PREPARED BY-SAYAMDEEP ROY

B.PHARM 3rd YEAR, 6th SEM

REG NO.-112080210015ROLL NO.-20801911015

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

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’.

Intrinsic pump failure

Increased workload on

the heart

Impaired filling of cardiac

chamber

Systolic dysfunction

Diastolic dysfunction

Poor supply of O2 &

nutrients

1 2

PATHOPHYSIOLOGY OF

CHFCONGESTIVE HEART FALIURE

ACE

Angiotensinoge

n

SYMPTOMS OF CHF

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.

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

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

RENIN (from kidney)

ANGIOTENSIN CONVERTING

ENZYME

ANGIOTENSIN

CONVERTING

ENZYME (ACE)

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.

These include postural hypotension, renal

insufficiency, hyperkalemia, angioedema.

ARBs are contraindicated in pregnancy.

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

ß-blocker is not a drug of choice in CHF , because it have various adverse effects--

BRADYCARDIA

INCREASED FREQUENCY OF URINATION

Etc.

DIURETIC

S

Decrease

circulating

volume of heartDecrease 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

Some adverse effects are –

THIAZIDE GROUP- LOSS OF Na+

LOOP DIURETICS GROUP- LOSS OF

ELECTROLYTE

INSTEAD OF THIS-

INCREASED FREQUENCY OF URINATION,

HYPOTENSION,

Etc.

ORGANIC NITRATES (GLYCERYL TRINITRATE ,

ISOSORBIDE DINITRATE)

MECHANISM OF ACTION OF

VENODILATORS

NITRIC OXIDE5-NITROSOTHIOL

Metabolized in vascular

endothelial cell

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

GTP cGMP

GUANYLYL

CYCLASE

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

METABOLIZED IN

ENDOTHELIAL CELLS AND

RBC

MECHANISM OF ACTION OF PHOSPHODIESTERASE III (PDE III) INHIBITOR

ATP cAMP 5’AMP

PDE III

PDE III inhibitor (milrinone , amrinone)

Increase Ca2+ influxin myocardial muscle

Increase force of contraction ofheart (positive inotropic effect)

Some adverse effects are--

THROMBOCYTOPENIA

NAUSEA

DIARRHOEA

ABDOMINAL PAIN

LIVER DAMAGE

FEVER

CARDIAC ARRHYTHMIA

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

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

Ca2+ entry through L-type Ca2+

channel

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.

• 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

REFERENCE