Incidence of Heart Failure
Heart failure is a major public health problem. About 550,000 new cases occur each year in the United States, and in 1999, heart failure contributed to approximately 287,200 deaths. Approximately 1.7 % to 2% of the adult population in the United States carries a diagnosis of congestive heart failure. Over 12 million office visits and 2.5 million hospitalizations as the result of heart failure occurred in 2001. It is estimated that currently, one in five Americans over the age of 40 will develop heart failure.

The incidence of heart failure developing in women with just hypertension and without myocardial infarct is slightly less (1:6). In contrast, the risk of men without a heart attack developing heart failure is nearly 1:9. Statistics indicate that even modest hypertension (under 140/90) is a major risk in both women (12%) and men (14.8%). When age-adjusted variables are equalized, slightly more men than women develop heart failure, but more women than men die of heart failure.( Petrie, Mark C. BSc, et al. Failure of Women's Hearts. Circulation. 1999;99:23342341.) (2002 Heart and stroke statistical update. Dallas: American Heart Association, 2001.)

The incidence of heart failure more than doubles each decade from age 45 to 75 years, and the disease represents the most common medical discharge diagnosis for patients over age 65 years (Massie BM, Shah NB. Evolving trends in the epidemiologic factors of heart failure: Rationale for preventive strategies and comprehensive disease management. Am Heart J. 1997;133(6):703-712.)

Historical perspective
From a historical perspective, one should realize that for many years, clinicians stated that patients with congestive heart failure should not be physically challenged. They refused to prescribe exercise for patients with the heart failure diagnosis. Heart failure was considered by many to be a literal death sentence and exercise would only hasten their demise. Bedrest was considered the best remedy at augmenting diuresis in those pre-loop diuretic days. (McHenry, MM. Medical screening of patients with coronary heart disease: criteria for entry into exercise conditioning programs. American Journal of Cardiology, 1974: 33: 752-56.)

Fortunately, in the 1980s, definitive studies showed that exercise could improve the quality of life, if not prolong the life itself. (Jensen, D, et al. Improvement in ventricular function during exercise studied with radionuclide ventriculography after cardiac rehabilitation. American Journal of Cardiology 1980; 46: 770-777) (Sullivan, MJ, Higginbotham, MB, Cobb, FR: Exercise training in patients with severe left ventricular dysfunction; hemodynamic and metabolic effects. Circulation 1988; 78: 506-15) (Sullivan, MJ, Higginbotham, MB, Cobb, FR: Exercise training in patients with chronic heart failure delays ventilatory anaerobic threshold and improves submaximal exercise performance. Circulation 1989; 79: 324-9.)

Despite numerous studies that showed improvements and benefits from exercise therapy, there was an occasional review that indicated a worsening of symptomatalogy and physiology of heart disease with exercise: (Arvin, S. Exercise performance of the high-risk acute myocardial infarction patient after cardiac rehabilitation. American Journal of Cardiology 1998, 62: 197-201) (Jugdutt, BI et al. Exercise training after anterior Q wave myocardial infarction: Importance of regional left ventricular function and topography. JACC, 1988. 12: 362-372.)

Current literature
As the 1990's progressed, cardiologists recognized the advantages of adding aerobic exercise training to their increasing pharmaceutical armament for their patients with compromise left ventricular function. Studies documented the improvement of vasodilatation and oxidation capacity in the majority of patients with heart failure, when moderate aerobic exercise was added to a regimen of diuretics, ACE inhibitors, BetaBlockers and occasionally digitalis. However, the mechanisms for the improvement were not completely understood at the cellular level.

There is now overwhelming evidence that a multi-tiered approach to the treatment of heart failure could reduce mortality by about 50 percent. Medication, life style modification, including a regular exercise program, smoking cessation, control of hypertension and weight loss as well as invasive vascular procedures have all aided in the improvement of life quality as in longevity. (Pifla IL, Apstein CS, Balady GJ, et al. Exercise and heart failure: a statement from the American Heart Association Committee on Exercise, Rehabilitation, and Prevention. Circulation. 2003; 107: 1210-1225.)

The Stages of Heart Failure - NYHA Classification
In order to determine the best course of therapy, physicians often assess the stage of heart failure according to the New York Heart Association

(NYHA) functional classification system. This system relates symptoms to everyday activities and the patient's quality of life.

The physiology of heart failure symptoms
It is easily seen that the exercise intolerance in patients with heart failure is demonstrated as significant shortness of breath at low workloads, muscle fatigue, generalize fatigue and occasionally, angina. The result of inadequate cardiac output due to a hypertrophied, dilated or stiff left ventricle is the decreased blood flow to the myocardial, pulmonary and skeletal vasculature. At rest, the already decreased stroke volume (and therefore cardiac output) is often able to just meet the oxygen needs required for the non-active lifestyle often with less than 50% of expected cardiac output as compared to a non-failure heart. As the oxygen demands increase, as with activity, the compromised ventricle is unable to meet those demands.

Heart failure results in physiological consequences as impaired myocardial contractility, elevated systemic vascular resistance, decreased peripheral vascular vasodilatation response and a reduction of the myocardial beta adrenergic receptor sites (which normally would improve tissue response). There are also a myriad of catecholamine and endothelia cell alterations that catalyst and enhance the changes. With the "normal", stroke volume impaired, there is often a hypotensive response to exercise due to the myocardial ischernia caused by the inability of the cardiac output to meet the increased needs of the myocardium.

Brief Pharmacology overview
When patients are diagnosed with heart failure, most are prescribed a diuretic, an ACE inhibitor and often a beta blocker. Controlling blood pressure and reducing the energy expended by the myocardiurn are key components in improving the symptoms of heart failure. Early diagnosis, early pharmaceutical treatment and aggressive life style modification may help to maintain a near normal cardiac output, reduce the energy needs of the myocardium,

Other frequent medications prescribed may be Digoxin, ARBs, nitrates and (if diastolic pathology is present) Calcium channel blockers. Less commonly prescribed medications include anticoagulants, antiarrhythmics, hBNP and potassium supplements.

Benefits of aerobic exercise
Since 197 1, over 25 studies have looked at the benefits of exercising patients with CHF. Changes in such physiological measurements as stroke volume (cardiac output), peripheral vascular endothelium, lactic acid accumulation, catecholamine release and ventilatory exchange were documented. Improvements in quality of life perception, as well as reduction in mortality were also measured.

Numerous studies did not find significant increases in the stroke volume, cardiac output or ventricular wall remodeling after participation in numerous exercise programs. Some studies did document modest improvements in stroke volume at higher workloads but the improvements were not noted at rest. Most researchers agreed that the improved in exercise tolerance was the result of the effects had on other physiologically impaired processes.

Studies that focused on the peripheral (skeletal) vasculature mechanism for clearing lactic acid, oxidative capacity and increase capillary blood flood found improvements in all three measurements after even modest exercise programs.

It is of little surprise that a reduction of circulating catecholamines (thereby reducing vasoconstriction and increased metabolic demand on the heart) were noted early in most well designed studies. Decreases in norepinephrine levels paralleled the increased mitochondrial density (increasing energy, eliminating C02 and lactic acid) and improving oxidative capacity. (Belardinelli, et al. Low intensity exercise training in patients with chronic heart failure. JACC, 26(4), 975-982).

Ventilatory exchange (V02 max) improved (example 48.6 to 78.9 L/min). Pulmonary musculature strength improved with peak exercise V02 increasing from 11.4 to 13.3 niL/kg/min. (Mancini DM, Henson D, LaManca J, et al. Benefit of selective respiratory muscle training on exercise capacity in patients with chronic congestive heart failure. (Circulation. 1995; 91: 320-329.) However, it was also noted in numerous studies that the measurable improvements in pulmonary functioning could not account for the significant improvements noted by the patients.

Quality of Life questionnaires revealed that heart failure patients who exercised on a regular basis felt that their exercise ability and for the majority of the responders, that their quality of life was also improving.

Contraindications to exercise
Patients with severe stenotic or regurgitant valvular heart disease should not participate in an exercise training program. Patients who have heart failure due to mild to moderate stenotic or regurgitant valvular disease should not be exercised. Denying entrance to an exercise program on the basis of a patient's ejection fraction percentage should not be done. In numerous studies, there is poor reliability between ejection fraction and functional capacity or survival. (Balady, GJ and Pina, IL. 1997. Exercise and Heart Failure. AHA Monograph Series. New York).

The program
Initial assessment must include a walk test that evaluates not only the heart rate and blood pressure, but also the oxygen saturation levels. Setting the exercise guidelines must follow the results of the initial evaluation. Exercise prescriptions based on heart rate may not be accurate due to a reduced chronotropic reserve and changes made to beta blocker prescriptions. A number of programs reported that the combination of BORGs and individual 02 saturation monitors were used to guide the workloads of each patient. Training effects were found beneficial with reported BORGs of 12 and 13. Anaerobic or ventilatory thresholds were reported at 13 to 15 BORGs.

Patients with heart failure may need a longer warm up period. Initially, some may need to sit during warm up for their first weeks in the class. The use of hand weights or resistant bands should not be included in the warm up period but rather included as an addition to the aerobic period or in the recovery / cool down period.

During the aerobic period, interval training has shown to be the most effective method for improvement of the myocardial, skeletal and pulmonary functioning. Using treadmills, bicycles, and other modalities that use major muscle groups is recommended. The duration of the aerobic period should be between 20 and 30 minutes. Debilitated patients may need to rest in-between modalities. The rest period should not be subtracted from their total exercise time, which may complicate a class type setting. Patients who are limited by fatigue may need to have their work loads or modality session time reduced. Patients must be encouraged to continue their aerobic training to a total of 5 or 6 days a week.

There is no consensus of cardiac monitoring for heart failure patients. Though AACVPR recommends direct monitoring and supervision, especially in the initial training sessions, numerous studies have documented successful home based programs without complications. It is prudent, however, to recommend monitoring of the patients who have exercise induced arrhythmias as well as significantly compromise patients.

Following the AACVPR recommendations, monitoring of disease process, compliance to medication and instructions, nutrition guidance and risk reduction education should also be included with the supervised sessions.

The recovery or cool down period is essential for the heart failure period. Gradually normalizing the cardiovascular process helps to prevent hypotensive response at the end of exercise. It also permits; the oxidative capacity and skeletal endothelium to remove lactic build up. Slow and static stretching of the large muscles assists in both processes.

The use of resistive training has not been well established but has strong support by the AHA Science Advisory. Using 1, 2 or 5 pound free weights, resistance bands or repetitive isolated muscle training helps to improve strength and endurance without ventilatory or cardiac compromise.

Providing a CHF exercise program is a challenge on many fronts.

• It is not considered a reimbursable activity by many insurance companies.
• Participating in self-pay programs (even low cost programs) may be impossible for many patients as they are already financially over-extended due to the high cost of medications, frequent physician and hospital visits.
• Patients are often in a physically compromised state that prohibits regular attendance in a 3 time a week program.
• It is difficult to combine Class III CHF patients with Cardiac Rehab classes since they have additional needs and their own timing on exercise modalities.
• Controversy over monitoring may leave some physicians and patients unsure of what program to choose.

However, there is little controversy over the benefits of regular exercise for all CHF patients. The challenge must be creatively met in order to provide this large, vulnerable population the education, exercise and support that they need and deserve.

Proposals for free CHF exercise and educational programs are being made to hospital administrations in an effort to document the benefits of the program by a few Cardiac Rehabilitation programs. Those benefits would include fewer emergency department visits, fewer hospitalizations, fewer physician visits, improved medication compliance, less daily fatigue and weight stabilization. If any of those programs succeed in their appeals to their administrations, CSCR will inform the membership on the progress of those programs.

Heart Failure, Overview and Exercise Post- Test Questions:

Write your answers on a piece of paper. Open your e-mail and send an e-mail message to Jane Hedgpeth CSCR Education Chairperson.jane_dot_ hedgpeth_at_jmmdhs_dot_com . Give her your name, title, e-mail address, license #, and phone #. Make a list 1-8 and indicate your answer to each question. Jane will e-mail your CEU certificate. This offer is free to CSCR members.

CHF causes approximately
a. 125,000 deaths a year
b. 290,000 deaths a year
c. 500,000 deaths a year
d. 750,000 deaths a year

2. The incidence of heart failure more than doubles each decade from age 45 to 75.
a. True
b. False

3. Following the New York Heart Association CHF functional class system, which "class" of patient would one not non-nally see in Cardiac Rehab:
a. Class I
b. Class II
c. Class III
d. Class IV

4. What alterations would one not expect to see in non-exercising patients with CHF?
a. Increase in catecholarnmes
b. Increase in mitochondria
c. Impaired stroke volume
d. Dilated, stiff or bypertropbied left ventricles.

5. What of the following would one not expect to see in exercising CHF patients?
a. Improved clearing of skeletal lactic acid.
b. Increased peripheral and capillary blood flow.
c. Increased mitochondrial density.
d. Significant improvement in stroke volume.

6. The cardiac output or stroke volume is a good determinant of physical ability or survival.
a. True
b. False

7. When developing an exercise program, what should not be included?
a. Longer, slower warm ups
b. Keeping BORGs between 12 and 13
c. Periodically challenging the patients to increase BORGs to 13 and 14
d. Permitting rest if needed, in-between interval training, but not including the rest time in the total exercise time of 20 to 30 minutes.

8. Cool down, using slow and static stretching of the large muscles, is essential for CHF patients because it permits the skeletal endothelium to remove lactic acid build up.
a. True
b. False