Heart Failure

Prepared by:
Dr. Zacharia (MD)
Learning Objectives
By the end of this session, students are expected to be able to:
Define heart failure
Discuss causes of heart failure
Mention types of heart failure
Describe a brief account of epidemiology of heart failure
Describe clinical feature of heart failure
Discuss differential diagnoses of heart failure
Describe management of heart failure
Definition
Heart failure: Is a complex syndrome that can result from any
structural or functional cardiac disorder that impairs the ability of the
heart to function as a pump to support a physiological circulation.
Heart failure (HF) can also be defined as the pathophysiologic state in
which an abnormality of cardiac function is responsible for the failure
of the heart to pump blood at a rate commensurate with the
requirements of the metabolizing tissues and/or allows it to do so
only from an abnormally elevated diastolic volume.
Heart failure may be caused by myocardial failure.
Heart failure always causes circulatory failure.
Types of Heart Failure
1. Right sided heart failure
2. Left sided heart failure
3. Congestive heart failure (Bilateral cardiac failure)
Epidemiology of Heart Failure
Heart failure is a worldwide problem.
The most common cause of heart failure in industrialized countries is
ischemic cardiomyopathy.
Valvular cardiomyopathy assumes a more important role in
underdeveloped countries than in the United States.
However, as underdeveloped countries urbanize and become more well
off, the rate of heart failure increases in concordance with rates of
Diabetes
Hypertension
More processed diet
More sedentary lifestyle
Despite recent advances in the management of patients with heart
failure, morbidity and mortality rates remain high, with an estimated 5-
year mortality rate of 50%
Progressive renal insufficiency is common in patients with long-
standing heart failure as well as acutely decompensated heart failure.
The higher prevalence of heart failure in African Americans, Hispanics,
and Native Americans is directly related to the higher incidence and
prevalence of hypertension and diabetes.
The prevalence of heart failure increases with age.
The prevalence is 1-2% of the population younger than 55 years and
increases dramatically to a rate of 10% of those older than 75 years.
Nonetheless, heart failure can occur at any age, depending on the
cause.
Aetiology
It is a common end point for many diseases of cardiovascular system
that can be caused by
Inappropriate work load (volume or pressure overload)
Restricted filling
Myocyte loss
Causes of heart failure include:
Ventricular volume overload
o Left Ventricle (LV) volume overload (e.g. Mitral or Aortic
Regurgitation, Arteriovenous fistulae)
o Ventricular Septal defect (VSD)
o Right Volume overload (e.g.Atrial Septal defect)
o Increased metabolic demand (high output)
Ventricular outflow obstruction (pressure overload)
o Systemic hypertension, Aortic Stenosis (Left Heart Failure)
o Pulmonary hypertension, pulmonary valve stenosis (Right heart
failure)
Ventricular inflow obstruction
o Mitral stenosis,
o Tricuspid stenosis
Reduced ventricular contractility (loss of muscles)
o Post myocardial infarction (MI-Segmental dysfunction)
o Chronic ischemia
o Connective tissue diseases
o Myocarditis/Cardiomyopathy (global dysfunction)
o Infection
o Poisons (alcohol, cobalt, doxorubicin)
Restricted Filling (diastolic dysfunction)
o Pericardial diseases
o Restrictive cardiomyopathy
o Left ventricular hypertrophy and fibrosis
o Cardiac temponade
Arrythmia
o Atrial fibrillation
o Tachycardia cardiomyopathy
o Complete heart block
Pathophysiology
Hemodynamic changes
Neurohormonal changes
Cellular changes
Hemodynamic Changes
From hemodynamic stand point HF can be secondary to systolic
dysfunction or diastolic dysfunction
Neurohormonal Changes
Cellular Changes
Changes in Ca+2 handling
Changes in adrenergic receptors
o Slight ↑ in α1 receptors
o β1 receptors desensitization → followed by down regulation
Changes in contractile proteins
Programmed cell death (Apoptosis)
Increase amount of fibrous tissue in heart muscles
Left sided-heart Failure
CLINICAL FEATURES

Breathlessness, a cardinal symptom of left ventricular failure, may

manifest with progressively increasing severity as
Exertional dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea
Dyspnea at rest
Acute pulmonary edema
Other cardiac symptoms of heart failure include
Chest pain/pressure
Palpitations (awareness of heart beats)
Patients often manifest non cardiac symptoms of heart failure like
Anorexia
Nausea
Weight Loss
Bloating
Fatigue
Weakness
Oliguria
Nocturia
Cerebral symptoms of different severity ranging from anxiety to
memory impairment and confusion
Exertional Dyspnea
The principal difference between exertional dyspnea in patients who
are healthy and exertional dyspnea in patients with heart failure is the
degree of activity necessary to induce the symptom.

As left ventricular (LV) failure advances, the intensity of exercise

resulting in breathlessness progressively declines.
Orthopnea
Defined as dyspnea that develops in the recumbent position and is
relieved with elevation of the head with pillows.
The number of pillows required to relieve orthopnea is important in
assessing the severity of the dyspnoea.
Orthopnea occurs rapidly, often within a minute or two of recumbency,
and develops when the patient is awake.
Cough, particularly during recumbency, may be an ‘orthopnea
equivalent.’
This nonproductive cough may be caused by pulmonary congestion
and is relieved by the treatment of heart failure.
Paroxysmal Nocturnal Dyspnea

Paroxysmal nocturnal dyspnea usually occurs at night and is defined

as the sudden awakening of the patient, after a couple hours of sleep,
with a feeling of severe anxiety, breathlessness, and suffocation.

The patient may bolt upright in bed and gasp for breath.
Dyspnea at Rest
Acute pulmonary edema
Is defined as the sudden increase in pulmonary capillary pressure
(usually more than 25mm Hg) as a result of acute and fulminant left
ventricular failure.
It is a medical emergency and has a very dramatic clinical
presentation.
Patient appears extremely ill, poorly perfused, restless, and sweaty,
with an increased work of breathing and using respiratory accessory
muscles, tachypneic, tachycardic, hypoxic and coughing with frothy
sputum that on occasion is blood tinged.
Predominant Right-sided Heart Failure
There is reduction in right ventricular output for any given right atrial pressure.
Causes of isolated heart failure include: chronic lung disease (cor pulmonale),
multiple pulmonary emboli and pulmonary valvular stenosis.
Patient may develop fluid in the abdominal cavity (ascites)
Congestive hepatomegaly and right upper quadrant (RUQ) abdominal pain
Anasarca (Generalized edema including pedal, ankle, pretibial and sacral edema)
Other gastrointestinal symptoms, caused by congestion of the hepatic and
gastrointestinal venous circulation, include anorexia, bloating, nausea, and
constipation.
Biventricular heart failure
Failure of the left and right heart. May develop because of:
Disease process affects both ventricles e.g., dilated cardiomyopathy,
ischaemic heart disease
Disease of the left heart leads to chronic elevation of the left atrial
pressure, pulmonary hypertension and right heart failure.
Presents with clinical features of left and right heart failure.
Physical Examination
General appearance
May be dyspnoic, anxious, malnourished and sometimes even
cachectic
Central cyanosis and icterus may be evident in patients with severe
heart failure
Dusky discoloration of the skin
The pulse may be weak, rapid, and thread
Evidence of increased adrenergic activity
Tachycardia
Diaphoresis
Pallor
Peripheral cyanosis with pallor and coldness of the extremities
Pulmonary rales
Rales heard over the lung bases are characteristic of heart failure of
at least moderate severity
With acute pulmonary edema, rales are frequently accompanied by
wheezing and expectoration of frothy, blood-tinged sputum
The absence of rales certainly does not exclude elevation of
pulmonary capillary pressure due to LV failure
Edema
Edema, in the absence of dyspnea or other signs of LV or RV failure, is
not solely indicative of heart failure and can be observed in many
other conditions including
Chronic venous insufficiency
Nephrotic syndrome
Hypoproteinemia or osmotic imbalance
Hepatomegaly (enlargement of the liver)
Hepatomegaly is prominent in patients with chronic right-sided heart
failure, but it may occur rapidly in acute heart failure.
When occurs acutely, the liver is usually tender.
Hydrothorax (pleural effusion). This is most commonly observed in
patients with hypertension involving both systemic and pulmonary
systems.
Hydrothorax is usually bilateral, although when unilateral, it is
usually confined to the right side of the chest.
Ascites
This finding occurs in patients with increased pressure in the hepatic
veins and in the veins draining into the peritoneum.
Ascites usually reflects long-standing systemic venous hypertension.
Cardiomegaly (enlargement of the heart)
Fever: May be present in severe decompensated heart failure
because of cutaneous vasoconstriction and impairment of heat loss.
Staging Heart Failure
A classification of patients with heart disease based on the relation
between symptoms and the amount of effort required to provoke
them has been developed by the New York Heart Association (NYHA).
Class I: No limitations. Ordinary physical activity does not cause undue
fatigue, dyspnea, or palpitations.
Class II: Slight limitation of physical activity. Such patients are
comfortable at rest. Ordinary physical activity results in fatigue,
palpitations, dyspnea, or angina.
Class III: Marked limitation of physical activity. Although patients are
comfortable at rest, less-than-ordinary activity leads to fatigue,
dyspnea, palpitations, or angina.
Class IV: Symptomatic at rest. Symptoms of Congestive Heart Failure
are present at rest; discomfort increases with any physical activity
Based on cardiac output heart failure can be classified in low-output
failure (most of the conditions) or high-output failure (beriberi, paget
disease, pregnancy, anemia, AV fistula, sepsis).

Based on the ventricle affected, heart failure can be classified in LV

failure, RV failure, or biventricular failure.

Based on the onset of symptoms, heart failure can be acute or

chronic.
Differential Diagnoses of Heart Failure
Anaemia
Protein loosing enteropathy
Nephrotic syndrome
Chronic renal insufficiency
Pneumonia
Acute respiratory distress syndrome
Asthma
Myocardial infarction or pericardial diseases
Pulmonary edema
Pneumothorax
Pneumocystis carinii pneumonia
Pulmonary embolism
Pulmonary fibrosis
Liver disease
Management (Investigations & Treatment)
of Heart Failure
Patients with heart failure should be referred to hospitals for
evaluation and initiation of treatment. This is because most of the
services for diagnosis of complications of HF are lacking in the primary
health care facilities (dispensaries and health centres). Even some of
the drugs for the treatment of HF might not be available in the
dispensaries and health centres.
Laboratory Studies
CBC count: Assesses aggravating causes e.g. severe anemia, infection
Electrolytes
Renal function tests e.g. BUN and serum creatinine
Liver function tests to rule out primary liver disease as well as
complications of heart failure. In severe cases of acute RV or LV
failure, frank jaundice may occur.
Imaging Studies
Chest radiography
Chest radiographs are helpful in distinguishing cardiogenic pulmonary
edema (CPE) from other pulmonary causes of severe dyspnea.
Classic radiographic findings demonstrate cardiomegaly (in patients
with underlying CHF) and alveolar edema with pleural effusions and
bilateral infiltrates in a butterfly pattern.
Echocardiography
Determines LV/RV size and function, LV wall motion abnormalities,
valvular function and abnormalities, diastolic function, presence or
absence of pericardial abnormalities or intracardiac masses; evaluates
intracardiac filling pressures.
Electrocardiography (ECG)
The presence of left atrial enlargement and LV hypertrophy is
sensitive (although nonspecific) for chronic LV dysfunction.
ECG may suggest an acute tachyarrhythmia or bradyarrhythmia as the
cause of heart failure.
It may also aid in the diagnosis of acute myocardial ischemia or
infarction as the cause of heart failure.
Pulse oximetry
This is highly accurate at assessing the presence of hypoxemia and,
therefore, the severity of heart failure.
It is also useful for monitoring the patient's response to supplemental
oxygen and other therapies.
Note: For selected patients in specialized hospitals as indicated by
history and physical findings the following can be done.
Nuclear Cardiology-Radionuclide Angiography
Cardiac MRI
Positron Emission Tomography (PET)
Cardiac Catheterization
Cardiac biopsy if infiltrative diseases are suspected e.g Amyloidosis
Treatment
Patients with heart failure should be referred to hospitals for evaluation
and initiation of treatment. In the primary health facilities, only pre-
referral care can be offered such as provision of a diuretic (furosemide)
The treatment of heart failure (HF) may be divided into four
components:
Removal of the precipitating cause
Correction of the underlying cause
Prevention of deterioration of cardiac function
Control of the congestive HF state
Treat all chest infections and restore sinus rhythm in a patient with
atrial fibrillation. This will prevent development of heart failure

The prevention of deterioration of cardiac function, involves the

administration of angiotensin-converting enzyme (ACE) inhibitors and
beta-adrenergic blockers as well as reduction of cardiac work load.

Control of the congestive heart failure state requires reduction of the

excessive retention of salt and water as well as enhancement of
myocardial contractility.
Following effective treatment, recurrence of the clinical manifestations of
HF can often be prevented by continuing those measures that were
originally effective e.g. continuous use of medications and change of life
style.
As symptoms of heart failure develop simple measures such as moderate
restriction of activity and sodium intake and oral diuretics should be tried.
If these measures are insufficient, the next step is more rigorous
restriction of salt intake and higher doses and multiple diuretics.
If HF persists, hospitalization with rigid salt restriction, bed rest,
intravenous vasodilators, and positive inotropic agents are tried.
Angiotensin-Converting Enzyme (ACE) Inhibitors
The pharmacologic reduction of impedance to left ventricular
ejection with an ACE inhibitor represents an important component of
the management of HF.
ACE inhibition should not be used in hypotensive patients.
Lisinopril in doses of 20 mg qd or enalapril 10 mg bid or captopril
25mg tid have been shown to be useful in the management of heart
failure.
Angiotensin Receptor Blockers
In patients who cannot tolerate ACE inhibitors (because of cough,
angioneurotic edema, leukopenia), an angiotensin II receptor blocker
(e.g. losartan 50 mg qid) may be used instead.
Aldosterone Antagonist
Spironalactone is a specific competitive antagonist to aldosterone,
producing a weak diuresis but with a potassium sparing action.
Studies have shown that its use resulted in 30% reduction in all-cause
mortality in patients with moderate to severe heart failure. Similar
results were found with use of Eplerenone, another aldosterone
antagonist. Spironolactone is used in dosages of 12.5-25 mg/d. Risk
factors for developing hyperkalaemia increases when higher doses of
spironolactone are used or in patients with renal failure when used
together with ACE inhibitors. Potassium should be measured 5 days
after initiating spironolactone, until levels are stable, then every 1-3
months.
Beta-Adrenoceptor Blockers
There is considerable evidence to support the use of beta blockers in
patients with chronic stable heart failure. These drugs help to
counteract the deleterious effects of enhanced sympathetic
stimulation and reduce the risk of arrhythmias and sudden death.
When initiated in standard doses they may precipitate acute-on-
chronic heart failure, but when given in small incremental doses,
metoprolol and bisoprolol can increase ejection fraction, improve
symptoms, exercise tolerance, left ventricular function, reduce the
frequency of hospitalization and reduce mortality in patients with
heart failure of any cause.
Bisoprolol started at dose of 1.25 mg daily increased gradually over
12 weeks to a target maintenance dose of 10 mg daily. Carvedilol
started at 3.125 mg PO bid and titrated over a period of months
rather than days to maximally tolerated dose or to maximum of 25-
50mg bid.
Reduction of Cardiac Work Load
This consists of reducing physical activity, instituting emotional rest,
and reducing after load.
Modest restriction of physical activity in mild cases and rest in bed or
in a chair in severe failure are useful.
In acute, severe failure, meals should be small in quantity, but more
frequent, and every effort should be made to diminish the patient's
anxiety; sometimes drugs such as diazepam (2 to 5 mg tid) for several
days are useful.
Physical and emotional rest tends to lower arterial pressure and
reduce the load on the myocardium by diminishing the requirements
for cardiac output.
Reduced physical exertion should be continued for several days after
the patient's condition has stabilized.
The hazards of phlebothrombosis and pulmonary embolism which
occur with bed rest may be reduced with anticoagulants, leg
exercises, and elastic stockings.
Absolute bed rest is rarely required or advisable, and the patient
should ordinarily be encouraged to sit in a chair.
Regular, non exhausting exercise such as walking should be employed
once the patient has become compensated
Weight reduction by restriction of caloric intake in obese patients
with HF also diminishes cardiac work load and is an essential
component of the therapeutic program
Control of Excessive Fluid
Many of the clinical manifestations of HF result from expansion of the
extracellular fluid volume.
A negative sodium balance can be achieved by reducing the dietary
intake and increasing the urinary excretion of this ion with the aid of
diuretics.
Rarely, in severe HF, mechanical removal of extracellular fluid by
means of thoracocentesis and paracentesis may be necessary.
Frusemide 40-80 mg once daily orally in patients without edema and
40-120mg IV in patients with edema until edema subsides.
Diet
In patients with mild HF, symptomatic improvement may result
simply from reducing the sodium intake, particularly if accompanied
by periods of physical rest.
The normal diet contains approximately 6 to 10 g sodium chloride;
this intake can be reduced by half simply by excluding salt-rich foods
and salt added at the table.
Enhancement of Myocardial Contractility
Digitalis (Digoxin)
The improvement of myocardial contractility by means of cardiac
glycosides is useful in the control of HF.
Digitalis is particularly effective in patients with systolic HF
complicated by atrial flutter and fibrillation and a rapid ventricular
rate, who benefit from both slowing of the ventricular rate and the
positive inotropic effect.
Although digitalis does not improve survival in patients with systolic
HF and sinus rhythm, it reduces the need for hospitalization.

Digoxin is given orally at doses of 1.0-1.5mg over 24 hours loading

and maintenance of 125 - 250μg (i.e., 0.125-0.25mg) once daily. Dose
may be divided according to body mass, renal function and in atrial
fibrillation, on heart-rate response. Elderly patients may require lower
loading doses.
Complications of Heart Failure
These can also be complications of treating heart failure (drugs)
Renal failure
Hypokalaemia
Hyperkalaemia
Hyponatraemia
Impaired liver function
Thromboembolism
Atrial and ventricular arrythmias
THANX