This Slideshare includes the introduction of congestive heart failure, signs and symptoms, pathogenesis, epidemiology, etiology, pathophysiology, classification of drugs which is used to manage CHF, and recent drugs used to manage CHF.

1. CONGESTIVE HEART FAILURE

2. INTRODUCTION
2
By
Miss. Shruti Rajendra Rudraksha
Department of Clinical Pharmacy
M. Pharm First year
Guide
Dr. S. D. Patil
Dr. K. R. Patil
Mrs. H. E. Choudhary
R. C. Patel
Institute of Pharmaceutical Education and Research, Shirpur - 425405, Dist. Dhule (M.S.)

3. 3
CONTENTS
Definition
Signs and Symptoms
Pathogenesis
Epidemiology
Etiology
Pathophysiology
Classification
Recent Drugs

4. 4
Definition
Congestive heart failure in which the heart is
unable to maintain an adequate circulation of
blood in the bodily tissue or to pump out the
venous returned to it by veins.
It is a chronic progressively condition that
affects the pumping power of human heart
muscle.

5. 5
Signs
Symptoms
o Exercise intolerance
o Shortness of breath
o Fluid retention and
swelling
Complications
o Impaired liver function
o Headache
o Vomiting
o Diarrhoea

6. 6
Non Pharmacological Management
• Diet
• Compliance
• Salt- Advise patient to avoid high salt content
foods and not to add salt
• Alcohol- Advice moderate alcohol consumption
• Exercise- Regular exercise should be
encouraged

7. 7
Pathogenesis
Renin + Angiotensinogen
Angiotensinogen I
Angiotensinogen II
Peripheral constriction Aldosterone secretion
Increase afterload salt and water retention
Increased plasma volume
Decrease cardiac output Increases preload
Increased cardiac workload

8. 8
Sympathetic Nervous System Stimulation = Activation of adrenaline and
nor adrenaline cause increase heart rate, increase contractility and
peripheral contraction.
VENTRICULAR HYPERTROPHY
The left ventricular hypertrophy
Systolic/Diastolic
dysfunction
Atrial fibrillation
ventricular arrhythmia
Congestive
Heart
Failure

9. EPIDEMIOLOGY
 3-5% in the population over 65 years old
 Between 8% and 16% of those aged over 75 years.
9
I No symptoms with ordinary physical activity (such as walking or
climbing stairs)
II Slight limitation with dyspnoea on moderate to severe
exertion(climbing stairs or walking uphill)
III Marked limitation of activity, less than ordinary activity causes
dyspnoea( restriction walking distance and limiting climbing to one
flight of stairs)
IV Severe disability, dyspnoea at rest(unable to carry on physical
activity without discomfort)
New York Heart
Association(NY
HA)
classification
status of the
patient with
heart failure

10. ETIOLOGY
10
CHF is a weakening of heart caused by an underlying heart or blood vessel
problem.
 Cardiomyopathy(weakened heart muscle)
 Coronary artery disease(cholesterol deposition)
 Damaged heart valve
 High blood pressure
 Congenital heart defects(defect in the structure of heart)
 Inflammation of heart muscle(myocarditis)
 Cardiac arrhythmia(irregular heart beat)
🔑

11. 11
Systolic dysfunction
Ventricles of the heart are not able to
generate enough stroke volume.
Decrease in cardiac output and
ejection fraction.
1. Reduction in muscle mass (e.g.,
myocardial infarction)
2. Dilated cardiomyopathy
3. Bradyarrhythmia
Diastolic dysfunction
Ventricle wall is thickened.
Decrease in preload and increase in
afterload.
1. Ventricular hypertrophy
2. Infiltrative myocardial disease
3. Myocardial ischemia and
infarction
• Mitral or tricuspid valve stenosis
• Pericardial disease.
Congestive heart failure can result from any disorder that affects the ability of the heart to
contract (systolic dysfunction) or relax(diastolic dysfunction).
Mainly 2 types:
Systolic dysfunction
Diastolic dysfunction

12. 12

13. 13

14. PATHOPHYSIOLOGY
 To understand the pathophysiology processes in heart failure, basic
understanding of normal cardiac failure is necessary.
 Cardiac output(CO) is defined as the volume of blood ejected per unit time and
is the product of heart rate(HR) and stroke volume (SV)
 CO =HR *SV
Mainly depends upon 4 factors (on the basis of Starling’s law)
1. Preload- volume and pressure of blood in ventricles during diastole.
2. Afterload- volume and pressure of blood in ventricles during systole.
3. Contractility
4. Heart rate
14

15. 15
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 force of contraction.
3. Myocardial hypertrophy(increase in size and weight) to increase amount of
contractile tissue and hence contractability.
When the compensatory mechanism become insufficient or when they are active
for a long period they become ineffective and contribute to heart failure.

16. 16
Damage to cardiac myocytes and extracellular matrix leads to changes in the size, shape
and function of the heart and cardiac wall stress
These changes lead to systemic neurohormonal imbalance
This may lead to fibrosis, apoptosis, hypertension, hypertrophy, cellular and molecule
alteration, myotoxicity
Hemodynamic alterations, salt
and water retention
Morbidity and mortality
Arrhythmia, pump failure
HF symptoms
dyspnea, edema, fatigue
Progressive remodeling
and worsening of LV
function

17. COMPENSATORY
MECHANISM
 Chronic activation of sympathetic system which leads to tachycardia and
increased contractility.
 Renin angiotensin aldosterone system (loss of myocyte and causes hypertrophy
which leads to decrease in pumping function).
 Vasoconstriction and increased afterload. Vasoconstriction occurs due to
number of neurohormones like norepinephrine, angiotensin 2 and vasopressin.
 Vasoconstriction increases peripheral vascular resistance and hence decreases
cardiac output.
 Ventricular hypertrophy and remodeling.
17

18. CLASSIFICATION
Angiotensin converting enzyme- Captopril, Enalapril, Ramipril
Angiotensin receptor blocker- Candesartan, Losartan, Telmisartan
Beta adrenoreceptor blocker- Atenolol, Carvedilol, Metoprolol
Diuretic- Bumetanide, Furosemide, Hydrochlorothiazide
Direct vasodilator- Hydralazine, Isosorbide dinitrate
Ionotropic agent- Digoxin, Dobutamine
Aldosterone antagonist- Spironolactone
18

19. ACE INHIBITOR
19

20. DECREASE
ANGIOTENSIN 2 CAUSES-
Decrease output of sympathetic nervous system
 Increase vasodilation of vascular muscles
 Decrease retaining of sodium and water
 Increase levels of Bradykinin
Decreases preload and afterload
Increases cardiac output
20
Phloretin
Contraindication-
Pregnant women
1.Postural
hypotension
2. Renal
insufficiency
3.Dry cough
Adverse effects

21. CAPTOPRIL
Mechanism of action
Inhibits ACE hence inhibits the conversation of angiotensin II:
 Reduce afterload and preload
 Reduction in aldosterone secretion
 Reduce Na+ and water reabsorption
Adverse effects:
 Cough due to increase in the plasma level of bradykinin.
 Angioedema
 Hyperkalemia
 Teratogenicity
 Hypotension
21

22. 22
Angiotensin receptor blocker
• It improve systolic function
• Reverse cardiac remodeling
• Decrease sympathetic outflow from CNS
• Inhibition of renin release.
Losartan
Mechanism of action
• Angiotensin II, a vasoconstrictor is
concerned with ventricular
remodeling and fluid retention.
• These drug inhibit the binding of
angiotensin II to its AT1 receptor
• These agents do not exert any action
on bradykinin and thus do not
produce cough.
• Has comparable effect to ACE I
• Can be used in certain conditions
when ACE I are contraindicated.
Adverse drug
reaction
• Hypotension
• Impairment of renal
functioning

23. 23
Beta blocker
Mechanism of action
Standard beta blocker-
• Reduction in damaging sympathetic influences in the
heart(tachycardia, arrhythmia, remodeling)
• Inhibition of renin release
Carvedilol
• Beta blockade effect
• Peripheral vasodilation via alpha 1 adrenoreceptor
blockade

24. ADVERSE EFFECTS
 Bronchoconstriction
 Can produce some CNS symptoms like depression and sleep
disturbance
24

25. 25
Diuretics
 It relieves pulmonary congestion and peripheral
edema
 Reduce symptoms of volume overload
 Decrease plasma volume and venous return(preload)
to heart.
 Decrease cardiac work and decrease oxygen demand
 Decrease plasma volume decreases after load
decreases blood pressure
 They increase salt and water elimination Decreases
blood volume Decreases venous pressure

26. 26
Furosemide
Mechanism of Action of Loop Diuretics :
• Loop diuretics act on the Na-K-2Cl symporter in the thick ascending limb of the
loop of Henle to inhibit sodium and chloride reabsorption. Because magnesium
and calcium reabsorption in the thick ascending limb is dependent on sodium and
chloride concentration.
• Loop diuretics cause vasodilation of the veins and of the kidney’s blood vessels ,
mechanically causing a decrease in blood pressure. The collective effects of
decrease blood volume and vasodilation on decrease blood pressure.

27. DIRECT
VASODILATOR
 Hydralazine
 Mechanism of action- These agents reduce pulmonary congestion and increase
cardiac output by reducing preload or afterload. They also prevent remodeling of
heart.
 Nitrate receptor which is present on smooth muscle possess –SH group which
reduces nitrates to nitrite and nitric oxide.
 NO itself gets converted to an intermediate reactive nitrosothiol which activates
intracellular guanylate cyclase(GC) to convert GTP to cGMP results in vascular
smooth muscle relaxation.
27

28. ADVERSE EFFECTS
 Flushing face, palpitation, dizziness, tolerance develop rapidly used
orally in sustained release form or transdermally or by IV infusion
without drug free interval.
 DRUG INTERACTION
1. Sildenafil and other vasodilator potentiate the hypotensive action of
nitrates(inhibit the metabolizing enzyme PDE-IV and potentiate further
release of cGMP) sudden death occurs.
28

29. 29

30. 30
Contraindications
Ventricular fibrillation,
ventricular tachycardia, digitalis
toxicity
Adverse
reaction
Fatigue, headache,
blurred yellow or green
vision, seizures

31. 31
ALDOSTERONE ANTAGONIST
SPIRONOLACTONE
These enhances diuresis by promoting Na+ and water excretion (while
retaining K+) and prevents myocardial as well as vascular fibrosis which is
responsible for pathological remodeling of heart.
ADVERSE EFFECTS
Hyperkalemia is major risk during the therapy and require serum K+
monitoring.
Gynecomastia may occur in male patients after long term use.

32. 32

33. 33
MANAGEMENT AND TREATMENT
LAB FINDINGS
1. BUN (Blood Urea Nitrogen)
2. Liver Function Test
3. Kidney Function Test
4. B type Naturetic peptide test(BNP)
SURGICAL TREATMENT
1. Coronary Artery Bypass Graft Surgery
2. Valve Surgery
3. Left ventricular Reconstruction
4. Passive Cardiac Support
5. Artificial Cardiac Pacemaker
6. Cardiac transplantation
7. Implantable Cardiovascular Defibrillation
8. Ventricular Assist Devices

34. RECENT DRUGS
 Cardiac myosin activator (Omecamtive Mecarbil)
34
They accelerate transition of actin- myosin complex from a weakly
bound to strongly bound configuration.
Increase myosin head interaction with actin
Decrease nonproductive ATP hydrolysis
Increase duration of action further increase in stroke volume hence
improvement in myocardial systolic function and increases oxygen
consumption.

35. VASODILATOR
SERELAXIN
 Recombinant human relaxin- 2
 Relaxin- circulating peptide found in pregnant women
 Regulates systemic vasodilation
 Improves dyspnea significantly.
35

36. 36
THANKS…!
Suggesstions Please…….