Download DRUGS USED IN CARDIAD FAILURE CONGESTIVE CARDIAC

DRUGS USED IN CARDIAD FAILURE
CONGESTIVE CARDIAC FAILURE
Inability of the heart to pump sufficient blood to meet the metabolic needs of the body is
called heart failure.
ETIOLOGY
•IMPAIRED FUNCTION OF CARDIAC MUSCLES
•INCREASED DEMAND OF THE BLOOD BY THE TISSUE
CIRCULATION OF BLOOD
Through veins into Superior Vena cava and Inferior vena cava  Right atrium.
Right atrium  Right ventricle  Pulmonary arteries  Lungs (for oxygenation) 
Pulmonary vein  Left atrium  Left ventricle  Aorta  Tissues (Through arteries)
COMPENSATORY PHYSIOLOGICAL RESPONSE IN HEART FAILURE
In heart failure compensatory mechanisms are:
1) INCREASED SYMPATHETIC ACTIVITY:
Activation of -adrenergic receptors in heart results in increased force of contraction and
heart rate
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2) FLUID RETENTION:
During cardiac failure, the blood flow to the kidneys
reduces , causes increased renin secretion and
angiotensin-II synthesis.
3) MYOCARDIAL HYPERTROPHY:
The most important intrinsic compensatory mechanism is myocardial hypertrophy.
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Clinically cardiac failure is divided
into four classes
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Class I: No limitation to ordinary activities & symptoms occur only with greater than
ordinary exercise.
Class II: Slight limitation of ordinary activities, which result in fatigue and palpitation.
Class III: Results in no symptom at rest but fatigue, difficulty in breathing and other
symptoms occur at less than ordinary activities.
Class IV: Symptoms at rest.
SYMPTOMS & SIGNS
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DIFFICULTY IN BREATHING
PULMONARY EDEMA
BASAL CREPTS
RAISED JVP
PERIPHERAL EDEMA
DRUGS USED FOR THE TREATMENT OF Congestive Cardiac Failure
CARDIAC GLYCOSIDES:
DIGOXIN, DIGITOXIN
BIPYRIDINE DERIVATIVES:
AMRINONE, MILRINONE
-ADRENERGIC AGONISTS:
DOPAMINE, DOBUTAMINE
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ACE INHIBITORS:
CAPTOPRIL
ENALAPRIL
LISINOPRIL
FOSINOPRIL
VASODILATOR:
SODIUM- NITROPRUSSIDE
DIURETICS:
LOOP AND THIAZIDE DIURETICS.
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CARDIAC GLYCOSIDES
Digitalis are extracts of the plant
“Digitalis purpura” .
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Digoxin is most commonly used agent have low therapeutic index.
MECHANISM OF ACTION
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Digitalis inhibit directly the Na–K ATPase and increase the intracellular Ca+2.
Normally the Na+ is extruded from the cell by the Na–K ATPase (Na–K pump) at the end
of action potential, to bring the cell back the resting state. Another pump Na–Ca pump
causes efflux of Ca+2 in exchange of Na+. The activity of this pump depends upon the
intracellular Na+ level.
When Na–K ATPase is inhibited, Na+ levels inside the cell is increased, results in the
decreased activity of Na–Ca exchange, thus increase intracellular Ca+2 levels, that
increase the force of myocardial contraction.
Digitalis inhibit directly Na–K ATPase
Na+ levels inside the cell is increase
Activity of Na–Ca pump decrease
Intracellular Ca+2 levels increase
Force of contraction increase
PHARMACOLOGICAL ACTIONS
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DIRECT ACTIONS
MECHANICAL ACTIONS
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Increased force of contraction
Increased intra-cellular Ca concentration
Inhibition of Na+–K+
ELECTRICAL ACTIONS
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Trasient prolongation of APD
Shortening of APD due to intracellular K+ defeciency
Shorting of atrial & ventricular ERP
Delayed after depolarization due to increased intracellular Ca+2
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INDIRECT ACTIONS
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PARASYMPATHOMIMETIC
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Sensitization of baroreceptors.
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Central Vagal Stimulation.
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Facilitation of Muscarinic transmission at the cardiac muscle cell.
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SYMPATHOMIMETIC
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outflow increased at toxic dose
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sensitized the myocardium and exaggerates all the effect of the drug.
Effects on other organ
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Glycosides effect all excitable tissues i.e. Smooth muscle & CNS.
ECG CHANGES
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ST segment depression.
T wave inversion.
P–R interval prolongation.
Q–T interval shortening.
Decreased heart rate.
BLOOD VESSELS
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mild direct vasoconstrictor effects
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no prominent action on Blood pressure.
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Pulse pressure increased.
KIDNEY:
Diuresis, secondary to improvement in circulation and renal perfusion.
CENTRAL NERVOUS SYSTEM:
Digitalis has little CNS effects, high doses cause CTZ activation produces nausea
vomiting.
USES:
A) CONGESTIVE HEART FAILURE
Cardiac output is insufficient to meet the demands of tissue perfusion.
Low out-put failure e.g. Hypertension, Rh valvular defects, CHD, IHD, Myocarditis,
Arrhythmias.
Digitalis is beneficial in low output failure and results are best obtained when
myocardium is not primarily damaged
B. CARDIAC ARRHYTHMIAS:
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A) Atrial Fibrillation:
Drug of choice, reducing the ventricular rate in AF by decreasing the number of impulses
that pass down the A-V node and bundle of His.
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B) Atrial flutter:
(Atrial rate 200-300/min) regular & synchronous
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C) Paroxysmal supra-ventricular tachycardia.
Mostly due to reentry involving the SA & AV node
Digitalis increases the vagal tone and depresses the impulses through the SA / AV node.
ADVESE EFFECTS
Toxicity of Digitalis is high ,margin of safety is low, 25% developed toxic symptoms.
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EXTRA-CARDIAC.
Anorexia, Nausea Vomiting, Abdominal pain, Malaise, Fatigue, Headache, Mental
confusion, Restlessness, Hyperapnea, Disorientation, Psychosis & Visual disturbances.
Diarrhea occasionally
Skin rashes & Gynaecomazia rarely.
CARDIAC:
Arrhythmias
FACTORS INCREASING DIGITALIS TOXICITY
Age specially in old age
Route of administration
Hypokalemia
Diuretic therapy
Dialysis
Hypercalcemia
Hypernatremia
Hypothyroidism
Catecholamines
Drugs
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STEPS IN THE MANAGEMENT OF CCF
Reduce work load of the heart:
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Limit activity level.
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Reduce body weight.
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Control hypertension.
Keep the patient in prop up position.
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Restrict sodium (Salt) intake.
Give diuretics.
Give ACE inhibitors and digitalis.
Give  blockers to patients with stable class II–III heart failure.
Give vasodilators.
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REFERANCES
LIPPINCOTT’S ILLUSTRATED REVIEW PHARMACOLOGY
4TH EDITION
Pg # 183 – 195
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