HEART FAILURE- BASIC CONCEPTS

• Heart failure describes the clinical syndrome that develops when the heart cannot maintain
adequate output, or can do so only at the expense of elevated ventricular filling pressure.
• In mild to moderate forms of heart failure, symptoms occur only when the metabolic demand
increases during exercise or some other form of stress. In severe heart failure, symptoms may
be present at rest.
• In clinical practice, heart failure may be diagnosed when a patient with significant heart
disease develops the signs or symptoms of a low cardiac output, pulmonary congestion or
systemic venous congestion at rest or on exercise. Three types of heart failure are recognised.
 HEART FAILURE DEFINITION

• Cardiac output is inadequate for the body’s requirements.

• Prognosis is poor with ~25–50% of patients dying within 5yrs of diagnosis.
• Prevalence 1–3% of the general population; ~10% among elderly patients.
 CLINICAL ASSESSMENT

• Heart failure may develop suddenly, as in MI, or gradually, as in valvular heart disease.
• When there is gradual impairment of cardiac function, several compensatory changes take place.
The term compensated heart failure is sometimes used to describe the condition of those with
impaired cardiac function, in whom adaptive changes have prevented the development of overt
heart failure.
• However, a minor event, such as an intercurrent infection or development of atrial fibrillation, may
precipitate acute heart failure in these circumstances
• Similarly, acute heart failure sometimes supervenes as the result of a decompensating episode, on
a background of chronic heart failure; this is called acute-on-chronic heart failure.
ACUTE VERSUS CHRONIC HEART FAILURE
ACUTE HEART FAILURE
• is often used exclusively to mean
new onset acute or decompensation
of chronic heart failure characterized
by pulmonary and/or peripheral
oedema with or without signs of
peripheral hypoperfusion.
CHRONIC HEART FAILURE
• develops or progresses slowly.
• Venous congestion is common but
arterial pressure is well maintained
until very late.
 LEFT-SIDED VERSUS RIGHT-SIDED FAILURE
MAY OCCUR INDEPENDENTLY, OR TOGETHER AS
CONGESTIVE CARDIAC FAILURE (CCF)
LEFT VENTRICULAR FAILURE
(LVF)
• Causes: aortal valves diseases, mitral
regurgitation, hypertension, CAD
• Symptoms: Dyspnoea, poor exercise tolerance,
fatigue, orthopnoea, paroxysmal nocturnal
dyspnoea (PND), nocturnal cough (±pink frothy
sputum), wheeze (cardiac ‘asthma’), nocturia,
cold peripheries, weight loss, muscle wasting.
RIGHT VENTRICULAR
FAILURE (RVF)
• Causes: LVF, pulmonary stenosis, lung
disease (emphisema, pnemoslerosis)
• Symptoms: Peripheral oedema (up to thighs,
sacrum, abdominal wall), ascites, nausea,
anorexia, facial engorgement, pulsation in
neck and face (tricuspid regurgitation),
epistaxis.
 LEFT ATRIAL FAILURE
(LAF)

• Causes: mitral stenosis

• Symptoms: Dyspnoea, cyanosis,
paroxysmal nocturnal dyspnoea
(PND), nocturnal cough

• LAF lead to right ventricular failure

(RVF) due to pulmonary hypertension
 SYSTOLIC VERSUS DIASTOLIC FAILURE
NB: SYSTOLIC AND DIASTOLIC FAILURE
USUALLY COEXIST
SYSTOLIC FAILURE
• inability of the ventricle to contract
normally, resulting in decreasing of
cardiac output.
• Ejection fraction (EF) is <40%.
• Causes: IHD, MI, cardiomyopathy.
DIASTOLIC FAILURE
• inability of the ventricle to relax and fill
normally, causing filling pressures.
• EF is >50%.
• Causes: constrictive pericarditis,
tamponade, restrictive cardio myopathy,
hypertension.
 LOW-OUTPUT VERSUS HIGH-OUTPUT FAILURE
LOW-OUTPUT HEART FAILURE HIGH-OUTPUT HEART FAILURE
• Cardiac output is  and fails to  normally with • This is rare. Here, output is normal or
exertion.
increased in the face of needs.
• Causes: Pump failure: Systolic and/or diastolic HF (see
above), heart rate (eg -blockers, heart block, post • Failure occurs when cardiac output fails to
MI), negatively inotropic drugs (eg most antiarrhythmic meet these needs. It will occur with a
agents).
normal heart, but even earlier if there is
• Excessive preload: eg mitral regurgitation or fluid
heart disease. Causes: Anaemia, pregnancy,
overload (eg NSAID causing fluid retention). Fluid
overload may cause LVF in a normal heart if renal hyperthyroidism, Paget’s disease,
excretion is impaired or big volumes are involved arteriovenous malformation, beri beri.
• More common if there is simultaneous compromise of
cardiac function, and in the elderly.
• Consequences: Initially features of RVF;
later LVF becomes evident.
• Chronic excessive afterload: eg aortic stenosis,
hypertension.
 NEW YORK CLASSIFICATION OF HEART
FAILURE: SUMMARY

• I Heart disease present, but no undue dyspnoea from ordinary activity.

• II Comfortable at rest; dyspnoea on ordinary activities.
• III Less than ordinary activity causes dyspnoea, which is limiting.
• IV Dyspnoea present at rest; all activity causes discomfort.
 SIGNS

• To diagnose there should be symptoms of failure and objective evidence of

cardiac dysfunction (at rest).
• Diagnosis can be made using Framingham criteria
• Other signs: exhaustion, cool peripheries, cyanosis, BP, narrow pulse
pressure, pulsus alternans, displaced apex (LV dilatation), RV heave
(pulmonary hypertension), murmurs of mitral or aortic valve disease, wheeze
(cardiac asthma).
 FRAMINGHAM CRITERIA FOR CONGESTIVE
CARDIAC FAILURE (CCF)
MAJOR CRITERIA MINOR CRITERIA
• Paroxysmal nocturnal dyspnoea
• Bilateral ankle oedema
• Neck vein distention
• Crepitations • Nocturnal cough
• Acute pulmonary oedema
• Dyspnoea on ordinary exertion
• S3 gallop
• Hepatojugular reflux • Hepatomegaly
• Cardiomegaly (cardiothoracic ratio >50% on chest
radiography)
• Tachycardia (heart rate >120/min)
• Increased central venous pressure (>16cmH2O at • Pleural effusion
right atrium)
• Weight loss >4.5kg in 5 days in response to • Decrease in vital capacity by ⅓ from
treatment maximum recorded
 INVESTIGATIONS

• According to NICE, if ECG and B-type natriuretic peptide are

normal, heart failure is unlikely, and an alternative diagnosis
should be considered; if either is abnormal, then echocardiography
is required.
 INVESTIGATIONS

• Tests: FBC; U&E; BNP; CXR: cardiomegaly (cardiothoracic ratio >50%), prominent upper lobe
veins (upper lobe diversion), peribronchial cuffing, diffuse interstitial or alveolar shadowing,
classical perihilar ‘bat’s wing’ shadowing, fluid in the fi ssures, pleural effusions, septal (formerly
called ‘Kerley B’) lines (variously attributed to interstitial oedema and engorged peripheral
lymphatics .
• ECG may indicate cause (look for evidence of ischaemia, MI, or ventricular hypertrophy). It is rare
to get a completely normal ECG in chronic heart failure. Echocardiography is the key investigation.
• It may indicate the cause (MI, valvular heart disease) and can confirm the presence or absence of
LV dysfunction. Endomyocardial biopsy is rarely needed.
 FACTORS THAT MAY PRECIPITATE OR
AGGRAVATE HEART FAILURE IN PRE-EXISTING
HEART DISEASE
• Myocardial ischaemia or infarction
• Intercurrent illness
• Arrhythmia
• Inappropriate reduction of therapy
• Administration of a drug with negative inotropic (β-blocker) or fluid-retaining properties (non-steroidal anti-
inflammatory drugs, glucocorticoids)
• Pulmonary embolism
• Conditions associated with increased metabolic demand (pregnancy, thyrotoxicosis, anaemia)
• Intravenous fluid overload
 CLINICAL FEATURES OF LEFT AND RIGHT
HEART FAILURE
• Patients with chronic heart failure commonly follow a relapsing and remitting course, with periods of stability and episodes of
decompensation, leading to worsening symptoms that may necessitate hospitalisation.
• The clinical picture depends on the nature of the underlying heart disease, the type of heart failure that it has evoked, and the changes
in the SNS and RAAS that have developed
• Fatigue, listlessness and a poor effort tolerance; the peripheries are cold and the BP is low.
• To maintain perfusion of vital organs, blood flow is diverted away from skeletal muscle and this may contribute to fatigue and
weakness.
• Poor renal perfusion leads to oliguria and uraemia
• Pulmonary oedema due to left heart failure presents with dyspnoea and inspiratory crepitations over the lung bases. In contrast, right
heart failure produces a high JVP with hepatic congestion and dependent peripheral oedema. In ambulant patients the oedema affects
the ankles, whereas in bed-bound patients it collects around the thighs and sacrum. Ascites or pleural effusion may occur . Heart failure
is not the only cause of oedema
 HEART FAILURE IS NOT THE ONLY CAUSE OF
OEDEMA

LEFT HEART FAILURE RIGHT HEART FAILURE

• JVP +/++ • Raised JVP +++

• Pleural effusions • Hepatomegaly
• Pulmonary oedema Cardiomegaly • Ascites
• Pitting oedema +/++ • Peripheral pitting oedema +++
 DIFFERENTIAL DIAGNOSIS OF PERIPHERAL
OEDEMA

• Cardiac failure: right or combined left and right heart failure, pericardial constriction, cardiomyopathy
• Chronic venous insufficiency: varicose veins
• Hypoalbuminaemia: nephrotic syndrome, liver disease, protein losing enteropathy; often widespread, can
affect arms and face
• Drugs:
Sodium retention: fludrocortisone, non-steroidal anti- inflammatory drugs
Increasing capillary permeability: nifedipine, amlodipine •
• Idiopathic: women > men •
• Chronic lymphatic obstruction
CLINICAL FEATURES OF LEFT AND RIGHT
HEART FAILURE

• weight loss (cardiac cachexia), caused by anorexia and impaired absorption

due to gastrointestinal congestion, poor tissue perfusion due to a low cardiac
output, and skeletal muscle atrophy due to immobility.
 LEFT HEART FAILURE

• This is characterised by a reduction in left ventricular output and an increase in left

atrial and pulmonary venous pressure.
• If left heart failure occurs suddenly – for example, as the result of an acute MI – the
rapid increase in left atrial pressure causes pulmonary oedema.
• If the rise in atrial pressure is more gradual, as occurs with mitral stenosis, there is
reflex pulmonary vasoconstriction, which protects the patient from pulmonary
oedema. However, the resulting increase in pulmonary vascular resistance causes
pulmonary hypertension, which in turn impairs right ventricular function.
 RIGHT HEART FAILURE

• This is characterised by a reduction in right ventricular output and an

increase in right atrial and systemic venous pressure.
• The most common causes are chronic lung disease, pulmonary embolism and
pulmonary valvular stenosis.
• The term ‘cor pulmonale’ is used to describe right heart failure that is
secondary to chronic lung disease.
 BIVENTRICULAR HEART FAILURE

• Both sides of the heart are affected.

• Affects both ventricles or because disease of the left heart leads to chronic
elevation of the left atrial pressure, pulmonary hypertension and right heart
failure
• Causes: dilated cardiomyopathy or ischaemic heart disease
 EPIDEMIOLOGY

• Heart failure predominantly affects the elderly;

• The prevalence rises from 1% in those aged 50–59 years to over 10% in those aged 80–89 years
• Approximately 50% of patients with severe heart failure due to left ventricular dysfunction will
die within 2 years because of either pump failure or malignant ventricular arrhythmias.
• The most common causes are coronary artery disease and myocardial infarction but almost all
forms of heart disease can lead to heart failure.
• An accurate diagnosis is important because treatment of the underlying cause may reverse heart
failure or prevent its progression.
 PATHOGENESIS

• Heart failure occurs when cardiac output fails to meet the demands of the
circulation.
• Cardiac output is determined by preload (the volume and pressure of blood in
the ventricles at the end of diastole), afterload (the volume and pressure of
blood in the ventricles during systole) and myocardial contractility, forming
the basis of Starling’s Law .
 STARLING’S LAW

• Normal (A), mild (B), moderate (C) and severe (D) heart failure.
• Ventricular performance is related to the degree of myocardial stretching. An
increase in preload (end-diastolic volume, end-diastolic pressure, filling pressure or
atrial pressure) will therefore enhance function; however, overstretching causes
marked deterioration. In heart failure, the curve moves to the right and becomes
flatter.
• An increase in myocardial contractility or a reduction in afterload will shift the curve
upwards and to the left (green arrow).
 VENTRICULAR DYSFUNCTION IS THE MOST
COMMON CAUSE OF HEART FAILURE
• This can occur because of impaired systolic contraction due to myocardial disease, or diastolic
dysfunction where there is abnormal ventricular relaxation due to a stiff, non-compliant
ventricle. This is most commonly found in patients with left ventricular hypertrophy
• Systolic dysfunction and diastolic dysfunction often coexist, particularly in patients with CAD.
• Ventricular dysfunction reduces cardiac output, which, in turn, activates the sympathetic
nervous system (SNS) and renin–angiotensin–aldosterone system (RAAS). Under normal
circumstances, activation of the SNS and RAAS supports cardiac function but, in the setting of
impaired ventricular function, the consequences are negative and lead to an increase in both
afterload and preload .
 VENTRICULAR DYSFUNCTION

• A vicious circle may then be established because any additional fall in cardiac output causes further
activation of the SNS and RAAS, and an additional increase in peripheral vascular resistance. Activation
of the RAAS causes vasoconstriction and sodium and water retention. This is primarily mediated by
angiotensin II, a potent constrictor of arterioles, in both the kidney and the systemic circulation.
• Activation of the SNS also occurs and can initially sustain cardiac output through increased myocardial
contractility and heart rate. Prolonged sympathetic stimulation has negative effects, however, causing
cardiac myocyte apoptosis, cardiac hypertrophy and focal myocardial necrosis. Sympathetic stimulation
also contributes to vasoconstriction and predisposes to arrhythmias. Sodium and water retention is further
enhanced by the release of aldosterone, endothelin-1 (a potent vasoconstrictor peptide with marked
effects on the renal vasculature) and, in severe heart failure, vasopressin (antidiuretic hormone, ADH).
 VENTRICULAR DYSFUNCTION IS THE MOST
COMMON CAUSE OF HEART FAILURE
• Natriuretic peptides are released from the atria in response to atrial dilatation and
compensate to an extent for the sodium-conserving effect of aldosterone, but this mechanism
is overwhelmed in heart failure. Pulmonary and peripheral oedema occurs because of high
left and right atrial pressures, and is compounded by sodium and water retention, caused by
impairment of renal perfusion and by secondary hyperaldosteronism.
• If the underlying cause is a myocardial infarction, cardiac contractility is impaired and SNS
and RAAS activation causes hypertrophy of noninfarcted segments, with thinning, dilatation
and expansion of the infarcted segment . This leads to further deterioration in ventricular
function and worsening heart failure.
NEUROHUMORAL ACTIVATION AND COMPENSATORY
MECHANISMS IN HEART FAILURE
Increased
Increased blood
blood pressure
pressure and
and cardiac
cardiac work
work

Myocyte loss Increased

Increased Myocardial Heart failure intravascular
afterload fibrosis Reduced volume
cardiac output

Vasoconstriction Sodium and

water retention
Neurohumoral activation
Sympathetic nervous system Renin –
angiotensin system Vasopressin system
Endothelin system
 HIGH-OUTPUT FAILURE

• Sometimes cardiac failure can occur in patients without heart disease due to a
large arteriovenous shunt, or where there is an excessively high cardiac
output due to beri-beri , severe anaemia or thyrotoxicosis.
 VALVULAR DISEASE

Heart failure can also be caused by valvular disease:

• Impaired filling of the ventricles due to mitral or tricuspid stenosis;
• Obstruction to ventricular outflow, as occurs in aortic and tricuspid stenosis
and hypertrophic cardiomyopathy;
• The result of ventricular overload secondary to valvular regurgitation.
 MECHANISMS OF HEART FAILURE
Cause
Reduced ventricular contractility
Ventricular outflow obstruction
(pressure overload)
Ventricular inflow obstruction
Examples
Myocardial infarction (segmental
dysfunction)
Myocarditis/cardiomyopathy (global
dysfunction)
Hypertension, aortic stenosis (left heart
failure) Pulmonary hypertension,
pulmonary valve stenosis (right heart
failure)
Mitral stenosis, tricuspid stenosis
Features
In СAD, ‘akinetic’ or ‘dyskinetic’
segments contract poorly and may
impede the function of normal segments
by distorting their contraction and
relaxation patterns.
Progressive ventricular dilatation
Initially, concentric ventricular
hypertrophy allows the ventricle to
maintain a normal output by generating
a high systolic pressure. Later,
secondary changes in the myocardium
and increasing obstruction lead to failure
with ventricular dilatation and rapid
clinical deterioration
Small, vigorous ventricle; dilated,
hypertrophied atrium. Atrial fibrillation
is common and often causes marked
deterioration because ventricular filling
depends heavily on atrial contraction
 MECHANISMS OF HEART FAILURE
Cause Examples
Ventricular volume overload Left ventricular volume overload
(mitral or aortic regurgitation)
Ventricular septal defect Right
ventricular volume overload (atrial
septal defect) Increased metabolic
demand (high output)
Arrhythmia Atrial fibrillation
Tachycardia
Complete heart block
Features
Dilatation and hypertrophy allow the
ventricle to generate a high stroke
volume and help to maintain a normal
cardiac output. However, secondary
changes in the myocardium lead to
impaired contractility and worsening
heart failure
Tachycardia does not allow for
adequate filling of the heart, resulting
in reduced cardiac output and back
pressure
Prolonged tachycardia causes
myocardial fatigue
Bradycardia limits cardiac output,
even if stroke volume is normal
 MECHANISMS OF HEART FAILURE
Cause Examples
Diastolic dysfunction Constrictive pericarditis
Restrictive cardiomyopathy
Left ventricular hypertrophy and
fibrosis
Cardiac tamponade
Features
Marked fluid retention and peripheral
oedema, ascites, pleural effusions and
elevated jugular veins
Bi-atrial enlargement (restrictive
filling pattern and high atrial
pressures). Atrial fibrillation may
cause deterioration
Good systolic function but poor
diastolic filling
Hypotension, elevated jugular veins,
pulsus paradoxus, poor urine output
 COMPLICATIONS OF HEART FAILURE

• Renal failure
• Hypokalaemia
• Hyperkalaemia
• Hyponatraemia
• Impaired liver function
• Thromboembolism
• Atrial and ventricular arrhythmias related to hypokalaemia and hypomagnesaemia
• Sudden death due to ventricular fibrillation
 INVESTIGATIONS

1.Clinical symptoms: fatigue, listlessness and a poor effort tolerance

2. Determine the aetiology: MI, CAD, arterial hypertension,
rheumatism,cardiomyopathy
3. Interstitial oedema of ancles,ascites,pulse учащенный низкоамплитудный,
III tone, heart border moved
4. Serum urea, creatinine and electrolytes, hemoglobin and thyroid function,
cardiospesific enzymes
 INVESTIGATIONS

5. A chest X-ray: abnormal distension of the upper lobe pulmonary veins with the
patient in the erect position.
Vascularity of the lung fields becomes more prominent and the right and left
pulmonary arteries dilate. Subsequently, interstitial oedema causes thickened
interlobular septa and dilated lymphatics. These are evident as horizontal lines in the
costophrenic angles (septal or ‘Kerley B’ lines).
More advanced changes due to alveolar oedema cause a hazy opacification spreading
from the hilar regions, and pleural effusions
 INVESTIGATIONS

6. Echocardiography:
• to determine the aetiology
• to detect hitherto unsuspected valvular heart disease, such as occult mitral stenosis, and other
conditions that may be amenable to specific remedies
• to identify patients who will benefit from long-term drug therapy.
7. ECG& tredmill test
8. MRT, ventriculograpgy
9. Ultrasound of organs
 CHRONIC HEART FAILURE—MANAGEMENT

• Stop smoking.
• Eat less salt.
• Optimize weight & nutrition.
• Treat the cause (eg if dysrhythmias; valve disease).
• Treat exacerbating factors (anaemia, thyroid disease, infection, BP).
• Avoid exacerbating factors, eg NSAIDS (fl uid retention) and verapamil (–ve
inotrope).
 CHRONIC HEART FAILURE—MANAGEMENT
• Drugs: the following are used:
1 Diuretics
2 ACE-i:
3 Beta-blockers
4 Digoxin
5 Vasodilators