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Dr. Nikhilkumar S Sakle
Assistant Professor
Department of Pharmacology
Y. B. Chavan College of Pharmacy,
Aurangabad.
Drugs for Heart Failure
(Cardiac Glycosides)
1
 It means that the heart's pumping power is weaker than
normal.
 Blood moves through the heart and body at a slower
rate and pressure in the heart increases.
 As a result, the heart cannot pump enough oxygen and
nutrients to meet the body's needs.
2
 The chambers of the heart may respond by stretching
to hold more blood to pump through the body or by
becoming stiff and thickened.
 This helps to keep the blood moving, but the heart
muscle walls may eventually weaken and become
unable to pump as efficiently
3
 As a result, the kidneys may respond by causing the
body to retain fluid (water) and salt.
 If fluid builds up in the arms, legs, ankles, feet,
lungs, or other organs, the body becomes congested,
and congestive heart failure is the term used to
describe the condition.
4
5
Cardiac Glycosides
 They increase myocardial contractility and output in a
hypodynamic heart without a proportionate increase in
O2 consumption.
 These are glycosidic drugs having cardiac inotropic
property.
 Thus, efficiency of failing heart is increased.
6
 In contrast, ‘Cardiac Stimulants’ (Adr, theophylline)
increase O2 consumption rather disproportionately and
tend to decrease myocardial efficiency.
7
 Cardiac glycosides are found in several plants and in
toad skin (Bufotoxin).
 Digitalis lanata is the source of Digoxin, the only
glycoside that is currently in use. Others like Digitoxin
(from Digitalis purpurea) and Ouabain (from Strophan
thus gratus), etc. are no longer clinically used or
marketed.
8
PHARMACOLOGICAL ACTIONS
 Heart: Digitalis has direct effects on myocardial
contractility and electrophysiological properties.
Force of contraction Digitalis causes a dose dependent
increase in force of contraction of heart—a positive
inotropic action.
There is more complete emptying of failing and dilated
ventricles—cardiac output is increased and end-
diastolic volume is reduced.
9
 Rate: Heart rate is decreased by digitalis. In addition,
digitalis slows the heart by vagal and extravagal
actions.
10
Mechanism of action
11
 Blood vessels: Digitalis has mild direct
vasoconstrictor action.
 Kidney: Diuresis occurs promptly in CHF
patients, secondary to improvement in circulation
and renal perfusion. The retained salt and water
is gradually excreted. No diuresis occurs in
normal individuals or in patients with edema due
to other causes.
12
 CNS: Digitalis has little apparent CNS effect in
therapeutic dose. Higher doses cause CTZ activation
→ nausea and vomiting. Still higher doses produce
hyperapnoea, central sympathetic stimulation, mental
confusion, disorientation and visual disturbances.
13
ADVERSE EFFECTS
 Toxicity of digitalis is high, margin of safety is low
(Therapeutic index 1.5–3 ng/ml).
 Extracardiac Anorexia, nausea, vomiting and
abdominal pain are usually reported first: are due to
gastric irritation, mesenteric vasoconstriction and CTZ
stimulation. Fatigue, malaise, headache, mental
confusion, restlessness, hyperapnoea, disorientation,
psychosis and visual disturbances are the other
complaints. Skin rashes and gynaecomastia are rare.
14
 Cardiac Almost every type of arrhythmia can be
produced by digitalis: pulsus bigeminus, nodal and
ventricular extrasystoles, ventricular tachycardia and
terminally ventricular fibrillation. Partial to complete
A-V block may be the sole cardiac toxicity, or it may
accompany other arrhythmias. Severe bradycardia,
atrial extrasystoles, AF or AFl have also been noted.
15
PRECAUTIONS AND
CONTRAINDICATIONS
 Hypokalemia:
 Elderly, renal or severe hepatic disease
 Myocardial ischaemia:
 Thyrotoxicosis:
 Myxoedema:
 Ventricular tachycardia
 Partial A-V block:
 Acute myocarditis:
 Wolff-Parkinson-White syndrome:
16
INTERACTIONS
 Diuretics:
 Calcium:
 Quinidine:
 Adrenergic drugs:
 Digoxin absorption may be reduced by
metoclopramide, sucralfate, antacids, neomycin,
sulfasalazine.
 Absorption of digoxin is increased by atropinic drugs,
including tricyclic antidepressants.
 Propranolol, Verapamil, diltiazem and disopyramide:
17
TREATMENT OF CHF
18
 Heart failure occurs when cardiac output is
insufficient to meet the demands of tissue
perfusion, or is able to do so only by elevating
filling pressure. It is a progressive disease with
gradually deteriorating cardiac performance.
 Heart failure may primarily be due to systolic
dysfunction or diastolic dysfunction.
19
 Systolic dysfunction
 This refers to deficient pumping action of
ventricles, i.e. ventricles are unable to develop
sufficient wall tension to eject adequate
quantity of blood and get progressively dilated.
 The most important cause of systolic
dysfunction is coronary artery disease (CAD),
myocardial infarction (MI) and loss of functioning
myocardium.
 Other causes are valvular incompetence, dilated
cardiomyopathy, viral (including HIV) myocarditis,
tachyarrhythmias (mostly AF), etc
20
 Diastolic dysfunction
 The ventricular wall is thickened and unable to
relax normally during diastole; ventricular filling is
impaired and stroke volume is reduced, but the
EF may be normal.
 Long standing hypertension is the most common
cause of left ventricular hypertrophy (LVH) and
subsequent diastolic dysfunction. It is mostly
associated with ageing and myocardial stiffening.
Aortic stenosis, hypertrophic cardiomyopathy, A-V
shunts and congenital heart disease are the other
important causes.
21
 However, most patients, especially long standing
cases, have both systolic and diastolic dysfunction.
Symptomatically also both are similar. Several
compensatory mechanisms are brought into action to
overcome the reduced cardiac output (CO).
 These include:
 Elevation of filling pressure
 Increase in sympathetic tone
 Activation of RAS
 Over production of aldosterone
 Endothelin production
 Release of natriuretic peptides (ANP and BNP)
TREATMENT OF CHF
 There are two distinct goals of drug therapy in CHF:
(a) Relief of congestive/low output symptoms and restoration
of cardiac performance. This can be achieved by:
 Inotropic drugs—Digoxin, dobutamine/ dopamine,
amrinone/milrinone.
 Diuretics—Furosemide, thiazides
 RAS inhibitors—ACE inhibitors/ARBs
 Vasodilators— Nitrate (Veno), Hydralazine, nitroprusside
 β-blocker—Metoprolol, bisoprolol, carvedilol, Nebivolol
22
(b) Arrest/reversal of disease progression and
prolongation of survival, possible with:
 ACE inhibitors/ ARBs, β blockers
 Aldosterone antagonist—Spironolactone, eplerenone.
 Important nonpharmacological measures are rest and
salt restriction.
23
24
Uses
25
 1. Congestive Heart failure
 2. Cardiac arrhythmias
 Atrial fibrillation (AF)
 Atrial flutter (AFI)
 Paroxysmal supraventricular tachycardia (PSVT)

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Pharmacology of Drugs for Congestive Heart Failure

  • 1. Dr. Nikhilkumar S Sakle Assistant Professor Department of Pharmacology Y. B. Chavan College of Pharmacy, Aurangabad. Drugs for Heart Failure (Cardiac Glycosides) 1
  • 2.  It means that the heart's pumping power is weaker than normal.  Blood moves through the heart and body at a slower rate and pressure in the heart increases.  As a result, the heart cannot pump enough oxygen and nutrients to meet the body's needs. 2
  • 3.  The chambers of the heart may respond by stretching to hold more blood to pump through the body or by becoming stiff and thickened.  This helps to keep the blood moving, but the heart muscle walls may eventually weaken and become unable to pump as efficiently 3
  • 4.  As a result, the kidneys may respond by causing the body to retain fluid (water) and salt.  If fluid builds up in the arms, legs, ankles, feet, lungs, or other organs, the body becomes congested, and congestive heart failure is the term used to describe the condition. 4
  • 5. 5
  • 6. Cardiac Glycosides  They increase myocardial contractility and output in a hypodynamic heart without a proportionate increase in O2 consumption.  These are glycosidic drugs having cardiac inotropic property.  Thus, efficiency of failing heart is increased. 6
  • 7.  In contrast, ‘Cardiac Stimulants’ (Adr, theophylline) increase O2 consumption rather disproportionately and tend to decrease myocardial efficiency. 7
  • 8.  Cardiac glycosides are found in several plants and in toad skin (Bufotoxin).  Digitalis lanata is the source of Digoxin, the only glycoside that is currently in use. Others like Digitoxin (from Digitalis purpurea) and Ouabain (from Strophan thus gratus), etc. are no longer clinically used or marketed. 8
  • 9. PHARMACOLOGICAL ACTIONS  Heart: Digitalis has direct effects on myocardial contractility and electrophysiological properties. Force of contraction Digitalis causes a dose dependent increase in force of contraction of heart—a positive inotropic action. There is more complete emptying of failing and dilated ventricles—cardiac output is increased and end- diastolic volume is reduced. 9
  • 10.  Rate: Heart rate is decreased by digitalis. In addition, digitalis slows the heart by vagal and extravagal actions. 10
  • 12.  Blood vessels: Digitalis has mild direct vasoconstrictor action.  Kidney: Diuresis occurs promptly in CHF patients, secondary to improvement in circulation and renal perfusion. The retained salt and water is gradually excreted. No diuresis occurs in normal individuals or in patients with edema due to other causes. 12
  • 13.  CNS: Digitalis has little apparent CNS effect in therapeutic dose. Higher doses cause CTZ activation → nausea and vomiting. Still higher doses produce hyperapnoea, central sympathetic stimulation, mental confusion, disorientation and visual disturbances. 13
  • 14. ADVERSE EFFECTS  Toxicity of digitalis is high, margin of safety is low (Therapeutic index 1.5–3 ng/ml).  Extracardiac Anorexia, nausea, vomiting and abdominal pain are usually reported first: are due to gastric irritation, mesenteric vasoconstriction and CTZ stimulation. Fatigue, malaise, headache, mental confusion, restlessness, hyperapnoea, disorientation, psychosis and visual disturbances are the other complaints. Skin rashes and gynaecomastia are rare. 14
  • 15.  Cardiac Almost every type of arrhythmia can be produced by digitalis: pulsus bigeminus, nodal and ventricular extrasystoles, ventricular tachycardia and terminally ventricular fibrillation. Partial to complete A-V block may be the sole cardiac toxicity, or it may accompany other arrhythmias. Severe bradycardia, atrial extrasystoles, AF or AFl have also been noted. 15
  • 16. PRECAUTIONS AND CONTRAINDICATIONS  Hypokalemia:  Elderly, renal or severe hepatic disease  Myocardial ischaemia:  Thyrotoxicosis:  Myxoedema:  Ventricular tachycardia  Partial A-V block:  Acute myocarditis:  Wolff-Parkinson-White syndrome: 16
  • 17. INTERACTIONS  Diuretics:  Calcium:  Quinidine:  Adrenergic drugs:  Digoxin absorption may be reduced by metoclopramide, sucralfate, antacids, neomycin, sulfasalazine.  Absorption of digoxin is increased by atropinic drugs, including tricyclic antidepressants.  Propranolol, Verapamil, diltiazem and disopyramide: 17
  • 18. TREATMENT OF CHF 18  Heart failure occurs when cardiac output is insufficient to meet the demands of tissue perfusion, or is able to do so only by elevating filling pressure. It is a progressive disease with gradually deteriorating cardiac performance.  Heart failure may primarily be due to systolic dysfunction or diastolic dysfunction.
  • 19. 19  Systolic dysfunction  This refers to deficient pumping action of ventricles, i.e. ventricles are unable to develop sufficient wall tension to eject adequate quantity of blood and get progressively dilated.  The most important cause of systolic dysfunction is coronary artery disease (CAD), myocardial infarction (MI) and loss of functioning myocardium.  Other causes are valvular incompetence, dilated cardiomyopathy, viral (including HIV) myocarditis, tachyarrhythmias (mostly AF), etc
  • 20. 20  Diastolic dysfunction  The ventricular wall is thickened and unable to relax normally during diastole; ventricular filling is impaired and stroke volume is reduced, but the EF may be normal.  Long standing hypertension is the most common cause of left ventricular hypertrophy (LVH) and subsequent diastolic dysfunction. It is mostly associated with ageing and myocardial stiffening. Aortic stenosis, hypertrophic cardiomyopathy, A-V shunts and congenital heart disease are the other important causes.
  • 21. 21  However, most patients, especially long standing cases, have both systolic and diastolic dysfunction. Symptomatically also both are similar. Several compensatory mechanisms are brought into action to overcome the reduced cardiac output (CO).  These include:  Elevation of filling pressure  Increase in sympathetic tone  Activation of RAS  Over production of aldosterone  Endothelin production  Release of natriuretic peptides (ANP and BNP)
  • 22. TREATMENT OF CHF  There are two distinct goals of drug therapy in CHF: (a) Relief of congestive/low output symptoms and restoration of cardiac performance. This can be achieved by:  Inotropic drugs—Digoxin, dobutamine/ dopamine, amrinone/milrinone.  Diuretics—Furosemide, thiazides  RAS inhibitors—ACE inhibitors/ARBs  Vasodilators— Nitrate (Veno), Hydralazine, nitroprusside  β-blocker—Metoprolol, bisoprolol, carvedilol, Nebivolol 22
  • 23. (b) Arrest/reversal of disease progression and prolongation of survival, possible with:  ACE inhibitors/ ARBs, β blockers  Aldosterone antagonist—Spironolactone, eplerenone.  Important nonpharmacological measures are rest and salt restriction. 23
  • 24. 24
  • 25. Uses 25  1. Congestive Heart failure  2. Cardiac arrhythmias  Atrial fibrillation (AF)  Atrial flutter (AFI)  Paroxysmal supraventricular tachycardia (PSVT)