Congestive Heart Failure (CHF)

3.1.1. Definition
- Heart failure refers to a constellation of signs and
symptoms that result from the heart’s inability to pump
enough blood to meet the body’s metabolic demands.
- The pump itself is impaired and unable to supply
adequate blood to meet the cellular needs.
3.1.2. Causes of CHF
The causes of CHF are classified into two major classes as
underlying causes and precipitating (Secondary) causes.
I. Underlying causes
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- It is the main pathological lesion that is responsible for the
heart not to pump adequately.
-These include: -

Myocardial lesions

- Cardiomyopathy
- Myocarditis
- Myocardial infarction

Valvular & Endocardial lesions

- Endocarditis
- Congenital valvular- heart disease
- RHD (Rheumatic Heart Disease)

Pericardial – lesions

- Pericarditis
- Cardiac-tamponade
II. Precipitating (secondary) causes.
Normally in the absence of precipitating factors or causes, an
individual heart with those underlying lesions tries to
compensate by making multiple pathophysiologic changes.
But when the precipitating causes come to the picture the
individual heart goes in to full- blown clinical signs and
symptoms of CHF. The precipitating causes are abbreviated
by a phrase “heart-fails”.
H = Hypertension
E = Infective Endocarditis
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A = Anemia
R = Rheumatic –fever (Recurrence)
T = Thyrotoxicosis
F = Fetus (pregnancy)
A = Arrhythmias
I = Infections
L = Lung problems (pathologies)
S = Stress, salts, etc.
3.1.3. Pathophysiology of Heart Failure
The onset of heart failure may be acute or
insidious. It is often associated with systolic or
diastolic over loading and with myocardial
weakness. As the physiologic stress on the heart
muscle reaches a critical level, the contractility of
the muscle is reduced and cardiac output declines,
but venous input to the ventricle remains the same
or becomes increased which is responsible for
cardiac – over load.
When cardiac output is decreased; the body
undergoes alteration to compensate for the failure.
There are two types of compensatorymechanisms
for congestive-heart failure:-
I. Systemic compensatory mechanisms
A. Reflex increase in sympathetic activity.
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B. Release of rennin from the kidneys.
C. Anaerobic metabolism by affected tissues.
D. Increased extraction of oxygen by the
peripheral cells.
II. Cardiac compensatory mechanisms
a. Myocardial dilatation: -
In acute or short-term mechanisms, as the end-diastolic fiber
length increases, the ventricular muscle responds with
dilatation and increased force of contraction (starling’s law)
Example:- Acute myocardial infraction results in
ventricular –dilatations.
b. Myocardial Hypertrophy
In long-term mechanisms, ventricular hypertrophy increases
the ability of the heart muscle to contract and push its volume
into the circulation.
Example:- Hypertension results in ventricular
hypertrophy, which maintains pumping
blood for severeal years against
increased after-load.
A) Sympathetic response to heart Failure:-
A decrease in cardiac out put results in decreased blood
pressure, which causes a reflex stimulation of sympathetic
nervous system (SNS). The SNS causes increased force and
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rate of myocardial contraction. It also causes vasoconstriction
of arterioles throughout the body. These effects temporarily
prolong the patient’s life. But in the long run, it facilitates the
progress o f pumping f a i l u r e (cause cardiac
decompositions).
B) Rennin Angiotensin Aldosterone system:-
- It constantly works to maintain fluid volume and blood
pressure through the following cascades:-
Decreased perfusion of tissues.
Release of Rennin from juxtaglomerular cells of the
kidney.
Formation of Angiotensin- I (formed from
Angiotensinogen in the
liver by the action of
rennin )
Formation of Angiotensin –II ( by enzyme reaction in
thepulmonary-
capillary bed )
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Figure 3.1 Effects of angiotencin-II in congestive heart failure
NB. * After load- the arterial pressure against which the
ventricles must contract.
** Preload- It is the pressure during filling of the ventricles
or tension on myocardium due to congestion.
C) Anaerobic Metabolism
When cells do not receive adequate blood or oxygen,
metabolism decreases and alternative methods are
used to produce energy. The major alternative method
is anaerobic production of ATP, which results in
formation of lactic acid as a bi-product.
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85
Even if the formed ATP by this mechanism could
prolong the life of the tissues, the accumulation of the
metabolic bi-product (lactic acidosis) inhibits
myocardial contractility, which facilitates the pumping
failure.
D) Oxygen extraction from RBCS
Oxygen extraction from RBCS to the tissue increases
when the circulation is inadequate and the perfusion is
diminished.
Normally, about 30% of oxygen is extracted from
RBCS by the peripheral tissues, but greater amounts
can be extracted during periods of poor perfusion.

Subsequent effects of compensatory mechanisms

All of the compensatory mechanisms described above may

preserve the life of the individual but they usually aggravate
the underlying conditions:-
Sympathetic Responses: - Preserve life by
increasing blood flow to brain and heart. But
increases the cardiac work load by increasing
after load (vasoconstriction)
Rennin- Angiotensin-Aldosterone system: -
Maintain blood volume and pressure to life
initially, but the aldosterone effect results in
increase pre-load (fluid-over load) on the heart.
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Alsoincreasedafter-loaddueto
vasoconstriction effect of Angiotensin-II.
Anaerobic metabolism: - This also preserves
life by forming ATP. But its metabolic bi-product;
lactic acid accumulation results in depression of
the myocardial contractility.
Myocardial Hyper trophy and myocardial
Dilatation: - Increase oxygen demand by the
myocardium. Put more stress on the already
failed heart.
3.1.4. Classification of Heart-Failure
-Based on clinical manifestations heart failure has

been classified into two:-

I) Left-sided Heart Failure: - Forward or low out put
syndrome dominate.
II) Right-sided Heart Failure:- The congestive
phenomenon dominates.
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87

But, in reality both features are present in heart failure

just as both left-sided and right-sided because the heart and lungs are interconnected; what
affects one
side of the heart eventually affects the other.
I. Left Heart Failure (LHF)

-Left heart failure occurs when the output of the left

ventricle is less than the total volume of blood received

from the right side of the heart through the pulmonary
circulation. As a result, the pulmonary circuit becomes
congested with blood that cannot be moved forward
and the systemic blood pressure falls.
Causes
- Myocardial infraction (MI) commonest cause
- Systemic Hypertension
- Aortic stenosis or insufficiency
- Cardiomyopathy
- Mitral stenosis and insufficiency; also causes
symptoms of LHF
Pathophysiology of LHF

Back word effects of LHF

Because the left ventricle cannot pump out all of

its blood; blood dams back to the left atrium into

the four pulmonary veins and pulmonary
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capillary bed (PCB). As the volume of blood in
the lungs increases, the pulmonary vessels are
congested and fluid starts to pass in to the
interstitial spaces and alveoli to cause
pulmonary-edema. Some times, acute
pulmonary edema may occur which is a lifethreatening
condition by impairing gas
exchange.

These phenomena are congestive phenomena

of LHF that result from the volume over load of

the left ventricle. They are called the backward
effects of LHF.

Forward Effects of LHF

The left ventricle also cannot pump its normal

stroke volume out to the aorta. Thus, the

systemic blood pressure decreases. This
decrease is sensed by baro-receptors that cause
a reflex stimulation of sympathetic nervous
system (SNS), which results in increased heart
rate and peripheral vasoconstriction.

Decreased cardiac out-put cause decreased

tissue perfusions, which stimulate the RAAsystem

as a compensatory mechanism.
Angiotensin–II correct blood pressure by Vasoconstriction,
while aldosterone increases blood
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volume by sodium retention. These are called
the forward effects of LHF.
Signs and symptoms of LHF
Dyspnea
- The earliest manifestation
- Is because of fluid accumulation in the lung
interstitial space which impairs gas exchange,
so that respiratory rate increased to
compensate.
- Is on exercise first then at rest on late stage.
Orthopnea
- In ability to breathe in supine position
- Is because of lung congestion due to
decreased gravity effect resulting in increased
venous return while on supine positions.
Paroxysmal nocturnal dyspnea
- Is onset of acute episodes of dyspnea at night.
- The cause is unknown; but thought to be due to
improved cardiac
Performance at night during decumbency.
- The increased venous return results in
pulmonary congestion which causes acute
pulmonary edema.
Cardiac Asthma
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90
- Refers to wheezing due to bronchospasm
induced by heart failure.
- The bronchioles may react to the increased
fluid in the alveoli, Constrict and produce
characteristic wheezing.
Pulmonary-edema
- Is an acute, life-threatening condition that
usually results from back ward effect of
LHF.
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II) Right Heart Failure (RHF)

Right heart failure occurs when the output of the right

ventricle is less than the input from systemic venous

circulation. As the result, the systemic venous circuit is
congested and the out put to the lungs decreased.
Causes
- LHF because of back ward effect of LHF which
causes pulmonary vascular congestion
(hypertension)
-Chronicobstructivelungdisease
(corpulmonale)
- Pulmonary embolism
- Right ventricular infarction.
- Congenital heart disease.
Pathophysiology of RHF

Back ward or congestive effects of RHF

In RHF, the right ventricle cannot pump all

of its contents forward so blood dams back

from the right ventricle to the right atrium
causing an increased pressure in systemic
venous circuit. This results in congestion of
organs like liver and spleen with peripheral
edema due to oozing of fluid.

The Forward effects of RHF

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The right ventricle also cannot maintain its

output to the lung. This results in a

decreased pulmonary circulation and
decreased return to the left side of the
heart.

These forward effects of RHF cause all of

the forward effects of LHF.

Signs and symptoms of RHF
Pitting, dependant edema: - on the foot ,on the
sacrum, etc
Hepato splenomegally (enlarged spleen & liver)
because of congestion.
Respiratory distress: - because of acute pulmonary
congestion.
Neck veins distension: - because of congestions of the
veins.
Anasarca (generalized body swelling) occurs in severe
form of RHF.