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.

Individuals with Left Ventricular Assist Devices

Left ventricular assist devices have become more common as an interim intervention for an individual awaiting heart transplant. The donor pool is small, so many individuals may not survive the wait for surgery. The Jarvik heart is a left ventricular device designed as a long-term solution for heart failure. In an initial case study describing a patient with a Jarvik heart, exercise tolerance, myocardial function, and end-organ function all improved 6 weeks after surgery.¹⁶⁶ The Jarvik heart shows some promise for the management of end-stage heart failure; however, its success will depend on its mechanical dependability.

Individuals with Congenital Heart Disease

Guidelines for individuals with congenital heart disease warrant development. Barriers to exercise in this cohort have been reported to be their perceived physical limitations, lack of interest, and fear.¹⁶⁷ Currently, guidelines are suboptimal.

Individuals with Intermittent Claudication

Intermittent claudication (IC) is the symptom of exercise-induced muscle ischemia of peripheral arterial disease. IC is a systemic complication of atherosclerosis with or without overt ischemic heart disease. The disabling pain during walking results from muscle ischemia. The risk for cardiovascular morbidity and mortality far exceeds that of severe limb ischemia or limb loss.¹⁶⁸ A patient with IC must be managed as a patient with heart disease as well as one with peripheral arterial disease. Conservative management is a priority and should include physical activity and exercise programs, smoking cessation, weight loss and optimal nutrition, and stress management.

Claudication symptoms may mask cardiac symptoms. In addition, a comorbidity such as arthritis can complicate the clinical picture in such a way that the underlying vascular condition is neither manifested peripherally nor centrally. During exercise testing and training, arthritis may limit the capacity of the patient who may have well been restricted by claudication pain.¹⁶⁹ Even in this cases, exercise training can improve exercise tolerance in the absence of improved peripheral blood flow.¹⁶⁹ Exercise effects include reduced submaximal heart rates and oxygen cost and reduced postexercise lactate levels. In addition, lipid profiles can be improved.

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

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 vasculature¹⁸⁹ 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

As in other conditions, in the management of patients with COPD, individualized training programs based on heart rate as the gas exchange threshold (anaerobic threshold), as opposed to standard protocols based on 50% of heart rate reserve, produce superior therapeutic outcomes; that is, they reduce ventilatory requirements and are safer.¹⁹² Supervised training of individuals with COPD has been reported to have advantages over self-monitored exercise programs.¹⁹³ When two to eight programs were compared, the supervised treadmill program was superior to a community-based walking program with respect to training intensity in terms of improved , , , and heart rate in response to moderate-intensity workloads. Research is needed to design home-based programs for selected patients in order to maximize these programs’ effectiveness.

The 6-minute walk test is useful in the assessment and management of patients with COPD, for whom the test was originally developed. The discriminating capacity of the test can be increased by considering factors in addition to walking distance. Four factors based on an evaluation of 15 variables accounted for 78% of the variances in distance walked:¹⁹⁴

Based on a walking-distance test, the effect of an exercise program can be predicted on the basis of low pretraining walking distance and higher FEV₁.¹⁹⁵

Symptom-limited tests are used to estimate the effects of training on patients with COPD. In patients with low functional work capacity, objective submaximal indexes of training effects are useful. With respect to oxygen kinetics during constant work rate, the time constant of after training is reduced, and it reverts after detraining.¹⁹⁶ The O₂ pulse similarly increases and decreases with training and detraining, respectively, and serum lactate decreases with training and increases with detraining.

Rigorous training (80% of peak work rate, for 45 minutes, 3 times a week, for 6 weeks) results in significant training responses in individuals with severe COPD.¹⁹⁷ Peak work rate and exercise endurance increase. In response to constant work rate, the kinetics of O₂ uptake, CO₂ production, , and heart rate are reduced. Improved exercise tolerance may reflect changes in breathing pattern, specifically, increased tidal volume and reduced respiratory rate.

During the past decade, research that sought to elucidate the training responses of individuals with COPD and their adaptation to exercise has focused on peripheral muscle pathophysiology and adaptation. With refinement in exercise testing and training procedures and in measurement, changes in peripheral muscles have been found to be associated with the underlying disease. In addition, aerobic training responses reflect both central and peripheral adaptations.

Compared with healthy people matched for activity level, individuals with COPD have less muscle strength (70% to 80% of age-matched healthy people), which may be explained by deconditioning, a disease-related myopathy, or both.¹⁹⁸ In addition, mechanical efficiency may be impaired. Patients have large numbers of less efficient type II muscle fibers, but cross-sectional fiber area, capillarization, and mitochondrial density are comparable or reduced.^135,199 Although metabolic capacity is unchanged, differences in fiber type in COPD may explain the reduced mechanical efficiency.

Systemic factors contributing to exercise intolerance have been identified in individuals with chronic lung disease, and they appear to resemble those observed in individuals with chronic heart disease.²⁰⁰ Some individuals with COPD have impaired peripheral perfusion and oxygen extraction, which may be explained by the redistribution of cardiac output from the peripheral to the respiratory muscles during increasing work rates.¹⁸⁷ This may be a primary exercise limiter in these patients. In a study designed to distinguish central from peripheral limitations in the exercise responses of patients with COPD, central factors rather than peripheral muscle limitations were reported to be responsible (although not wholly) for their exercise intolerance.²⁰¹ Endurance training is associated with increased skeletal muscle activity and recruitment of slow-twitch fibers.²⁰²

Individuals with Primary Pulmonary Hypertension

Patients with primary pulmonary hypertension have impaired exercise responses that may resemble those of patients with COPD and secondary pulmonary hypertension. During incremental exercise, the lungs become less efficient as gas exchangers because of impaired lung perfusion.²⁰³

Individuals after Lung Volume Reduction Surgery

Lung volume reduction surgery has become a topic of increasing interest as an invasive means of correcting the hyperinflation in the lungs of patients with COPD. A good quality of life is correlated with reduced lung hyperinflation after surgery,²⁰⁴ and these improvements have been maintained for at least 18 months on follow-up.²⁰⁵ A commensurate reduced work of breathing appears to facilitate performance of activities of daily living. Improvement in functional capacity after surgery has been attributed to improved breathing mechanics during exercise, as well as at rest,²⁰⁶ and to improved respiratory muscle strength.²⁰⁷ Specifically, higher maximum levels of tidal volume and are achieved; in turn, these lead to improvements in and .

Individuals with Interstitial Lung Disease

Performing exercise testing in individuals with interstitial lung disease can elucidate the extent of the pathology and its functional consequences—diffusing capacity and alveolar arterial oxygen tension difference.²⁰⁸ These patients have less ability than healthy people to recruit the pulmonary capillary bed during increased exercise stress, so they can desaturate readily.^209,210 is correlated with impairment of gas exchange and circulation, rather than with ventilatory impairment. Thus the pathophysiology of the pulmonary vasculature is considered more important than impaired ventilatory mechanics in patients with interstitial lung disease.²¹¹ Abnormal exercise responses in individuals with pulmonary sarcoidosis may reflect subclinical right heart dysfunction.²¹²

One study that examined the contribution of diffusion limitation to exercise performance in this patient group showed evidence of a ventilatory impairment that was manifested by a decrease in alveolar oxygen tension.²¹³ Cardiac impairment such as impaired diastolic filling may occur secondary to pulmonary fibrosis during exercise or restriction of the pleurae and thoracic cavity. Changes in gas exchange during exercise may be the most sensitive indicator of physiological limitation in patients with subclinical evidence of interstitial lung disease.^214,215 However, in terms of prognostic capability, the results of an exercise test for evaluating gas exchange do not appear to augment standard pulmonary function testing.²¹⁶

Individuals after Lung Transplantation

Lung transplantation improves pulmonary function and quality of life in individuals such as those with cystic fibrosis. When exercise responses before and after bilateral lung transplantation are compared, exercise capacity remains low, although improved.²¹⁷ This observation has been explained on the basis of poor oxygen extraction.²¹⁸ Exercise conditioning is required in these patients postoperatively to maximize their functional capacity. However, maximum oxygen consumption may remain below that of healthy peers matched for age and gender, and anaerobiosis during exercise is achieved earlier. These responses reflect inadequate adaptation of cardiac output in these patients, as well as deconditioning.

Individuals with Asthma

There are several specific aspects to consider when testing and training individuals with exercise-induced asthma.²¹⁹ For those who are managed with medication, a low-intensity warm-up before exercise can optimize its therapeutic effect. A longer cool-down may also be beneficial. Individuals with asthma are taught to monitor their unique responses to their medication and its coordination with physical activity and exercise. They also monitor the ambient air (humidity and temperature) to anticipate the potential for bronchoconstriction and respiratory distress. With good knowledge of conditions and medication, individuals with asthma can participate in high-intensity exercise safely.

Individuals with Cystic Fibrosis

General health and wellness have become primary goals for individuals with cystic fibrosis (CF) Twenty years ago, management of people with this condition, primarily children, was based largely on passive removal of excessive secretions by means of postural drainage and vigorous percussion. Now people with cystic fibrosis are living longer, and comprehensive physical therapy management, including a regular program of exercise, is recognized as a central component of promoting general health and airway clearance.220,221

Although life expectancy continues to improve in people with CF, end of life usually results from respiratory infection, so exacerbations have to be prevented. With a basis of good health resulting from proper nutrition and exercise, exacerbations may occur less often and last for a shorter time. The exercise program is adjusted during these times and then ramped up afterwards. Medications, including bronchodilators, are coordinated with exercise to produce the best effects both during sessions and over the long term.²²²

Setting and Team Members

In addition to the physical therapist, the team consists of physicians, nurses, a psychologist, a social worker, a pharmacist, and in some centers, an exercise physiologist. Typically, the physical therapist is involved with exercise testing and training, program modification and progression, and eventual discharge. Additional roles involve education and risk-factor modification. A physical therapist applies the principles and practices of cardiovascular and pulmonary rehabilitation to any patient in any setting and to patients who have cardiovascular and pulmonary dysfunction or its risk factors as a primary or secondary diagnosis or concern. The guidelines and standards for assessment and exercise testing and training must be adhered to if the best service and the best and safest outcomes are to be achieved.²²⁹

Central to comprehensive physical therapy management is focusing on the individual rather than on the condition. Although this chapter emphasizes exercise testing and training in individuals with primary cardiovascular and pulmonary conditions, in reality, people present with comorbidities. Thus individuals with secondary cardiovascular and pulmonary dysfunction (see Chapters 25 and 32) are likely to have a high incidence of primary cardiovascular and pulmonary dysfunction or risk for it (in comparison with the general population). For this reason, underlying risk factors and disease must be examined in all patients, irrespective of their primary presenting diagnoses.

The history, lab tests, and investigations, including scans and ECGs, and the basic assessment of an individual with cardiovascular and pulmonary dysfunction are described in Part Two, but the aspects of the assessment that warrant particular attention in exercise testing and in training individuals with cardiovascular and pulmonary dysfunction are highlighted in this section. Although the cardiovascular and pulmonary systems may be the focus of rehabilitation, a complete review of all systems is necessary to determine limitations imposed by musculoskeletal, neurological, endocrine, hematological, or other conditions. These need to be considered in both testing and training.

The assessment comprises the examination of risk factors, including profiles of the patient’s nutrition intake, weight, smoking history, and stress management (including rest and sleep profiles), as well as physical activity and aerobic capacity. Before implementing any intervention, a detailed history, examination, and lab data are accumulated to provide an objective baseline. Within 6 to 8 weeks, elements of the assessment are repeated and outcome measures recorded to determine the degree to which the patient has progressed with respect to achieving short-term goals.

Predictors of long-term survival of myocardial infarction include several factors that need to be identified so that patients can be stratified according to risk. These factors include age, left ventricular ejection fraction, diabetes, hypertension, and elevated resting heart rate.²³⁰ Attention to these factors may help to detect changes in status early and prevent adverse exercise effects by judicious modification of an exercise program. Individuals who develop late-onset heart failure have a tenfold increased risk for mortality. Glucose abnormalities (hyperglycemia and hyperinsulinemia) in those who do not have diabetes are common in individuals with heart failure (43%).⁵¹ Further, these findings are associated with greater functional deterioration than that found in individuals with heart failure without glucose abnormalities. Thus knowledge of an individual’s glucose tolerance is essential at baseline and over time within the rehabilitation program.

Well-being extends beyond physical health. Rehabilitation programs record and monitor outcomes related to the subjective sense of well-being, the health-related quality of life, the general quality of life, and life satisfaction. Many scales and questionnaires are available to provide outcomes and fluctuations in these variables over time.

Clinical depression is associated with ischemic heart disease in two ways. First, depression is an independent risk factor for cardiovascular disease and related increased morbidity and mortality.²³¹ Second, up to 45% of individuals exhibit symptoms of major depression after acute myocardial infarction. Thus individuals referred to cardiac rehabilitation need to be screened for depression, and psychotherapy, counseling, or pharmacotherapy may be indicated. Remediation of depression associated with chronic disease may augment functional capacity independent of physical rehabilitation. Depression and peak aerobic capacity have been reported to be the best independent predictors of patient-reported physical function scores in older individuals with heart disease.²³² These findings suggest a role for depression management that is independent of exercise training but augments functional capacity.

The general assessment must also include an assessment of the individual’s learning style (see Chapter 1 and 28). Prochaska’s Transtheoretical Model of readiness to change has important implications for rehabilitation programs that are formalized (e.g., cardiac and pulmonary rehabilitation), as well as for individual rehabilitation programs. In addition to the goal of shifting an individual into a lower risk category, another objective is to shift an individual into a higher readiness-to-change category. An individual’s readiness to change health-related behavior is assessed, along with his or her intention to engage in the recommended risk-reduction behaviors, including dietary changes, physical activity and exercise, smoking cessation, and relaxation. Readiness to change may differ for each behavior. Barriers include time management, psychological adaptation, and laziness.²³³ Another component of the education is the assessment of the individual’s knowledge deficits regarding his or her condition.

Smoking Cessation

The risk for myocardial infarction is three times higher in patients who continue to smoke after a cardiac event.²⁴² When patients quit, the risk for reinfarction is reduced to that of nonsmokers prior to the first infarction.

Nutrition and Weight Control

Optimal nutrition and weight control are priorities. Individuals with cardiovascular dysfunction are at risk for fluid and electrolyte imbalances and related ECG irregularities, so these aspects of nutrition need to be included. In addition, patients with chronic heart failure have some special considerations. These patients rely more on fat substrate during exercise than on carbohydrates, which may contribute to increased catecholamines and free fatty-acid levels.²⁴³ These changes may compensate to protect muscle glycogen stores. However, given that fat metabolism is not energy-efficient, this shift may contribute to exercise intolerance.

Psychosocial Issues

Stress management and life-skills training are fundamental to rehabilitation programs in minimizing undue sympathetic arousal and impact on the cardiovascular and pulmonary systems. If indicated, help with depression control and anger and hostility management are provided by the appropriate professionals. Remediation of depression alone can enhance functional status.

Risk Reduction

Prevention and rehabilitation programs aim to reduce an individual’s cardiac risk factor category. Figure 24-2 shows an example of a scale for assessing cardiac risk and identifying an individual’s category of risk. Using such a scale provides objective markers for risk factor modification, and evaluating the degree of risk reduction with health behavior change, an important physical therapy outcome. Table 24-4 shows the distinctions among low, intermediate, and high risk for cardiac disease.²⁴⁴

Monitoring

Assessment and monitoring considerations for the individual with heart disease are described in Part Two and Chapter 31. At the onset of the program, a baseline assessment is made of the patient’s subjective sense of well-being, including health-related quality of life, impact of sickness and disability, quality of life, and life satisfaction. Related assessments are made throughout the program to observe the program’s effects on these outcomes and to assess the impact of the program at its completion.

An individual with primary cardiovascular dysfunction or its risk factors requires particular attention to his or her hemodynamic status. Risk factors, however, do not necessarily predict complications during supervised exercise.²⁴⁶ Serial lipid profiles, blood pressure, resting heart rate, and body weight are monitored regularly, and interventions are modified accordingly.²⁴⁷ Blood pressure, however, can be abnormal in individuals with exercise-induced left ventricular systolic dysfunction, which leads to unstable hemodynamic status.²⁴⁸ Blood pressure may not be a valid measure of exercise stress in such individuals. Further study is needed before exercise risk stratification guidelines can be used with any assurance to monitor supervised rehabilitation programs.

The absolute and relative changes in heart rate, blood pressure, rate pressure product, arterial saturation, and perceived exertion are particularly important. ECGs may be performed intermittently throughout exercise or continuously, as indicated. Recent evidence has questioned the conventional guideline of an ST-segment depression of greater than 1 mm in favor of a more conservative guideline, greater than 0.5 mm during or after exercise.²⁴⁹ This value is associated with risk for myocardial infarction, requiring bypass surgery, and risk for cardiac mortality.

Exercise-induced silent myocardial ischemia is an important indicator of increased risk for cardiovascular disease (3.5-fold) and stroke (2.2-fold) in men when they are compared with those without silent ischemia. Other risk factors include smoking, hypercholesterolemia, hypertension, and being overweight.²⁵⁰

Recovery data are important components of the exercise testing assessment and interpretation. Delayed heart rate recovery is a predictor of mortality,¹⁸⁴ irrespective of angiographic evidence of disease severity.²⁵¹ Heart rate recovery is calculated as the difference in heart rate from peak exercise to that recorded at 1, 2, and 3 minutes after exercise. Women have been reported to be more susceptible to postexercise hypotension than men; an active cool-down period may offset postexercise hypotension.²⁵² Signs and symptoms of overexertion must be monitored (Box 24-2).

Smoking Cessation

Smoking cessation is essential for the health and well-being of all people, in particular those with pulmonary disease. The physical therapist has a responsibility to address this modifiable risk as a priority of management (see Chapters 1 and 31).

Nutrition and Weight Control

The connection between nutrition and lung health has become a focus of research interest, and that research supports the role of good nutrition (in particular, the consumption of fruits, vegetables, and fish) in optimal lung health.274,275 Diet may be an important cofactor in the development of COPD. Whether good nutrition improves damaged lungs has not been substantiated, but good nutrition improves general health and thus should be a primary recommendation when managing these patients.

Psychosocial Issues

Patients with chronic conditions have higher incidences of depression and poorer psychosocial adjustment than do individuals in the general population. Although chronically poor blood gases can affect psychological and cognitive function, the remediation of any source of depression can independently improve function. Thus depression and other psychological issues must be assessed and managed independently.

Risk Reduction

Lifestyle modification and risk factor modification are fundamental components of the pulmonary rehabilitation program; these modifications include smoking cessation, nutrition and weight control, and stress management, in conjunction with physical activity and exercise. Optimal nutrition is encouraged as a lifelong change in patients with COPD, whose nutritional status is often suboptimal.²⁷⁶ Carbohydrate-rich foods, known to increase carbon dioxide production, have been targeted as a food group that should be limited in patients with COPD. Small changes in the carbohydrate constituents of diet have been reported to have a major effect on , exercise tolerance, and breathlessness.²⁷⁷ Smoking cessation is essential to limit further lung damage and has the potential to reverse impaired pulmonary function, improve oxygen transport capacity, and reduce or reverse smoking-related risk factors as the period of nonsmoking lengthens. Reduction of pulmonary and cardiac risk factors in an individual with primary lung dysfunction is essential.

Physical Activity and Exercise: Special Considerations

The principles and practice of exercise prescription are described in detail in Chapter 19. However, special considerations for this patient group, with respect to monitoring, testing, and training, are detailed here.