Congestive cardiac failure occurs when the heart cannot pump enough blood to meet the body's needs. It results from structural or functional abnormalities of the heart. The key functions of the heart are to supply oxygen and substrates to tissues through adequate blood flow and receive blood returning from tissues. When the heart cannot fulfill these functions due to issues with its structure, filling, contractility, heart rate, or afterload, congestive cardiac failure develops. Common causes include coronary artery disease, hypertension, diabetes, and valvular heart disease. Over time, compensatory mechanisms like increased sympathetic activity and fluid retention can worsen the condition. Treatment involves managing symptoms, improving cardiac function, and preventing further disease progression through medications, diet, exercise,

1. CONGESTIVE CARDIAC FAILURE(CCF)
VIGNESH M
1ST SEM M PHARM
PHARMACOLOGY DEPARTMENT
GOVERNMENT COLLEGE OF
PHARMACY

2. Heart is a vital muscular organ specialized for
pumping blood to the peripheral organs and brain.
Essential functions of the heart
 To cover metabolic needs of body tissue (oxygen,
substrates) by adequate blood supply
 To receive all blood coming back from the tissue
to the heart
Essential conditions for fulfilling these functions
 Normal structure and functions of the heart
 Adequate filling of the heart by blood

3. CCF Defn…..
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 to commensurate
with the requirements of the
metabolizing tissues.

5. Factor 1
Heart Rate
In general, the higher the heart rate, the lower the
cardiac output
With excessively high heart rates, diastolic filling time
begins to fall, thus causing stroke volume and thus CO
to fall.
60 beats/min x 80 ml = 4800 ml/min (4.8 L/min)
70 beats/min x 80 ml = 5600 ml/min (5.6 L/min)

6. Factor 2
Preload
The volume of blood/amount of fiber stretch in the
ventricles at the end of diastole (i.e., before the next
contraction)
Preload increases with:
Fluid volume increases
Vasoconstriction (“squeezes” blood from vascular system into
heart)
Preload decreases with:
Fluid volume losses
Vasodilation (able to “hold” more blood, therefore less returning
to heart)

7. Starling’s Law (Rubber band model)
Describes the relationship between preload and cardiac
output
The greater the heart muscle fibers are stretched (b/c
of increases in volume), the greater their subsequent
force of contraction – but only up to a point. Beyond
that point, fibers get over-stretched and the force of
contraction is reduced
Excessive preload = excessive stretch → reduced
contraction → reduced SV/CO

8. Factor 3
Afterload
The resistance against which the ventricle must pump.
Excessive afterload = difficult to pump blood →
reduced CO/SV
Afterload increased with:
Hypertension
Vasoconstriction
Afterload decreased with:
Vasodilation

10. Factor 4
Contractility
Ability of the heart muscle to contract; relates to the
strength of contraction
Contractility decreased with:
Infarcted tissue – no contractile strength
Ischemic tissue – reduced contractile strength.
Electrolyte/acid-base imbalance
Negative inotropes (medications that decrease contractility, such
as beta blockers).
Contractility increased with:
Sympathetic stimulation (effects of epinephrine)
Positive inotropes (medications that increase contractility, such
as digoxin, sympatho mimmetics)

11. Compensatory mechanisms activation
Ventricular hypertrophy
Increased mass of contractile elements- strength of
contraction
Increased sympathetic adrenergic activity
Increased HR, increased contractility
Increased activity of RAAS system

13. Etiology
Primary risk factors
 Coronary artery disease (CAD)
 Advancing age
 Alteration in sarcomeric proteins
 Anemia
Contributing Factors
 Hypertension
 Diabetes
 Obesity
 Valvular heart disease
 Pulmonary Embolism

14. Risk factor variation
• 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.
• Heart failure is more common in men than in women until age
65 years, reflecting the greater incidence of coronary artery
disease in men.

15. Types
• Ventricular dysfunction (Right / Left)
• Biventricular HF (both)
• Systolic dysfunction / Diastolic dysfunction
• Ischemic HF / Non-ischemic HF
• Acute HF / Chronic HF

16. Pathophysiology
Primary Effects
Reduced Cardiac Output
Excessive Sympathetic Discharge
Salt & Water Retention
Long-term Effects
Remodeling
Cardiac Hypertrophy
Cardiac Apoptosis

18. Risk 1
Cardiac Output
Preload: (Atrial Pressure) Increased in preload due to
increased blood volume and venous tone
Afterload: (Vascular Resistance) Increased due to reflex
sympathetic outflow and renin-angiotensin system
though elevated afterload may further reduce cardiac
output
Contractility: Reduction in intrinsic contractility and
therefore reduction in pump performance
Heart Rate: Increases through sympathetic NS
compensation

19. Risk 2
Sympathetic stimulation
 SNS stimulation: release of epinephrine/nor-
epinephrine
• Increase HR
• Increase contractility
• Peripheral vasoconstriction (increases afterload)
 Myocardial hypertrophy: walls of heart thicken to
provide more muscle mass → stronger contractions

20. Risk 3
Kidney
Hormonal response
 ↓’d renal perfusion interpreted by juxtaglomerular
apparatus as hypovolemia.
 Kidneys release renin, which stimulates conversion of
angiotensin I → angiotensin II,
• Aldosterone release → Na retention and water
retention (via ADH secretion)
• Peripheral vasoconstriction

21. Compensatory mechanisms may restore CO to near-
normal.
But, if excessive the compensatory mechanisms can
worsen heart failure because . .

22. Excess Vasoconstriction:
↑’s the resistance against which heart has to pump
(i.e., ↑’s afterload), and may therefore ↓ CO
Excess Na and water retention:
↑’s fluid volume, which ↑’s preload. If too much
“stretch” (too much fluid) → ↓ strength of contraction
and ↓’s CO
Excessive tachycardia
→ ↓’d diastolic filling time → ↓’d ventricular filling →
↓’d SV and CO

23. Ventricular overload progression

24. Acute Congestive Heart Failure Clinical
Manifestations
 Pulmonary edema
 Agitation
 Pale or cyanotic
 Cold, clammy skin
 Severe dyspnea
 Tachypnea
 Pink, frothy sputum

25. Chronic Congestive Heart Failure Clinical
Manifestations
 Behavioral changes
 Restlessness, confusion, attention span
 Chest pain ( CO and ↑ myocardial work)
 Weight changes ( fluid retention)
 Skin changes
 Dusky appearance

26. Left-sided failure
 This type of heart failure occurs as a result of
ineffective left ventricular contractile function.
 As the pumping ability of the left ventricle fails,
cardiac output falls. Blood is no longer effectively
pumped out into the body; it backs up into the left
atrium and then into the lungs, causing pulmonary
congestion, dyspnea, and activity intolerance.
 If the condition persists, pulmonary edema and right-
sided heart failure may result.
 Common causes include left ventricular infarction,
hypertension, and aortic and mitral valve stenosis.

27. Right-sided heart failure
 Right-sided heart failure results from ineffective right
ventricular contractile function.
 Consequently, blood is not pumped effectively through the
right ventricle to the lungs, causing blood to back up into
the right atrium and into the peripheral circulation.
 The patient gains weight and develops peripheral edema
and engorgement of the kidney and other organs.
 It may be due to an acute right ventricular infarction or a
pulmonary embolus.
 However, the most common cause is profound backward
flow due to left-sided heart failure.

28. Pulmonary Edema

29. Signs of identification
Right side failure Left side failure
Facial edema Tachypnea
Hepatomegaly Tachycardia
Jugular venous Cough
Enlargement Wheezing
Edema of feet Crepts in chest

30. Systolic dysfunction
 Systolic dysfunction occurs when the left ventricle
can't pump enough blood out to the systemic
circulation during systole and the ejection fraction
falls.
 Causes of systolic dysfunction include myocardial
infarction and dilated cardiomyopathy.

31. Diastolic dysfunction
Life is
drawing
without an eraser
 Diastolic dysfunction may occur as a result of left
ventricular hypertrophy, hypertension, or
cardiomyopathy.
 Diastolic dysfunction occurs when the ability of the
left ventricle to relax and fill during diastole is
reduced and the stroke volume falls. Therefore,
higher volumes are needed in the ventricles to
maintain cardiac output.
 Consequently, pulmonary congestion and peripheral
edema develop.

32. Symptoms
Dyspnea Orthopnea
Exercise intolerance Hemoptysis
Tachypnea Abdominal pain
Cough Anorexia
Fatigue Nausea
Nocturia Bloating
Paroxysmal nocturnal dyspnea
Poor appetite,
Ascites

33. Diagnosis
• Imaging
• Echocardiography
• Chest X-rays/ Chest Radiograph
• Electrocardiogram (ECG)
• Blood test
• Angiography Monitoring

34. Treatment
NON PHARMACOLOGICAL MANAGEMENT
• Bed rest (propped up position)
• Consuming small but frequent meals (4 to 6
daily)
• Moderate sodium restriction (2 to 4g / day)
• Smoking cessation
• Avoid alcohol intake
• Humidified oxygen

35. PHARMACOLOGICAL MANAGEMENT
Drugs Relief in acute decompensation
1. Inotropic agents Ex digoxin, dobutamine,
dopamine, milrinone.
2. Diuretics Ex Furosemide, Thiazides,
metolazone.
3. RAS inhibitors (ACE inhibitors/ARB’s)
4. Vasodilators Ex Hydralazine, nitrates, sodium
nitroprusside.
5. Beta blockers Ex Metoprolol, bisoprolol, carvedilol, nebivolol

36. Drugs for Arrest of disease progression
1. ACE Inhibitors Ex Captopril, Enalapril, Ramipril, Lisinopril,
Perindopril.
2. ARB’s Ex Losartan, Candesartan, Irbesartan, Valsartan,
Telmisartan.
3. Beta blockers
4. Aldosterone antagonists Ex Spironolactone, Eplerenone.
5. Neprilysin inhibitor Ex Sacubitril

37. Digoxin (Digitalization)
It is a purified cardiac glycoside extracted from the foxglove plant
Digitalis lanata.
Pharmacological actions:
HEART: Dose dependent increase force of contraction
(positive inotropic effect).
Systole is shortened, Diastole is prolonged.
Heart rate is decreased (bradycardia) Depression of SA node and
AV node, also vagal tone is increased.
Resting membrane potential is decreased with increasing doses
Phase 0 depolarization is reduced (marked in av node and
bundle of his
Slope of phase 4 depolarization is increased

38. BLOOD VESSELS: No prominent effect on BP.
Weak direct vasoconstrictor action (PR increases) but mild
Systolic bp increases Diastolic bp decreases.
KIDNEY: It causes diuresis in CHF patients, secondary to
improvement in circulation and renal perfusion.
CNS: High doses causes nausea and vomiting.
Hyperapnoea, central sympathetic stimulation, mental
confusion, disorientation and visual disturbances.

39. Pharmacokinetics
Absorption: 70 to 80% of an oral dose of digoxin is absorbed
mainly in the proximal part of the small intestine.
Onset: 15-30 min after oral admn, peak 2-5 hr.
Vd: 6-8 L/Kg
Plasma protein binding: 20 to 30% (albumin).
Distribution: Digoxin is extensively distributed in the heart and
kidneys, but the skeletal muscles form the largest digoxin
storage.
Elimination: elimination half life(36-48 hrs)
major renal excretion
25 per non renal routes(bile).

40. Mechanism

41. Contraindications
• Hypersensitivity
• Uncontrolled Ventricular Arrhythmias
• AV block
• Constrictive Pericarditis
• Idiopathic Hypertrophic Subaortic Stenosis.
Adverse effects
• Mental disturbances
• Diarrhea
• Headache
• Nausea
• Vomiting
• Maculopapular rash
• Dizziness

42. Digoxin is administered only under hospitalization due
to narrow therapeutic index
Antidigoxin Immunotherapy.
An effective antidote for life-threatening digoxin or digitoxin
toxicity is available in the form of antidigoxin immunotherapy
with purified Fab fragments from ovine antidigoxin antisera
(DIGIBIND).
A full neutralizing dose of Fab (based on either the estimated
total dose of drug ingested or the total body digoxin burden) can
be administered intravenously in saline solution over 30 to 60
minutes. For a more comprehensive review of the treatment of
digitalis toxicity

43. Diuretics

46. PDE 3 Inhibitors (amrinone, milrinone)

47. Sympathomimetic inotropics (Dopamine,
Dobutamine)
They are particularly used when heart failure Is accompanied by
low bp.
Dopaminergic D1 agonistic action has positive inotropic effect.
They are used to combat emergency pump failure, but the
benefits of this pump are short lasting due to development of
tolerance and their cardiotoxic potential.
Not used as long term therapy, used in case of emergency.

48. Neprilysin inhibitor (Sacubitril)
It prevents the degradation of ANP(atrial
natriuretic peptide), BNP( brain natriuretic
peptide) and other vasodilator peptides
producing vasodilation, natriuresis and diuresis.
Recently approved for use in advanced heart
failure

49. Be safe…..