Heart failure.

Two million or more Americans have congestive heart failure (CHF), and the 400,000 new cases that occur yearly require over 900,000 hospitalizations each year.[1,2] In addition, based on years of cardiovascular data compiled in Framingham, Mass, there appears to be a 1% prevalence of CHF in individuals aged 50 to 59 years.[3] The incidence of CHF increases with advancing age to approximately 10% of people aged 80 to 89 years.[3] Because of the increasing age of the American population and newer medications and technologies that have increased survival at the expense of increased cardiovascular morbidity, the population of patients with CHF is markedly increasing.[4] In view of this, many individuals with a wide variety of heart and lung diseases will very likely develop CHF at some time during their lives,[5,6] manifesting itself as pulmonary congestion or edema.[1]

The purposes of this article are to describe the pathophysiology and clinical manifestations of CHF and to review the important contributions physical therapists can make in treating patients with CHF.

Pathophysiology of Congestive Heart Failure

Causes of Congestive Heart Failure

Many of the signs and symptoms of CHF are the result of a "sequence of events with a resultant increase in fluid in the interstitial spaces of the lungs, liver, subcutaneous tissues, and serous cavities."[7(p471)] Congestive heart failure is often described as a syndrome in which pathophysiologic and compensatory mechanisms act upon the body to maintain an adequate ejection of blood from the left ventricle each minute (cardiac output) to the body's organs and tissues (cardiac index).

The primary cause of CHF is cardiac muscle dysfunction. Cardiac muscle can become dysfunctional for many reasons (Tab. 1). The conditions shown in Table 1 have the potential to impair the heart's ability to pump blood or for the ventricles to accept blood.7 Of these conditions, cardiomyopathy, congenital abnormalities, renal insufficiency, and aging are more commonly associated with chronic heart failure, whereas the other conditions tend to cause acute CHF. Acute and chronic heart failure can be more specifically described as either forward or backward, right-sided or left-sided, low-output or high-output, or systolic or diastolic heart failure.[7]

Table 1.
Causes of Cardiac Muscle Dysfunction(a)

1. Hypertension
2. Coronary artery disease (myocardial infarction/ischemia)
3. Cardiomyopathy
4. Cardiac dysrhythmias
5. Heart valve abnormalities and congenital or acquired heart
disease
6. Pericardial effusion/myocarditis
7. Pulmonary embolus/pulmonary hypertension
B. Renal insufficiency
9. Spinal cord injury
10. Aging

(a)"Adapted with permission from Cahalin LP. Cardiac muscle
dysfunction. In:
Hillegass E, Sadowsky HS, eds. Essentials of Cardiopulmonary
Physical Therapy.
Philadelphia, Pa: WB Saunders Go; 1993:124.

Types of Congestive Heart Failure

The terms "right-sided CHF" and "left-sided CHF" simply describe which side of the heart is failing, as well as the side initially affected and behind which fluid tends to localize. For example, left-sided CHF is frequently the result of left ventricular damage (eg, myocardial infarction, hypertension, aortic valve disease), which causes fluid to accumulate behind the left ventricle. This, in turn, produces an accumulation of fluid in the lungs, liver, abdomen, and ankles (because of the backward movement of blood).[7] In right-sided CHF, fluid backs up behind the right ventricle and produces an accumulation of fluid in the abdomen and ankles.[7] The backward movement of blood in right- and left-sided CHF is due to increased pressure in the chambers of the heart and produces backward CHF. Forward CHF is the result of a poor cardiac output. Both forward and backward CHF occur in most patients with chronic CHF.[7]

Low-output CHF is frequently associated with heart failure and is the result of a low cardiac output at rest or during exertion.[7] High-output CHF usually results from a volume overload, as occurs during pregnancy or with thyrotoxicosis (overactivity of the thyroid gland such as with Graves' disease) or renal insufficiency.[7-9] Although the term "high-output" implies a greater cardiac output, the output is still lower than it was before CHF developed.

"Systolic CHF" and "diastolic CHF" are perhaps the most informative and useful descriptors because optimal cardiac performance is dependent on proper systolic and diastolic function.[7] The impaired contraction of the ventricles during systole that produces an inefficient expulsion of blood is termed "systolic heart failure."[7] Diastolic CHF is associated with an inability of the ventricles to readily accept the blood ejected from the atria during diastole.[7] Both types of CHF often occur simultaneously. For example, after a massive anterior myocardial infarction, the anterior wall of the left ventricle fails to contract adequately (systolic heart failure) and may lead to diastolic CHF when the infarcted area is replaced with nondistensible fibrous scar tissue.

Pathophysiologic Processes

The pathophysiologic events associated with CHF appear to be due to the effects of nine independent, yet interrelated, systems (Tab. 2, Fig. 1). The systolic or diastolic dysfunction that frequently leads to CHF often produces a series of events that are due primarily to a reduction in cardiac output. A reduction in cardiac output may initially be well-tolerated because of the body's compensatory mechanisms. As the cardiac output decreases further, however, because of the body's inability to compensate for cardiac muscle dysfunction or because of increased physical activity, a threshold is reached, at which point CHF ensues with resultant effects on the systems described.[7]

Table 2.
Organs and Organ Systems Affected by Congestive Heart Failure

Organ System              Effects

Cardiovascular            Decreased myocardial
                          performance, with subsequent
                          peripheral vascular
                          vasoconstriction to increase
                          venous return
                               [down arrow]
Pulmonary                 Pulmonary edema because of a
                          "back up" of blood due to poor
                          cardiac performance and fluid
                          overload
                               [down arrow]
Renal                     Water retention because of
                          decreased cardiac output
                               [down arrow]
Neurohumoral              Increased sympathetic stimulation
                          that eventually desensitizes the
                          heart to [beta.sub.1]-adrenergic-receptor
                          stimulation and
                          decreases the heart's inotropic
                          effect
                               [down arrow]
Musculoskeletal           Skeletal muscle wasting and
                          possible skeletal muscle
                          myopathies as well as
                          osteoporosis from inactivity or
                          other accompanying diseases
                               [down arrow]
Hematologic               Possible polycythemia, anemia,
                          and hemostatic abnormalities
                          because of a reduction in
                          oxygen transport,
                          accompanying liver disease, or
                          stagnant blood flow in the
                          heart's chambers because of
                          poor cardiac function
                                [down arrow]
Hepatic                   Possible cardiac cirrhosis from
                          hypoperfusion due to an
                          inadequate cardiac output or
                          hepatic venous congestion
                                [down arrow]
Pancreatic                Possible impaired insulin secretion
                          and glucose tolerance as well as
                          the source of a possible
                          myocardial depressant factor
                                [down arrow]
Nutritional/biochemical   Anorexia that leads to malnutrition
                          (protein-calorie and vitamin
                          deficiencies) and cachexia

In CHF, the reduction in cardiac output stimulates the sympathetic nervous system to increase peripheral vascular vasoconstriction to increase venous return.[7] This baroreceptor-mediated reflex occurs in an attempt to improve the decreasing cardiac output and cardiac index. Unfortunately, this reflex often worsens the cardiac output by increasing the amount of blood in poorly contracting or filling ventricles (preload) and the amount of work imposed on the heart because of the increased peripheral vascular vasoconstriction (afterload). The increased blood in the ventricles increases the pressures in the chambers of the heart and drives blood backward into the lungs (producing pulmonary edema) and other areas (often producing the characteristic jugular venous distention and peripheral edema of CHF). The confounding effects of renal fluid retention, increased neurohumoral activity, deconditioning, and other musculoskeletal abnormalities, as well as abnormal hematologic, hepatic, pancreatic, and biochemical function, further impair cardiac performance and the exercise tolerance of patients with CHF.[7]

The inability to exercise or perform more than minimal functional activity and the pathophysiologic processes associated with CHF appear to greatly affect the skeletal muscles of patients with CHF. The skeletal muscles of patients with CHF have been observed to have a decrease in the average diameters of the type I and type II fibers, selective atrophy of type II fibers, pronounced nonselective myopathy and hypotrophy of type I fibers, increased intracellular acid phosphatase activity, and increased intracellular lipid accumulation.[10,11] Although it is unclear whether the etiology of these changes is primary (due to cardiac and skeletal muscle myopathy) or secondary (due to chronic CHF), the changes suggest that skeletal muscle fatigue in patients with CHF is at least in part due to intracellular acidosis and phosphocreatinine depletion as well as decreased skeletal muscle strength (by approximately 50%).[10-12]

The skeletal muscle abnormalities and the pathophysiologic processes described produce observable and measurable signs and symptoms that can be used to assist physical therapists in determining realistic and obtainable goals. The characteristic signs and symptoms of CHF occur when the heart's compensatory mechanisms are inadequate.[7]

Characteristics of Congestive Heart Failure

The characteristic signs and symptoms of CHF arc listed in Table 3. Identification of several of the signs and symptoms frequently suggests the presence of CHF, but radiologic and occasionally laboratory findings are usually needed to confirm the diagnosis and provide baseline from which to evaluate therapy.[6]

Table 3.
Characteristic Signs and Symptoms of Congestive Heart Failure(a)

Dyspnea
Tachypnea
Paroxysmal nocturnal dyspnea
Orthopnea
Peripheral edema
Cold, pale, and possibly cyanotic extremities
Weight gain
Hepatomegaly
Jugular venous distention
Crackles (rales)
Tubular breath sounds and consolidation
Presence of an [S.sub.3] heart sound
Sinus tachycardia
Decreased exercise tolerance or physical work capacity

(a)"Adapted with permission from Cahalin LP. Cardiac muscle
dysfunction. In:
Hillegass E, Sadowsky HS, eds. Essentials of Cardiopulmonary
Physical Therapy.
Philadelphia, Pa: WB Saunders Co; 1993:128.

Radiologic Findings in Congestive Heart Failure

Radiologic evidence of CHF is dependent on the size and shape of the cardiac silhouette (evaluating left ventricular end-diastolic volume) as well as the presence of interstitial, perivascular, and alveolar edema (evaluating fluid in the lungs).[7] Interstitial, perivascular, and alveolar edema are the radiologic hallmarks of CHF and generally occur when pulmonary capillary pressure (which reflect the left ventricular end-diastolic pressure) exceed 20 to 25 mm Hg.[7] Pleural effusions (parenchymal fluid accumulations) and atelectasis (collapsed lung segments) also may be present.

Laboratory Findings in Congestive Heart Failure

Proteinuria; elevated urine specific gravity, blood urea nitrogen (BUN), and creatinine levels; and decreased erythrocyte sedimentation rates (because of decreased fibrinogen concentrations resulting from impaired fibrinogen synthesis) are associated with CHF.[7] Occasionally, arterial partial pressure of oxygen ([PaO.sub.2]) and oxygen saturation levels will be reduced, and arterial partial pressure of carbon dioxide ([PaCO.sub.2]) levels will be elevated.[13] Catecholamine levels (eg, norepinephrine) may be elevated because of an overactivated sympathetic nervous system. Liver enzymes (serum glutamic oxaloacetic transaminase, alkaline phosphatase, and so on) are often elevated, and hyperbilirubinemia commonly occurs, resulting in subsequent jaundice.[7] Serum electrolytes are generally normal, but individuals with chronic CHF may demonstrate hyponatremia due to activation of the atrial natriuretic peptide system or rigid sodium restriction and diuretic therapy. Hypokalemia may occur as a result of aggressive diuretic therapy.[7] Hyperkalemia may occur for several reasons, but it is most often due to a marked reduction in the glomerular filtration rate (especially if individuals are receiving a potassium-retaining diuretic) or to overzealous potassium supplementation (when a non-potassium-retaining diuretic is used).[7]

Patients with CHF may be prescribed anticoagulant drugs (eg, heparin, Coumadin) to decrease the likelihood of embolus formation due to retention of blood in the ventricles. Frequent adjustments in anticoagulant drugs and other medical therapy are made based on assessment of prothrombin time and partial prothrombin time.[7]

Symptoms of Congestive Heart Failure

Dyspnea. Dyspnea is probably the most common finding associated with CHF and is frequently the result of poor gas transport between the lungs and the cells of the body. Poor gas transport at the lungs is often due to excessive blood and extracellular fluid in the alveoli, producing a shunt that is "characterized by a reduction of vital capacity as a consequence of the replacement of the air in the lungs with blood or interstitial fluid or both."[7](p476) The reduction in vital capacity and the potential reduction in oxygenation may produce easily provoked dyspnea or, in severe cases of CHF, dyspnea at rest. Poor ventilatory muscle strength and endurance also may be partly responsible for the dyspnea of individuals with chronic CHF.[14-16]

Paroxysmal nocturnal dyspnea. Another common complaint of individuals with CHF is paroxysmal nocturnal dyspnea, in which sudden, unexplained episodes of shortness of breath occur at night, usually after patients with CHF assume supine positions to sleep.7 After a period of time in a supine position, excess fluid fills the lungs, fluid that earlier in the day was in the lower extremities because of upright positions and activities. When fluid is in the lower extremities, it allows for more effective ventilation and perfusion of the lungs (correcting the ventilation-perfusion mismatch). When upright, the effects of gravity keep the lungs relatively fluid-free, depending on the degree of CHF (which, if severe, would fill the lungs even in upright positions). Individuals with paroxysmal nocturnal dyspnea frequently place the head of the bed on blocks or sleep with more than two pillows, and they often find it difficult to breath with fewer than two pillows. Patients with marked CHF often assume a sitting position to sleep and are sometimes found sleeping on a recliner instead of a bed.

Orthopnea. The term "orthopnea" describes the development of dyspnea in the recumbent position.7 Sleeping with two or more pillows puts the body in a more upright position and enables gravity to draw fluid from the lungs and to distribute the fluid to the more distal parts of the body. The severity of CHF can sometimes be inferred from the number of pillows used to prevent orthopnea. Thus, the terms "two-pillow orthopnea," "three-pillow orthopnea," "four-pillow orthopnea," and so forth indirectly allude to the severity of CHF (four-pillow orthopnea suggests more severe CHF than two-pillow orthopnea).

Signs Associated With Congestive Heart Failure

Breathing patterns. A rapid respiratory rate at rest, characterized by quick and shallow breaths, is common in patients with CHF. Such tachypnea is apparently not due to hypoxemia (which may or may not be of sufficient magnitude), but rather to stimulation of interstitial J-type receptors (stretch receptors in the interstitium).[13] The quick, shallow breathing of tachypnea may serve to assist the pumping action of the lymphatic vessels, thus minimizing or delaying the increase in in terstitial fluid.[13]

In many patients with CHF, there is extreme dyspnea after a change in position, most frequently when the person moves from a sitting to a standing position. This response appears to be occasionally but inconsistently associated with orthostatic hypotension and increased heart rate activity.[13,17] Orthostatic hypotension and dyspnea (tachypnea) may be the result of (1) lower-extremity muscle deconditioning, producing a pooling of blood in the lower extremities when standing, with a subsequent decrease in blood flow to the heart and lungs, or (2) attenuation of the atrial natriuretic factor (release of a regulatory hormone from the atria because of elevated atrial pressure, which produces a brisk diuresis to reduce fluid volume), which may suggest advanced atrial distention and poor left ventricular function.[17] The more pronounced the dyspnea is, the more severe the CHF will be, and vice versa. This clinical sign can be timed (time for the dyspnea to subside) and measured (blood pressure and heart rate) to document progress or deterioration in patient status.[17]

A breathing pattern characterized by waxing and waning depths of respiration with recurring periods of apnea also occurs in patients with CHF. "Cheyne-Stokes respiration," as it is called, has been observed in individuals with central nervous system damage (particularly those in comas), but it also occurs in individuals with CHF.[7]

Rales (crackles). Pulmonary rales, now referred to as crackles, are abnormal breath sounds that, if associated with CHF, occur during mid to late inspiration and represent the movement of fluid in the alveoli and subsequent opening of airways that were closed because of excessive fluid.7 Crackles are frequently heard at both lung bases in individuals with CHF (and sound like hair near the ears being rubbed between two fingers), but they may extend upward depending on the patient's position or severity of CHF. Therefore, auscultation of all lobes should be performed in a systematic manner, allowing for bilateral comparison.

The importance of the presence and magnitude of crackles was addressed in 1967 and provided data for the Killip classification of patients with acute myocardial infarction.[18] Classes I through IV were developed to categorize the approximate mortality associated with less severe CHF (classes I and II) and more severe CHF (classes Ill and IV). Individuals with crackles extending over more than 50% of the lung fields were observed to have a far poorer prognosis.[18]

Heart sounds. Heart sounds can provide a great deal of information regarding cardiopulmonary status, but unfortunately are forgotten in most physical therapy examinations. The normal heart sounds include a first heart sound ([S.sub.1]), representing closure of the mitral ([M.sub.1]) and tricuspid ([T.sub.1]) valves, and a second sound ([S.sub.2]), representing closure of the aortic (A2) and pulmonic ([P.sub.2]) _valves. The most common abnormal heart sounds of CHF are the third ([S.sub.3]) and fourth ([S.sub.4]), which occur at specific times in the cardiac cycle as a result of abnormal cardiac mechanics. The [S.sub.3] heart sound is normal in children, young adults, and pregnant women, but in patients with heart disease it is suggestive of a stiff, noncompliant ventricle and is considered the hallmark of CHF.[19,20] The [S.sub.3] heart sound occurs during early diastole, and [S.sub.4] is a presystolic sound.

Splitting of [S.sub.1] and [S.sub.2] also is occasionally heard and represents the closure of both the mitral and tricuspid valves in [S.sub.1] and the aortic and pulmonic valves in [S.sub.2]. Differentiating between a split [S.sub.1] and [S.sub.4] or a split [S.sub.2] and S3 can be done by alternating light and firm pressure with the bell of the stethoscope. The [S.sub.3] and [S.sub.4] are lower-frequency sounds and thus are heard best with light pressure using the bell of the stethoscope, whereas firm pressure on the bell accentuates higher-frequency sounds and diminishes lower-frequency sounds. Therefore, if with light pressure an extra sound is heard and the sound disappears with firm pressure, it is an [S.sub.3] or [S.sub.4]; a split [S.sub.1] or [S.sub.2] will become louder with firm pressure.

Different areas of auscultation also will produce differences in the heart sounds. The four main areas, which are typically named for the area of the heart that is best heard on the chest wall, are the aortic (base), pulmonic, atrial (apex), and tricuspid areas. In general, the mitral (apex) area yields the greatest amount of information because [S.sub.1] and [S.sub.2] are usually heard well here, and [S.sub.3] and [S.sub.4] are typically easier to identify in this area. Auscultation of all areas should be performed in a systematic manner to evaluate heart sounds.[19,20]

Peripheral edema. Peripheral edema frequently accompanies CHF, but may be absent even when patients have CHF.[7] In patients with CHF, fluid is retained because the heart's ability to maintain an adequate cardiac output is often impaired, which is detected by the pressoreceptors as a decreased volume of blood. The autonomic nervous system attempts to increase the cardiac output by decreasing the elimination of fluid from the kidneys.[21] Unfortunately, this retention of fluid compounds the problem and makes the heart work even harder, which further decreases its ability to pump. The retained fluid commonly accumulates bilaterally in the dependent extracellular spaces of the periphery.[7]

Jugular venous distention. Jugular venous distention (JVD) also results from fluid overload. As fluid is retained and the heart's ability to pump is further compromised, the retained fluid "backs up" not only into the lungs but also into the venous system, of which the jugular veins are the simplest to identify and evaluate. The external jugular vein lies medial to the external jugular artery and in a 45-degree semirecumbent position can be readily measured for signs of distention (although individuals with marked CHF may demonstrate JVD in all positions). The highest point of visible pulsation is determined as the trunk and head arc elevated, and the vertical distance between this level and the level of the sternal angle of Louis is recorded, as well as the angle of elevation of the patient.[19,22]

Pulsus alternans. Pulsus alternans (mechanical alteration of the femoral or radial pulse characterized by a regular rhythm and alternating strong and weak pulses) can frequently be used to identify severely depressed myocardial function and CHF in general. This diagnostic test is performed using light pressure, with the patient's breath held in mid-expiration (to avoid the superimposition of respiratory variation on the amplitude of the pulse).[19] Sphygmomanometry can more readily detect this phenomenon, which commonly demonstrates [greater than or equal to]20 mm Hg of alternating systolic blood pressure. Characteristically, if pulsus alternans exists, a [less than or equal to]20-mm Hg decrease in systolic blood pressure occurs during breath-holding because of increased resistance to left ventricular ejection. A difference exists between pulsus alternans and pulsus paradoxus, the latter of which is characterized by a marked reduction of systolic blood pressure [greater than or equal to]20 mm Hg) and strength of the arterial pulse during inspiration.[19]

Pulsus paradoxus. Pulsus paradoxus also can be detected by sphygmomanometry and is represented by a [greater than or equal to]20-mm Hg decrease in systolic blood pressure during inspiration.[19] Pulsus paradoxus is occasionally seen in CHF but is more frequently associated with cardiac tamponade and constrictive pericarditis. This phenomenon is primarily due to increased venous return and right heart volume during inspiration, which bulges the interventricular septum into the left ventricle, thus decreasing the amount of blood present in the left ventricle and the amount of blood ejected from it.19

Weight gain. As fluid is retained, total body fluid increases, as does total body weight. Fluctuations of a few pounds from day to day is usually considered normal, but an increase of 2 lb (0.9 kg) or more per day suggests CHF in a patient with cardiac muscle dysfunction.[7] Measurement of body weight using the same scale at approximately the same time of day with similar clothing is valuable in tracking patients with CHF.

Cold, pale, and cyanotic extremities. Occasionally, the extremities of patients with CHF will be cold and will appear pale and cyanotic. This is due to the overactivation of the sympathetic nervous system, which decreases peripheral blood flow because of increased peripheral vascular vasoconstriction.[7]

Sinus tachycardia. Sinus tachycardia or other tachydysrhythmias may occur in patients with CHF as the pressoreceptors and chemoreceptors of the body detect an abnormal cardiac output and potentially reduced oxygen levels, respectively.7 The sympathetic nervous system attempts (via increased heart rate) to increase the cardiac output and oxygen to the peripheral tissues where it is needed. Unfortunately, these increases, much like the message to the kidneys to retain fluid, only compound the problem and make the heart work even harder, which further deteriorates the heart's pumping ability.

Decreased exercise tolerance. Decreased exercise tolerance is the culmination of the pathophysiologic and compensatory events associated with CHF. When an individual, at rest, becomes short of breath, gains weight, and develops a rapid heart rate, the ability to exercise is dramatically decreased. This phenomenon has repeatedly been observed in patients with CHF.[7]

The methods of measuring exercise tolerance in patients with CHF have improved in the past few years, but many clinicians continue to use the criteria set forth by the New York Heart Association (NYHA) in 1964.23 These criteria categorize patients into one of four classes depending on the development of symptoms and the amount of effort required to provoke the symptoms. Patients in class I have no limitation in ordinary physical activity, whereas patients in class IV are unable to carry on any physical activity without discomfort. Classes 11 and Ill are characterized by slight limitation and marked limitations in physical activities, respectively.

The Minnesota Living with Heart Failure Questionnaire is a comprehensive instrument designed to measure patients' perceptions of the effects of CHF on their lives and has been found to be correlated to the NYHA classification.[24] Several recent trials have used this 21-item, self-administered questionnaire to measure physical, socioeconomic, and psychologic impairments that patients relate to their CHF.[25,26]

Measurement of Exercise Tolerance

Traditional Exercise Testing

Exercise tolerance in patients with CHF is usually evaluated via traditional exercise testing.[27-33] Measurement of peak oxygen uptake, anaerobic threshold, and the change in oxygen consumption to change in work rate above the anaerobic threshold are methods that appear to be useful and relatively reliable in determining cardiorespiratory function, prognosis, and survival in patients with CHF.[27-33] Measurement of peak oxygen consumption has been used as the major predictor of survival in patients With CHF [31,32] and is used to determine the appropriateness and timing of cardiac transplantation.33 Patients with a peak oxygen consumption of <14 mL/kg/min are often considered to be ideal candidates for cardiac transplantation because of their poor survival rate, whereas patients with a peak oxygen uptake of >14 mL/kg/min are frequently considered too "healthy" for transplantation and have a greater rate of survival.[33]

Nontraditional Exercise Testing

Unfortunately, many physical therapists do not have access to equipment to measure respiratory gases. Assessing symptoms, heart rate and rhythm, blood pressure, respiratory rate, and oxygen saturation at specified work loads during physical therapy sessions can provide important and useful information that can be used to compare patient responses from day to day and to establish a progressive exercise conditioning program. A standardized evaluation such as the 6-minute walk test also is useful for such comparisons.[25] Through these types of assessments, progress or deterioration can be documented and appropriate therapy can be implemented.

Cahalin and colleagues[34] recently found that the 6-minute walk test effectively predicts peak oxygen consumption and early survival in patients with CHF. Univariate and multivariate analysis of 24 patient characteristics identified the 6-minute walk test distance ambulated as the strongest predictor of peak oxygen consumption and age-gender-adjusted peak oxygen consumption (Figs. 2 and 3). The model-predicted peak oxygen consumption and the model-predicted percentage of predicted peak oxygen consumption using information obtained from the 6-minute walk test correlated well to the observed peak oxygen consumption and the observed percentage of predicted peak oxygen consumption (r=.81 and .71, respectively) but accounted for only 65% and 51% of the variability, respectively.[34] The distance ambulated during the 6-minute walk test also was helpful in evaluating short-term (6-month) survival. Forty percent of patients ambulating <300 m died or were admitted to a hospital for inotropic or mechanical support as a bridge to transplantation, compared with only 12% of those patients ambulating >300 m (Fig. 4).[34] The 6-minute walk test may provide an inexpensive, simple method for assessing functional capacity and short-term prognosis in patients with advanced heart failure.

Exercise Training in Congestive Heart Failure

Traditional Exercise Training

Exercise training of patients with CHF due to systolic or diastolic dysfunction and of patients with cardiac muscle dysfunction has been shown to produce improvements in exercise tolerance and many other variables (Tab. 4).[35-56] One of the earliest studies evaluating the effects of exercise on CHF was done by a team of physicians and physical therapists who studied patients with mild CHF (left ventricular ejection fraction of [less than or equal to]40%).[35] The subjects were able to increase their exercise duration (mean increase from 6.4 to 7.4 minutes) without change in heart rate or blood pressure at maximal exertion after a 12- to 42-month exercise training program. Resting heart rates were decreased (from 71 to 63 beats per minute [bpm]) as well as heart rates during standardized submaximal work (from 117 to 109 bpm), Cardiac catheterization revealed no change in resting left ventricular ejection fraction, left ventricular end-diastolic pressure, or left ventricular end-diastolic volume, all of which further suggested the importance of peripheral adaptation in skeletal muscle.[35] Pulmonary artery pressures were slightly lower after the exercise training.

[TABULAR DATA 4 OMITTED]

Recent investigations into the issue of CHF and exercise have focused on exercise tolerance and anaerobic metabolism. Many patients with CHF have lower anaerobic thresholds, and the resultant anaerobic metabolism becomes the limiting factor (because of lactate acidosis) for further exercise. The lower anaerobic threshold may be due in part to reduced blood flow to exercising muscles in patients with CHF and is probably the reason that these patients were observed to have a 40% to 50% lower exercise capacity than a group of control subjects.[39] Some Studies[39-43] have shown that exercise training of patients with mild to severe CHF improves the oxidative capacity of skeletal muscle and reduces lactate production, thereby increasing exercise capacity.

Sullivan et al[39] evaluated the effects of exercise training in patients with chronic CHF due to left ventricular dysfunction (ejection fraction of 24%[+ or -]10%). Twelve patients with stable symptoms underwent a 4- to 6-month training program of stationary bicycling, walking, jogging, and stair climbing 4 hours per week at approximately 75% of peak oxygen consumption. After the training period, central hemodynamic and peripheral metabolic adaptations to heart failure were improved, which produced an increased exercise tolerance and peak oxygen consumption. Four complications (one sudden death unrelated to exercise, one orthopedic injury, one progressive CHF, and one patient with prolonged fatigue) were observed during the training period.[39]

Similar results but without complication were observed by Coats et al,[56] who evaluated the effects of physical training in 11 patients with chronic heart failure due to ischemic heart disease. The subjects had very low ejection fractions (mean of 19%) and underwent 8 weeks of home-based exercise training (5 days per week for 20 minutes at 70%-80% of maximal heart rate) and 8 weeks of activity restriction in this physician-blind, random-order, crossover trial. Exercise training increased exercise duration (from 14.2 minutes to 16.8 minutes) and peak oxygen consumption (from 14.3 mL/kg/min to 16.7 mL/kg/min) and reduced heart rates at submaximal work loads, rate-pressure products, and patient-rated symptom scores.[56] A follow-up study by Coats et al43 of six additional patients demonstrated similar findings as well as improved cardiac output at submaximal exercise (5.9-6.7 L/min) and at peak exercise (6.3-7.1 L/min), systemic vascular resistance, and autonomic nervous system activity (a 51% increase in parasympathetic activity and a 21% decrease in sympathetic activity, as well as a 16% decrease in norepinephrine). The absence of complications (although the patients were provided sophisticated pulse-rate monitors, cycle ergometers, and thorough exercise instructions) and the improvements in patients with markedly reduced left ventricular ejection fractions are two very important findings.

Improvements without major complications were found in the first study conducted to evaluate the effects of exercise training in patients with CHF due to diastolic rather than systolic dysfunction.[44] In this controlled study of 55 patients (mean left ventricular ejection fraction of 27%) with idiopathic cardiomyopathy (n = 18) and ischemic cardiomyopathy (n = 37), improvements in work load, peak oxygen consumption, anaerobic threshold, and diastolic filling were observed after 8 weeks of cycle ergometry performed for 40 minutes at 60% of peak oxygen consumption, three times per week.[44]

It is surprising that no studies of weight training in patients with CHF have been published. The results of simple weight training with elderly subjects[57] suggest that similar weight training in elderly patients and possibly even younger patients with CHF may be very helpful. Future investigation of weight training with patients with CHF is needed.

Nontraditional Exercise Training

Ventilatory muscle training. Ventilatory muscle training has been shown to be helpful for patients with pulmonary disease by increasing ventilatory muscle, force and endurance and by decreasing dyspnea, need for medications, emergency department visits, and number of hospitalizations.[58,59] Recently, individuals with chronic CHF have been found to have poor ventilatory muscle strength,[14-16] and one study[60] has demonstrated improvements in ventilatory muscle force and endurance, submaximal and maximal exercise capacity, and dyspnea after 3 months of aggressive ventilatory muscle training in eight patients with chronic CHF.

Cahalin et al[61] observed improvements in maximal inspiratory and expiratory pressures and degree of dyspnea as early as 2 weeks after ventilatory muscle training was initiated with the Threshold inspiratory muscle trainer(*) at 20% of maximal inspiratory pressure, three times a day, for 5 to 15 minutes. The improvement in ventilatory muscle strength was associated with less dyspnea at rest and with exercise. The authors did not, however, evaluate the effects of ventilatory muscle training on ventilatory muscle endurance, which may be the most important effect of ventilatory muscle training. Improvement in ventilatory muscle force may decrease the dependency, impairment, and possibly even cost associated with chronic CHF. Increased ventilatory muscle force also may enhance early postoperative recovery in patients undergoing cardiac transplantation or cardiac surgery.

Exercise training during continuous intravenous dobutamine infusion. Many patients with severe CHF are hospitalized for prolonged periods, receiving continuous intravenous (IV) dobutamine infusion for inotropic support (to improve cardiac muscle contraction) while awaiting cardiac transplantation.[62] It is becoming common practice for patients with severe CHF to occasionally be hospitalized for IV dobutamine infusion ("dobutamine holiday") to transiently improve myocardial performance.[63] Many patients are being sent home with portable IV dobutamine pumps, and their physical activity is therefore less restricted due to the absence of large IV pumps.[64] Exercise training during continuous IV dobutamine infusion, however, has received little attention.[65]

In view of these practices, my colleagues and I sought to investigate the safety and effects of increased physical activity and exercise training in 40 patients (34 men and 6 women, mean age [[+ or -]SD]=49 [+ or -]8 years) with severe CHF (mean left ventricular ejection fraction =20%[+ or -]6%) (LP Cahalin, TG Disalvo, MJ Semigran, GW Dec; unpublished data; January 1996). The majority of patients were hospitalized, awaiting cardiac transplantation and receiving a mean dosage of 200 [mu]g of IV dobutamine as well as standard medical management of CHF (digoxin, diuretics, and angiotensin-II converting enzyme inhibitors). No complications occurred during more than 1,000 patient-hours of exercise training, and no increase in baseline ectopy was observed during exercise. The exercise was gradually progressed from sitting active-range-of-motion exercises to bicycling and walking at a Borg rating of perceived exertion of 3/10 (representing a mean heart rate of 120 bpm, 70% of age-predicted maximal heart rate) for a mean of 20 minutes, five times per week. Further investigation of exercise training in this patient population is needed.

Continuous positive airway pressure. Continuous positive airway pressure (CPAP) and bi-level positive air-way pressure (BiPAP) have been observed to improve the exercise performance of patients with obstructive lung disease.[66-68] Despite the lack of research on the effects of CPAP or BiPAP on the exercise performance of patients with CHF, resting myocardial performance has repeatedly been observed to improve with CPAP in patients with CHF[69-71] and in patients with CHF and coexistent obstructive or central sleep apnea.[72-74] The beneficial effect of CPAP on cardiac performance is postulated to be due to increased intrathoracic pressure, which reduces cardiac preload (by impeding cardiac filling) and afterload (by reducing left ventricular transmural pressure).[69,70] Increased intrathoracic pressure also unloads the inspiratory muscles, which may increase lung compliance.[71] The effects of CPAP or BiPAP on exercise performance in patients with CHF are unknown, but limited pilot work suggesting an improvement in exercise tolerance and symptoms[75] and the beneficial effects of CPAP seen at rest[69-74] indicate a need for further investigation.

Left ventricular assist devices. Improved technology has enabled patients, who otherwise were immobilized because of intra-aortic balloon pump placement or nonmobile left ventricular assist device (LVAD) placement, to become mobile and to ambulate with a cart that provides left ventricular assistance via a portable pneumatic pump.[76] A recent investigation of the safety and benefits of exercise conditioning in patients awaiting cardiac transplantation and using LVADs has revealed that patients can safely exercise for prolonged periods and obtain specific training effects.[77] Patients using LVADs underwent 1,173.6 hours of exercise conditioning without major complications and with only four minor complications (3.4 incidents per 1,000 patient-hours). Improvements in exercise tolerance and functional capacity continued until week 6 of conditioning, after which further improvements were minimal. The investigators suggest that delaying cardiac transplantation until 6 weeks of exercise conditioning have been performed may improve postoperative recovery and surgical success.[77] Further investigation in this area is warranted.

Guidelines for Exercise Training in CHF

The studies that demonstrated improvements in exercise tolerance and in patient symptoms were all performed differently, with varying modes, intensities, durations, and frequencies of exercise. Guidelines for exercise training of patients with CHF are difficult to implement because patient status frequently changes. Patients with decompensated (uncontrolled) CHF are typically very dyspneic with limited exercise tolerance and therefore should not begin aerobic exercise training until the CHF is compensated.[78,79] Exercise training guidelines are listed in Table 5 and include the attainment of a cardiac index of 1.8 L/min/[m.sup.2] or greater (for invasively monitored patients in the hospital) before aerobic exercise training is implemented and the maintenance of an adequate pulse pressure (not less than a 10-mm Hg difference between systolic and diastolic blood pressures) during exercise. The development of marked dyspnea and fatigue, [S.sub.3] heart sound, or crackles during exercise requires the modification or termination of exercise.

Table 5.
Exercise Training Guidelines for Patients With Congestive Heart
Failure

I. Relative criteria necessary for the initiation of an aerobic
exercise training program
  a. Compensated congestive heart failure
    1. Ability to speak without signs or symptoms of dyspnea
able to speak comfortably with a respiratory rate of <30
breaths/min)
    2. Less-than-moderate fatigue
    3. Crackles (rales) present in more than half of the lungs
    4. Resting heart rate of < 120 bpm
    5. Cardiac index of [greater than or equal to] 1.8 L/min/[m.sup.2] (for
invasively monitored patients)
    6. Central venous pressure of < 12 mm Hg (for invasively
monitored patients)

II. Relative criteria indicating a need to modify or terminate
exercise training
  a. Marked dyspnea or fatigue (eg, Borg Scale rating of
>3/10)
  b. Respiratory rate of >40 breaths/min during exercise
  c. Development of an S3 heart sound or pulmonary crackles
  d. Increase in pulmonary crackles
  e. Increase in the sound of the second component of the
second heart sound
  f. Poor pulse pressure (<10-mm Hq difference between the
systolic and diastolic blood pressures)
  g. Decrease in heart rate or blood pressure of > 10 bpm or
mm Hg, respectively, during continuous (steady-state) or
progressive (increasing work loads) exercise
  h. Increased supraventricular or ventricular ectopy
  i. Increase of > 10 mm Hq in the mean pulmonary artery
pressure (For invasively-monitored patients)
  j. Increase or decrease of >6 mm Hg in the central venous
pressure (for invasively monitored patients)
  k. Diaphoresis, pallor, or confusion

Progression of an exercise conditioning program for patients with CHF can be done as outlined in the Appendix. Although this protocol is designed for hospitalized patients, it can be applied to patients with CHF in outpatient clinics, nursing homes, and their own homes. For most patients, ambulation may be the most effective and functional mode of exercise to administer and prescribe, beginning with frequent short walks and progressing to less frequent, longer bouts of exercise. Occasionally, patients may be so deconditioned that gentle strengthening exercises, restorator cycling, or ventilatory muscle training is the preferred mode of exercise conditioning. As strength and endurance improve, patients can be progressed to upright cycle ergometry or ambulating with a rolling walker.

Such progression is based on an individualized prescription that is gradual and pyramidal in nature. Figure 5 demonstrates the importance of an exercise prescription that first utilizes the most appropriate and effective mode of exercise (such as ventilatory muscle training for those patients who are most debilitated. and dyspneic) and then utilizes the proper combination of the key elements of an exercise prescription (with emphasis placed on the intensity of exercise during the later stages of exercise conditioning). A very important aspect of an exercise prescription for patients with CHF is compliance with exercise and adequate rest periods. Rest should follow all exercise conditioning and must be considered in the pyramidal scheme of the exercise prescription.

Because dyspnea is the most common complaint of patients with CHF, the level of dyspnea or the Borg rating of perceived exertion appears to be an acceptable method for prescribing an exercise program.80 This is supported by the observation that dyspnea and exertion scales correlate well with training heart rate ranges in this patient population.[81] Therefore, a basic guideline of increasing the exercise intensity to a level that produces a moderate degree of dyspnea (eg. conversing with modest difficulty, ability to count to five without taking a breath, a Borg rating of 3/10) may be the simplest and most effective method for prescribing exercise for patients with CHF. Such a guideline also appears to be an effective method for progressing a patient's exercise prescription.[80,81] The exercise prescription of patients with CHF can be progressed when the cardiopulmonary response to exercise is adaptive (Tab. 5) and work loads that previously produced moderate dyspnea (eg, Borg rating of 3/10) produce mild dyspnea or less (eg, Borg rating of [greater than or equal to] -2/10).

This same principle appears to be useful for determining patient appropriateness for entry into an outpatient cardiac rehabilitation program.81 Determining the suitability of patients with CHF for exercise training in cardiac rehabilitation programs appears to depend on the patient performing any level of exertion for several minutes without excessive dyspnea or fatigue and without adverse hemodynamic effects, dysrhythmias, or evidence of myocardial ischemia.[81]

The performance of exercise without excessive dyspnea or fatigue and the performance of exercise without an adverse cardiopulmonary response are supported by two important studies of patients with left ventricular dysfunction.[82,83] Arvan[82] demonstrated that to obtain training effects, patients with left ventricular dysfunction must not exhibit electrocardiographic signs of myocardial ischemia. Jugdutt et al[83] evaluated which patients with left ventricular dysfunction (due to acute anterior myocardial infarctions) would benefit most from exercise training. If left ventricular dysfunction was below a specific echocardiographic index of contractility and exercise training was performed, left ventricular function actually deteriorated, decreasing the ejection fraction and functional capacity.[83]

Counseling, Education, and Lifestyle Modifications for Patients With Congestive Heart Failure

Counseling and education have been observed to improve patient outcomes and decrease unnecessary hospitalizations in patients with CHF.[84] Patients with CHF benefit most when educated about sodium and fluid restrictions and other dietary issues as well as the pathophysiology of CHF, medications, signs and symptoms of worsening CHF, and activity or exercise.[84]

Conclusion

Physical therapists can provide programs that profoundly improve the exercise tolerance and functional status of patients with CHF. Medical treatment can be more objectively implemented by utilizing information obtained during physical therapy assessments and treatments. Simple tests implemented by a physical therapist, such as the 6-minute walk test, may be helpful in predicting peak oxygen consumption and early survival as well as in implementing a proper exercise conditioning program for patients with advanced heart failure.

Aerobic exercise training of patients with compensated CHF can produce improvements in cardiovascular and muscular function. Such improvements can be achieved with an individualized, carefully progressed exercise prescription that is implemented in a pyramidal manner with emphasis on the most appropriate and effective mode of exercise and the proper combination of the key elements of the exercise prescription. The exercise prescription of patients with CHF can be progressed when their cardiopulmonary response to exercise is adaptive and work loads that previously produced moderate dyspnea (eg, Borg rating of 3/10) produce mild dyspnea or less (eg, Borg rating of [less than or equal to] 2/10).

The material presented in this article demonstrates the widespread occurrence of CHF and its potential implications for physical therapy. Physical therapists will undoubtedly encounter and continue to be challenged by patients with CHF.

Acknowledgments

Sincere appreciation is extended to H Steven Sadowsky, PT, RRT, CCS, for assistance with the graphic depiction of material in this article and to Randolph G Ice, PT, CCS, Raymond L Blessey, PT, and David H Nielsen, PhD, PT, for their persistent clinical inquisitiveness.

[Figures 1 to 5 ILLUSTRATION OMITTED]

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LP Cahalin, PT CCS, is Clinical Specialist, Physical Therapy Services, Massachuetts General Hospital, Bigelow 858, Boston, MA 02114 (USA)