The document provides an overview of congestive heart failure including its definition, epidemiology, etiology, types, risk factors, pathogenesis, signs and symptoms, diagnosis, management goals, and pharmacological and surgical treatment options. It discusses how heart failure results from the heart's inability to pump sufficient blood and covers compensatory mechanisms and factors that can precipitate or exacerbate the condition. Treatment focuses on improving quality of life, relieving symptoms, and slowing disease progression through lifestyle changes, medications like diuretics, ACE inhibitors, beta-blockers, and surgery in some cases.

1. M.Asiyabi., M.Pharm (First year)
Department of pharmacology

2. Agenda
1.Introduction
2.Terminology
3.Definition
4.Epidemiology
5.Etiology
6.Types
7.Risk factors
8.Pathogenesis
9.Signs and Symptoms
10.Diagnosis
11.Management (Treatment Goals)
12.Pharmacological Treatment

3. What is congestive cardiac failure or Heart
failure..??
Lets go….

4. Congestive heart failure
• Heart failure does not mean the heart has
stopped working.
• Rather, it means that the heart's pumping
power is weaker than normal.
• With heart failure, blood moves through the
heart and body at a slower rate, and pressure in
the heart increases.
• As a result, the heart cannot pump enough
oxygen and nutrients to meet the body's needs.
Introduction :-

5. Introduction
-Heart failure is a clinical syndrome caused by the inability of the heart to
Pump sufficient blood to meet the metabolic needs of the body.
- Heart failure can result from any disorder that reduces ventricular filling
(diastolic dysfunction) and or myocardial contractility (systolic dysfunction)
-The leading causes of heart failure are coronary artery disease and
hypertension.
-The primary manifestations of the syndrome are Dyspnea,fatigue, and
fluid retention
-Diseases that adversely affect ventricular diastole (filling),ventricular
systole (contraction), or both can lead to heart failure

6. Terminology
–Chronic heart failure (CHF), also called congestive cardiac failure(CCF), is an
ongoing condition in which the heart muscle is weakened and can't pump as
well as it normally does.
–CHF specifically refers to the stage in which fluid builds up around the heart
and causes it to pump inefficiently.

7. Definition (Pictorial representation)

8. Epidemiology
<65 years < 65 years
More common in men
Risk of coronary artery disease
is more.
80% of men will die within 8
years.
11.4% chance for men at age 40
Women less affected than men
Hypertension is the leading
epidemiology
70% of women will die within 8
years
15.4% chance for women at age 40
Two to three percent of the population have heart failure, but in those 70 to 80 years old, it
occur in 20–30 Percent.

9. Etiology
Reduction in muscle mass
(e.g.,myocardial infarction)
Dilated cardiomyopathies
Ventricular hypertrophy
Pressure overload
(e.g.,systemic or pulmonary
hypertension,aortic or
pulmonic valve stenosis)
Volume overload
(e.g.,valvular regurgitation,
shunts,high-output states)
Systolic dysfunction
(decreased contractility)

10. Etiology (cont..)
Increased ventricular stiffness
Ventricular hypertrophy
(hypertrophic cardiomyopathy)
Infiltrative myocardial diseases
(e.g.,amyloidosis,sarcoidosis,
endomyocardial fibrosis)
Myocardial ischemia and
Infarction
Mitral or tricuspid valve
Stenosis
Pericardial disease
(e.g.,pericarditis,pericardial
tamponade)
Diastolic dysfunction
(restriction in ventricular
filling)

12. Types of Heart failure
In right-sided heart failure, the right ventricle
loses its pumping function, and blood may back
up into other areas of the body, producing
congestion
Right Sided Heart Failure
Inability of the left heart to maintain its circulatory load,
with corresponding rise in pressure in the pulmonary
circulation usually with pulmonary congestion and
ultimately pulmonary edema.
Left Sided Heart Failure
Heart Failure can divided into two types

13. Types based on contractility
Systolic heart failure (Inability to relax)
The left ventricle loses its ability to contract normally.The heart can't
pump with enough force to push enough blood into circulation.
Diastolic heart failure (Inability to contract)
Diastolic dysfunction refers to an abnormality in how the heart fills
with blood during diastole. The heart muscles do not relax in a
normal manner and the heart may fill too slowly with an elevation in
filling pressure only.

15. Clinical manifestations

16. Clinical manifestations

17. Signs and symptoms
Pulmonary rales
Pulmonary edema
S3 gallop
Cool extremities
Pleural effusion
Cheyne-Stokes respiration
Tachycardia
Narrow pulse pressure
Cardiomegaly
Peripheral edema
Jugular venous distension
Hepato jugular reflux
Hepatomegaly

18. Risk factors
• Coronary artery Diseases
• Myocardial Infarction
• Hypertension
• Diabetes
• Heart Valve Disease ( e.g.Aortic Stenosis)
• Smoking
• Obesity
• Previous heart attack
• Congenital heart defects
• Cardiomyopathy
• Infection of heart muscles
• Conduction defects
• Large amount of salt intake

19. Pathophysiology

21. Normal Cardiac Function
– To understand the pathophysiologic processes in heart failure,a basic understanding
of normal cardiac function is necessary.
– The relationship between CO and mean arterial pressure(MAP)is:
CO = HR ×SV
MAP = CO ×systemic vascular resistance (SVR)

22. Frank-Starling mechanism
–Represents the relationship between stroke volume and end diastolic volume.
–The law states that the stroke volume of the heart increases in response to an
Increase in the volume of blood in the ventricles,before contraction (the end diastolic
volume),when all other factors remain constant.

23. Compensatory Mechanisms In Heart Failure
Regardless of the index event,the decrease in the heart’s pumping capacity
results in the heart having to rely on compensatory responses to maintain an adequate
cardiac output.
These compensatory responses include
(a)Tachycardia and increased contractility through sympathetic nervous system(SNS)
activation,
(b)TheFrank-Starling mechanism,whereby an increase in preload results in an increase
in stroke volume,
(c)Vasoconstriction,and
(d)Ventricular hypertrophy and remodeling.

24. Factors Precipitating/Exacerbating Heart Failure
Negative ionotropic effect
Antiarrhythmics (eg.,Disopyramide,flecainide,propafenone)
Β-blockers ( propranalol, metaprolol)
Calcium channel blockers (Verapramil,diltiazem)
Itraconazole
Terbinafine
Cardiotoxic
Doxorubicin
Daunomycin
Cyclophosphamide
Imatinib
Amphetamines
Ethanol
Sodium and water retention
NSAID
COX-2 inhibitors
Rosiglitazone and pioglitazone
Androgens and estrogens
Salicylates (high dose)
Sodium containing drugs (Ticarcillin disodium)

25. Diagnostic evaluation
1.Patient history collection
2.Physical examination
3.Electrocardiogram
4.Echocardiogram
5.Blood Tests
6.Dobutamine Stress Echo Cardiography
7.MRI
8.Cardiac Catheterization
9.Chest X-Ray

26. Stages of heart
failure with
examples

27. Desired outcome
To improve quality of life,
Relieve or reduce symptoms,
Prevent or minimize hospitalizations,
Slow disease progression and
Prolong survival.
The therapeutic goals for chronic HF

29. Treatment of chronic heart failure
General Approach
–The first step in managing chronic HF is to determine the
etiology or precipitating factors.Treatment of underlying
disorders(e.g,anemia,hyperthyroidism) may obviate the need
for treating HF.
–Non pharmacologic interventions include cardiac
rehabilitation and restriction of fluid intake(maximum 2L/day
from all sources) and dietary sodium (approximately 2 to 3g
of sodium per day).

30. Pharmacologic
theraphy
Drug therapies for selected patients :Drug therapies for routine use :
1.Diuretics
2.Angiotensin-Converting Enzyme
(ACE) Inhibitors
3.β-Blockers
1. Angiotensin II Receptor Blockers
2. Aldosterone Antagonists
3. Digoxin
4. Nitrates and Hydralazine
Surgical management

31. Diuretics
–Compensatory mechanisms in HF stimulate excessive sodium and water retention,
often leading to systemic and pulmonary congestion.
–However,because they do not alter disease progression or prolong survival, they are not
considered mandatory therapy for patients without fluid retention.
–Thiazide diuretics(e.g.,hydrochlorothiazide) are relatively weak diuretics and are used alone
infrequently in HF. However, thiazides or the thiazide like diuretic metolazone can be used in
combination with a loop diuretic to promote effective diuresis.

32. Angiotensin-Converting Enzyme (ACE) Inhibitors
– ACE inhibitors decrease angiotensin II and aldosterone,
– Clinical trials have produced unequivocal evidence that ACE
inhibitors improve symptoms, slow disease progression, and
decrease mortality in patients with HF and reduced LVEF(stageC).
– These patients should receive ACE inhibitors unless contraindications
are present.
– ACE inhibitors should also be used to prevent the development of
HF in at-risk patients (i.e.,stages A and B).

33. β-Blockers
–Beneficial effects of β-blockers may result from antiarrhythmic effects,
–β-Blockers are also recommended for asymptomatic patients with a reduced LVEF (stageB) to
decrease the risk of progression to HF.
–Because of their negative inotropic effects, β-blockers should be started in very low doses with
slow upward dose to avoid symptomatic worsening.
–Carvedilol, 3.125mg BD initially; target dose, 25 mg BD.
–Metoprolol succinate CR,12.5 to 25mg Od initially; target dose, 200 mg OD
–Bisoprolol,1.25mg once daily initially; target dose,10mg once daily.

34. Angiotensin II receptor blocker
–The angiotensin II receptor antagonists block the angiotensin II receptor subtype AT1, preventing
the deleterious effects of angiotensin II.
–Cough and angioedema are the most common causes of ACE inhibitor intolerance.
–ARBs are not alternatives in patients with hypotension,hyperkalemia,or renal insufficiency due to
ACE inhibitors because they are just as likely to cause these adverse effects.
–Candesartan,4 to 8mg once daily initially; target dose,32mg once daily.
–Valsartan,20 to 40mg twice daily initially; target dose,160mg twice daily.

35. Aldosterone antagonists
–Spironolactone and eplerenone block the mineralocorticoid receptor, the target site for
aldosterone.
–In the kidney,aldosterone antagonists inhibit sodium reabsorption and potassium excretion.
–Effects in the heart attenuate cardiac fibrosis and ventricular remodeling.
–Initial doses should below (spironolactone 12.5mg/day; eplerenone 25mg/day), especially in the
elderly and those with diabetes or creatinine clearance <50mL/min.

36. Digoxin
–Although digoxin has positive inotropic effects, its benefits in HF are related to its neurohormonal
effects.
–Mechanism : Digoxin attenuates the excessive sympathetic nervous system activation present in HF
patients,perhaps by reducing central sympathetic out flow.
–It also increases parasympathetic activity in HF patients and decreases heart rate thus
enhancing diastolic filling.
–Digoxin does not improve survival in patients with HF but does provide symptomatic benefits.
–Doses should be adjusted to achieve plasma digoxin concentration of 0.5 to1ng/mL.
–Higher plasma levels are not associated with additional benefits but may increase the risk of toxicity.

37. Digoxin toxicity
Non-cardiac (mostly CNS)
adverse effects
Anorexia, nausea, vomiting,
abdominal pain
Visual disturbances
Halos, Photophobia,
problems with color perception
(i.e.,red-green or yellow-green vision),
Scotomata
Fatigue, weakness, dizziness,
headache, neuralgia,confusion
Cardiac adverse effects
Ventricular arrythmias
Premature ventricular depolarisation,
bigeminy,trigeminy
AV junctional escape rythms
Atrial arrythmias
Paroxysmal atrial tachycardia
Sinus bradycardia

38. Nitrates and Hydralazine
–Nitrates(e.g.,ISDN) and hydralazine were combined originally in the treatment of HF because of
their complementary hemodynamic actions.
–Nitrates are primarily venodilators producing reductions in preload.
–Hydralazine is a direct vasodilator that acts predominantly on arterial smooth muscle to reduce
systemic vascular resistance(SVR) and increase stroke volume and cardiac output.
–A fixed-dose combination product is available that contains ISDN 20mg and hydralazine 37.5mg.
–The combination is also appropriate as first-line therapy in patients unable to tolerate ACE
Inhibitors or ARBs because of renal insufficiency,hyperkalemia,or possibly hypotension.

39. Nitroglycerine
–The major hemodynamic effects of IV nitroglycerin are decreased preload
–In higher doses,nitroglycerin displays potent coronary vasodilating properties and beneficial
effects on myocardial oxygen demand and supply making it the vasodilator of choice.
–Nitroglycerin should be initiated at 5 to 10 mcg/min (0.1 mcg/kg/min) and increased every 5 to 10
minutes as necessary and tolerated.
–Maintenance doses usually range from 35 to 200 mcg/min (0.5 to 3 mcg/kg/min).

40. Surgical management
Coronary Artery Bypass Graft (CABG) Surgery
Coronary Angioplasty
Implantable Cardiac Defibrillator
Intra Aortic Balloon Pump
Left Ventricular Assist Device
Valve Repair Or Valve Replacement Surgery
Pacemaker Insertion
Heart Transplantation