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Heart Failure

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0% found this document useful (0 votes)
9 views

Heart Failure

Uploaded by

David Vinc
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd
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HEART FAILURE

Definition
• A pathophysiologic state in which impaired cardiac function is
unable to maintain an adequate circulation for metabolic
needs of the body.
• Congestive Heart Failure-This is chronic heart failure
evidenced by congestion of peripheral circulation and lungs.
Occurs as a result of heart disease and mainly involves both
right and left heart failures.
Etiology
a) Intrinsic Pump Failure
This is the most common cause that is characterized by
weakening of ventricular muscle due to diseases thus the heart
fails to act as an efficient pump.
Diseases likely to cause this condition include:
Ischemic heart diseases
Myocarditis
Contd’
Cardiomyopathies
Metabolic disorders e.g. beriberi
Disorders of rhythm e.g. atrial fibrillation and flutter
Contd’
b) Increased workload on heart
Leads to increased myocardial demand resulting in myocardial
failure. This can be in the form of
Increased pressure load in cases of:
-Systemic and pulmonary hypertension
-Valvular disease e.g. mitral and aortic stenosis
-Chronic lung disease
Contd
Increased volume load
The ventricle is required to eject more than the normal volume of
blood leading to cardiac failure.
This is seen in:
a) Valvular insufficiency
b) Severe anemia
c) Thyrotoxicosis
Contd’
c)A-V shunts
d)Hypoxia due to lung diseases
c)Impaired filling of cardiac chambers

• This causes a decrease in cardiac output and cardiac failure


may result from extra cardiac causes or defects in filling of the
heart i.e.
-Cardiac tamponade e.g. haemopericardium ,hydropericardium
-Constrictive pericarditis
Contd’
• CVS adapts to decreased myocardial contractility or increased
hemodynamic burden by
i) Activation of neurohumoral systems which include:
-Release of NT- NE which increases heart rate and myocardial
contractility
-Activation of RAAS system
-Release of ANP that causes vasodilation, naturesis and diuresis.
ii) Frank Sterling mechanism
Contd’
• Compensated Heart Failure. This occurs when the dilated
ventricle is able to maintain CO at a level that meets patient’s
body requirements.
• Decompensated HF. This is when the dilated ventricle is
unable to maintain CO at a level that meets bodily
requirement.
In this situation of decompensated heart failure , the ventricles
hypertrophy.
Contd’
Cardiac cells have a decreased capacity to regenerate thus
hypertrophy either as
a) Concentric hypertrophy characterized by increase in the
thickness of the ventricular wall with no increase in chamber
size caused by pressure overload.
b) Eccentric hypertrophy characterized by increase in length of
fiber length thus increase in heart size and thickness of the
wall mainly caused by volume overload
Types of heart failure

Classified either as
a) Acute and chronic
b) Right sided and left sided heart failure
c) Forward and backward failure
ACUTE AND CHRONIC HF

Depends on the rate of development of the heart failure either


rapidly or slowly.
ACUTE HF
Heart failure occurs sudden and rapidly. HF occurs in the
following conditions
 Larger myocardial infarction
 Valve rupture
 Cardiac tamponade
 Massive pulmonary embolism
 Acute viral myocarditis
 Acute bacterial toxemia
Contd’
• This form of HF is characterized by a sudden decrease in CO
resulting in systemic hypotension and absence of edema
• Cardiogenic shock and cerebral edema develops.
CHRONIC HF
• HF develops slowly.
This is seen in;
a) Myocardial ischemia from atherosclerotic coronary artery
disease.
b) Multivalvular heart disease
c) Systemic arterial hypertension
d) Chronic lung diseases causing hypoxia and pulmonary
arterial hypertension
e) Progression from acute HF to chronic HF
Contd’
Compensatory mechanisms i.e. tachycardia, cardiac dilatation
and cardiac hypertrophy try to make adjustments thus maintain
CO.
There is well maintained arterial pressure
LEFT SIDED HF
Stress to the left heart resulting in HF is seen in the following
conditions:
a) Systemic hypertension
b) Mitral/aortic valve stenosis
c) Ischemic heart disease
d) Myocardial diseases e.g. cardiomyopathies, myocarditis
e) Restrictive pericarditis
Morphology
Characterized by;
-Left ventricular hypertrophy and dilation except in mitral valve
stenosis or other processes that restrict left ventricular size.
-Hypertrophied and fibrotic myocardium
-Secondary enlargement of left atrium hence atrial fibrillation
that can decreases SV and causes stasis of blood and
subsequently thrombus formation.
Contd’
-Pulmonary congestion and edema due to pressure in pulmonary
veins and capillaries
-Heavy and boggy lungs that histologically present with
transudate, alveolar septal edema and intra-alveolar edema.
-Capillary leakiness that causes accumulation of
erythrocytes( phagocytized by macrophages hence presence of
hemosiderin in macrophages called ‘Heart Failure Cells’
Clinical Manifestations

• These present due to decreased left ventricular output thus


accumulation of fluid upstream in the lungs and diminished
peripheral blood pressure and flow.
• Clinical features include:
1) Dyspnea
2) Cough
3) Orthopnea
4) Hypoxic encephalopathy
5) Skeletal muscle weakness and fatigue
6) Ischemic acute tubular necrosis
RIGHT SIDED HF
Mainly occurs as a consequence of LSHF.
Pressure increase in pulmonary circulation increases burden on
right side of heart.
Causes of right sided HF include;
a) Cor pulmonale due to intrinsic lung injury disease
b) Pulmonary/tricuspid Valvular disease
c) Pulmonary hypertension secondary to pulmonary
thromboembolism.
d) Myocardial diseases affecting right heart
e) Congenital heart disease with left to right shunt.
Morphology
Affects the liver and portal system
-Increase in size and weight of the liver.
-Liver cut section reveals passive congestion. Called a nutmeg
liver.
-Liver lobules have congested centers with pallor and fat.
-Centrilobular necrosis
-Sinusoidal congestion
-Cardiac cirrhosis due to necrosis
Contd’
Increased pressure in portal vein and its tributaries thus enlarged
spleen (Congestive splenomegaly)
Chronic edema in bowel thus decreased absorption of nutrients.
Ascites-Fluid accumulation in peritoneal cavity.
Clinical Features
In this HF, there is upstream of right heart e.g. systemic and
portal venous congestion and reduced cardiac output.
Pathologic changes include;
-Systemic venous congestion in the liver,spleen,kidney and leg
veins.
-Reduced cardiac output thus circulatory stagnation causing
anoxia , cyanosis and coldness of extremities.
Clinical features
These include:
 Systemic and portal venous congestion
 Hepatic and splenic enlargement
 Peripheral edema
 Pleural effusions
 Ascites.
Backward and Forward HF
Backward HF
Either of the ventricles fails to eject blood normally thus
increased EDV in ventricle causing an increase in volume and
pressure in atrium that is transmitted backward producing
increase in venous pressure.
Forward HF
• Failure of the heart to pump blood thus causing diminished
blood flow to tissues i.e. decreased renal perfusion thus
activation of RAAS.
.
Evolution of congestive heart failure and its effects.

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