Cardiovascular Pathophysiology Congestive Cardiac Failure (CCF)/ Congestive Heart Failure (CHF)/ Heart Failure (HF)

1. Cardiovascular Pathophysiology
Congestive Cardiac Failure (CCF)/
Congestive Heart Failure (CHF)/
Heart Failure (HF)
Dr. Vishal Balakrushna Jadhav
Assistant Professor (Pharmacology)
School of Pharmaceutical Sciences (SOPS), SUN
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2. Content
 Definition of Congestive Heart Failure (CHF)
 Etiopathogenesis of CHF- Etiology and Pathogenesis
 Types of Heart Failure
 Pathological Changes
 Clinical Features
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3. Definition of Congestive Heart Failure (CHF)
 The pathological state of the heart in which an impaired cardiac function
is not able to maintain an adequate circulation for metabolic need of the
tissues of the body.
 May be acute (rapid in onset and short but severe lasting) or chronic (slow
in onset but long lasting and recurrent).
 CCF/CHF is the chronic form of heart failure with evidence of congestion
(excessive accumulation of blood or other fluid in body part) of peripheral
as well as pulmonary (lung) circulation.
 CHF is the end result of various forms of cardiac diseases.
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4. Etiopathogenesis of CHF
Etiology
 Heart failure may caused by one of the following factors either individually or in
combination.
A) Intrinsic pump failure
 Weakening of the ventricular muscles due to disease fails the heart fails to acts as
an efficient pump.
 Various diseases causing pump failure are- Ischaemic heart disease (IHD),
Myocarditis, Cardiomyopathy (a disorder, usually of unknown origin, of myocardial
muscles), Metabolic disorders, e.g. Beriberi (deficiency of vitamin B1, thiamine)
Disorder of rhythm like atrial flutter and fibrillation.
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5. B) Increased cardiac workload
 It leads to an increase in myocardial O2 demand thereby caused myocardial failure.
The resultant increase in heart workload may be in the form of pressure or volume
load.
 Pressure load increases in systemic and pulmonary hypertension, valvular diseases
like mitral stenosis, aortic stenosis, pulmonary stenosis, and chronic lung diseases.
 Volume load is seen when ventricles ejects more than normal volume of blood,
may leads to heart failure as seen in valvular insufficiency, severe anemia,
thyrotoxicosis, atrioventricular shunts, and hypoxia due to lung disease.
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6. C) Impaired filling of cardiac chambers
Decreased cardiac output and cardiac failure may results from extracardiac causes or
defect in filling of heart. This may be due to-
 Cardiac tamponade, e.g. haemopericardium or hydropericardium,
 Constrictive pericarditis
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7. Pathogenesis
 Three primary compensatory mechanisms attempts to maintain cardiac functions
in the situation of cardiovascular exercise and stress are-
1) Reflex sympathetic stimulation to increase myocardial contractility which in turn
results in vasoconstriction and increased cardiac workload,
2) Retention of sodium and water to increase venous return and thus cardiac fluid
volume to stretch the ventricular fibers and hence increase in the force of contraction,
and
3) Myocardial hypertrophy (increase in size and weight) to increase the amount of
contractile tissue and hence contractility.
Insufficiency or persistent activation of these compensatory mechanisms contribute to
heart failure.
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Activation of NA and ANP Activation of RAAS
Increased
myocardial
contractility
Tachycardia Sodium and water retention
Increased
cardiac
workload
Further myocardial stress
Congestive heart failure (CHF)
Cell stretching
Compensatory hypertrophy and dilatation

10. Types of heart failure
 Acute or chronic, left sided or right sided, forward or backward heart failure.
a) Acute or chronic heart failure- Depends on the development of the heart failure,
either slow or fast; it may be acute or chronic respectively.
Acute heart failure seen in-
 Larger MI,
 Cardiac tamponade,
 Massive pulmonary embolism,
 Acute viral myocarditis, and
 Acute bacterial toxaemia.
 Sudden reduction in the systemic hypotension, but edema does not occur.
 A stage of cardiogenic shock and cerebral hypoxia develops.
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11. Chronic heart failure seen in-
 Myocardial ischemia from coronary atherosclerosis,
 Multivalvular heart disease,
 Systemic arterial hypertension, and
 Chronic lung disease resulting in hypoxia and pulmonary arterial hypertension.
 Compensatory mechanisms like tachycardia, cardiac dilatation and cardiac
hypertrophy try to maintain an adequate cardiac output.
 Well maintained arterial pressure and fluid accumulation (edema).
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12. b) Left sided and right sided heart failure-
The clinical manifestations results from the accumulation of excess fluid upstream to the left
and right cardiac chamber whichever firstly affected.
Left sided heart failure- It is initiated by stress to the left side of heart, and seen in-
 Systemic hypertension,
 Mitral or aortic valve stenosis,
 IHD, and
 Myocardial diseases, e.g. cardiomyopathies, myocarditis, restrictive pericarditis.
Clinical characteristics
 Pulmonary congestion and edema causing dyspnoea and orthopnoea.
 Decreased left ventricular output causing hypoperfusion and diminished oxygenation of
tissues, e.g. in kidneys causing ischaemic acute tubular necrosis, in brain causing hypoxic
encephalopathy and in skeletal muscles causing muscular weakness and fatigue.
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13. Right sided heart failure occurs more often as a consequence of left sided heart failure, and in
some conditions affect right ventricles like-
 Consequence of left ventricular failure,
 Cor pulmonale in which right sided heart failure occurs due to intrinsic lung disease,
 Pulmonary or tricuspid valvular disease,
 Pulmonary hypertension, secondary to pulmonary thromboembolism,
 Myocardial disease affecting right side, and
 Congenital heart disease with left to right shunt.
Clinical characteristics
 Systemic and portal venous congestion in different tissues and organs, e.g. subcutaneous
edema on dependent parts, passive hepatic congestion, passive congestion of spleen and
kidneys, leg veins and neck veins etc.
 Reduced cardiac output results in circulatory stagnation, causing anoxia, cyanosis and
coldness of extremities. 13

14. Pathological changes
 Myocardial hypertrophy without dilatation is referred to as concentric and
when associated with dilatation is called as eccentric myocardial hypertrophy.
 The weight of the heart increased above the normal often over 500 g.
However, an excessive epicardial fat is not indicative of true hypertrophy.
 Grossly, the thickness of the left ventricular wall above 1 mm is an indication
of significant hypertrophy. In the concentric hypertrophy, the lumen of the
chamber is smaller than usual while in an eccentric one, the lumen is dilated.
 Microscopically, there is an increase in the size of individual muscle fibers.
There may be multiple minute degenerative changes and necrosis in the
hypertrophied myocardium.
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15. Clinical Features
 Various grades of dyspnoea like paroxysmal nocturnal dyspnoea, orthopnoea,
shortness of breath.
 Fatigue- Reduced cardiac output and hence hypoperfusion of the skeletal
muscle is responsible for fatigue.
 Cerebral symptoms- Confusion, reduced concentration, headache, sleep
disturbances, anxiety are commonly seen due to reduced cerebral blood flow.
 Chest pain
 Gastrointestinal symptoms- Congestion of gastric mucosa, live and portal
venous system results in nausea, loss of appetite, abdominal pain etc.
 Nocturia and oliguria.
 Edema- Blood flowing into the right side of the heart leads to swelling in the
feet, ankles, legs, liver, abdomen etc.
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