Exercise Testing and Training

Primary Cardiovascular and Pulmonary Dysfunction

Elizabeth Dean, Donna Frownfelter and Eduard Gappmaier

The principles of physical therapy practice in the management of individuals with primary cardiovascular and pulmonary conditions can be applied in formally structured programs or in one-on-one sessions. Exercise testing and training are primary components of comprehensive physical therapy management, which is detailed in Chapter 31. This chapter describes these principles. Structured cardiac and pulmonary rehabilitation programs are therapeutic multidisciplinary programs that encompass the essentials of the best physical therapy practice (Box 24-1). The distinctions among structured programs lie in the primary patient populations they serve rather than in the principles of physical therapy management, which are comparable when applied on a one-to-one basis. The general principles of comprehensive care include teamwork, patient education, exercise testing and training, long-term sustainable lifestyle change, and follow-up, and these are common across patient groups. This chapter extends the basic principles of exercise testing and training outlined in Chapter 19. The chapter highlights state-of-the-art literature and the physical therapist’s central role as clinical exercise physiologist and health educator in addressing the needs of individuals with primary cardiovascular and pulmonary conditions.

Box 24-1 Definition of Cardiovascular and Pulmonary Rehabilitation

The goal of cardiovascular and pulmonary rehabilitation is to maintain or return an individual with cardiovascular and pulmonary dysfunction to full participation in life with a high level of life satisfaction.

Cardiovascular and pulmonary rehabilitation consists of a comprehensive interdisciplinary management program, including physical activity and exercise, education, and behavioral change designed to improve the physical and emotional status of individuals with cardiovascular and pulmonary dysfunction or their risk factors.

The role of the physical therapist as health coach and advocate to promote lifelong health and well-being is further emphasized in the management of these patient groups. These principles are also applied when primary cardiovascular and pulmonary dysfunction is a secondary diagnosis—that is, for example, in a patient whose primary diagnosis is a frozen shoulder but who has history of ischemic heart disease or its risk factors. This underlying condition has major implications for the modification of an exercise program for the frozen shoulder in addition to implementing management to specifically address it.

Over the past decade, an extensive number of position statements, clinical practice guidelines, and consensus statements have been published to guide contemporary practice in cardiac and pulmonary rehabilitation programs. The major goal of these programs is to improve quality of life and tolerance of daily activities. An overriding objective is to institute lifelong healthy practices, including secondary prevention.¹ The application of these principles is central to the management of cardiovascular and pulmonary conditions, whether they are primary or secondary conditions. In general practice today, patients (including children) presenting to the physical therapist with musculoskeletal or neuromuscular complaints have a high probability of having underlying cardiac or pulmonary pathology, or one or more associated risk factors (see Chapter 1). Established guidelines for cardiac rehabilitation programs do not replace the expert clinical judgment of rehabilitation professionals and goal-directed, patient-centered service delivery.² Consistent with the World Health Organization’s definition of health (see Chapter 1), both cardiac and pulmonary rehabilitation programs focus on the enhancement and maintenance of cardiovascular and pulmonary health through individualized programs designed to optimize physical, psychological, social, vocational, and emotional status overall. In addition, they promote secondary prevention through risk-factor identification and modification in an effort to prevent disease progression and the recurrence of cardiovascular and pulmonary events.²

A criticism of conventional cardiac and pulmonary rehabilitation programs is that they are structured with little individualization.³ The physical therapist, who is uniquely qualified as an applied clinical exercise physiologist and health coach, needs to ensure that all components—in particular, exercise—are prescribed to meet the specific needs and comorbidities of each individual. For reference purposes, we include elements of international standards and guidelines for cardiac and pulmonary rehabilitation programs in Appendixes A and B. We caution, however, that these elements need to be tailored to an individual (based on a detailed history, assessment, and examination, and ongoing evaluation) and that such standards may change as new evidence emerges. Nonetheless, they will provide useful guidelines to physical therapists involved with setting up facilities related to cardiac and pulmonary rehabilitation.

This chapter extends the information in Chapter 31 concerning the management of chronic, primary cardiovascular and pulmonary dysfunction. In the review of the state-of-the-art literature, was often reported in studies and was used to mean (see Chapter 18 for elaboration of this physiological distinction). Despite this, we have retained the term used by the original investigators in each study in our summary of these studies.

Cardiac and Pulmonary Rehabilitation: Evidence Base, Efficacy, and Practicalities

Although an interprofessional team approach is fundamental to both cardiac and pulmonary programs, individuals who regularly participate in moderate exercise experience greater control of symptoms and increased functional capacity than do those treated with drugs alone.⁴ Self-management strategies learned in a pulmonary education program also contribute to perceived control of symptoms and to self-confidence.⁵ This sense of control is perhaps the single best argument supporting the exploitation of noninvasive interventions for the management of chronic conditions. This component may be singularly important in determining long-term outcomes, such as reduced demands for health care and lower health care costs.⁶

The effectiveness of cardiac and pulmonary rehabilitation has been established at the highest level of evidence 2,7–19 and this is true irrespective of stage of disease.^20,21 With the aging of the population, cardiac rehabilitation has been shown to benefit octogenarians as well as younger people. Because of the issues associated with exercise testing older people, the use of a mobility index, such as the Rivermead Mobility Index, to evaluate exercise performance has been proposed even in absence of a formal exercise test.²² Because of common lifestyle behaviors, ischemic heart disease as a primary lifestyle-related condition will remain prevalent for the foreseeable future.

These interprofessional programs have internationally recognized standards that are well described and are recommended for all patients with cardiovascular and pulmonary conditions. They specialize in patient education (including smoking cessation, nutrition and weight control, and promotion of self-management and training) that has sustained, lifelong, positive effects on cardiovascular and pulmonary status and sense of well-being.23–26 The term end stage needs to be revisited, given the efficacy of rehabilitation in severely compromised individuals.²⁷ Considering these benefits and the enormous economic implications of keeping people healthy and out of hospitals and physicians’ offices, rehabilitation can be supported as a primary intervention rather than a secondary priority after suboptimal effects of pharmacotherapy or surgery.²⁸

Noninvasive cardiac and pulmonary rehabilitation is more cost-effective than medical and surgical treatments, and it offers long-term health benefits and reduced risk. However, there is a significant discrepancy between the actual provision and practice of cardiac rehabilitation and that advocated in published guidelines. These evidence-based, noninvasive, cost-effective interventions are being grossly underused, and participation rates are low.²⁹ Referral to cardiac rehabilitation has been reported to reflect selected groups, namely, younger age groups, those who have participated previously, those admitted to hospital with outpatient cardiac rehabilitation services, and those having a discharge diagnosis of myocardial infarction or coronary artery bypass surgery.^30,31 Significant barriers also have been reported to exist with respect to availability, referral, and utilization of these programs; payment issues are another factor.³² Only a small proportion of individuals are referred, and of those, only a small proportion can access the programs.^33–35 Phase I inpatient cardiac rehabilitation has been reported to be a declining trend.³⁶ Physicians and surgeons may not have knowledge and awareness of the effectiveness of noninvasive approaches to health problems that have been managed primarily with drugs and surgery, so suitable candidates are not always referred.³⁷ In addition, there are psychosocial reasons for underutilization of these resources. Women are referred less commonly than men, and their drop-out rates are higher.^38,39 Thus there is a selection bias in the individuals sampled for studies of cardiac rehabilitation.⁴⁰ The participation of women is associated with insurance, level of education, bypass surgery, and transportation availability.⁴¹ Cost containment and increasing accessibility are two primary barriers to participation in cardiac rehabilitation.⁴² Low participation rates (particularly by women, minority group members, and older people) and means of increasing access have become primary areas of interest.⁴³

Of the multiple facets of a cardiac rehabilitation program, different components may have different effects on individual heart health. In addition, physiological distinctions between men and women affect the incidence and manifestation of cardiovascular conditions between the two sexes and, in turn, their responses to cardiac rehabilitation. Women tend to have lower systolic blood pressure and pulse pressure than men and to have more favorable lipid and homocysteine levels.⁴⁴ However, the compliance of women’s small blood vessels tends to be lower, which may reflect female sex hormones and the higher mortality rates of premenopausal women hospitalized for myocardial infarction. Women also tend to have more “silent” ischemic heart disease than men, which is more often associated with sleep disturbance in women. The results of one descriptive study also showed that women were less likely to adhere to diet and exercise modification guidelines compared with regimens for smoking cessation, medication, and stress management.⁴⁵

Special attention needs to be paid to motivating individuals to participate in rehabilitation programs (identify facilitating factors and barriers to participation), to generalize their new skills to home activities and the community, and to continue their new lifestyle behaviors beyond formal enrollment in the program.⁴ Given that education and exercise are core components of cardiac and pulmonary rehabilitation, physical therapy is uniquely positioned to implement care for individuals with cardiac or pulmonary conditions as primary or secondary diagnoses and to mobilize an interprofessional health care team for a given individual if no formal program exists. Education materials should be individualized to the learner’s needs and capacities; otherwise, resources will be wasted. A marked disparity exists between the average American’s reading ability (eighth grade level) and the readability levels of cardiac rehabilitation materials.⁴⁶ The large number of polysyllabic words is a primary factor.

Cardiac and pulmonary rehabilitation programs are typically conducted in formal centers in large communities. The vast majority of patients, however, do not have access to cardiac and pulmonary rehabilitation. Furthermore, long-term participation and adherence to the principles of the program have been disappointing, particularly for women.⁴⁷ The principles of these programs reflect fundamental physical therapy practice, which can be implemented on a one-to-one basis in a private practice (in a large or small community) or in a hospital that does not have a formal program in cardiac or pulmonary rehabilitation; in such settings, the outcomes are comparable to those in formal programs.^48–50 A close-to-home philosophy of care is emerging in the field of health care, including cardiac rehabilitation, in an effort to improve access to underserved people and groups.⁵¹ When well constructed, a home-based cardiac rehabilitation program can have long-term outcomes comparable to those of a center-based program—for example, improved total cholesterol, smoking reduction, anxiety reduction, and self-reported improved physical activity and diet.⁵² Patients who are stable after bypass surgery do as well (in terms of improved exercise capacity and risk reduction) in an individualized detailed home program as those participating in a supervised center-based rehabilitation program.⁵³

As patients become more active, their pharmacokinetics change. Medications must be reviewed on an ongoing basis and prescriptions modified accordingly.⁵⁴ These changes reflect the long-term metabolic effects of exercise, in addition to improved health and potential weight loss. Close teamwork is needed to monitor a patient’s medications and ensure that drug prescriptions are changed so that they promote weaning from medication commensurate with the benefits of noninvasive intervention, including education and exercise. Eliminating or reducing the needs for medication and pharmacological support is an important physical therapy outcome consistent with the philosophy of exploiting noninvasive care as much as possible.

Formal exercise testing and training—primary physical therapy skills—are warranted in patient diagnosis, evaluation, and exercise prescription. Early intervention with exercise for heart and lung conditions has become an established practice to counter the deleterious effects of deconditioning and the loss of cardiac and pulmonary function and to maximize remaining oxygen-transport reserve.⁵⁵

Addressing the psychosocial components of care in cardiac and pulmonary rehabilitation is an element of the internationally accepted definition of rehabilitation. Psychosocial factors, however, constitute few, if any, aspects of the workup and assessment of an individual with heart or lung disease. A structured assessment tool to assess and monitor psychosocial factors and changes in patients with heart disease has been proposed.⁵⁶ Guidelines concerning the psychosocial component of cardiac rehabilitation are the sole focus of a position paper currently being developed in Europe. This position paper is designed to promote active psychological as well as physical well-being.⁵⁷ Given the aging of the populations of high-income countries, cardiac rehabilitation programs must pay particular attention to the needs of older adults with respect to nutrition, physical activity and exercise, program adherence, smoking cessation, psychological issues, and methods of teaching the older learner.⁸ Doing so will help to reduce the high exclusion rate of this cohort of the population from cardiac rehabilitation programs.

Finally, with the advent of databases and outcome measures, projects such as the Wisconsin Society for Cardiovascular and Pulmonary Rehabilitation (WISCVPR) Web-based Outcomes Project, which focuses on outcomes for cardiac rehabilitation, are being used to develop benchmarks and further refine best practice guidelines.⁵⁸ Outcomes of pulmonary rehabilitation include quality of life, which for those with chronic lung disease, is reflected in the St George’s Respiratory Questionnaire and the 36-item Short-Form Health Survey. A simple linear analog quality-of-life scale has also been shown to be valid in evaluating disease-specific, health-related quality-of-life issues in older individuals with chronic lung disease.⁵⁹ With databases and outcomes evaluation, physical therapists will be able to individualize programs to promote more immediate, more effective, and more long-lasting effects.⁶⁰ In addition, programs are being evaluated that will enhance the quality of prevention strategies initiated by health care providers through hospital-based programs for patients at risk.

Quality-improvement initiatives are becoming a focus in the literature. In 2008, one such initiative that used interactive training of hospital teams with Web-based teaching tools, enhanced adherence to prevention guidelines in hospitalized patients with cardiac disease.⁶¹ From baseline to 1 year, this initiative reported marked improvements in smoking cessation, lipid control, blood pressure control, and cardiac rehabilitation referral. Quality-improvement initiatives for activities related to cardiac rehabilitation produce marked benefits. In addition to structured exercise, cardiac rehabilitation focuses on counseling and teaching about risk reduction in order to promote lifelong health; however, long-term studies are needed to address the issue of deterioration with respect to risk factors and lifestyle behaviors over time.⁶² In 1998, a multistate outcome program for cardiovascular and pulmonary rehabilitation was shown to be feasible; it was possible to benchmark data across programs.²¹ Outcomes included the SF-36 Health Survey, a patient knowledge test, and a 6-minute-walk test distance. All outcomes improved in both cardiac and pulmonary rehabilitation programs. Such outcomes are needed to systematically evaluate the effects of cardiac and pulmonary rehabilitation programs.

Although cardiac rehabilitation reduces cardiac deaths, it remains unclear whether exercise alone or the comprehensive range of interventions associated with cardiac rehabilitation is responsible.⁶³ The answer to this question is singularly important in refining the principles and practices of cardiac rehabilitation programs.

Studies of the efficacy of cardiac rehabilitation have been methodologically marred by selection bias: subjects tend to be low-risk, middle-aged men, whereas those who might benefit most are often excluded, namely, those who are older, at high risk, and have multiple comorbidities.⁶³ Those individuals who do not attend cardiac rehabilitation programs tend to be older, less aware of their cholesterol values, and less likely than attenders to believe their condition was controllable and that their lifestyle may have contributed.⁶⁴ Attention to exercise and motivational profiles has been proposed as a means of enabling rehabilitation program participants to continue with exercise.⁶⁵ Promoting self-efficacy should therefore be an important focus in tailoring cardiac rehabilitation programs. Finally, the ethnicity of program participants is rarely reported. Given the needs of the aging population, the number of people with multiple conditions, and the increasing ethnic diversity in the United States and Canada, the reports on the effects of cardiac rehabilitation, to date, have relatively limited generalizability.

As a handy reference for clinicians, key points in the assessment, evaluation, and exercise testing and prescription of patients with primary cardiovascular and pulmonary conditions are summarized in Appendix C.

Patients with Chronic Cardiac Dysfunction: Exercise Responses

Cardiac dysfunction includes a range of types of pathology, causes (acquired or congenital), and severity that may be managed medically, surgically, or in both ways (see Chapter 31 for the principles of comprehensive physical therapy management). The most common cause is ischemic heart disease and myocardial infarction. The muscle that is infarcted never recovers, so remodeling of the heart occurs, and that alters the heart’s electrical functions (as shown on an electrocardiogram [ECG]) and mechanical functions (evidenced by ECG and echocardiogram). Remodeling takes place over time and with exercise. Ejection fraction (right ventricle) at rest is a poor indicator of cardiac function and exercise capacity.⁶⁶ In fact, heart failure can occur in the presence of a normal ejection fraction,⁶⁷ a form of disorder that typically occurs in women who have histories of hypertension and increased left ventricular mass.

Patients can range from being asymptomatic and having risk factors to being in severe distress and having minimal functional capacity, requiring high levels of supplemental oxygen and pharmacological support, and awaiting heart transplantation. Patients with extremely severe disease may require mechanical ventilation. To be able to classify patients’ functional capacity in a semi-quantitative manner, the New York Heart Association classification of function is commonly used (see Box 31-2). Exercise is now considered an essential component in the management of individuals with stable heart failure and in those who have undergone transplantation.⁶⁸ Surgical options include keyhole surgery, open-heart surgery (e.g., coronary artery bypass surgery, valve repair, and aneurysm repair), and heart transplantation.

There is an interaction between circadian rhythms and the pathogenesis of heart rate and blood pressure variability. These rhythms are under the influence of adrenal, autonomic, hypothalamic, and pituitary activity. Thus physical exertion, sleep deprivation, emotional stress, and high-fat meals are major triggers of myocardial ischemia, angina, infarction, sudden cardiac death, and stroke, which have a higher incidence in the second quarter of the day, between 0600 and 1200.⁶⁹ Heart rate and blood pressure variation have been implicated in the pathogenesis and progression of atherosclerosis, heart failure, and thrombosis, and are independent risk factors. During this period, vitamins C and E are lower than during the rest of the day; it has been postulated that regulating the intake of these vitamins and exercising may minimize the variability of heart rate and blood pressure. Whether such regulation can then modulate cardiovascular events warrants further study.

Although dyspnea is a common limiter to exercise in cardiac failure, the other factors that contribute to exercise limitation are multiple. In addition to central hemodynamic impairments, exercise capacity is affected by impaired ventilatory control, lung function, peripheral circulation, and skeletal muscle function.⁷⁰ Exertional dyspnea has been attributed to the regulation of arterial pH during exercise.⁷¹ Pulmonary hypertension and systemic hypotension can also limit exercise performance.⁷² Explanations for these limiters include baroreceptor dysfunction, beta-receptor downregulation, abnormal vascular adaptation, and poor cardiac output in relation to elevated right ventricular afterload. The delayed responses (delayed oxygen kinetics or time constant for this variable) are associated with lactate production and early anaerobiosis.⁷³ Maladaptive gait changes have been ruled out as a factor influencing ventilation in patients with chronic heart failure.⁷⁴

The physiological capacity of patients with cardiac dysfunction to adapt to exercise depends on the type and severity of impairment in the heart and in other steps in the oxygen transport pathway. Reduced alveolar-capillary membrane-diffusing capacity ⁷⁵ and a ventilation to perfusion mismatch have been proposed⁷⁶ and may reflect chronically elevated pulmonary capillary pressure. A primary ventilation-perfusion mismatch defect in patients with heart failure may explain their increased ventilatory response to exercise, but this theory has been questioned.⁷⁷ Patients with severe left ventricular dysfunction enhance their aerobic capacity primarily by improving oxygen extraction at the tissue level rather than by means of central adaptation. Similarly, with aerobic exercise, these patients improve the collateralization of peripheral capillaries so as to improve blood flow to working muscles and increase nitric oxide production in the blood vessels, which mediates endothelium-dependent relaxation.⁷⁸ This effect is correlated with functional capacity. Thus evaluation of vasomotor reactivity has been proposed as a means of explaining the effects of interventions, including exercise and medications. Aortic wall elasticity modulates left ventricular function and coronary blood flow. Pulse wave velocity is a marker of arterial stiffness and is an independent predictor of .⁷⁹ The exercise intolerance observed in individuals with dilated cardiomyopathy may be explained by an increase in arterial stiffness.

Although guidelines for exercise prescription have been commonly adopted for people with uncomplicated heart disease, the optimal prescription is still being refined. Moderate aerobic exercise performed alternate days for 20 to 40 minutes is generally accepted. Nonetheless, despite the general health benefits that are associated with this level of exercise, more moderate levels including brisk walking have been reported to be equally protective.⁸⁰ Such findings are important particularly for individuals who are disinclined to formally exercise at the recommended level for cardioprotection. Brisk walking is more easily integrated into daily life hence likely to be adhered to.

Individuals with Chronic Cardiac Dysfunction and Failure

The cardiac dysfunction managed by physical therapists can range from mild to severe. With increasing severity of disease, an individual’s response and adaptation to exercise are altered markedly, which has major implications for exercise testing and training. Today, patients with even severe heart dysfunction may be able to participate in some level of exercise.¹⁹ However, this needs to be done under the supervision of a competent health care team to ensure the benefits are maximized and the risks minimized.

Chronic heart failure is usually hallmarked by left ventricular dysfunction. In health, normal left stroke volume coupled with increased heart rate leads to greater cardiac output and greater metabolic demand, as during exercise. As the left ventricle becomes increasingly compromised, the individual with heart failure depends more on heart rate to increase cardiac output and peripheral oxygen extraction. Left ventricular ejection fraction during exercise is not consistently associated with resting ejection fraction,⁸¹ even in people with objective signs of myocardial ischemia and increased heart rates during exercise. Thus the left ventricular ejection fraction at rest must be interpreted cautiously in the context of exercise and predicted exercise responses.

Determining which patients will benefit from a rehabilitation program has been the subject of debate. Goebbels and colleagues (1998)⁸² reported that patients with depressed left ventricular function benefit, whereas patients whose left ventricular function has been preserved, such as may occur after myocardial infarction and coronary artery bypass surgery, tend to improve spontaneously within 3 months.⁸³ Proponents of selecting patients for cardiac rehabilitation however, have failed to address the past history of patients, their comorbidities, access to rehabilitation, return to work, and secondary prevention strategies to maximize their care and long-term outcomes. Noninvasive practices need to be exploited before, during, and after a myocardial event or surgery to maximize long-term gains, including reduced recurrence of the problem and need for doctor- and hospital-based care, reduced risk factors and morbidity, and prolonged quality of life. Physical therapy has a commitment to long-term outcomes, including reduced doctor- and hospital-based care, reduction or elimination of medications, and reduced probability of repeat surgeries.

Conservative management of patients with heart failure who utilize physical therapy has emerged as a major focus in the literature, in part because of the cost of surgery and an inadequate supply of organ donors. The benefits include reduction of deconditioning, including restoration of normal autonomic balance and, potentially, some primary effects on the underlying pathology.⁸⁴ Patients with chronic heart failure respond to aerobic exercise favorably, showing improvement in functional class as defined by the New York Heart Association.⁸⁵ Both and anaerobic threshold improve. In addition, there is a reduction in the exaggerated ventilatory response at maximal and submaximal work rates that is usually observed in these patients. As a result, symptoms are reduced. Exercise benefits persist after patients shift from a supervised center-based to a home-based program. This finding has important practical and economic implications.

Over recent years attention has turned to exercise training of patients with cardiac failure and the role of ventilatory changes in exercise-induced dyspnea. The periodic breathing of patients with cardiovascular disease is well known clinically; however, the mechanism underlying the cycling hyperpnea and hypopnea is not clear. Fluctuations in pulmonary blood flow have been proposed as a mechanism for this periodic breathing.⁸⁶ With respect to other ventilatory correlates of heart failure, ventilatory efficiency, the ratios of and , have yielded important prognostic information.⁸⁷ When used in combination with (≥15 mL/kg/min), (≥50 L/L) can be useful in defining a high-risk group that should be prioritized for heart transplantation.⁸⁸

At rest, individuals with more severe heart failure have more restrictive lung pathology and impaired gas exchange.⁸⁹ During exercise, these patients have increased dead space, impaired gas exchange, and greater submaximal ventilatory responses than individuals whose disease is less severe. Exercise limitation in patients with chronic heart failure correlates with reduced FEV₁ and FVC, implicating airway resistance in the increased work of breathing in exercise intolerance.⁹⁰ In addition, an exercise-induced diffusion defect has been identified.⁹¹ Alveolar-capillary membrane conductance has been identified as the best lung function predictor of in patients with chronic heart failure.⁹² The impairment in ventilatory efficiency is associated with reduced exercise tolerance and pulmonary artery pressures.⁹³ Pulmonary vasoconstriction has been implicated in leading to pulmonary hypertension and alveolar hypoperfusion. Overall, exertional dyspnea observed in patients with heart failure is not the result of abnormal ventilatory function.⁹⁴

Ventilatory exercise parameters, including , , and , are strong predictors of mortality.95,96 , however, may be underestimated, given the slowed O₂ kinetics in this population.⁹⁷ Gas exchange, therefore, should continue to be monitored throughout recovery. Submaximal respiratory gas indexes have been proposed as being more sensitive than peak for assessing functional impairment⁹⁸ and for predicting survival in ambulatory patients with chronic heart disease.⁹⁹ Nonetheless, ventilatory capacity is not likely to limit exercise performance in patients with stable chronic heart failure.¹⁰⁰ Ventilatory and heart rate responses are, however, strong and powerful predictors of mortality in these patients, and they are superior to the use of .¹⁰¹ Inspiratory capacity varies inversely with pulmonary capillary wedge pressure in individuals with chronic heart failure, and it is a strong independent predictor of functional capacity.¹⁰²

Patients with severe chronic heart failure often have high ventilatory demands during exercise, and they have respiratory alkalosis, which is consistent with significant wasted ventilation on exertion,¹⁰³ and increased respiratory drive;¹⁰⁴ only a relatively small effect is attributed to ventilation-perfusion mismatch. However, increased ventilatory drive, as evidenced by the ventilatory equivalent of carbon dioxide (), has been reported to occur infrequently.¹⁰⁵ Knowledge and understanding of which patients exhibit this response and which do not would be clinically useful.

Patients with severe chronic heart failure have a reduced ratio of increase in to increase in work rate during incremental exercise.¹⁰⁶ The reduced DO₂ due to severely compromised cardiac output is not fully compensated by an increase in oxygen extraction. These patients do tend to show improved exercise response through improved peripheral oxygen extraction. Changes in cardiac performance may reflect the Frank-Starling effect rather than changes in contractility.¹⁰⁷ Low cardiac output, particularly in less intense exercise, does not necessarily result in lower exercise capacity.¹⁰⁸ This phenomenon has been attributed to a unique mechanism that regulates arteriovenous oxygen content difference to optimize DO₂ to the tissues in patients with severe heart failure. At peak exercise, fractional oxygen extraction in the muscle is greater in patients with chronic heart failure than in healthy people in proportion to the level of the patient’s impairment.¹⁰⁹ This observation supports the importance of peripheral adaptation to aerobic training in patients with heart failure.

Heart failure can be categorized as either diastolic or systolic; the former may be the dominant form in elderly people.¹¹⁰ In stable outpatients, mortality due to diastolic failure is about half that of mortality due to systolic failure. However, when patients are hospitalized, the rates are comparable. Because of its strong prevalence among the elderly, diastolic failure exceeds systolic failure in being the cause of mortality. In diastolic failure, the Frank-Starling mechanism is impaired, causing reduced maximal cardiac output, heart rate, stroke volume, and left ventricular filling pressure. Vascular stiffness is also increased. Acute exacerbations result in pulmonary edema and are associated with hypertension, sodium intake, and lack of adherence to medication schedule. A primary goal is to reduce blood pressure, which improves symptoms and reduces exacerbations.

Exercise testing is an important means of establishing the prognosis of an individual with chronic heart failure with respect to treatment response, morbidity, and mortality. Peak pulse, ( rate), and lean body mass adjusted for O₂ pulse are useful prognosticators.¹¹¹ Postexercise blood pressure response has shown to be a reliable and valid predictor of adverse cardiac events in individuals with dilated cardiomyopathy.¹¹² The postexercise blood pressure response is defined as the ratio of systolic blood pressure at 3 minutes postexercise to that at peak exercise, with a criterion of 0.79 or greater to predict complications. The 6-minute walk test has been reported not to replace as a prognosticator in individuals with advanced heart failure.¹¹³

Prediction of the prognosis of individuals with chronic heart failure can be improved with a two-step exercise-test protocol.¹¹⁴ This test combines maximal and low-intensity exercise to improve accuracy and reproducibility. In addition, a distance of less than 300 meters walked in the 6-minute walk test (see Chapter 19) has been reported to be a useful prognostic marker of subsequent cardiac death in individuals with mild to moderate heart failure.¹¹⁵ Exercise testing has also been reported to provide good prognostic value in determining postoperative outcomes (mitral and aortic regurgitation).¹¹⁶ An important role for exercise testing in prognosis is emerging.

Although tests of can be used to stratify patients with cardiac failure according to risk factors, these tests can be invalid as a result of premature termination by the tester or lack of motivation by the patient. Tests of anaerobic threshold may be less influenced by these factors in such a potentially compromised group.¹¹⁷ Rather, the combination of a at an anaerobic threshold (gas exchange threshold) of less than 11 mL/kg/min and a versus slope of more than 34 is a better predictor of mortality at 6 months than is , and it may provide a guide when prioritizing patients for heart transplantation. Submaximal and endurance tests and determining the anaerobic threshold have been advocated over maximal tests for clinical evaluation of patients with heart failure because they are relatively easy to perform, are associated with less risk, and are more valid indexes of a patient’s capacity for daily activity.^118,119

Individuals with heart failure have a higher incidence of glucose intolerance compared with healthy individuals (20% lower).¹²⁰ After an aerobic exercise program, glucose uptake can increase by 25%. The mechanism of the reduction in glucose tolerance in individuals with heart failure and the remediating effects of aerobic exercise have yet to be elucidated. Whether secondary improvement in insulin sensitivity from aerobic exercise occurs in these individuals comparable to that in healthy people warrants clarification.

Body position may be an important factor to consider when exercising patients with chronic heart failure who often complain of orthopnea. However, when exercise responses in the erect and supine positions were compared in one study, no change was reported in breathlessness, and no change occurred in . However, was greater in the upright position.¹²¹

Patients with chronic heart failure can benefit from aerobic training. Exercise training of patients with impaired left ventricular function is associated with improved ventilatory function.¹²² In addition to improved cardiac output, long-term high-intensity exercise resulted in reduced ventilatory dead space and improved ventilatory efficiency. In men with reduced left ventricular function, high-intensity exercise (2 hours of walking daily in combination with high-intensity, monitored cycle ergometry at 70% to 80% of peak capacity for 40 minutes, four times a week for 8 weeks) has been reported to result in marked increases in secondary to increased cardiac output and widening of the A-aO₂ difference.¹²³ No improvement in myocardial contractility tends to be observed in these patients after such an exercise program. High-intensity exercise does not impair hemodynamic status or lead to further myocardial damage. Low-intensity exercise in individuals with chronic heart failure has been shown to improve autonomic tone and reactivity to vagal and sympathetic stimulation.¹²⁴

The effects of exercise training on pulmonary function in individuals with heart failure are becoming better understood. After training, individuals with coronary artery disease have been reported to show no change in pulmonary function, with the exception of the respiratory exchange ratio at peak exercise.¹²⁵ Also, alveolar-capillary diffusing capacity may contribute to improvement in exercise tolerance after training.¹²⁶ Pretraining pulmonary function is not correlated with improvement in exercise performance.

With aerobic exercise training, respiratory muscle endurance improves, and that contributes to improved overall exercise capacity.¹²⁷ Breathlessness is also reduced. The reverse occurs too—that is, respiratory muscle training can improve , as well as respiratory muscle endurance in patients with chronic heart failure. The combination of muscle and endurance training is superior to endurance training alone in this patient cohort with respect to improved left ventricular function, , and strength.^128,129

An understanding of skeletal muscle function in individuals with chronic heart failure is important because improvements in aerobic capacity may be largely dependent on maximizing peripheral oxygen extraction. Strength training in combination with aerobic training improves walking distance in the 6-minute walk test, which is an independent prognosticator in individuals with chronic heart failure.¹³⁰ Regular endurance exercise increases oxidative enzymes in the working muscles and is associated with a shift from type II to type I fibers.¹³¹ These skeletal muscle adaptations are independent of peripheral circulatory adaptations.

Adaptation to resistance muscle training reflects changes in the myosin heavy chain of peripheral skeletal muscle and a shift from slow aerobic to fast glycolytic and fast oxidative characteristics.¹³² These findings are associated with , O_2pulse, and tidal volume. Reduced strength of the knee flexors and extensors in patients with chronic heart failure is associated with impaired ventilatory response to exercise; thus muscle dysfunction has been proposed as a contributing factor to symptoms.¹³³ Improved functional outcomes, increased walking distance, and reduced muscle area with increased interstitial space after exercise training support the theory that these effects are mediated by improved capillary density and flow reserve to exercising muscle.¹³⁴

Peripheral myopathy in individuals with chronic heart failure may contribute to exercise intolerance and training capacity.¹³⁵ Features include reduced proportion of type I fibers, shift to type II fibers, biochemical shift consistent with increased muscle fatigability, reduced mitochondrial density, and reduced capillary density.¹³⁶ However, some of these changes, such as altered capillary density, appear to be gender-specific, which may have implications for training.¹³⁷ Skeletal muscle appears to adapt to central impairment of oxygen transport in heart failure. There is histochemical and gas exchange evidence showing that physiological recovery is delayed in patients with heart failure.¹³⁸ Interestingly, markers of skeletal muscle oxygenation, including myoglobin and its derivatives, are reduced during incremental aerobic exercise to maximum, and during the recovery. As the capacity for aerobic exercise declines, patients may have greater reliance on anaerobic metabolism (but this cannot be sustained/attained in the same way), which is consistent with increasing reliance on anaerobic pathways for metabolism during exercise. Inflammatory cytokines have been implicated in the myopathy associated with heart failure.¹³² However, the possibility that this outcome reflects deconditioning cannot be ruled out because patients typically are unable to achieve high exercise intensities.¹³⁹

The recovery process in patients with heart failure has important implications for optimizing exercise training parameters and, thereby, training effects. However, further study of differences in exercise recovery characteristics between patients with heart failure and healthy people is warranted.140,141 Evidence supports the idea that exercise intolerance in these patients is characterized by slower adaptation to acute exercise and recovery and to reduced maximal exercise capacity compared with healthy people.¹⁴²

After angiography, positioning and mobilization have important roles after several hours of bed rest.¹⁴³ Limiting restricted mobility after cardiac catheterization to 2 hours from 6 hours has been reported to be safe, and it may limit complications.¹⁴⁴

Different types of exercise stress (aerobic or resistance) have differential effects on the heart and circulation.¹⁴⁵ In health, for example, static exercise exerts a pressure load on the heart that can be distinguished from the normal hemodynamic response to dynamic exercise, which involves a volume load on the heart. Static exercise leads to concentric cardiac hypertrophy (left ventricular), and dynamic training is associated with eccentric hypertrophy. Static exercise can produce effects that have been associated with aerobic training. Isotonic exercise using hand weights has been reported to be associated with increases in systolic and diastolic blood pressure, rate pressure product, serum norepinephrine, and perceived exertion.¹⁴⁶ Pulmonary capillary wedge pressure, incidence of dysrhythmias, and ST-segment changes do not differ from rates recorded at rest. Generally, isotonic exercise is tolerated well by individuals with heart failure, and no angina or dyspnea occurs.

Low to moderately intense strength training may cause fewer cardiovascular complications than aerobic exercise training in individuals who have undergone myocardial infarction.¹⁴⁷ Resting blood pressure can be reduced, albeit to a lesser extent, suggesting reduced sympathetic and baroreceptor activity. In addition, lipid profiles may improve. These benefits can be observed in patients with cardiac and circulatory pathology without adverse effects. Even older, frail patients may tolerate weight training at 40% to 60% of maximal voluntary contraction. Qualitatively similar hemodynamic responses occur in response to resistance exercise, as in aerobic exercise in individuals with heart failure.¹⁴⁸ In general, resistance training with multiple repetitions of moderate weight produces the most beneficial effects. To ensure that a patient is able to perform optimally the activities of daily living, which require a certain degree of muscle strength, strength training is considered an integral component of a cardiac rehabilitation program.

The effect of cardiac dysfunction on regional circulation has been of interest, particularly with respect to cerebral perfusion. A recent study has shown that patients with left ventricular dysfunction can have impaired cerebral perfusion. During exercise, the adequacy of cerebral perfusion is dependent on the adequacy of cardiovascular and pulmonary function; it is compromised in patients whose cardiac output fails to increase appropriately in response to exercise.¹⁴⁹

Some individuals with chronic heart failure have been reported to have sick euthyroid syndrome, in which serum-free triiodothyronine is reduced in the presence of normal free L-thyroxin and thyrotropin.¹⁵⁰ Sick euthyroid syndrome is a sign of poor prognosis in individuals with chronic heart failure. Exercise, however, can normalize the free triiodothyronine levels and reverse the syndrome, in turn improving exercise capacity.

Individuals with persistent life-threatening cardiac rhythms may require artificial pacemakers. Advances in this area have included biventricular pacing for individuals with systolic left ventricular failure with prolonged duration of the QRS complex. Preliminary reports suggest that these pacemakers are safe and effective.¹⁵¹ Further, biventricular pacing can improve symptoms and quality of life by improving walking times and ejection fraction.¹⁵² These effects persisted at the 6-month follow-up, and the 2-year survival rate was excellent. There are few specific guidelines for these individuals with respect to exercise testing and prescription. Similarly, there are few guidelines for individuals with automatic implantable cardioverter defibrillators.¹⁵³ Preliminary reports suggest that exercise and lifestyle recommendations are needed for individuals with pacemakers and implanted cardioverter defibrillators and that with due modification, exercise testing and training are feasible.

Ventricular dysrhythmias contribute to a significant number of deaths. Despite improved survival, this cohort of high-risk individuals may be considered inappropriate for cardiac rehabilitation. With careful patient screening and monitoring, however, some patients with ventricular dysrhythmias may safely participate in cardiac rehabilitation.¹⁵⁴

Individuals after Heart Transplantation

Heart transplantation has become an accepted therapy for end-stage heart failure over the past 20 years, with its ultimate goal being the return of function and a good quality of life (see Chapter 17). Postoperatively, the resting heart rate for heart transplant recipients is higher than normal. In the early postoperative period, the peak and work rate of people who have had heart transplants are 50% of those of healthy people.¹⁵⁵ At ventilatory threshold, the and work rate were also 50% of normal. Peak heart rate, which increases for up to 3 minutes after peak exercise, is also significantly lower. This evidence supports the need for mandatory rehabilitation so as to maximize the benefits of this high-risk surgery, including optimizing functional work capacity, return to work, and life satisfaction.

Without training, exercise tolerance remains severely limited over the first 16 months postoperatively. This has been explained by the reduced capacity to respond to the Frank-Starling mechanism and the residual low cardiac index.¹⁵⁶ Rehabilitation begins preoperatively and continues for 1 year after discharge.¹⁵⁷ The principles of cardiac rehabilitation are applied; however, response of the denervated heart to exercise requires extended warm-up and cool-down periods and limits the maximal heart rate and that can be achieved. Reinnervation of the sympathetic nerves to the heart is associated with improved heart rate response to exercise and contractile function.¹⁵⁸ Hemodynamic responses to exercise are initially dependent on exogenous catecholamines rather than on the fast-responding sympathetic release from nerve endings. Systolic blood pressure is more appropriate than heart rate for assessing exercise response and recovery.¹⁵⁹ Anaerobiosis is achieved early. The degree to which neuroplasticity can be influenced by exercise training to promote autonomic reinnervation to the heart after transplant has yet to be established.

When compared with patients after bypass surgery in postoperative cardiac rehabilitation programs (phase II; up to 3 months postoperatively), patients with heart transplants have comparable functional outcomes.¹⁶⁰ However, after graduation from this program and being on a home-based program for 9 months, patients with transplants had lower and were significantly more limited at the 1-year follow-up. Thus phase I only, combined with recommendations for a home program, may be inadequate for patients after heart transplantation; they may benefit from long-term supervised training programs.

Persistently low after transplant reflects in part intrinsic skeletal muscle abnormalities.161,162 In addition to intensive aerobic exercise, resistance muscle training has an important role in countering the effects of corticosteroid-related osteoporosis and peripheral myopathy. With respect to predicting the prognosis of patients with heart failure who undergo heart transplantation, is considered a superior indicator of submaximal indexes of exercise capacity.¹⁶³

Isometric exercise and activities requiring postural stabilization are largely avoided in people who have had heart transplants because of potential hemodynamic stress. Light isometric exercise (handgrip) attenuates increases in heart rate, blood pressure, and systemic vascular resistance. Whole-body isometric exercise also attenuates these hemodynamic variables.¹⁶⁴ At rest, heart rate, blood pressure, and rate pressure product are higher in individuals who have had transplants than those rates in healthy people.

Some patients who receive heart transplants have low pulmonary diffusion capacity, and this is associated with lower exercise tolerance than is found in patients who do not have this impairment.¹⁶⁵ Poor diffusion capacity, however, is not associated with exercise-induced hypoxemia and thus is not considered a primary contributor to impaired exercise tolerance.

The exercise responses of patients with IC also exhibit a slowed response related to impaired muscle perfusion.¹⁷⁰ The associated delayed ventilatory response has been associated with the hyperemic response in the exercising muscle rather than with ischemia.

Outcome measures, including ankle-brachial index performed in a vascular laboratory to assess changes in peripheral stenoses with exercise training, are useful.¹⁷¹ Ultrasound can be used to assess pulses, particularly when they are weak. Palpation of skin temperature is a crude indicator of perfusion in that skin is highly sensitive to ambient temperature. Using the back of the hand, however, and scanning bilaterally down the legs, so that skin temperature can be compared in the legs, may have some utility for identifying gross differences in blood supply.

Individuals with Anemia

The exercise responses of patients with anemia have not been well described. The capacity of the blood to transport oxygen is determined by the hemoglobin concentration and the binding characteristics of the hemoglobin. Patients who develop acute anemia are more likely to complain of dyspnea than patients who develop anemia gradually. Rather than a primary cardiac, pulmonary, or muscle compensatory mechanism, this adaptation is mediated by increased diphosphoglycerate, which decreases the affinity of hemoglobin for oxygen in the tissue. Patients with sickle cell anemia have a low and a low anaerobic threshold in the presence of a high heart rate reserve but no gas exchange abnormalities.¹⁷² The disease is characterized by restrictive lung pathology, increased alveolar dead space, and hypoxemia.¹⁷³ Increased dead space may reflect impaired pulmonary capillary perfusion due to the sickle cells. Exercise hyperventilation is thought to be associated with increased anaerobiosis.

Individuals with Hypertension

Hypertension remains the silent killer for which effective nonpharmacological interventions are underused. Hypertension is associated with sedentary lifestyle, diet, obesity, smoking, and stress. Further, hypertension has long been linked to type 2 diabetes mellitus as well as vascular changes typically seen with aging.174,175 Modifying one or more of these factors can reduce high blood pressure and its lethal sequelae and eliminate, or at least reduce, the need for medication. Chronic sympathetic overdrive associated with hypertension promotes left ventricular hypertrophy, cardiac dysrhythmias, and atherogenesis.¹⁷⁶ Further, inhibiting sympathetic overactivity may help reduce cardiovascular risk. Regular physical activity and a formal exercise program reduce the risk for hypertension or modify it. This effect is likely mediated through a decrease in total peripheral vascular resistance. African American men are particularly at risk for hypertension, and this risk can be detected by an exaggerated blood pressure response to exercise.¹⁷⁷ Endurance training reduces this exaggerated response and thereby may reduce the risk for developing hypertension. Along with eating a healthy low-salt diet and not smoking, exercise is a potent noninvasive intervention that can prevent, as well as control, high blood pressure. Despite the efficacy of many antihypertensive medications, potential deleterious effects of low perfusion to the vital organs with intensive blood pressure control cannot be overlooked clinically.¹⁷⁸

Individuals with Type 2 Diabetes Mellitus

Type 2 diabetes mellitus is a strong risk factor for coronary artery disease and sudden cardiac death. This condition is associated with reduced baroreceptor sensitivity and heart rate variability, which are also risk factors for morbidity and mortality. Exercise training improves baroreceptor sensitivity in people with type 2 diabetes as well as glucose sensitivity, exercise tolerance, and muscle strength.¹⁷⁹ Prognosis may well be improved with exercise.

Type 2 diabetes mellitus results in multiple deficits to exercise capacity, both central and peripheral. Muscle blood flow may be impaired at the level of microcirculation in the absence of overt peripheral vascular disease.¹⁸⁰ In patients with chronic diabetes, exercise capacity is compromised by reduced oxygen delivery. A reduction in the arteriovenous oxygen difference may contribute to a reduction in .¹⁸¹ When smoking is controlled, individuals with diabetes mellitus who are insulin dependent and have complications have been reported not to exhibit impaired pulmonary gas exchange during exercise despite thickening of the alveolar basal lamina.¹⁸² Individuals with non–insulin-dependent diabetes mellitus have reduced glucose transport in skeletal muscles, and this may contribute to exercise intolerance.

Diabetes mellitus is an independent risk factor for reduced left ventricular ejection fraction during exercise, as is severity of coronary artery disease.¹⁸³

Role of Medications: Augmenters and Attenuators of Outcome

Among the factors that can confound exercise responses of patients are medications. Medications can enhance, limit, or have no effect on exercise performance. Patients with cardiovascular dysfunction, particularly those under a physical therapist’s care, are likely to be taking one or more potent medications. The timing of their ingestion of these medications in relation to their performing an exercise test should be recorded in order to standardize testing procedures from one time to the next; at the very least, it is important to be aware of the confounding effects of a medication that could explain improved or worsened responses. Beta blockers are commonly taken by patients with cardiac dysfunction to improve the rhythm and contractile force of the heart. Long-term use of beta blockers causes no significant improvement in delayed heart rate recovery, which is a predictor of mortality in patients with heart failure.¹⁸⁴ These drugs can contribute to fatigue and exercise intolerance. Many patients are taking angiotensin-converting enzyme (ACE) inhibitors to enhance cardiac function. This classification of drug improves diffusion capacity and exercise capacity, an effect mediated through prostaglandin activity. However, this activity can be mitigated by aspirin, another drug commonly taken by patients with heart failure.¹⁸⁵ Thus a change in aspirin administration in combination with ACE inhibitors can worsen exercise tolerance. Captopril, a commonly prescribed ACE inhibitor, has a demonstrable beneficial effect on exercise responses in patients after myocardial infarction.¹⁸⁶ Ventilatory efficiency is improved, as is evidenced by a reduction in at submaximal workloads. Reduced perception of exertion and improved capacity to perform the activities of daily living may result from a reduction in ventilatory demand. Concurrent with physical therapy management, an inventory of the patient’s medications and medication changes should be maintained and considered when conducting an exercise test or interpreting exercise test data.

Individuals with Chronic Pulmonary Dysfunction: Exercise Responses

Of individuals who participate in pulmonary rehabilitation programs, the largest proportion is made up of those with emphysema. Smoking is the primary cause of emphysematous changes in the lungs and the associated systemic complications (see Chapter 5). Patients with moderate or severe pulmonary distress may be referred to pulmonary rehabilitation. Other groups that may be referred are individuals with cystic fibrosis, asthma, interstitial lung disease, and alpha₁-antitrypsin deficiency. Patients with lung cancer are typically underrepresented in rehabilitation programs and warrant being targeted as a group that could benefit.

Like patients with chronic cardiac dysfunction, those with chronic pulmonary dysfunction may have a history of being managed pharmacologically or surgically. Surgical options include lung volume reduction surgery, segmentectomies, lobectomies, pneumonectomies, and lung transplantation.

Individuals with Chronic Obstructive Lung Disease

Deconditioning in patients with chronic lung disease is an anticipated consequence of the downward spiral of pathophysiological compensation for the structural and functional damage to the lungs. In individuals with severe disease, exercise intolerance may reflect limited peripheral perfusion and oxygen extraction due to the disproportionate demand on the respiratory muscles.¹⁸⁷ These individuals are unable to exercise at an intensity that induces a high level of aerobic conditioning, and they experience early onset of dyspnea. On experiencing dyspnea with exercise, a person with chronic obstructive pulmonary disease (COPD) reduces his or her activity level, which leads to deconditioning. With impaired aerobic capacity, anaerobic glycolysis has an increasingly important role in supporting physical activity. This leads to increased blood lactate, which needs to be buffered with bicarbonate, thereby producing additional carbon dioxide. This further increases ventilatory load and dyspnea and leads to further inactivity and deconditioning. These individuals frequently have secondary cardiac and hematological changes. The goal of physical therapy is to relieve dyspnea and increase exercise tolerance, hence, quality of life. After smoking cessation, exercise is the single best intervention for controlling dyspnea in individuals with COPD.

Exercise testing has become an established component of the workup of an individual with impaired functional capacity, including patients with chronic lung disease. Although estimating the ventilatory capacity of patients with COPD on the basis of whether a patient can climb one or two flights of stairs is no longer considered a tenable test, symptom-limited stair climbing can be used to evaluate cardiovascular and pulmonary reserve.¹⁸⁸ Stairs climbed in a symptom-limited stair-climbing test correlate with , , heart rate, and respiratory rate in response to a maximal cycle ergometer test.

During acute exercise, patients with COPD have elevated heart rates and blood pressures and show increased hypoxemia and desaturation with incremental or prolonged constant work-rate exercise. Impaired exercise capacity reflects physical damage to the lungs, including impaired pulmonary vasculature ¹⁸⁹ as well as cardiac and skeletal muscle abnormalities. Exercise capacity is marked by a disproportionate ventilatory response and differences in FEV₁, but these responses explain only a fraction of the variability in .¹⁹⁰ Variability in the ventilatory response to exercise is a primary determinant of variability in the exercise capacity of patients with COPD. In the absence of right heart failure, right ventricular end diastolic volume is highly correlated with and cardiac index in patients with COPD, suggesting that right ventricular end diastolic volume compensates optimally.¹⁹¹