|Home | About | Journals | Submit | Contact Us | Français|
Over 80% of all heart failure patients are 65 years and older. The diagnosis and management of heart failure in older adults can be challenging. However, with the correct clinical skill and experience, most geriatric heart failure can be properly diagnosed and managed. Management of geriatric heart failure can be simplified by following this useful mnemonic: DEFEAT–Heart Failure. This covers the essential aspects of geriatric heart failure management: Diagnosis, Etiology, Fluid, Ejection frAcion, and Treatment. The process begins with a clinical Diagnosis, which must be established, before ordering an echocardiogram as nearly half of all geriatric heart failure patients have normal left ventricular ejection fraction. Because heart failure is a syndrome and not a disease, an underlying Etiology must be sought and determined. Determination of the Fluid volume status by careful examination of the external jugular veins in the neck is vital to achieve euvolemia. An echocardiography should be ordered to obtain left ventricular Ejection frAction to assess prognosis and guide Therapy. However, if left ventricular ejection fraction cannot be determined, as in many developing nations, all geriatric heart failure patients should be treated as if they have low ejection fraction, and should be prescribed an angiotensin-converting enzyme inhibitor and a beta-blocker. Diuretic and digoxin should be prescribed for all symptomatic patients with heart failure. An aldosterone antagonist may be used in select patients with advanced systolic heart failure, carefully avoiding hyperkalemia.
Heart failure is a geriatric syndrome as most heart failure patients are older adults. Heart failure is also a cardiac syndrome with complex and rapidly evolving pathogenesis and treatment. However, heart failure is ultimately a syndrome, as most heart failure patients are managed by generalist physicians and it is also a leading cause of hospitalization among older adults. Further, unlike other cardiovascular disorders, heart failure is a clinical diagnosis that can be made at bedside and the established evidence-based therapy for heart failure can be easily implemented by generalist physicians. The diagnosis and management of heart failure in the elderly can be complicated by multiple co-morbidities and polypharmacy.1 The management of heart failure in a 75-year-old elderly woman with normal left ventricular ejection fraction may be complicated by lack of evidence to guide therapy, comorbidities such as hypertension, atrial fibrillation, diabetes mellitus, osteoarthritis, chronic kidney disease, and depression, and polypharmacy related to these conditions. The management of heart failure in the elderly is further made difficult by atypical presentation of heart failure in older adults.2 Heterogeneity is another name of aging, and geriatric heart failure is no exception. Geriatric heart failure patients may present with a wide range of phenotypic heterogeneity, as can be seen from the cases presented.
An 80-year-old man with prior history of hypertension and myocardial infarction presented with progressive dyspnea on exertion and leg swelling for the past 6 months. He denied dyspnea at rest, orthopnea, paroxysmal nocturnal dyspnea, cough, wheezing, or chest pain. He reported no emergency room visits or hospitalizations due to his dyspnea. A physical examination revealed only mild pitting lower extremity edema. He had neither jugular venous pressure elevation nor hepatojugular reflux. On cardiac auscultation, his first and second heart sounds were regular; a third or fourth heart sound could not be appreciated. On pulmonary examination, there were no râles or wheezing. He had normal sinus rhythm on his electrocardiogram. A chest x-ray revealed no cardiomegaly or pulmonary venous congestion. He had a left ventricular ejection fraction of 35% by an echocardiogram done a week later.
An 84-year-old woman with known heart failure presented with dyspnea for 4 weeks during which time she developed dyspnea and fatigue on minimal exertion and even at rest. She also complained of orthopnea and reported that most of the past week she slept sitting in a recliner. Prior to sleeping on a recliner, she had had one episode of paroxysmal nocturnal dyspnea. Her past medical history was remarkable for hypertension. She denied chest pain, palpitation or dizziness. She also reported right upper quadrant pain associated with nausea and loss of appetite but no vomiting. She had chronic leg swelling which has gotten so severe over the past several weeks that she could not wear her shoes. She responded to her worsening symptoms by restricting her activities and did not see her physician. At the emergency department, her jugular venous pressure was elevated at 15 cm of water. She had positive hepatojugular reflux, a right-sided third heart sound and an enlarged soft tender liver. She had no pulmonary râles or wheezing. She had severe bilateral pitting edema in both of her legs up to mid-thigh areas with multiple blisters over lower legs. She also had evidence of venous insufficiency with brown pigmentation and induration of skin. A loud second heart sound at left fourth intercostal space suggested that her estimated pulmonary artery systolic pressure was elevated at 40–45 mm Hg. She had normal sinus rhythm by an electrocardiogram. Her chest radiograph was remarkable for marked cardiomegaly and pulmonary venous congestion. Her prior left ventricular ejection fraction was unknown and a subsequent echocardiogram revealed a left ventricular ejection fraction of >55%.
A 78-year-old man hospitalized for a syncopal episode was found to have a left ventricular ejection fraction of 30% on an echocardiogram during a workup. He later admitted to have progressive dyspnea on exertion during past several months. He did not report his symptoms to his doctors and instead restricted his physical activities to avoid symptoms. He denies dyspnea at rest, orthopnea, paroxysmal nocturnal dyspnea or chest pain. He had normal sinus rhythm by an electrocardiogram and a chest x-ray revealed cardiomegaly. His coronary angiogram was normal. He had lower extremity edema and he was discharged on furosemide 80 mg daily. His dyspnea on exertion worsened after discharge and his furosemide was increased to 160 mg daily. His symptoms improved and he lost weight. However, his furosemide was continued at 160 mg/day dose and several weeks later he developed fatigue and dyspnea on exertion. On physical examination his systolic blood pressure was low at 90 mm Hg and his jugular venous pressure was low at 3 cm of water water. His symptoms improved and he gained nearly 10 lbs in one week after his furosemide was decreased to 80 mg daily.
An 83-year-old woman presented with a one-year history of dyspnea at rest, chest tightness, and dizziness. Her past medical history was remarkable for hypertension and coronary artery disease. Her symptoms worsened three times during the past year when she went to the emergency department and was hospitalized each time. An echocardiogram, a cardiac catheterization and a magnetic resonance imaging of her brain done during hospitalization revealed no pathology upon which she was discharged from her last hospitalization. However, she continued to remain symptomatic and was somewhat frustrated that she was discharged based on normal test results and no attention was paid to her continuing symptoms. She denied having dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea or leg swelling. On further questioning she revealed that her husband of 45 years died about two years ago and since then she sold their home and moved to live near her daughter in another town. She is a retired teacher and volunteers at the Sunday school in her church. She had no signs of heart failure. A diagnosis of somatizatioin with geriatric depression was made and her symptoms were completely resolved within four weeks of therapy with sertraline 50 mg daily.
Dyspnea and fatigue, with or without some degree of leg swelling, are the cardinal symptoms of heart failure (Table 1). The American College of Cardiology / American Heart Association guidelines for chronic heart failure defines heart failure as “a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood.”3 The Heart Failure Society of America heart failure guidelines define heart failure as a “syndrome caused by cardiac dysfunction, generally resulting from myocardial muscle dysfunction or loss and characterized by left ventricular dilation or hypertrophy.”4
Because heart failure is a progressive condition, clinical manifestations of heart failure vary depending on the stages in its natural history. Stage A is a pre-clinical stage in which there is neither clinical heart failure nor structural myocardial damage. However, these patients have one or more of the known risk factors for heart failure, such as hypertension or coronary artery disease, and are at high risk of developing heart failure. The importance of identifying patients at this stage is early primary prevention of heart failure. Stage B is characterized by structural myocardial damage but these patients are still asymptomatic and do not have clinical heart failure. However, due to structure myocardial damage, these patients may be at a higher risk of developing heart failure than those in Stage A. The importance of identifying patients at this stage is late primary prevention of heart failure. Stage C patents are those who have already developed clinical symptoms and signs of heart failure. Once patients are in Stage C, they are always in Stage C even if they are currently asymptomatic. Patients at this stage may be amenable to secondary prevention from other complications of heart failure. Stage D heart failure patients are symptomatic and terminal, and are often refractory to therapy.
Dyspnea or fatigue on exertion, with or without some degree of lower extremity swelling, is generally the most common early symptom of heart failure (Cases 1 – 3). With progression of disease, especially in the absence of appropriate treatment, dyspnea on exertion or fatigue gradually becomes more severe and appears with decreasing exertion (Case 2), and eventually at rest. Older adults often attribute their dyspnea on exertion or fatigue on exertion to aging, and respond to their early symptoms by restricting their physical activities, thus delaying clinical manifestations and diagnosis. It is important to take that into consideration while inquiring about dyspnea on exertion from older adults. Clinicians should also routinely screen their geriatric patients with high risk for heart failure (Stage A and Stage B) for symptoms and signs of dyspnea on exertion, exertional fatigue, leg edema and other common heart failure symptoms to make an early diagnosis of heart failure. This is important as early initiation of therapy may be associated with long-term survival benefit.5 When a patient presents with dyspnea at rest, it is important to determine its duration and if it was preceded by dyspnea on exertion. Dyspnea at rest without dyspnea on exertion is almost never organic in etiology, and may represent somatization in older adults (Case 4).6
Orthopnea and paroxysmal nocturnal dyspnea are relatively specific symptoms for heart failure in older adults.2, 7 Orthopnea usually occurs soon after lying down and is also relieved promptly by sitting or standing up. Paroxysmal nocturnal dyspnea occurs 2–3 hours after onset of sleep, and causes patients to wake up from sleep with dyspnea, which may be followed by cough and/or wheezing. Relief starts with sitting up, but complete relief of symptoms may take between five minutes to half an hour. Patients sleeping with multiple pillows or on a recliner to avoid orthopnea may not experience paroxysmal nocturnal dyspnea. It can also be caused by chronic obstructive pulmonary disease, in which case, it often begins with cough later leading to dyspnea and may be relieved with the expectoration of the clogged mucus, even without sitting up.8 However, these symptoms are relatively infrequent in older adults with heart failure and may not be reported until fluid overload is severe, as in Cases 2.9, 10 Many older adults with heart failure may sleep in a chair or a recliner to avoid orthopnea, and may not voluntarily report that unless specifically asked.
Lower extremity edema associated with heart failure is generally bilateral. However, bilateral leg edema is a relatively non-specific symptom and may also be caused by chronic venous insufficiency, obesity, prolonged sitting or standing, or medications such as calcium channel blockers. Edema generally begins with foot and ankle, extending proximally to leg, but when prolonged and left untreated, may also affect more proximal lower extremity, scrotal area, and abdomen. Edema associated with heart failure is always symmetric and pitting. A history of past trauma or surgery may explain why edema may be greater in one leg over the other. Edema may be marked during evening hours in ambulatory patients, and over sacral area in bed-bound patients. Chronic severe edema may lead to skin changes including erythrema, brown pigmentation, and induration. Older adults are more prone to skin blisters with severe and longstanding edema. Other less common and atypical symptoms of heart failure in older adults include fatigue, syncope, angina, nocturia, oliguria, and changes in mental status. Weight gain almost always accompanies symptomatic heart failure, but is rarely reported as a symptom by older heart failure patients.
An elevated jugular venous pressure is the most specific sign of fluid overload in heart failure and is the most important physical examination in the initial and subsequent examinations of an elderly heart failure patient.11 Euvolemia or a normal fluid balance is essential for two reasons: it allows patients to lead a symptom-free life, and it also makes it possible to initiate and maintain life-prolonging therapies with drugs such as an angiotensin-converting enzyme (ACE) inhibitor or a beta-blocker. However, to achieve euvolemia, one must first be able to identify conditions of volume overload and hypovolemia. Assessment of fluid volume status can often be done by careful estimation of the jugular venous pressure in the neck. As easy as it sounds, the estimation of jugular venous pressure using external jugular veins is a difficult clinical skill that needs to be acquired through diligent practice. Because estimation of the jugular venous pressure is the most important physical examination in heart failure, it must be done very carefully, and may take several minutes even for the most experienced clinicians.
Despite text book recommendations and traditional classroom and bedside teachings, internal jugular vein is not suitable for the estimation of jugular venous pressure in chronic heart failure. For most of its course in the neck, the internal jugular veins lie deep in the neck behind the large sternocleidomastoid muscles. It is only subcutaneous in a small triangular area at the root of the neck in between the two heads of the sternocleidomastoid muscle. Therefore, the use of internal jugular veins is not suitable for the estimation of jugular venous pressure and is likely to underestimate jugular venous pressure. In one study of older adults, mean age 70 years, who presented with dyspnea at the emergency department, only 14% had elevated jugular venous pressure.10 In two large clinical trials of chronic heart failure patients (total population >10,000), in which all patients were evaluated by cardiologists, slightly >10% had elevated jugular venous pressure.12, 13 In one of the largest registries of hospitalized acute heart failure patients in United States (total population >40,000), only <30% had elevated jugular venous pressure at the time of hospital admission.14
External jugular veins are subcutaneous and their pulsation can be more easily visible for estimation of jugular venous pressure (Figure 1).15 However, as superficial veins, they are also prone to external pressure or internal occlusions. Thus thrombosis or screlosis of their valves may cause partial or complete occlusion of their lumen, giving a distended appearance proximal to the obstruction. Therefore, a non-pulsatile distended external jugular vein may not be useful for jugular venous pressure estimation. Estimation of the jugular venous pressure involves estimation of the distance from the right atrium to the top of the external jugular venous pulsation and is a two-step process. The process of jugular venous pressure estimation begins with the estimation of the distance from the top of the jugular venous pulsation to the sternal angle and that from sternal angle to the right atrium. Jugular venous pressure can be estimated in 90–95% of all heart failure patients if this examination technique is used properly.
The process begins with proper positioning of the patient at an elevation so that the top of the external jugular venous pulsation can be visualized in the middle of the neck. If the examination begins with the patient lying supine and a distended external jugular vein is visualized, then the head of the patient should be gradually elevated by about 10 degrees at a time until the top of the jugular venous pulsation can be seen in the middle of the neck. For patients in a sitting position, the external jugular vein may not be visible, although in the very elderly, the path of a hardened empty vein may be visible. However, when the patient’s head is gradually lowered, by about 10 degrees at a time, the top of the pulsation would often appear at the root of the neck and would be in the middle of the neck with little further lowering of the head. External jugular venous pulsation should be examined on both sides of the neck. The movement of the top of the venous pulsation in response to changes in the patient’s position may be used as an indication that the external jugular vein is not occluded. This can also be done the hepatojugular reflux. Hepatojugular reflux occurs when a noncompliant right ventricle cannot handle a rapid venous return that is caused by a firm but gentle pressure over an abdomen whose veins may already be congested with blood.16 Some degree of reflux is not uncommon in heart failure, and for hepatojugular reflux to be considered positive, the top of the jugular venous pulsation must rise by 2–3 cm and should remain elevated for about 10 seconds when a gentle yet firm pressure is applied to the mid-abdomen area. A positive reflux is indicative of increased right atrial pressure and confirms fluid overload, especially in the presence of elevated jugular venous pressure.16, 17 A positive hepatojugular reflux in the presence of a normal jugular venous pressure may be an early sign of fluid buildup in a patient presenting with dyspnea or may indicate mild residual fluid overload for stable asymptomatic patients, which may be baseline for that patient.
Once the top of the jugular venous pulsation has been identified, its vertical distance from the sternal angle should be estimated, to which should be added the estimated distance between the sternal angle and the right atrium. The distance between the right atrium and sternal angle has been traditionally taught to be 5 cm regardless of body position. However, recent evidence based on computed tomography of the chest suggest that the distance varies with the position of the patient.18 While the distance is 5 cm in supine position, it increases to 10 cm in positions at or above 45 degrees (Figure 1). Therefore, the position at which the top of the jugular venous pulsation is visible in the middle of the neck needs to be taken into account when estimating jugular venous pressure. When the top of the jugular venous pulsation is below the sternal angle, the distance between sternal angle and top of jugular venous pulsation, should be subtracted from the position-appropriate distance between the right atrium and sternal angle (Figure 1). In chronic heart failure patients this is often due to overdiuresis. Hypoperfusion and hypovolemia due to overdiuresis may cause myocarardial ischemia, hypotension, dizziness, fatigue, renal failure, and paradoxical worsening of dyspnea. Therefore, it is important to recognize hypovolemia and an early intervention may be an appropriate lowering of the dose of the diuretics (Case 3). Other physical signs such as pulmonary râles, a third heart sound or leg edema may not always be present in chronic heart failure and may be caused by conditions other than heart failure, and thus less reliable and useful.8, 11, 19
Because heart failure is a syndrome and not a disease, it is always associated with an underlying cause. Hypertension and coronary artery disease are the two most common causes of heart failure in all ages, including older adults.20, 21 The presence of these risk factors may often be determined from history and other tests. It is important to identify the presence of these comorbidities, as their presence may lead to continued myocardial damage, disease progression, and poor outcomes. When primary care physicians cannot determine an underlying cause or when an underlying cause such as continued myocardial ischemia or valvular heart disease requires specialized treatment, patients should be referred to cardiologists
The most clinically relevant classification of clinical heart failure into systolic and diastolic heart failure is based on left ventricular ejection fraction. An echocardiogram is the most commonly used test to determine left ventricular ejection fraction. Determining if heart failure is systolic or diastolic has both prognostic and therapeutic implications.22, 23 Other descriptive classifications of heart failure are less clinically relevant and are briefly discussed below. Systolic heart failure is clinical heart failure with left ventricular ejection fraction <45%.24–30 Systolic heart failure is characterized by a large but weak left ventricle that is unable to eject enough blood to produce a normal stroke volume and cardiac output (Table 1). Most randomized clinical trials in heart failure have been restricted to systolic heart failure.24–30 It is also the predominant type of heart failure among younger adults, especially those seen in large academic medical centers.31
However, epidemiological data from the past several decades suggest that over 50% of all heart failure patients may have diastolic heart failure.32–37 Diastolic heart failure is defined as clinical heart failure with normal or near normal left ventricular ejection fraction, generally 55% or greater. However, clinical presentation and prognosis of heart failure patients with left ventricular ejection fraction between 45% and 55% are similar to those with left ventricular ejection fraction >55% and thus can be considered to have diastolic heart failure for all practical purposes.14 Diastolic heart failure is characterized by a strong but small ventricle that is stiff and cannot relax fully to fill up the ventricle during diastole and thus does not have enough blood to pump to produce a normal stroke volume and cardiac output (Table 1). Clinical manifestations of systolic and diastolic heart failure are very similar and often cannot be clinically distinguished.3, 4, 14, 38–40 The Case 2 presented with classic text-book symptoms and signs of heart failure yet was later found out to have normal left ventricular ejection fraction.
A transthoracic two-dimensional echocardiography with or without Doppler imaging is usually the preferred test to assess left ventricular ejection fraction. Left ventricular ejection fraction can also be measured using other techniques,41 but echocardiography is most commonly used. It is widely available, safe, non-invasive, not uncomfortable, and provides excellent images of not only the heart, but also the great vessels and paracardiac structures.42 It can also provide an estimate of left ventricular diastolic dysfunction. Assessment of left ventricular ejection fraction is important as it is of crucial therapeutic and prognostic significance.3, 4, 38, 40 However, left ventricular ejection fraction should not be assessed until after a clinical diagnosis has been made, as over half of all geriatric heart failure patients have normal left ventricular ejection fraction, a fact that can confound the diagnostic process.
A determination of diastolic dysfunction is not essential to make a clinical diagnosis of diastolic heart failure.36 Significant abnormalities in active and passive relaxation are common in most diastolic heart failure patients.35, 43 Doppler studies of velocity of transmitral blood flow can determine ventricular filling patterns. In diastolic heart failure, the peak transmitral E velocity (represents early filling during active ventricular relaxation) is decreased, while there is a relative increase in the peak A velocity (due to a compensatory increase in atrial contraction in late diastole). Thus, the E:A ratio is decreased, and even reversed to <1 in diastolic heart failure.35, 44, 45 However, E:A ratio may also be decreased with normal aging,46 and may be normalized with progressive diastolic heart failure (pseudo-normalization).47, 48 However, mitral annular tissue Doppler imaging can distinguish normal from pseudo-normal filling patterns, and if combined with transmitral flow Doppler imaging and clinical history, can accurately determine severity of diastolic abnormalities.35, 47, 48 There is evidence that severity of diastolic dysfunction may be associated with increased mortality.35
Heart failure has also been classified as left-sided versus right-sided, forward versus backward, low versus high output, and acute versus chronic heart failure. However, none of these classifications are of much clinical relevance. Theoretically, pure left-sided heart failure may result in either pulmonary congestion, or hypoperfusion, or both, and may result in left-sided symptoms such as dyspnea, cough, wheezing, fatigue, hypotension, tachycardia, confusion, syncope, delirium, and oliguria, pulmonary râles, and left-sided third heart sound. Right-sided heart failure, on the other hand, may lead to right-sided symptoms and signs such as dyspnea, fatigue, leg swelling, nausea, vomiting, epigastic and upper abdominal pain, elevated jugular venous pressure, hepatojugular reflux, hepatomegaly, right-sided third heart sound, prominent pulmonic component of the second heart sound, and dependent edema. Even though most early heart failure involves left ventricle, most advanced heart failure is biventricular. Thus, most advanced heart failure patients have both left- and right-sided heart failure as noted in Case 2. However, symptoms and signs related to bi-ventricular heart failure may also be seen in early heart failure (Cases 1 and 3), who presented with dyspnea on exertion and leg edema. A classification of left-sided or right-sided heart failure has no therapeutic or prognostic implication.
A weak heart as in systolic heart failure may cause forward failure leading to symptoms of hypoperfusion, and a non-complaint heart as in diastolic heart failure may cause backward failure leading to symptoms related to congestion.49–51 However, most clinical heart failure patients have some degree of both systolic and diastolic heart failure and have symptoms and signs related to hypoperfusion and congestion (Cases 1–3).6 A classification of backward or forward heart failure has no therapeutic or prognostic implication.
Although most elderly heart failure patients have low cardiac output heart failure (Cases 1–3), heart failure associated with high-output heart failure may occur due to hyperdynamic conditions such as severe anemia, thyrotoxicosis, and arteriovenous fistula, including those used for hemodialysis.52–54 Anemia rarely causes high-output heart failure in the absence of other cardiac disease or unless hemoglobin is very low (<5 gm/dl).3, 6 However, milder anemia (hemoglobin between 5 and 10 mg/dl) may cause exacerbation of symptoms in patients with existing heart failure. Thyrotoxicosis alone also rarely causes high-output heart failure. Except for warm extremities, clinical features of high- and low-output heart failure may be indistinguishable. Laboratory tests for anemia, kidney function, and thyroid function are usually sufficient to screen heart failure patients for high-output situations.3, 4, 45
Finally, acute heart failure may indicate both severity (mild to moderate versus severe) and onset (sudden versus gradual) of symptoms, and can occur both during initial presentation and in patients with chronic heart failure (Cases 2 and 4).55, 56 Over two-thirds of all hospitalized heart failure patients have known chronic heart failure.57 This may be due to noncompliance with drugs, salt or fluid, acute myocardial ischemia, severe hypertension, or natural disease progression. Clinical manifestations of ambulatory chronic heart failure and hospitalized acute heart failure are generally similar, but may be more severe in the latter group.
The general principle for the treatment of heart failure in older adults is similar to that in younger adults and can generally be divided into symptom-relieving treatment and disease-modifying or life-prolonging treatment. Symptom-relieving therapy for heart failure is similar for both systolic and diastolic heart failure. However, because evidence for disease-modifying therapy is primarily derived from younger systolic heart failure, there is little evidence to guide therapy for elderly diastolic heart failure patients. Evidence-based therapy for systolic heart failure involves the use of drugs that suppress neurohormones (renin-angiotensin-aldosterone system and sympathetic nervous system) and includes an ACE inhibitor or angiotensin receptor blocker and a beta blocker, and in select patients, an aldosterone antagonist. Clinicians should be familiar with the use of these drugs and follow recommendations of chronic heart failure guidelines.3
All elderly systolic heart failure patients should be treated with an ACE inhibitor or an angiotensin receptor blocker, if a patient cannot tolerate an ACE inhibitor due to cough or angioedema. Chronic renal insufficiency is common in heart failure, and should not be a reason for nonuse of these drugs.58, 59 All elderly systolic heart failure patients should also be treated with an approved beta-blocker, namely, carvedilol, metoprolol extended release, or bisoprolol. There is no need to maximize the dose of an ACE inhibitor (or an angiotensin receptor blocker) before initiating therapy with a beta-blocker. Metoprolol may be better tolerated by patients with low systolic blood pressure.60 An aldosterone antagonist, such as spironolactone, may be used in advanced heart failure patients.29, 61 However, it would be used with caution as it may cause hyperkalemia, especially in those with impaired renal function. Aldosterone antagonists may also be used in patients with chronic hypokalemia receiving diuretics.
Digoxin should be used in low doses for patients who are symptomatic despite appropriate therapy with an ACE inhibitor (or an angiotensin receptor blocker) and a beta-blocker.62–64 A daily dose of 0.125 mg may be sufficient for most patients and may not require monitoring of serum digoxin levels. Most heart failure patients need loop diuretics to achieve euvolemia and remain euvolemic.3 Diuretics are known to activate neurohormones and may be potentially harmful.65, 66 Therefore, after euvolemia is achieved diuretics should be used in the lowest possible doses needed to maintain euvolemia. Hypokalemia should be avoided and should be treated as appropriate.67 The importance of salt and fluid restriction must be emphasized in all heart failure patients, especially in those who are volume overloaded, and require an increase of their diuretic dosage.
There are little evidence-based guidelines for therapy of diastolic heart failure patients. All symptomatic diastolic heart failure patients, like systolic heart failure patients, should be treated with diuretics, to achieve euvolemia. There is currently no evidence that the use of ACE inhibitors or beta-blockers reduces mortality or morbidity in diastolic heart failure. However, diastolic heart failure patients are often elderly and suffer from multiple comorbidities such as hypertension, diabetes, coronary artery disease, atrial fibrillation, and chronic kidney disease, which may benefit from the use of these drugs. Digoxin and candesartan may be beneficial in reducing heart failure hospitalizations in these patients.68, 69
Most geriatric heart failure patients in the developing nations may not be able to afford echocardiography. When left ventricular ejection fraction is unknown, all heart failure patients should be considered as systolic heart failure and should be treated accordingly. Heart failure patients who cannot afford or tolerate ACE inhibitors and beta-blockers should be prescribed digoxin in low doses. Digoxin is inexpensive, and may reduce morbidity and mortality in these patients.62, 64, 68
Management of geriatric heart failure may be simplified by the mnemonic DEFEAT: Diagnosis, Etiology, Fluid volume status, Ejection frAcion, and Treatment. Careful history and physical examination often may help make a clinical Diagnosis of heart failure in older adults and determine an underlying Etiology of heart failure. Determination of Fluid volume status by careful examination of the external jugular veins is the single most important physical examination during initial and subsequent visits. Determination of left ventricular Ejection frAction is the single most important test after a clinical diagnosis of heart failure has been made, which should be used to guide Therapy. When ejection fraction cannot be determined, all heart failure patients should be treated as systolic heart failure, and should be prescribed an ACE inhibitor and a beta-blocker, and an aldosterone antagonist for selected patients with advanced heart failure. Low-dose digoxin should be prescribed for all heart failure patients who cannot afford or tolerate ACE inhibitors or beta-blockers. Diuretics should be used judiciously to achieve and maintain euvolemia.
Grant Support: Dr. Ahmed is supported by the National Institutes of Health through a grant from the National Heart, Lung, and Blood Institute (R01-HL085561) and a generous gift from Ms. Jean B. Morris of Birmingham, Alabama.