CONGESTIVE CARDIAC FAILURE PATHOPHYSIOLOGY, DIAGNOSIS AND TREATENT

1. Presented by
Mrs Reshma V.Pawar
M.Pharm Pharmacology
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Genba Sopanrao Moze College of Pharmacy, Wagholi, Pune

2. Contents
 The disease
 Etiology
 Epidemiology
 Types of heart failure
 Pathophysiology
 Compensatory mechanism
 Common causes
 Sign and symptoms
 Diagnosis
 Management
 References
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3.  Defined as the pathophysiologic states in which impaired cardiac
function is unable to maintain adequate circulation to meet
demands of body
 It is gradually developing inability of heart to pump sufficient
blood i.e. It fails to function as efficient pump
 Inadequate cardiac output
 Venous congestion
 Salt and water retention
 Renal perfusion due to hypo perfusion
 During early stages of heart failure compensatory mechanism
works
 Frank starling mechanism-kidney retains NA and water and
increases blood volume
 Baroreceptor reflex- sympathetic activity is increased
catecholamines increased, increase heart rate and cardiac output
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4. Normal heart Congestive Heart Failure
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5.  Heart failure is a common, costly, disabling, and potentially
deadly condition.
 In developing countries, around 2% of adults suffer from heart
failure, but in those over the age of 65, this increases to 6–10%.
 Mostly due to costs of hospitalization it is associated with a high
health expenditure; costs have been estimated to amount to 2% of
the total budget of the National Health Service in the United
Kingdom, and more than $35 billion in the United States.
 Heart failure is associated with significantly reduced physical and
mental health, resulting in a markedly decreased quality of life.
 With the exception of heart failure caused by reversible
conditions, the condition usually worsens with time. Although
some patients survive many years, progressive disease is
associated with an overall annual mortality rate of 10%.
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6.  Gender-
 Women generally develop heart failure after menopause.
 Women tend to become more depressed than men
 Women have similar symptoms but the intensity is more
pronounced.
 Women usually survive a lot longer with heart failure than men.
 Race
New information suggests that elements of heart failure in African
Americans and Caucasians may be different
 Age-
Heart failure is a progressive medical disorder. As the heart gets
weaker, symptoms and signs become prominent. Heart failure can
affect the entire heart or only the right or left side. In the majority
of cases, both sides of the heart are affected. HF can occur at any
age depending on the cause. In general heart failure does increase
with age.
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7.  Heart failure may be caused by one of following
1) Intrinsic Pump Failure:
Weakening of ventricular muscle due to disease so that
heart fails to act as efficient pump. Reasons are,
 Ischeamic heart disease
 Myocarditis
 Cardinomyopathies (damaging function of myocardium)
 Metabolic disorders i.e. beriberi
 Disorders of rhythm i.e. atrial fibrillation and flutter
2) Increased workload on the heart
Increased myocardial load on heart results in increased
myocardial demand resulting in myocardial failure. It may be
pressure load or volume load
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8.  Increased pressure load is occuring in
 systemic and pulmonary hypertension
 Vulvular disease e.g. aortic stenosis, pulmonary stenosis
 Chronic lung disease
 Increased volume load occurs when ventricle is required to eject
more than normal volume of blood resulting in cardiac failure
 Severe anemia
 Thyrotoxicosis
 Hypoxia due to lung disease
3) Impaired filling of heart chamber
 Cardiac temponade i.e hemopericardium, hydropericardium
 pericarditis
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9. Heart failure may be acute or chronic, right sided or left sided,
forward or backward
1. Acute and chronic heart failure (rapidly or slowly)
 Acute heart failure:
i) Large myocardial infarction
ii) Valve rupture
iii) Cardiac temponade
iv) Pulmonary embolism
v) Myocarditis
 Chronic heart failure
i) Multivalvular heart disease
ii) Arterial hypertension
iii) Chronic lung disease resulting in hypoxia
iv) Acute into chronic conditions
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10. 2. Left sided and right sided heart failure
 Left sided heart failure
Initiated by stress to left heart. Causes are..
 Hypertension
 Valve disease
 Ischemic heart disease and
 Myocardial disease
The left sided heart failure results from accumulation of fluid
upstream in lungs and have major pathologic changes
 Pulmonary congestion and edema casing dysapnea and
orthopnea
 decreased left ventricular output causing hypoperfusion and
diminished oxygenation to tissues.
 Right sided heart failure
occurs as a consequence of left sided heart failure.
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11. But even some causes are
 Left ventricular failure
 Lung disease
 Pulmonary or tricuspid valvular disease
 Pulmonary hypertension
 Myocardial disease affecting right side.
Accordingly pathologic changes are as under
 systemic venous congestion in different tissues and organs as liver,
spleen, kidneys veins
 Reduced cardiac output resulting in cynosis, anoxia.
Left sided heart
failure
Pulmonary congestion,
decreased left ventricular
output
Right sided heart
failure
Systemic venous congestion,
involvement of liver and
spleen
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12. 3. Backward and forward heart failure
 Backward heart failure
 In this ventricles fails to eject blood normally
 results in rise of diastolic volume in ventricles and increase in
volume and pressure in atrium
 It transfer backward producing elevated pressure in veins
 Forward heart failure
Heart fails to pump blood causing diminished flow of blood to the
tissues, especially diminished renal perfusion and activation of
renin angiotensin aldosterone system
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13.  Forward Failure
Decreased cardiac output
Tissue anoxia
Renal perfusion
Activation of renin angiotensin
system
Sodium and water retention
PULMONARY CONGESTION AND
EDEMA
 Backward failure
 Blood in left ventricle
 Increased Left atrial pressure
and volume
 Increased pressure in
pulmonary venous circulation
 Pulmonary hypertension
 Increased right ventricular
pressure
 VENOUS CONGESTION AND
EDEMA
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14.  Reduced contractility, or force of contraction, due to overloading of
the ventricle.
 A reduced stroke volume, as a result of a failure of systole, diastole
or both. Increased end systolic volume is usually caused by reduced
contractility. Decreased end diastolic volume results from impaired
ventricular filling – as occurs when the compliance of the ventricle
falls (i.e. when the walls stiffen)
 Reduced spare capacity. As the heart works harder to meet normal
metabolic demands, the amount cardiac output can increase in
times of increased oxygen demand (e.g. exercise) is reduced. This
contributes to the exercise intolerance commonly seen in heart
failure. This translates to the loss of one's cardiac reserve. The
cardiac reserve refers to the ability of the heart to work harder
during exercise or strenuous activity. Since the heart has to work
harder to meet the normal metabolic demands, it is incapable of
meeting the metabolic demands of the body during exercise.
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15.  Increased heart rate, stimulated by increased sympathetic activity
in order to maintain cardiac output. Initially, this helps compensate
for heart failure by maintaining blood pressure and perfusion, but
places further strain on the myocardium, increasing coronary
perfusion requirements, which can lead to worsening of ischemic
heart disease. Sympathetic activity may also cause potentially fatal
arrhythmias.
 Hypertrophy (an increase in physical size) of the myocardium,
caused by the terminally differentiated heart muscle fibres
increasing in size in an attempt to improve contractility. This may
contribute to the increased stiffness and decreased ability to relax
during diastole.
 Enlargement of the ventricles, contributing to the enlargement and
spherical shape of the failing heart. The increase in ventricular
volume also causes a reduction in stroke volume due to mechanical
and contractile inefficiency
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16.  In order to maintain normal cardiac output, several
compensatory mechanism play a role. These are
1) Enlargement of heart (cardiac hypertropy, cardiac dilatation
or both.
2) Tachycardia (increased heart rate) due to release of NE, and
renin angiotensin system
3) Starlings law- the failing dilated heart, to maintain cardiac
performance, increases myocardial contractility, and maintain
blood volume.
Cardiac hypertrophy-
increase in size and weight of myocardium
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17.  It generally results from increase pressure load or increased volume
load
 Basic mechanism is not known but caused due to stretching of
myocardial fibers in response to stress induces the cells to increase
in length.
 Elongated fibers receive better nutrition and increase in size.
 Cardiac dilatation-
 Stress leading to accumulation of excessive volume of blood in a
chamber of heart causes increase in length of myocardial fibers and
hence causes cardiac dilatation.
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18.  Myocardial infarction
 ischemic heart disease,
 Hypertension,
 Cigarette smoking
 Valvular heart disease,
 Cardiomyopathy.
 Shortness of breath coughing, chronic venous congestion,
 Exercise intolerance.
 Obesity
 Diabetes
 Sedantary life style
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19.  Orthoapnea, dyspnea
 Nocturnal dysapnea
 Dizziness
 confusion
 Hepatomegaly (enlargement of the liver)
 Pulmonary edema (fluid in the alveoli).
 Gallop rhythm (additional heart sounds)
 Coagulopathy (problems of decreased blood clotting)
 Nocturia (night urination)
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20. 1) Imaging
 Echocardiography is
commonly used to support a
clinical diagnosis of heart
failure. This modality uses
ultrasound to determine the
stroke volume (SV, the
amount of blood in the heart
that exits the ventricles
with each beat), the end-
diastolic volume (EDV, the
total amount of blood at the
end of diastole).
 Chest X-rays are frequently
used to aid in the diagnosis
of CHF. In the compensated
patient, this may show
cardiomegaly (visible
enlargement of the heart),
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21. 2) Electrocardiogram
An electrocardiogram (ECG/EKG) may be used to identify arrhythmias,
ischemic heart disease, right and left ventricular hypertrophy, and
presence of conduction delay or abnormalities (e.g. left bundle branch
block).
3) Blood Tests
Blood tests routinely performed include electrolytes (sodium,
potassium), measures of renal function, liver function tests, thyroid
function tests, a complete blood count, and often C-reactive protein if
infection is suspected.
4) Angiography
Heart failure may be the result of coronary artery disease, and its
prognosis depends in part on the ability of the coronary arteries to
supply blood to the myocardium (heart muscle). As a result, coronary
catheterization may be used to identify possibilities for
revascularisation through percutaneous coronary intervention or bypass
surgery.
5) Food balance and body weight monitoring
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22.  Acute management-
In acute decompensated heart failure (ADHF), the immediate goal is to re-
establish adequate perfusion and oxygen delivery to end organs. This
entails ensuring that airway, breathing, and circulation are adequate.
Immediated treatments usually involve some combination of vasodilators
such as nitroglycerin, diuretics such as furosemide, and possibly non
invasive positive pressure ventilation (NIPPV).
 Chronic management-
ACE inhibitors improve survival and quality of life in heart failure patients,
and have been shown to reduce mortality in patients with left ventricular
dysfunction in numerous randomized trials.
In addition to pharmacologic agents (oral loop diuretics, beta-blockers,
ACE inhibitors or angiotensin receptor blockers, vasodilators, and in severe
cardiomyopathy aldosterone receptor antagonists), behavioral modification
should be pursued, specifically with regards to dietary guidelines regarding
salt and fluid intake.
Exercise should be encouraged as tolerated, as sufficient conditioning can
significantly improve quality-of-life.
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23.  In patients with severe cardiomyopathy, implantation of an automatic
implantable cardioverter defibrillator(AICD) should be considered. A select
population will also probably benefit from ventricular resynchronization.
 In select cases, cardiac transplantation can be considered. While this may
resolve the problems associated with heart failure, the patient generally
must remain on an immunosuppressive regimen.
 Sodium and fluid restrictions
 Smoking should be stopped
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24.  Diuretics- for relief of dysapnea and signs of sodium and water
retentions
 ACE inhibitors- cause decrease in angiotensin II and rise in renis. They
decrease circulating catecholamines and activates additional
vasodialtor mecanism. They further reduces symptoms, reduces
chances of hospitalization and mortality.
 Angiotensin antagonist- similar to ACE inhibitors
 ß blockers- improves symptoms, reduces sympathetic activation in
heart failure and blocks NE and E. they improve cardiac function by
reducing heart rate, resulting in lower myocardial energy
expenditure, prolonged diastolic filling and increase blood flow
 Aldosterone antagonist.
 Digoxin
 Nitrates and antiarrythmic drugs
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25.  Textbook of pathology, fifth edition 2005, by Harsh Mohan
 Lecture notes on cardiology by H. Gray, K.Dawkins, 5th
edition, Blackwell publishing, page 137-145
 Wikipedia.com
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Thanking
you