Congestive Heart

Failure
 Epidemiology
• Heart failure is a common syndrome that is
increasing in incidence and prevalence

• It is primarily a disease of aging, with over

75% of existing and new cases occurring in
individuals over 65 years of age

• The prevalence of heart failure rises from

< 1% in individuals below 60 years to
nearly 10% in those over 80 years of age
 Pathophysiology
• Systolic function of the heart is
governed by four major determinants:

1. Contractile state of the myocardium

2. Preload of the ventricle (the end-
diastolic volume and the resultant
fiber length of the ventricles prior to
onset of the contraction)
3. Afterload applied to the ventricles (the
impedance to LV ejection)
4. Heart rate.
• Cardiac function may be inadequate as a result of
alterations in any of these determinants

• In most instances, the primary derangement is

depression of myocardial contractility caused either by
loss of functional muscle (due to myocardial infarction,
etc) or by processes diffusely affecting the myocardium

• The heart may fail as a pump because preload is

excessively elevated, such as in valvular regurgitation

• The heart may fail as a pump because afterload is

excessive, such as in aortic stenosis or in severe
hypertension

• Pump function may also be inadequate when the heart

rate is too slow or too rapid
 High-output heart failure:

• Cardiac pump function may be supranormal

but nonetheless inadequate when metabolic
demands or requirements for blood flow are
excessive. This situation is termed high-
output heart failure and, though
uncommon, tends to be specifically treatable

• Causes of high output include thyrotoxicosis,

severe anemia, arteriovenous shunting
(including dialysis fistulas), Paget's disease of
bone, and thiamine deficiency (beriberi)
 Diastolic Cardiac Failure
• Manifestations of cardiac failure can also occur as a result of
isolated or predominant diastolic dysfunction of the heart

• In these cases, filling of the LV or RV is abnormal, either

because myocardial relaxation is impaired or because the
chamber is noncompliant ("stiff") due to excessive hypertrophy
or changes in composition of the myocardium

• Even though contractility may be preserved, diastolic pressures

are elevated and cardiac output may be reduced, potentially
causing fluid retention, dyspnea, and exercise intolerance

• The most frequent cause of diastolic cardiac dysfunction is LVH,

commonly resulting from hypertension, but conditions such as
hypertrophic or restrictive cardiomyopathy, diabetes, and
pericardial disease can produce the same clinical picture
 Pathophysiological
• When the heartAdaptations
fails, a number of adaptations occur both
in the heart and systemically

• If the stroke volume of either ventricle is reduced by

depressed contractility or excessive afterload, end-
diastolic volume and pressure in that chamber will rise

• This increases end-diastolic myocardial fiber length,

resulting in a greater systolic shortening (Starling's law of
the heart)

• If the condition is chronic, ventricular dilation will occur.

• Although this may restore resting cardiac output, the

resulting chronic elevation of diastolic pressures will be
transmitted to the atria and to the pulmonary and
systemic venous circulation. Ultimately, increased
capillary pressure may lead to transudation of fluid with
• Reduced cardiac output, particularly if associated with reduced arterial pressure
or perfusion of the kidneys, will also activate several neural and humoral systems

Sympathetic nervous system activation

• It will stimulate myocardial contractility, heart rate, and venous tone

• Tachycardia and increased contractility may precipitate ischemia in patients with

underlying CAD, and the rise in preload may worsen pulmonary congestion

• Increases peripheral vascular resistance

• This adaptation is designed to maintain perfusion to vital organs, but when it is

excessive it may itself reduce renal and other tissue blood flow

• Peripheral vascular resistance is also a major determinant of LV afterload, so that

excessive sympathetic activity may further depress cardiac function
Renin–angiotensin–aldosterone system activation

• The renin–angiotensin–aldosterone system is also

activated, leading to further increases in peripheral
vascular resistance and LV afterload as well as sodium
and fluid retention

• Heart failure is associated with increased circulating

levels of arginine vasopressin, which also serves as a
vasoconstrictor and inhibitor of water excretion

• Release of atrial natriuretic peptide is increased in

heart failure owing to the elevated atrial pressures,
there is evidence of resistance to its natriuretic and
vasodilating effects
Left and Right heart failure
Left heart failure:
• Patients with left heart failure have symptoms of
low cardiac output and elevated pulmonary venous
pressure; dyspnea is the predominant feature.

Right heart failure:

• Signs of fluid retention predominate in right heart
failure, with the patient exhibiting edema, hepatic
congestion, and, on occasion, ascites

• Most patients exhibit symptoms or signs of both right-

and left-sided failure, and LV dysfunction is the
primary cause of RV failure

• Although we will discuss mainly, cardiac failure due to

systolic LV dysfunction, patients with diastolic heart
failure experience many of the same symptoms and
may be difficult to distinguish clinically.
 Causes of Cardiac Failure
• CAD with resulting myocardial infarction and loss of functioning
myocardium (ischemic cardiomyopathy) is the most common cause

• Systemic hypertension remains an important cause of

CHF

• Valvular heart diseases: degenerative aortic stenosis

and chronic aortic or mitral regurgitation—are not infrequent causes
of heart failure.

• Dilated or congestive cardiomyopathy also

leads to CHF

 Characterized by LV or biventricular dilation and generalized systolic

dysfunction
 Most common causes are alcoholic cardiomyopathy, viral myocarditis
(including infections by HIV), and dilated cardiomyopathies with no
obvious underlying cause (idiopathic cardiomyopathy)
 Rare causes of dilated cardiomyopathy include infiltrative diseases
(hemochromatosis, sarcoidosis, amyloidosis, etc), other infectious
agents, metabolic disorders, cardiotoxins, and drug toxicity
 Clinical Findings
Symptoms
• The most common complaint is shortness of breath,
chiefly exertional dyspnea at first and then progressing to
orthopnea, paroxysmal nocturnal dyspnea, and rest
dyspnea

• A more subtle symptom of heart failure is a chronic

nonproductive cough, which is often worse in the
recumbent position

• Nocturia due to excretion of fluid retained during the day

and increased renal perfusion in the recumbent position
is a common nonspecific symptom of heart failure

• Patients with heart failure also complain of fatigue and

exercise intolerance
• Patients with right heart failure may experience right
upper quadrant pain due to passive congestion of the
liver, loss of appetite and nausea due to edema of the
gut or impaired gastrointestinal perfusion, and
peripheral edema

• Patients may also present with acute heart failure

• Causes of acute heart failure include myocardial

infarction, myocarditis, and acute valvular
regurgitation due to endocarditis or other conditions

• These patients usually present with pulmonary edema

• Patients may also present with acute exacerbations of

chronic, stable heart failure
 New York Heart Association
classification of Heart failure
• Patients with heart failure are often
categorized by the New York Heart
Association classification
• Class I (asymptomatic)
• Class II (symptomatic with mild activity)
• Class III (symptomatic with moderate
activity)
• Class IV (symptomatic at rest)
 Signs
Appearance:
• Many patients with heart failure, including
some with severe symptoms, appear
comfortable at rest
• Others will be dyspneic during conversation or
minor activity, and those with long-standing
severe heart failure may appear cachectic or
cyanotic

Vitals:
• The vital signs may be normal, but
tachycardia, hypotension, and reduced pulse
pressure may be present
• Patients often show signs of increased
sympathetic nervous system activity, including
cold extremities and diaphoresis
 Peripheral signs of heart failure;

Neck:
• RA pressure may be estimated through the height of
the pulsations in the jugular venous system
• Examination of the carotid pulse may allow estimation
of pulse pressure as well as detection of aortic stenosis
• The thyroid examination is important, since occult
hyperthyroidism and hypothyroidism are readily
treatable causes of heart failure

Lungs:
• In the lungs, crackles at the lung bases reflect
transudation of fluid into the alveoli
• Pleural effusions may cause bibasilar dullness to
percussion
• Expiratory wheezing and rhonchi may be signs of heart
failure
 Abdomen:
• Patients with severe right heart failure may have
hepatic enlargement—tender or nontender—due to
passive congestion

• Sustained moderate pressure on the liver may increase

jugular venous pressure (a positive hepatojugular reflux
is an increase of > 1 cm)

• Ascites may also be present

• Peripheral pitting edema is a common sign in patients

with right heart failure and may extend into the thighs
and abdominal wall.
 The Cardiac examination:

• Cardinal signs in heart failure are a parasternal lift,

indicating pulmonary hypertension
• An enlarged and sustained LV impulse, indicating LV
dilation and hypertrophy
• A diminished first heart sound, suggesting impaired
contractility
• S3 gallops originating in the LV and sometimes the RV
• An S4 is usually present in diastolic heart failure
• Murmurs should be sought to exclude primary valvular
disease
• Secondary mitral regurgitation and tricuspid regurgitation
murmurs are common in patients with dilated ventricles
• In chronic heart failure, many of the expected signs of
heart failure may be absent despite markedly abnormal
cardiac function and hemodynamic measurements
 Laboratory Findings
• A blood count may reveal anemia, a cause of high-
output failure and an exacerbating factor in other
forms of cardiac dysfunction

• Biochemical studies may show renal insufficiency

as a possible compounding factor

• Serum electrolytes may disclose hypokalemia,

which increases the risk of arrhythmias;
hyperkalemia, which may limit the use of inhibitors
of the renin–angiotensin system; or hyponatremia,
an indicator of marked activation of the renin–
angiotensin system and a poor prognostic sign
 Assays of BNP
• Assays of serum BNP or amino terminal pro-BNP can
be a useful adjunct to the clinical history and
physical examination in the diagnosis of heart failure

• Measurement of serum BNP has been shown to add

to clinical assessment in differentiating dyspnea due
to heart failure from noncardiac causes

• BNP is expressed primarily in the ventricles and is

elevated when ventricular filling pressures are high.
• Thyroid function should be assessed in older
patients to detect occult thyrotoxicosis or
myxedema

• In unexplained cases, appropriate biopsies

may lead to a diagnosis of amyloidosis, and
additional assessment should include iron
studies to exclude hemochromatosis

• Myocardial biopsy may exclude specific

causes of dilated cardiomyopathy but rarely
reveals specific reversible diagnoses
 ECG

• Underlying or secondary arrhythmia

• Myocardial infarction

• Nonspecific changes that often

include low voltage, intraventricular
conduction defects, LVH, and
nonspecific repolarization changes
 Chest Radiography

• Chest radiographs provide information about the size

and shape of the cardiac silhouette

• Cardiomegaly is an important finding

• Evidence of pulmonary venous hypertension includes

relative dilation of the upper lobe veins, perivascular
edema (haziness of vessel outlines), interstitial edema,
and alveolar fluid

• In acute heart failure, these findings correlate

moderately well with pulmonary venous pressure

• Patients with chronic heart failure may show relatively

normal pulmonary vasculature despite markedly
elevated pressures

• Pleural effusions are common and tend to be bilateral or

 Additional Studies

• Echocardiogram:
• The most useful test is the echocardiogram
• This will reveal the size and function of both ventricles and of
the atria
• It will also allow detection of pericardial effusion, valvular
abnormalities, intracardiac shunts, and segmental wall motion
abnormalities suggestive of old myocardial infarction as
opposed to more generalized forms of dilated cardiomyopathy

• Stress imaging procedures such as perfusion scintigraphy or

dobutamine echocardiography are often indicated
 Cardiac Catheterization:

• Left heart catheterization is necessary when significant

valvular disease must be excluded and when the presence
and extent of CAD must be determined

• The latter is particularly important when LV dysfunction

may be partially reversible by revascularization

• The combination of angina or noninvasive evidence of

significant myocardial ischemia with symptomatic heart
failure is often an indication for coronary angiography if
the patient is a potential candidate for revascularization

• Right heart catheterization may be useful to select and

monitor therapy in patients refractory to standard therapy
 Treatment
Pharmacologic Treatment
Correction of Reversible Causes
• The major reversible causes of chronic heart failure include
valvular lesions, myocardial ischemia, uncontrolled
hypertension, arrhythmias (especially persistent
tachycardias), alcohol- or drug-induced myocardial
depression, intracardiac shunts, and high-output states

• Calcium channel blockers, antiarrhythmic drugs, and

nonsteroidal anti-inflammatory agents are important causes
of worsening heart failure

• Some metabolic and infiltrative cardiomyopathies may be

partially reversible, or their progression may be slowed;
these include hemochromatosis, sarcoidosis, and
amyloidosis

• Reversible causes of diastolic dysfunction include

Diuretic Therapy
• Diuretics are the most effective symptomatic
relief to patients with moderate to severe CHF

• Excessive diuresis can lead to electrolyte

imbalance and neurohormonal activation

• A combination of a diuretic and an ACE inhibitor

should be the initial treatment in most
symptomatic patients

• When fluid retention is mild, thiazide diuretics or

a similar type of agent (hydrochlorothiazide, 25–
100 mg; metolazone, 2.5–5 mg; chlorthalidone,
25–50 mg; etc) may be sufficient
• Patients with more severe heart failure should be treated with
one of the loop diuretics.

• These include furosemide (20–320 mg daily), bumetanide (1–8

mg daily), and torsemide (20–200 mg daily)

• These agents have a rapid onset and a relatively short duration

of action

• In acute situations or when gastrointestinal absorption is in

doubt, they should be given intravenously

• The potassium-sparing agents spironolactone, triamterene, and

amiloride are often useful in combination with the loop diuretics
and thiazides

• Spironolactone is a specific inhibitor of aldosterone, which is

often increased in CHF and has important effects beyond
potassium retention

• Combinations of potassium supplements or ACE inhibitors and

potassium-sparing drugs can produce hyperkalemia but have
been used with success in patients with persistent hypokalemia.
 • Inhibitors of the Renin–
Angiotensin–Aldosterone
System
• The renin–angiotensin–aldosterone system
is activated early in the course of heart
failure and plays an important role in the
progression of this syndrome

• Inhibition of this system with ACE

inhibitors should be considered part of the
initial therapy of this syndrome based on
their favorable effects on prognosis.
• ACE inhibitors
• ACE inhibitors block the renin–angiotensin–aldosterone
system by inhibiting the conversion of angiotensin I to
angiotensin II, producing vasodilation by limiting angiotensin
II-induced vasoconstriction, and decreasing sodium retention
by reducing aldosterone secretion

• Because ACE is also involved in the degradation of bradykinin,

ACE inhibitors result in higher bradykinin levels, which in turn
stimulate the synthesis of prostaglandins and nitric oxide

• ACE inhibitors reduce mortality in patients with symptomatic

heart failure and have been shown also to prevent
hospitalizations, increase exercise tolerance, and reduce
symptoms in these patients
• ACE inhibitors should be part of first-line treatment of
patients with symptomatic LV systolic dysfunction (EF <
40%), usually in combination with a diuretic

• Because ACE inhibitors may induce significant

hypotension, particularly following the initial doses, they
must be started with caution

• Patients prone to hypotension should generally be

started at low dosages (captopril 6.25 mg three times
daily, enalapril 2.5 mg daily, or the equivalent), but
other patients may be started at twice these dosages
• ACE inhibitors should be titrated (captopril 50 mg three
times daily, enalapril 10 mg twice daily, lisinopril 10 mg
daily, or the equivalent) over a period of 1–3 months.

• The most common side effects of ACE inhibitors in heart

failure patients are dizziness (often not related to the
level of BP) and cough
•Angiotensin II receptor
blockers
• Another approach to inhibiting the
renin–angiotensin–aldosterone system
is the use of specific ARBs) which will
block or decrease most of the effects
of the system

• ARBs, specifically candesartan or

valsartan, provide important benefits
as an alternative, and in addition, to
ACE inhibitors in chronic heart failure
•Spironolactone
• Aldosterone may mediate some of the major
effects of renin–angiotensin–aldosterone system
activation, such as myocardial remodeling and
fibrosis, as well as sodium retention and
potassium loss at the distal tubules

• Spironolactone should be considered as a

neurohormonal antagonist rather than narrowly as
a potassium-sparing diuretic

• Potassium levels should be monitored closely

during initiation of spironolactone (after 1 and 4
weeks of therapy), particularly for patients with
even mild degrees of renal insufficiency, and in
patients receiving ACE inhibitors
• β-Blockers
• β-blockers have traditionally been considered to be
contraindicated in patients with heart failure because they
may block the compensatory actions of the sympathetic
nervous system, there is now strong evidence that these
agents have important beneficial effects in this patient
population

• The mechanism of this benefit remains unclear, but it is likely

that chronic elevations of catecholamines and sympathetic
nervous system activity cause progressive myocardial
damage, leading to worsening LV function and dilation

• Carvedilol, a nonselective β1- and β2-receptor blocker with

additional weak α -blocking activity, was the first β-blocker
approved for heart failure

• Others are metoprolol and Bisoprolol.

• Digitalis Glycosides
• The digitalis glycosides (primarily digoxin) are the only orally active
positive inotropic agents currently available

• They bind to the sodium–potassium ATPase on the sarcolemmal

membrane, inhibiting the sodium pump and thereby increasing
intracellular sodium

• This facilitates sodium–calcium exchange, with a resultant increase

in cytosolic calcium, which enhances contractile protein cross-
bridge formation and force generation

• Digoxin should be used for patients who remain symptomatic when

taking diuretics and ACE inhibitors as well as for patients with heart
failure who are in atrial fibrillation and require rate control

• The oral maintenance dose of Digoxin, may range from 0.125 mg

three times weekly to 0.5 mg daily

• Digoxin toxicity is also a very important concern because

therapeutic-to-toxic ratio is quite narrow
•Vasodilators
• Agents that dilate arteriolar smooth muscle and lower
peripheral vascular resistance reduce LV afterload

• Medications that diminish venous tone and increase venous

capacitance reduce the preload of both ventricles as their
principal effect

• Because most patients with moderate to severe heart failure

have both elevated preload and reduced cardiac output, the
maximum benefit of vasodilator therapy can be achieved by
an agent or combination of agents with both actions

• The combination of hydralazine and isosorbide dinitrate has

also improved survival, but to a lesser extent than ACE
inhibitors

• It is now prudent to use this combination in addition to other

effective therapies in African Americans with severe heart
failure
•Nitrates
• Intravenous vasodilators (sodium nitroprusside or
nitroglycerin) are used primarily for acute or severely
decompensated chronic heart failure

• sosorbide dinitrate is also used

• Nitroglycerin ointment, 12.5–50 mg (1–4 inches)

every 6–8 hours, appears to be equally effective
although somewhat inconvenient for long-term
therapy

• Nitrate therapy is generally well tolerated, but

headaches and hypotension may limit the dose of all
agents

• The development of tolerance to long-term nitrate

therapy is now generally acknowledged.
• Nesiritide
• This agent, a recombinant form of human brain
natriuretic peptide, is a potent vasodilator that
reduces ventricular filling pressures and improves
cardiac output

• Its hemodynamic effects resemble those of

intravenous nitroglycerin with longer duration of
action

• Because most patients with acute heart failure

respond well to conventional therapy, the role of
nesiritide may be primarily in patients who
continue to be symptomatic after initial treatment
with diuretics and nonparenteral
• Hydralazine

• Oral hydralazine is a potent arteriolar

dilator and markedly increases
cardiac output in patients with CHF

• The combination of nitrates and oral

hydralazine produces greater
hemodynamic effects
• Positive Inotropic Agents

• Intravenous agents, such as the α1-agonist dobutamine and

the phosphodiesterase inhibitor milrinone, are sometimes
used on a long-term or intermittent basis

• The role of positive inotropic agents appears to be limited to

patients with symptoms and signs of low cardiac output
(primarily hypoperfusion and deteriorating renal function)
and those who do not respond to intravenous diuretics

• In some cases, dobutamine or milrinone may help maintain

patients who are awaiting cardiac transplantation.
 Nonpharmacologic
Treatment
Case Management:
• Strategies to prevent clinical deterioration, such as case
management include home monitoring of weight and
clinical status, and patient adjustment of diuretics, can
prevent rehospitalizations and should be part of the
treatment regimen of advanced heart failure
Diet:
• Patients should routinely practice moderate salt
restriction (2–2.5 g sodium or 5–6 g salt per day)
• More severe sodium restriction is usually difficult to
achieve and unnecessary because of the availability of
potent diuretic agents
Exercise Training:
• Exercise training improves activity tolerance significantly
by reversing the peripheral abnormalities associated
with heart failure and deconditioning
• In severe heart failure, restriction of activity may
facilitate temporary recompensation
• In stable patients, a prudent increase in activity or a
regular exercise regimen can be encouraged
• Gradual exercise program is associated with diminished
symptoms and substantial increases in exercise capacity

Coronary Revascularization
• Since underlying CAD is the cause of heart failure in the
majority of patients, coronary revascularization may
both improve symptoms and prevent progression
• In general, bypass surgery is preferable to PTCA in the
setting of heart failure because it provides more
complete revascularization.
Biventricular Pacing (Resynchronization)

• Many patients with heart failure due to systolic

dysfunction have abnormal intraventricular conduction
that results in dyssynchronous and hence inefficient
contractions

• Resynchronization therapy is indicated for patients with

moderate to severe heart failure and LV dyssynchrony

Cardiac Transplantation
• Because of the poor prognosis of patients with
advanced heart failure, cardiac transplantation has
become widely used

Other Surgical Treatment Options

• Cardiomyoplasty
• Ventricular reduction surgery
• Externally powered and implantable ventricular assist
devices
• Palliative Care

• Despite the technologic advances of

recent years, it should be remembered
that many patients with chronic heart
failure are elderly and have multiple
comorbidities

• Many of them will not experience

meaningful improvements in survival with
aggressive therapy, and the goal of
management should be symptomatic
improvement and palliation
 Prevention
• Because many of the processes leading to heart failure
are of long standing and progress gradually, heart
failure is often preventable by early detection of
patients at risk and early intervention

• In patients who are at risk for developing heart failure

(such as patients with hypertension or CAD),
development of heart failure can be prevented with
interventions such as the aggressive treatment of
hypertension, modification of coronary risk factors, and
reduction of excessive alcohol intake

• In patients who have structural heart disease e.g.

patients with previous myocardial infarction, ACE
inhibitors and β-blockers prevent heart failure.
• In patients with LVH, or asymptomatic valvular disease,
more aggressive treatment of hypertension and early
surgical intervention are effective