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Transcript
“CARDIAC FAILURE”
“LEARNING OBJECTIVE”
At the end of lecture, the student should be able to know:
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What is cardiac failure?
Etiology of cardiac failure,
Diagnosis and its criteria,
Symptoms,
Physical signs,
Different mechanisms,
Pathophysiology,
Types of cardiac failure,
Complications of cardiac failure,
Investigations of cardiac failure,
Management of cardiac failure,
Diffential diagnosis.
“CARDIAC FAILURE”
DEFINITION:
A state in which the heart cannot provide sufficient cardiac
output to satisfy the metabolic needs of the body.
“CARDIAC FAILURE”
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In mild cases, the cardiac output is adequate at rest and becomes
inadequate only when increased cardiac output is required,eg in
exercise.
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Heart failure may involve either side of the heart, but as both sides
pump in parallel, failure of one side usually results in failure of
other.
“ETIOLOGY”
It is a common end point for many diseases of cardiovascular system.
It can be caused by :
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Inappropriate work load (volume or pressure overload)
Restricted filling
Myocyte loss
“DIAGNOSIS OF CARDIAC FAILURE FAILURE”
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Heart failure may be diagnosed whenever a patient with
signifificant heart disease develops the sign or symptoms of:
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Low Cardiac Output,
Pulmonary Congestion,
Systemic Venous Congestion.
“MAJOR CRITERIA”
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Paroxysmal nocturnal dyspnea.
Jugular venous distension.
Rales.
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Cardiomegaly.
Acute Pulmonary Edema.
S3 Gallop.
↑ venous pressure > 16 cm H2O
“MINOR CRITERIA”
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Lower limb edema,
Night cough.
Dyspnea on exertion.
Hepatomegaly.
Pleural effusion.
↓ vital capacity by 1/3 of normal.
Tachycardia 120 bpm.
“SYMPTOMS”
• SOB (shortness of breath) ,Orthopnea, paroxysmal
nocturnal dyspnea
• LOW CARDIAC OUTPUT SYMPTOMS
• ABDOMINAL SYMPTOMS:
- Anorexia,
- Nausea,
- Abdominal fullness,
- Rt hypochondrial pain.
“PHYSICAL SIGNS”
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High diastolic BP & occasional decrease in systolic BP
Jugular venous distension
Rales (Inspiratory)
Displaced and sustained apical impulses
Third heart sound – low pitched sound that is heard
during rapid filling of ventricle
Vibration of the ventricular wall by blood
filling
Fourth heart Sound (S4)
- Usually at the end of diastole
- Exact mechanism is not known
Could be due to contraction of
atrium against stiff ventricle
“MECHANISMS OF CARDIAC FAILURE”
CAUSE:
REDUCED VENTRICULAR CONTARACTILITY.
EXAMPLE:
• Myocardial infarction(segmental dysfunction),
FEATURES:
• In coronary artery contract poorly and may impede the
function of normal segments by distorting their contraction
and relaxation patterns.
EXAMPLE:
• Myocarditis/cardiomyopathy(global dysfunction)
FEATURES:
• Progressive ventricular dilation
“MECHANISMS OF CARDIAC FAILURE”
CAUSE
• VENTRICULAR OUTFLOW OBSTRUCTION(PRESSURE
OVERLOAD)
EXAMPLE:
Hypertension,Aortic Stenosis(left heart failure),pulmonary
Hypertension,Pulmonary Valve stenosis(right heart failure)
FEATURES:
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Initially concentric ventricular hypertrophy
Secondary changes in the myocardiumand increasing obstruction
eventually lead to failure with ventricular dilation and rapid clinical
detoriation.
“MECHANISMS OF HEART FAILURE”
CAUSE:
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VENTRICULAR INFLOW OBSTRUCTION.
EXAMPLE.
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Mitral stenosis,tricuspid stenosis.
FEATURES.
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Small vigorous ventricle,
dilated hypertrophied atrium.
Atrial fibrillation is common.
“MECHANISMS OF CARDIAC FAILURE”
CAUSE:
• VENTRICULAR VOLUME OVERLOAD.
EXAMPLE.
• LV volume overload(e.g mitral or aortic
regurgitation,atriovenoue fistulae)
• Ventricular septal defect)
• Increase metabolic demand(high output)
FEATURES.
• Dilation and hypertrophy allow the ventricle to
generate a high stroke volume and help to maintain a normal cardiac
output.
“MECHANISMS OF CARDIAC FAILURE”
CAUSE:
• ARRYTHMIA
EXAMPLE.
• Atrial fibrillation,
• Tachycardia cardiomyopathy,
• Complete heart block.
FEATURES.
• Tachycardia doesnot allow for adequate filling of the heart,resulting in
reduced cardiac output and back pressure.
• Bradycardia limits cardiac output even if stroke volume is normal
“MECHANISMS OF CARDIAC FAILURE”
CAUSE :
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DIASTOLIC DYSFUNCTION.
EXAMPLE.
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Constrictive pericarditis
FEATURES.
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Marked fluid retesion.
Peripheral oedema.
Ascites.
Pleural effusions.
Elevated jugular veins.
“PATHOPHYSIOLOGY”
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Hemodynamic changes
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Neurohormonal changes
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Cellular changes
“HEMODYNAMIC CHANGES”
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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:
• Slight  in α1 receptors
• β1 receptors desensitization  followed by down regulation
 Changes in contractile proteins
 Program cell death (Apoptosis)
 Increase amount of fibrous tissue
“TYPES OF CARDIAC FAILURE”
Heart failure can be described or classified in several ways.
#LEFT,RIGHT AND BIVENTRICULAR CARDIAC FAILURE.
#FORWARD AND BACKWARD CARDIAC FAILURE.
#DIASTOLIC AND SYSTOLIC DYSFUNCTION.
#HIGH OUTPUT FAILURE.
#ACUTE AND CHRONIC CARDIAC FAILURE
“LEFT,RIGHT AND BIVENTRICULAR HEART FAILURE”
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The LEFT SIDE of the heart is term for LEFT ATRIUM,LEFT
VENTRICLE,MITRAL AND AORTIC VALVE.
The RIGHT SIDE of the heart is term the RIGHT ATRIUM,RIGHT
VETRICLE,TRICUSPID AND PULMONARY VALVE.
LEFT SIDED HEART FAILURE
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Reduction in the left ventricular output or increase
in the left atrium pressure (may cause pulmonary
congestion or pulmonary edema or pulmonary venous
pressure)
“RIGHT SIDED CARDIAC FAILURE”
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Reduction in right ventricular output for any given
right atrial pressure.
Causes chronic lung disease(corpulmonal),multiple
pulmonary emboli
“BIVENTRICULAR CARDIAC FAILURE”
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Failure of Lf and Rt heart may develop because of disease
process(eg dilated cardiomyopathy or ischemic heart
disease)affects both ventricles.OR because disease of the
lf heart leads to chronic elevation of the Lf atrial
pressure,pulmonary hypertension and right heart failure
“FORWARD AND BACKWARD CARDIAC FAILURE”
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in heart failure the predominant problem is an inadequate cardiac
output(forward failure)
Whilst other patients may have a normal or near normal cardiac output
with marked salt and water retension causing pulmonary and
systemic venous congestion(backward failure)
“DIASTOLIC AND SYSTOLIC DYSFUNCTION”
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Heart failure develop result of impaired myocardial
contraction(systolic dysfunction)
due to poor ventricular filling and high filling pressure caused by
abnormal ventricular relaxation(diastolic dysfunction),is found in
patients with left ventricular hypertrophy and occurs in
hypertension and ischaemic heart disease
Systolic and diastolic dysfunction often coexist,particularly in
patients with coronary artery disease
“HIGH OUTPUT FAILURE”
Conditions that are associated with a very high cardiac output ,eg
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large atriovenous shunt,
beri beri,
severe anaemia
or thyrotoxicosis can ocasionally cause heart failure. (Body
metabolism is increased and overworks the heart)
“ACUTE AND CHRONIC CARDIAC FAILURE”
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Heart failure may develop suddenly as in myocardial infaction
or gradually as in progressive valvular heart disease
“ACUTE CARDIAC FAILURE”
A sudden diminution in output of blood from both ventricles may causes
acute reduction in the oxygen supply to all the tissues.Recovery from
the acute phase may be followed by chronic failure,or death may occur
due to anoxia of vital centres in the brain.the commonest causes are.
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Severe damage to an area of cardiac muscle due to ischaemia.
Pulmonary embolism.
Acute toxic myocarditis.
Severe cardiac arrythemia.
Rupture of heart chamber or valve cusp.
Severe malignant hypertension.
“CHRONIC CARDIAC FAILURE”
This develops gradually and in the early stages there may be no symptoms
because the heart compensates by increasing the rate and force of
contraction and the ventricles dilate.
Myocardial cell hypertrophy increase the strength of the muscle.
When further compensation is not possible there is gradual decline in
myocardial efficiency.
During the development of chronic failure hypoxia and venous
congestion cause changes in other systems,making still greater
demands on the heart eg renal,endocrine,respiratory.
underlying causes include:
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Chronic hypertension,,myocardial fibrosis,valvular disease,anaemia.
Previous acute cardiac failure.
Degenerative changes in old age.
“COMPLICATIONS”
In advanced cardiac failure a number of non specific
complications may occur.
• Renal failure.
• Hypokalaemia.
• Hyperkalaemia.
• Hyponatramia.
• Impaired liver function.
• Thromboembolism.
• Atrial and ventricular arrythmias.
“INVESTIGATIONS”
SIMPLE TESTS
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urea
electrolytes
hemoglobin
thyroid functions
ECG
chest X ray
These may help to establish the nature and severity of the underlying
heart disease and detect any complication.
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ECHOCARDIOGRAPHY
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A useful investigation and
should be considered in all patients with significant heart failure in order
to:
Determine the aetiology.
Detect unsuspected valvular heart disease
Identify patients who will benefit from long term therapy with drugs
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such as ACE inhibitors
Also known as a cardiac ultrasound, it uses
standard ultrasound techniques to image twodimensional slices.
CHEST X-RAY
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Size and shape of heart
Evidence of pulmonary venous congestion (dilated or upper lobe veins
→ perivascular edema)
Pleural effusion
ECHOCARDIOGRAM
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Function of both ventricles
Wall motion abnormality that may signify CAD.
Valvular abnormality
Intra-cardiac shunts
BRAIN NATRIURETIC PEPTIDE(BNP)
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BNP elevated in heart failure and can be screening test in breathless
patients and those with oedema.
CARDIAC CATHETERIZATION
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When CAD or valvular is suspected
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If heart transplant is indicated
“MANAGEMENT OF ACUTE CARDIAC FAILURE”
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Sit the patient up in order to reduce pulmonary congestion.
Give oxygen(high flow,high concentraion),non invasive positive
pressure ventilation(continuous positive airway pressure,CPAP,of
face mask results in a more
rapid improvement in the patients of clinical state.
• Administer nitrates
• Administer loop diuretics such as furosemide
50-100mg iv.
5-10 mmhg) by a tight fitting
“MANAGEMENT OF CHRONIC CARDIAC FAILURE”
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Good management depends on the accurate aetiological
diagnosis,because in some situations a specific remedy may be
available,but mainly because the nature of pathophysiology guides
logical drug therapy .
“TREATMENT OPTIONS”
The more common forms of heart failure
cannot be cured, but can be treated
Lifestyle changes
Medications
Surgery
“LIFE STYLE CHANGES”
Stop smoking
Loose weight
Avoid alcohol
Avoid or limit caffeine
Eat a low-fat, low-sodium diet
Exercise
Reduce stress
Keep track of symptoms and weight and report any changes or
concern to the doctor
Limit fluid intake
See the doctor more frequently
“MEDICTIONS”
ACE Inhibitors
• Cornerstone of heart failure therapy
• Proven to slow the progression of heart failure
• Vasodilator – cause blood vessels to expand lowering
blood pressure and the hearts work load
DIURETICS (WATER PILLS)
• Prescribed for fluid build up, swelling or edema
• Cause kidneys to remove more sodium and water from
the bloodstream
• Decreases workload of the heart and edema
• Fine balance – removing too much fluid can
strain kidneys or cause low blood pressure
POTASSIUM
• Most diuretics remove potassium from the body
• Potassium pills compensate for the amount lost
in the urine
• Potassium helps control heart rhythm and is
essential for the normal work of the nervous
system and muscles
“MEDICATIONS”
VASODILATORS
Cause blood vessel walls to relax
Occasionally used if patient cannot tolerate ACE
Decrease workload of the heart
DIGITALIS PREPARATIONS
Increases the force of the hearts contractions
Relieves symptoms
Slows heart rate and certain irregular heart beats
BETA-BLOCKERS
Lower the heart rate and blood pressure
Decrease the workload of the heart
BLOOD-THINNERS (COUMADIN)
Used in patients at risk for developing blood clots
in the blood vessels, legs, lung and heart
Used in irregular heart rhythms due to risk of stroke
“TREATMENT OPTION”
Surgery and other Medical Procedures
Not often used in heart failure unless there is a
correctable problem
Coronary artery bypass
Angioplasty
Valve replacement
Defibrillator implantation
Heart transplantation
Left ventricular assist device (LVAD)
“CARDIAC TRANSPLANT”
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It has become more widely used since the advances in
immunosuppressive treatment
Survival rate
– 1 year 80% - 90%
– 5 years 70%
“ANGIOPLASTY”
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Angioplasty is the technique of mechanically widening
a narrowed or obstructed blood vessel typically wire,
known as a balloon catheter, is passed into the
narrowed locations and then inflated to a fixed size
using water pressures some 75 to 500 times normal as
a result of atherosclerosis.An empty and collapsed
balloon on a guide blood pressure (6 to 20
atmospheres). The balloon crushes the fatty deposits, so
opening up the blood vessel to improved flow, and the balloon
is then collapsed and withdrawn.
“ANGIOGRAPHY”
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Angiography or Arteriography is a medical
imaging technique used to visualize the inside, or
lumen, of blood vessels and organs of the body,
with particular interest in the arteries, veins and the
heart chambers. This is traditionally done by
injecting a radio-opaque contrast agent into the
blood vessel and imaging using X-ray based techniques
such as fluoroscopy
“DIFFERENTIAL DIAGNOSIS”
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Pericardial diseases
Liver diseases
Nephrotic syndrome
Protein Losing Enteropathy
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