DEFEAT Heart Failure: A Guide to Management of Geriatric

Heart Failure by Generalist Physicians

Ali Ahmed, MD, MPH, FGSA, FACC, FAHA, FESC [Associate Professor]
Medicine and Epidemiology, Director, Geriatric Heart Failure Clinics, University of Alabama at
Birmingham, and Veterans Affairs Medical Center, Birmingham, Alabama
Abstract
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: DEFEATHeart
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.
Keywords
Heart failure; older adults; clinical manifestations; diagnostic assessment; etiology
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
Ali Ahmed, MD, MPH, University of Alabama at Birmingham1530 3
rd
Ave South, CH19-219, BirminghamAL 35294-2041
Telephone number: (205) 637-9632, Fax number: (205) 975-7099 aahmed@uab.edu.
NIH Public Access
Author Manuscript
Minerva Med. Author manuscript; available in PMC 2010 August 3.
Published in final edited form as:
Minerva Med. 2009 February ; 100(1): 3950.
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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.
Geriatric Heart Failure: Case Scenarios
Case 1
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 rles 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.
Case 2
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 rles 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 4045 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%.
Case 3
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
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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.
Case 4
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.
Definition and Stages of Heart Failure
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.
Symptoms of Geriatric Heart Failure
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
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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 23 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.
Signs of Geriatric Heart Failure
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
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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. J ugular
venous pressure can be estimated in 9095% 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 patients
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
patients 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 23 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
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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 rles, 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
Etiology of Geriatric Heart Failure
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
Determination of Left Ventricular Systolic Function
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%.
2430
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.
2430
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.
3237
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
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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, 3840
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
Other Classification of Heart Failure
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 rles, 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
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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.
4951
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 13).
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.
5254
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.
Treatment of Geriatric Heart Failure
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
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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.
6264
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
Summary: DEFEAT Heart Failure
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.
Acknowledgments
Grant Support: Dr. Ahmed is supported by the National Institutes of Health through a grant fromthe National
Heart, Lung, and Blood Institute (R01-HL085561) and a generous gift fromMs. J ean B. Morris of Birmingham,
Alabama.
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Figure 1.
Techniques for the estimation of jugular venous pressure (J VP) using external jugular veins
(EJ V) in older adults with chronic heart failure. The goal is to find a position between supine
and sitting in which the top of the EJ V pulsation is visible in the middle of neck (blue line in
neck). Then the vertical distance between the top of the EJ V pulsation and sternal angle is
measured, to which is added (subtracted, if the top of the EJ V pulsation is below the sternal
angle) the position-appropriate distance between sternal angle and right atrium (5 cm at
supine, 8 cm at 30 degrees and 10 cm at 45 degrees) (Adopted from Ahmed A, J ones L,
Hays CI. DEFEAT heart failure: assessment and management of heart failure in nursing
homes made easy. J Am Med Dir Assoc. 2008;9:3839.)
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Ahmed Page 15
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Minerva Med. Author manuscript; available in PMC 2010 August 3.