chf by sayamdeep roy b.pharm
DESCRIPTION
congestive heart failure & its treatment. Various drugs used , their mechanism of action & adverse effect.TRANSCRIPT
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