Heart failure occurs when the cardiac output is inadequate to meet the circulatory needs of the body. It is the most commonly coded diagnosis in Medicare patients, representing 1 million hospital admissions per year as a primary diagnosis and 3 million as one of the top three diagnoses.¹ It is the only cardiovascular disease that is increasing in both incidence and prevalence in the United States. It has an increased incidence with age that is exponential, exceeding 40% of the population by age 90. There are 5.5 million people in the United States with heart failure, including nearly 500,000 newly diagnosed each year and 300,000 who die annually. Because 90% of deaths and 80% of hospitalizations due to heart failure occur in patients older than 65 years, it is the quintessential geriatric ailment.²,³ Heart failure consumes one fourth of all Medicare expenditures. Medicare paid an average of $16,514 for reimbursement for medical care for patients with heart failure in 1996, which was 431% of the average cost of $3,831 spent for
other Medicare beneficiaries.⁴ The annual cost of care of patients with heart failure is estimated to be nearly three times greater than that for patients with cancer and two times greater than that for patients with acute myocardial infarction.⁴

The heart, which is primarily a pump, shows indications of failing when there is low cardiac output relative to the circulatory needs of the body. The resulting neurohormonal activation, with an elevation of natriuretic peptides and troponins, is a physiologic attempt to preserve cardiac output, although it occurs at the expense of further cardiac and vascular stress. In order to increase the effective circulatory volume, retention of sodium occurs—and continues to occur—even in the presence of established volume overload. Because sodium distributes equally between the plasma and the interstitial space (which together comprise the so-called sodium space), massive quantities of fluid can be retained over time if uncorrected. In the inadequately treated patient, the degree of fluid retention will exceed the degree of sodium retention as a consequence of the presence of other osmotically active molecules beside the sodium, and a relative hyponatremia will result.⁵ Indeed, persistent hyponatremia in the geriatric patient most commonly indicates volume expansion, and every attempt should be made to treat the heart failure sufficiently to correct it. Morbidity increases from pneumonia in “wet lungs” or from hypoxia-induced (from the pulmonary edema and hypoperfusion) myocardial infarction.

Although heart failure often presents as an acute event such as a myocardial infarction or an acute change in functional ability, as was the case here, the underlying disease process has frequently been present—and undetected—for a number of years. This particular patient, on additional questioning, not only had gradual onset of symptoms of heart failure over a 6-month period, but she also presented with mild untreated hypertension. Hypertension is the most common cause of diastolic heart failure. It is likely that the hypertension had been present for 10 to 20 years, causing chronic increased cardiac afterload that ultimately caused her heart failure.

The etiology of heart failure is often multifactorial in the elderly although the final pathway of disease is one of two cardiac dysfunctions: Inadequate ventricular filling and/or inadequate ventricular emptying. Contributing factors to heart disease can be traced to the four basic structural components of the heart: Muscle, valves, coronary arteries, and electrical conduction system. Cardiac muscle disease includes cardiomyopathies (hypertrophic, restrictive, congestive, infiltrative, hypertensive). Valvular disease includes stenosis or regurgitation of any of the four valves (particularly stenosis of the aortic valve and regurgitation of the mitral valve). Coronary artery disease includes myocardial ischemia and myocardial infarction. Electrical disturbances include atrial fibrillation and other arrhythmias. Of these, coronary artery disease is the most common cause and accounts for nearly 70% of cases of heart failure.⁶ Hypertension is the second most common cause and may account for up to 60% of cases in African Americans.⁷ Valvular heart disease is the third most common cause. Consequently, treatment of ischemia is essential. It is the most important strategy to maximize myocardial function. Hypertension, insufficiently treated in two thirds of patients, should be treated proactively long before heart failure has the opportunity to develop. Finally, surgery for valvular heart disease can be considered regardless of age. Outcome is more dependent on general fitness than on age alone.⁸

Heart failure has traditionally been defined as decreased cardiac output associated with a left ventricular ejection fraction (LVEF) of <45%. This is the prototypical systolic dysfunction. In the past two decades, however, there has been increased recognition that the cardiac pump can fail due to one of two mechanisms: Inadequate filling (ventricular charge) or inadequate emptying (ventricular discharge). For many years, large double-blinded, randomized placebo-controlled trials of heart failure focused on patients with a decreased ejection fraction. More recent information has
shown that most patients with heart failure have a normal ejection fraction.⁹ Until large trials in diastolic dysfunction are published, treatment with diuretics, ACE inhibitors, and β-blockers is based on extrapolation from studies on systolic dysfunction, expert opinion, and empiric observation.

Systolic dysfunction accounts for approximately one third of the cases of heart failure; diastolic heart failure is present alone in another third of cases and combines with systolic heart failure in another third (see Table 27.1). Diastolic dysfunction increases with age, particularly in women. Men with heart failure have a normal LVEF 22% of the time when diagnosed at age 60. Prevalence with a normal LVEF increases to 33%, 41%, and 47% respectively when their age is in the seventies, eighties, and nineties. In women, heart failure with a normal LVEF occurs more frequently, at rates of 37%, 44%, 59%, and 73% when thier age is in the sixties, seventies, eighties, and nineties, respectively.¹⁰ Seventy-three percent of hospitalized patients with heart failure and an LVEF of 50% or greater are women.⁹

The most common symptoms—fatigue, exercise intolerance, and weakness—are nonspecific and occur in well over 90% of heart failure cases. These symptoms are often incorrectly attributed to noncardiac causes including normal aging. Dyspnea on exertion occurs in 95% of patients with systolic heart failure and 85% of patients with diastolic heart failure. Orthopnea occurs in 60% to 70% of cases, and is slightly more common in systolic heart failure. Paroxysmal nocturnal dyspnea occurs approximately 50% of the time in both types.¹¹

Signs, like symptoms, may be nonspecific and require a high index of suspicion. Because an insidious onset permits the gradual development of compensatory physiologic processes, the physical examination may be essentially normal despite markedly reduced cardiac function. Rales, a displaced apical impulse and the presence of an S3 or S4 gallop occur approximately two thirds of the time in uncompensated heart failure. These signs occur almost twice as frequently as edema, which is present approximately one third of the time.¹¹

The constellation of signs and symptoms is more sensitive for the diagnosis of heart failure than any individual test. Monitoring signs and symptoms is essential for determining the efficacy of therapeutic interventions. One highly useful clinical sign is dry weight. Unfortunately a patient’s dry weight cannot be calculated from a formula. Dry weight is the weight at which the patient feels well and demonstrates optimized signs, symptoms, and laboratory parameters (particularly sodium, blood urea nitrogen, creatinine, and brain natriuretic protein).