This document provides an overview of congestive heart failure (CHF), including its etiology, pathophysiology, symptoms, management, and treatment with various drugs. CHF is defined as the heart's inability to pump sufficient blood due to problems with filling or ejecting blood. Common causes include intrinsic pump failure, increased workload, impaired filling, and poor oxygen/nutrient supply. The pathophysiology involves neurohormonal activation leading to fluid retention. Symptoms include fatigue, shortness of breath, and edema. Treatment focuses on lifestyle changes, medications like ACE inhibitors, beta-blockers, diuretics, and vasodilators to block neurohormonal activation and reduce preload and afterload. Ad

1. PREPARED BY-SAYAMDEEP
ROY
B.PHARM
3rd YEAR, 6th SEM
REG NO.-112080210015
ROLL NO.-20801911015

2.  CHF
 ETIOLOGY OF CHF
 EPIDEMIOLOGY OF CHF IN INDIA
 PATHOPHYSIOLOGY OF CHF
 SYMPTOM ,MANAGEMENT OF CHF
 VARIOUS DRUGS USED IN CHF
 MECHANISM OF ACTION, ADVERSE
EFFECT OF THE DRUGS
 REFERENCE

3.  Heart failure (HF) is a complex, progressive
disorder in which the heart is unable to pump
sufficient blood to meet the need of the body.
HF is due to an impaired ability of the heart
to adequately fill with and/or eject blood. It is
often accompanied by abnormal increases in
blood volume and interstitial fluid in cardio-pulmonary
system, hence the term
‘congestive’.

4.  Intrinsic pump failure
 Increased workload on
the heart
 Impaired filling of cardiac
chamber
 Systolic dysfunction
 Diastolic dysfunction
 Poor supply of O2 &
nutrients

5. 1 2

6. PATHOPHYSIOLOGY OF
CHF
CONGESTIVE HEART FALIURE
Angiotensinoge
ACE
n

7. SYMPTOMS OF CHF

8.  Weigh yourself daily.
 Try to read food labels.
 Follow a low-sodium diet. Keep total sodium intake to less than
2,000 mg (2g) per day.
 Exercise.
 Take prescribed medicine.
 Do not take NSAIDS—Advil® (Ibuprofen), Aleve® (Naproxen), Orudis®
(Ketoprofen), or other anti-inflammatory drugs.
 Avoid: Alka-Seltzer®, Metamucil Instant®, and all effervescent drugs.
 Lose weight (if overweight).
 Get support of friends and family.
 Quit smoking.
 Limit alcohol (if your heart failure is caused by alcohol, avoid it
completely).
 Take care of other medical conditions such as high blood pressure
and diabetes.
 Consult with a registered doctor.

9. DRUGS USED IN CHF
 RENIN-ANGIOTENSIN
SYSTEM BLOCKERS
ACE inhibitors ARBs
 ß-BLOCKERS
 DIURETICS
thiazides
High ceiling
K+sparing
/loop diuretics
 VASODILATORS
mixed
dilator Venodilator
Arteriolar
dilator
 CARDIAC
GLYCOSIDES /
INOTROPIC AGENTS
 ALDOSTERONE
ANTAGONISTS

10.  ACE inhibitors –
CAPTOPRIL
ENALAPRIL
QUINAPRIL
RAMIPRIL
 ANGIOTENSIN RECEPTOR
BLOCKER-LOSARTAN
VALSARTAN
TELMISARTAN
 β-BLOCKERS-ATENOLOL
PROPRANOLOL
CARVEDILOL
METOPROLOL
 HIGH CEILING /LOOP DIURETICS-FUROSEMIDE
TORSEMIDE
 K+ SPARING-SPIRONOLACTONE
 THIAZIDE DIURETICS-HYDROCHLOROTHIAZIDE
 VENODILATOR-ISOSORBIDE
DINITRATE
GLYCERYL TRINITRATE
 ARTERIOLAR DILATOR-HYDRALAZINE
MINOXIDIL
 MIXED DILATOR-SODIUM
NITROPRUSSIDE
 CARDIAC GLYCOSIDE-DIGITOXIN
DIGOXIN
PHOSPHODIESTERASE III (PDE III)
INHIBITOR-MILRINONE
AMRINONE

11. RENIN (from
kidney)
ANGIOTENSIN
CONVERTING
ENZYME

12. ANGIOTENSIN
CONVERTING
ENZYME (ACE)

13.  These include postural hypotension,
renal insufficiency, hyperkalemia,
angioedema, and a persistent dry
cough. The potential for symptomatic
hypotension with ACE inhibitor therapy
requires careful monitoring. ACE
inhibitors should not be used in pregnant
women, because they are fetotoxic.

15. These include postural hypotension, renal
insufficiency, hyperkalemia, angioedema.
ARBs are contraindicated in pregnancy.

16. ß-blocker inhibits the changes that occurs due
to activation of Sympathetic Nervous System
Decrease Heart Rate
Inhibition of renin secretion from kidney
Decreased Angiotensin II formation
Increased Cardiac Output

17. ß-blocker is not a drug of choice in CHF ,
because it have various adverse effects--
 BRADYCARDIA
 INCREASED FREQUENCY OF URINATION
Etc.

18. DIURETIC
S
Decrease
circulating
volume of heart
Decrease venous
return to heart
(preload)
Improve ventricular
efficiency
Decrease cardiac
workload & O2 demand
of heart
Decrease
afterload
by
decreasin
g plasma
volume
Decrease
the blood
pressure
Removin
g
periphera
l edema
&
pulmonar
y
congesti
on

19. Some adverse effects are –
THIAZIDE GROUP- LOSS OF Na+
LOOP DIURETICS GROUP- LOSS OF
ELECTROLYTE
INSTEAD OF THIS-
 INCREASED FREQUENCY OF URINATION,
 HYPOTENSION,
Etc.

20. MECHANISM OF ACTION OF
VENODILATORS
ORGANIC NITRATES (GLYCERYL TRINITRATE ,
ISOSORBIDE DINITRATE)
Metabolized in vascular
endothelial cell
5-NITROSOTHIOL NITRIC OXIDE
GUANYLYL
CYCLASE
GTP cGMP
Decreased Ca2+ entry in
Vascular cell
RELAXATION
DEPHOSPHORYLATION OF
MYOSIN LIGHTCHAIN KIASE
(MLCK)
DUE TO ABSENCE OF
PHOSPHORYLATED MLCK,
MYOSIN IS NOT ACTIVATED
NO ACTIN MYOSIN
INTERACTION

22. METABOLIZED IN
ENDOTHELIAL CELLS AND
RBC
GTP
RELAXATION OF
VASCULAR
MUSCLE
DEPHOSPHORYLATION OF
MYOSIN LIGHTCHAIN KIASE
(MLCK)
DUE TO ABSENCE OF
PHOSPHORYLATED MLCK,
MYOSIN IS NOT ACTIVATED
NO ACTIN MYOSIN
INTERACTION

23. MECHANISM OF ACTION OF
PHOSPHODIESTERASE III (PDE III) INHIBITOR
PDE III
ATP cAMP 5’AMP
PDE III inhibitor
(milrinone , amrinone)
Increase Ca2+ influx
in myocardial muscle
Increase force of contraction of
heart (positive inotropic effect)

24. Some adverse effects are--
 THROMBOCYTOPENIA
 NAUSEA
 DIARRHOEA
 ABDOMINAL PAIN
 LIVER DAMAGE
 FEVER
 CARDIAC ARRHYTHMIA

25. Na+-K+ATPase transport system moves Na+ ion out of the cell & brings 2k+ion in to the cell
Na+-k+ ATPase transporter molecule is blocked by cardiac glycosides
increased intracellular accumulation of Na+ions
Exchange of Na+ions with Ca2+ion through Na+-Ca2+ antiporter system is increased
Ca2+ entry through L-type Ca2+
Increase intra cellular concentration of Ca2+ ion
Ca2+ ion stored in Sercoplasmic Reticulum (SR)
Ca2+ release from SR
Ca2+ binds to troponin c to form troponin c-Ca2+ complex which activate actin
Actin-myosin interaction
Increased cardiac muscle contraction
channel

27. Occurrence of adverse drug reaction is common
due to its narrow therapeutic index. Some adverse
effects are --
Extra cardiac adverse effects-anorexia,
nausea, vomiting, diarrhoea, fatigue, headache,
mental confusion, restlessness, depression, blurred vision
Cardiac adverse effect-all
types of cardiac arrhythmia occurs like ventricular
extrasystole, ventricular tachycardia etc.

28. REFERENCE
• ESSENTIALS OF MEDICAL PHARMACOLOGY
KD TRIPATHI
6th edition , pp.-493-507
• LIPPINCOTT’S ILLUSTRATED REVIEWS
PHARMACOLOGY
RICHARD FINKEL, LUIGI X. CUBEDDU, MICHELLE A. CLARK
6th edition , pp.-151-157