phase 1, but with a longer recovery period extending their hospitalized care to an acute or subacute rehabilitation setting before discharge.
Training Phase (Phase 2)
Classically, phase 2 cardiopulmonary rehabilitation starts after a symptom limited full level ETT for patients with cardiac disease or a CPET for patients with complex pulmonary disease. This allows for setting target heart rates and target exercise intensity from the exercise. A target heart rate of 85% of the maximum heart rate on an ETT or a CPET is generally regarded as safe for patients at low risk. Exercise intensity targets are lower for patients at higher risk or those with underlying conditions. In patients with life-threatening arrhythmias or chest pain, target heart rates are chosen that are below notable end points. Because hypoxemia can add risk and limits participation with exercise, it is important to provide supplemental oxygen as needed (up to a rate of 15 L/min as needed) to maintain saturation above 90% for safe exercise. A target heart rate of 65% to 75% of maximum is safe and effective in a regular exercise program for patients at higher risk, and with target rates as low as 60% still providing a training benefit. Monitoring also needs to be customized to accommodate the underlying risk profile.
Classically, a cardiopulmonary training program is three sessions per week for 8 to 12 weeks. Cardiac rehabilitation is covered by most insurance plans, but the major limitation is a lack of referral and/or a lack of facilities in many areas. Creative and innovative care delivery programs have been developed to increase access and include home programs (patients at low risk), telemedicine programs, and community-based programs in nonmedical facilities. Because training continues after the 8- to 12-week period, it is important for patient self-efficacy that they learn to perform self-monitoring following the guidelines presented in standard references. Patients need to learn to begin exercise with a stretching session, then a warm-up session, a period of training exercise at designated intensity, followed by a cool-down period. The principles of specificity of training need to be remembered because training benefits generally are seen in the specific muscles exercised.
Maintenance Phase (Phase 3)
Although the maintenance phase of a cardiopulmonary rehabilitation is the most important part of the program, it often receives the least attention. The benefits of a phase 2 program can be lost in as little time as a few weeks if a patients ceases to exercise. Because of this, patient education of the importance of making exercise a part of their new health habits has to be emphasized and the patient needs to integrate exercise as a part of a healthy lifestyle. To maintain capacity, patients should perform moderate exercise at the target intensity learned in their rehabilitation program for at least 30 minutes three times a week. With low-level exercise, the frequency has to be increased to five times a week for maintenance of gains. Although telemetry monitoring is usually not used with patients with cardiac disease, patients with pulmonary disease can benefit from the use of home pulse oximetry and should be taught to adjust their supplemental oxygen as needed with exercise to maintain adequate oxygenation.
Cardiac Rehabilitation Programs in Specific Conditions
Angina Pectoris
Cardiac rehabilitation for angina aims to lower heart rate at rest and with given levels of activity to decrease angina by improving fitness. Exercise benefits for patients with angina include improved peripheral efficiency and improved coronary artery collateralization.
Cardiac Rehabilitation After Revascularization Procedures
Postcoronary Artery Bypass Grafting
Cardiac rehabilitation after coronary artery bypass grafting (CABG) emphasizes secondary prevention aims to improve conditioning and fitness. For patients with low ejection fractions and heart failure, closer telemetry monitoring should be done. If a patient had a sternotomy, arm exercises will have to be limited until sternal healing occurs, usually at approximately 6 weeks after surgery. Patients who have had percutaneous interventions usually pursue the program immediately and it is similar to the program after CABG.
Cardiac Rehabilitation for Patients After Cardiac Transplantation
Because most patients after cardiac transplantation have severe heart failure and debility before transplantation, involvement in a heart failure pretransplant program can help to limit deconditioning and help to treat depression and anxiety. Heart transplantation usually improves cardiac function, therefore a posttransplant program can focus on conditioning, education, and secondary prevention. An added feature is that many patients after transplantation may have vascular and neurologic complications, which may mean a phase 1B program is needed before starting the phase 2 outpatient program. This is often done in either acute or subacute rehabilitation settings.
Remembering the alterations of cardiac physiology in the patients after transplantation is important. Transplanted hearts are denervated and have no direct sympathetic or vagal central regulation. In many patients, the loss of vagal inhibition creates a resting tachycardia of 100 to 110 beats per minute. By contrast, because there is a loss sympathetic innervation, the chronotopic response to exercise is in response to circulating catecholamines, leading to a delayed and blunted heart rate response to exercise. Posttransplant, peak heart rates are usually 20% to 25% lower than in matched controls. Other cardiovascular effects that are seen include resting hypertension from the renal effects of calcineurin inhibitors (e.g., cyclosporine and tacrolimus) and prednisone, along with diastolic dysfunction in some patients. Combined, these effects usually reduce maximum work output and maximum oxygen by approximately one third compared with age-matched individuals. Of interest, despite no denervation of the heart, similar decreases in exercise capacity are also seen in patients after lung transplantation. With exercise, patients after transplantation have a lower work capacity, reduced CO, lower peak heart rate, and lower oxygen uptake, with higher resting heart rate and SBP than normal individuals. Additionally, resting and exertional diastolic blood pressures are usually higher for patients after heart transplantation. The net effect of these alterations in exercise response is higher than normal perceived exertion, minute ventilation, and ventilatory equivalent for oxygen at submaximal exercise levels.
The focus of a cardiopulmonary rehabilitation program after transplantation is on conditioning and education. Target intensity for aerobic exercise is usually approximately 60% to 70% of peak effort for 30 to 60 minutes three to five times weekly. Intensity can be regulated with rating of perceived exertion target at 13 to 14 on the Borg Scale, approximately 5 to 6 on the modified Borg Scale, with the goal being to consistently increase the level of activity. Education focuses on learning the complicated medical regimen and vocational and psychological needs. For patients after cardiac transplantation, a program of rehabilitation can help to assist them to improve work output and exercise tolerance, with some patients able to participate in competitive athletics.
Cardiomyopathy
Fortunately, cardiac rehabilitation for heart failure is now covered by insurance plans, since Medicare regulations started to cover rehabilitation for heart failure in March of 2014 (42 C.F.R. § 410.49(b)(1)(vii)). An important consideration for heart failure rehabilitation is the increased risk of complications such as sudden death, depression, and chronic cardiac disability. Closer monitoring of telemetry and vital signs is also needed because some patients with heart failure have inconsistent responses to exercise with increased fatigue, possible exertional hypotension, and syncope. Most patients also exhibit low endurance and chronic fatigue as a result of their low-exercise capacity. However, a positive effect can be realized in their fatigue and function with even a small improvement in V o 2 . These changes in capacity can lead to a marked improvement in quality of life and may help patients with heart failure to continue to live independently.
Because of the increased risk for complications in patients with heart failure, a graded exercise tolerance test is helpful before starting a cardiac rehabilitation program. Long warm-up and cool-down periods with gentle exercise at a limited workload helps to compensate for an impaired ability to generate a dynamic exercise response, and dynamic exercise is preferred to isometric exercise because isometric exercise can lead to an increase in diastolic pressure and cardiac afterload. Heart rate targets are usually set 10 beats per minute below any notable end point found with cardiopulmonary exercise testing. Cardiac rehabilitation begins with cardiac monitoring especially when severe left ventricular dysfunction is present. Once the patient has demonstrated stability with an exercise program and has learned how to self-monitor, the patient should be taught a self-monitored program. Education of patients with heart failure also includes doing a daily body weight (to observe for fluid accumulation) and monitoring their blood pressure and heart rate responses to exercise.
Patients who are on pharmacologic inotropic support or left ventricular mechanical support for end-stage heart failure can also exercise in a cardiac rehabilitation program with similar precautions to other patients with congestive heart failure. Rehabilitation after an LVAD usually follows a classical postsurgical course, and may include phase 1 and phase 1B rehabilitation followed by phase 2 and phase 3 programs. Patients with an LVAD seen in acute and subacute units require staff training, close cooperation with the LVAD team, and familiarity with the devices that are used locally. Because an LVAD often restores a reasonable CO, exercise tolerance is often only limited by the peak flow of the device. In addition to normal secondary prevention education, LVAD-specific family and patient education are also essential parts of post-LVAD rehabilitation.
Valvular Heart Disease
Cardiac rehabilitation for valvular heart disease resembles the program for cardiac heart failure. Postsurgical considerations are the same as for CABG, with the added consideration of anticoagulation for patients with mechanical valves. Because anticoagulation increases the risk of hemarthrosis and bruising, patients need to avoid impact exercises and need education regarding injury avoidance. The overall training program is similar to that discussed for the patient post-CABG.
Cardiac Arrhythmias
An essential consideration for patients with cardiac arrhythmias is the need for telemetry monitoring with increases in intensity of exercise and new exercises. Patients at high risk can benefit from an automatic implantable cardiac defibrillator (AICD), which may offer protection form ventricular arrhythmias. Cardiac rehabilitation for patients with AICD needs to be done at intensities that avoid the heart rates at which the device is set to respond to ventricular tachyarrhythmias. An exercise stress test can help to set appropriate target heart rates for an exercise program. In addition to secondary prevention and education, AICD-specific education and emotional support are important to include in the rehabilitation program.
Pulmonary Rehabilitation Programs in Specific Conditions
Emphysema
Rehabilitation for patients with COPD is the standard for pulmonary rehabilitation. Goals of a pulmonary rehabilitation program include improving disease management and exercise capacity. Because pulmonary rehabilitation does not improve lung function, the goal of the rehabilitation program is to improve peripheral efficiency and decrease dyspnea. Energy conservation education (how to do a given activity at a lower level of exertion), anxiety reduction, and improved endurance all contribute to improved function and decreased dyspnea. Longer duration exercise of moderate intensity is often used, rather than high-intensity exercise. Recent investigations have started to evaluate a possible role for high-intensity interval training for patients with COPD, but this has not yet been proven to be more effective than the standard training program. Because isometric exercises increase intrathoracic pressures, they should be avoided in patients with COPD. Appropriate supplemental oxygen should be given to maintain saturation above 90%, with education to lower supplemental oxygen after exercise back to baseline levels to prevent resting hypercarbia. Patients with COPD generally have relatively modest oxygen needs and can often maintain their oxygen saturation levels with 1 to 6 L of oxygen via a nasal cannula. Bilevel ventilation may have a role for patients with sleep apnea or ventilatory failure, and education for these patients should include the proper use of this modality. For patients being considered for lung volume reduction surgery, pulmonary rehabilitation is considered essential both to qualify for the surgery and after surgery to assure adequate outcomes.
Airway clearance and chest physical therapy has a role in the pulmonary rehabilitation of patients with substantial secretions. A combination of external percussion devices, vibration devices, and inhaled saline in combination with cough training and huffing may help to mobilize secretions. It is also important to include family training and education about inhaled medications, supplemental oxygen use, and management of equipment.
Interstitial Lung Disease
The basics of a program of pulmonary rehabilitation for interstitial lung disease are the same as for COPD. An essential issue for patients with interstitial lung disease is often profound hypoxemia that requires high-flow oxygen with exercise to maintain adequate saturation for activity. It is essential in this group of patients to avoid chronic hypoxemia to prevent secondary pulmonary hypertension because the coexistence of interstitial lung disease and pulmonary hypertension can lead to a markedly decreased life expectancy. Exercise intensity is often limited in patients with interstitial lung disease by oxygenation rather than dyspnea, and airway secretions are usually not an important issue. For some individuals with severe end-stage disease, there may be ventilatory failure with hypercarbia, but in those patients rehabilitation may no longer be possible.
Because interstitial lung disease is often progressive, transplant evaluation and education or end-of-life planning may be needed to permit as many patient goals as possible to be achieved.
Pulmonary Hypertension
Patients with pulmonary hypertension have similar limitations as patients with heart failure and share many similar precautions. Effective medical treatment for pulmonary hypertension has made a once-fatal condition into a chronic disease for many patients. Patients with pulmonary hypertension now have a much longer life expectancy and improved functional status is essential for maintaining an active life. Major concerns for pulmonary rehabilitation are preventing debility and improving dyspnea. Because hypoxemia can worsen pulmonary hypertension, it is important to maintain oxygen saturation with exercise, and cardiac monitoring may be needed for patients with a history of arrhythmias and right ventricular failure. Education for this group of patients should include a review of their vasodilating medications and supplemental oxygen use. Intravenous and continuous subcutaneous vasodilator infusion is appropriate for a pulmonary rehabilitation program, but similar to patients with heart failure there may need to be long warm-up and cool-down periods. For patients with severe pulmonary vascular disease, the program should start with moderate- to low-level exercise. Definitive research of the efficacy and safety of pulmonary rehabilitation for patients with pulmonary hypertension is still ongoing.
Ventilatory Failure
For alert patients on either invasive or noninvasive ventilation for ventilatory failure, a program of pulmonary rehabilitation can help to increase mobility and prevent complications. Exercise programs for patients on nocturnal or intermittent ventilatory support aim to improve efficiency and decrease fatigue while off the ventilator. The details of ventilatory support for patients requiring noninvasive ventilation is beyond the scope of this chapter. Table 27-6 provides an overview of the types of patients who may present with ventilatory failure. A summary of the indications for ventilatory support is listed in Table 27-7 .
Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
