CCF, DEFINITION, CLASSIFICATION, MGT.

1. Presented by;
Aiswarya.A.T,
First year M.Pharm.,
Dept. of Pharmacy
Practice,
Grace college of pharmacy.

2. Heart failure is a clinical
syndrome in which an
abnormality of cardiac
structure or function is
responsible for the
inability of heart to
eject or fill with blood at
a rate commensurate
with the requirements
of the metabolizing
tissues.

3. CLASSIFICATION
 Left ventricular dysfunction
 Right ventricular dysfunction
 Biventricular HF
 Left ventricular systolic dysfunction
 Left ventricular diastolic dysfunction
 Ischaemic HF
 Non-ischaemic HF
 Acute HF
 Chronic HF
 Low output HF
 High output HF
 Forward HF
 Backward HF
 Compensated HF

4.  Cardiac failure is a common condition with a prevalence
ranging from 3-5% in the population over 65 years old &
between 8-16% of those aged over 75years.
 It is the leading cause for hospitalization in people older than
65. In developed countries, the mean age of patients with heart
failure is 75years old.
 Heart failure is more common in men than in women until age
65 years, reflecting the greater incidence of coronary artery
disease in men.
 Improved survival of patients after myocardial infarction is a
likely contributor to the increased incidence and prevalence of
heart failure.
EPIDEMIOLOGY

5.  Infection
 Arrhythmias
 Physical, Dietary, Fluid, Environmental &
Emotional Excesses
 Myocardial Infarction
 Pulmonary Embolism
 Anemia
 Thyrotoxicosis & Pregnancy
 Aggravation of Hypertension
 Rheumatic, Viral & Other Forms of Myocarditis
 Infective Endocarditis
AETIOLOGY

6. ETIOPATHOGENESIs
ADAPTIVE AND MALADAPTIVE MECHANISMS
1. The Frank-Starling mechanism
2. Compensatory hypertrophy
3. In ventricular remodeling
4.Redistribution of a subnormal cardiac
REDUCTION IN CARDIAC EFFICIENCY
ALTERATIONS IN ENERGY METABOLISM
ALTERATIONS IN SARCOMERIC PROTEINS
MYOCARDIAL CELL DEATH
ABNORMALITIES OF EXCITATION-CONTRACTION
COUPLING

7. Loss of contractile function due to;
•Pressure overload of the heart
•Work overload of the heart
•Loss of myocardium
•Generalized decrease in contractility
Impaired cardiac function(congestive signs & symptoms)
Compensatory mechanisms:
Cardiac compensatory mechanism
•Ventricular dilation
•Ventricular hypertrophy
Peripheral compensatory mechanism
•Increased sympathetic activity
•Activation of RAAS
•Increased afterload
•Increased blood volume
•Receptor changes
PATHOPHYSIOLOGY

8. CLINICAL MANIFESTATIONS
Signs
■ Pulmonary rales
■ Pulmonary edema
■ Cool extremities
■ Pleural effusion
■ Tachycardia
■ Narrow pulse pressure
■ Cardiomegaly
■ Peripheral edema
■ Jugular venous distension
■ Hepatojugular reflux
■ Hepatomegaly
Symptoms
■ Dyspnea, particularly on exertion
■ Orthopnea
■ Paroxysmal nocturnal dyspnea
■ Exercise intolerance
■ Tachypnea
■ Cough
■ Fatigue
■ Nocturia
■ Hemoptysis
■ Abdominal pain
■ Anorexia
■ Nausea
■ Bloating
■ Poor appetite, early satiety
■ Ascites
■ Mental status changes

9. DIAGNOSIS
IMAGING
•Echocardiography
•Chest X-rays/ Chest Radiograph
ELECTROPHYSIOLOGY
Electrocardiogram (ECG/ EKG)
BLOOD TESTS
ANGIOGRAPHY
MONITORING

10. MANAGEMENT
NON PHARMACOLOGICAL MANAGEMENT
•Bed rest
•Consuming small but frequent meals (4 to 6 daily)
•Moderate sodium restriction (2 to 4g / day)
•Smoking cessation
•Avoid alcohol intake

11. PHARMACOLOGICAL MANAGEMENT
•ACE’s
Captopril, Enalapril, Lisinopril, Perindopril, Ramipril, Trandolapril
•ARB’s
Candesartencilexetil, Eprosartan, Irbesartan, Losartan, Olmesartan, Telmisartan,
Valsartan
•Beta adrenergic blocking agents
Bisoprolol, Metoprolol, Carvedilol
•Diuretics
Thiazide- Chlorothiazide, Hydrochlorothiazide, Indapamide, Chlorthalidone
Loop diuretics- Furosemide, Ethacrynic acid, Bumetanide, Torsemide
Potassium sparing diuretics- Amiloride, Spironolactone, Triamterene
•Aldosterone antagonists
Spironolactone, Eplerenone
•Vasodilators
Nitroprusside, Hydralazine, Prazosin, Nitrates
•Digitalis glycosides
Digitalis (Digoxin)
•Calcium channel blockers
•Inotropic agents
Dopamine i.v, Dobutamine, Inamrinone, Milrinone, Nesiritide