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DRUGS USED IN THE

TREATMENT OF CONGESTIVE
HEART FAILURE
Dr.dr. Asep Sukohar, M.Kes

Dept of pharmacology and therapy


Medical school Lampung University

CONGESTIVE HEART FAILURE


CHF is a condition in which the heart is unable to
pump suffient blood to meet the needs of the body.
Underlying disease:
Hypertensiv Heart Disease
Coronary Heart Disease
Valvular Heart Disease
Cardiomyopathy
Congenital Heart Disease
Others

Underlying disease
Cardiac
Failure
Venous pressure

Cardiac output

Sympathetic activity

Blood pressure
Renal blood flow
Renin, angiotensin II
Aldosteron
Sodium retention

capillary filtration
Edema

DRUG USED TO TREAT CHF


I.

INTROPIC AGENT
Increase the strength of contraction of
cardiac muscle

II. DIURETICS
Decrease ECF volume
III. VASODILATOR
Reduce the load on the myocardium

I. INTROPIC AGENT
1. CARDIAC GLICOSIDES
- Digoxin
- Digitoxin
- Quabain
1. ADRENERGIC AGONIST
- Dobutamin
- Dopamin
1. PHOSPNO DIESTERASE INHIBITORS
- Amrinone
- Milrinone

DIGOXIN
Therapeutic use of digoxin is confounded by
1.variable pharmacokinetics
2.Numerious drug interaction
3.Naroow theurapeutic index
Digoxin comentry is associated with high
mortallity

DIGOXIN
MECHANISM OF ACTION
D. inhibit Na+ - K+ exchange by Na +/K+
ATPase
- intracellular Na+
- intracellular Ca++
(+) inotropic
CO
Modifying autonomic neural discharge

PHARMACOKINETICS
First Pass Metabolism, by microba in
intestinum
Distributed to all tissue included CNS
Metabolism : 30%, is activated by
enzyme liver

SIDE EFFECT & TOXIC OF DIGOXIN


Gastrointestinal
Anorexia, nausea, vomiting, abdominal pain
Neurologic
Malaise fatigue, confusion, facial pain,
insomnia, depression, vertigo, colored
vision (green or yellow halos around light)
Cardiac
Arrhytmia
Ventricular fibrillation and cardiac arrest
(are the most common cause of death)

FACTORS PREDISPOSING TO
DIGITALIS TOXICITY
Electrolite Disturbances
Hypokalemia
Hypomagnesia
Hypercalcemia
Drugs
Thiazid
Renal Failure

Management of :
1. Phenytoin
Lidocain
blocker
2. Monoclonal digoxin : specitic antibodies
(F. ab fragments)

DRUG INTERACTION
Increased digitalis
Concentration may
occur during
Concurrent therapy

Amiodarone
Erythromycin base
Quinidine
Tetracycline
Verapamil

Enhanced potential
potential
Enhanced
for cardiotoxicity
cardiotoxicity
for

Decreased levels of
Blood potassium

Corticosteroids
Thiazide diuretics
Loop diuretics

INDICATION
Congestive Heart Failure (systolic CHF)
Arrhythmias
Supraventricular Arrhytmias

CONTRAINDICATION:
AV heart block

BETA ADRENERGIC AGONIST


DOPAMINE

Adrenergic dopamin
Effect

Effect

receptor
Effect

II. DOBUTAMIN
Asynthetic analog of dopamin
Dopamine increase Cardiac Output with
little change in the HR and does not
significantly elevated oxygen demands of
the myocard.

DOPAMIN - DOBUTAMIN
Indication:
Refractory Heart Failure
Severe acute myocardial failure
(after cardiac
surgery)
Cardiogenic
shock

EFFECT OF DIURETIC ON CHF


Relieve peripheral edema
Relieve pulmonary congestion
symptoms: orthopnea, paroxysmal
nocturnal dyspnea.
Decreased plasma volume
preload
cardiac load and O2
afterload
demand
BP
Hypokalemia

VASODILATOR
I. 1. ACEI (angiotensin converting enzym inhibitor)
*captropil
*lisinopril
2. ARB (angiotensin Receptor Blocking agent)
*losartan
*valsartan
II. Others

Nitrat organic (isosorbid-nitroglicerin)

ACE INHIBITOR

Captopril
Enalapril
Lisinopril
Benazepril

Quinapril
Rapipril
Fosinopril

MECHANISM OF ACTION

MECHANISM OF ACTION
Angiotensin I

bradikinin active
ACEI 1

ARB Angiotensin 2

bradikinin active

Vasodilatation

level of bradikinin

retention of Na-water

*Vasodilatation

Outflow of symphatetic

*Cough
*Angioneurotic E

PRELOAD
AFTER LOAD

ADR
Skin rash, dysgeusia and proteinuria
Angioedema
Neutropenia, agranulocytosis,
glomerulonephritis (rare)

INDICATION
CHF in a symptomatic patient (left
ventricular dysfunction)
Patient who have had a recent
myocardial infarction

DOPAMINE
1. Heart : inotropic (cardiac contracitas)
2. Renal
Dilare renal and splanenic arteriole
Increase blood flow (RBF)
Vascular and smooth muscle
inhigh dose
DOBUTAMINE
Little change in HR

SVR=systemic vascular resistance

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