This document discusses congestive heart failure (CHF), which occurs when the heart cannot pump enough blood to meet the body's needs. It defines two types of CHF based on ejection fraction - systolic and diastolic dysfunction. Several causes of CHF are listed, including arrhythmias, myocardial infarction, hypertension, and obesity. The body compensates via the sympathetic nervous system and renin-angiotensin-aldosterone system. Drug classes used to treat CHF are discussed in detail, including cardiac glycosides like digoxin, beta blockers, ACE inhibitors, angiotensin receptor blockers, aldosterone antagonists, and vasodilators. Side effects of each class are

1. Prepared by – Shagufta Farooqui
Assistant Professor
Department of Pharmacology
Nanded Pharmacy College, Nanded

2. Congestive Heart Failure
It is a Condition Where heart is not able to pump sufficient
blood to various parts of the body.
It is Chronic progressive Condition where heart is
unable to pump blood enough through the body to meet
the body’s need for blood and oxygen.

3. Symptoms

4. Causes
Arrhythmias
Myocardial Infraction
Hypertension
Atherosclerosis
Infection
obesity
Alcohol and tobacco use

5. 1. Systolic Dysfunction:
A Heart failure in which the heart muscle becomes weak and cannot
squeeze as much as blood out. Poor contractility leads to reduction in the
amount of blood pumped out of the ventricles which refer to ejection fraction.
Normal ejection fraction-50-75%
Heart failure due to systolic dysfunction is typically associated with an ejection
fraction less than 40%. For this reason the systolic heart failure is commonly
known as heart failure with reduced ejection fraction.
2. Diastolic Dysfunction:
In diastolic the heart squeezes normally but become stiff and cannot
adequately relax to allow for normal ventricular filling.
As a result patients with diastolic heart failure relatively normal ejection
fraction although stroke volume and cardiac output is reduced.
So diastolic failure is known as heart failure with preserved ejection fraction.
The body try to compensate via two mechanism-
1. Sympathetic Nervous system
2. Renin Angiotensin Aldosteron System

6. Mechanism

8. ATP CAMP Inactive
Adenyl cyclase Phodphodiesterase
Sympathomimetics PDE inhibitors
e.g Dobutamine e.g Amrinone
Mirinone
Drugs which Increases the level of CAMP

9. Cardiac Glycosides
They are group of chemically similar compounds that can increase the
contractility of the heart muscle and therefore are used in the
treatment of heart failure.
A. Digitalis
1. Digitalis Purpurea- Digitoxin
2.Digitalis lanata- Digoxin
Family- Scrophulariaceae
B. Strophanthus
1. Strophanthus Kombe- Strophanthin
2. Strophanthus gratus- ovabin
C. Thevetia
1.Thevetia Nerifolia
Apocynacea
D. Squill
Bulb of urgeniea indica kunth.
Family-Liliaceae

10. Ionotropic Agents: Which increase force of contraction. It Increase
cardiac output e.g Digoxin and Dobutamine
Digoxin is used to increase cells contractility i.e cardiac contractility
Digoxin inhibit NA+/K+ ATPase pump in cardiac muscle which is
responsible for moving sodium ion out of the cell and bringing K+ into the cell.
As a result of this inhibition, When Na+ conc. In cardiac cell increases another
electrolyte mover known as NA+-CA++ exchanger pushes the excess NA+ ions
out of cell while bringing CA++ ions in the cell.
This Causes Increase Intracellular CA+. Which causes increased Force of
contraction and cardiac output.

11. Pharmacokinetics:
Cardiac Glycosides are high Plasma Protein Bound Drugs.
Hence They have very longer duration of action.
Cardiac Glycosides are having very narrow therapeutic
index. Hence drugs are highly toxic.
Side effects:
1.Hypokalemia
2. Cumulative toxicity
3.Nausea Vomiting
4. Visual Disturbance
Antidote-Digibind

12. Beta Blockers:
Heart failure is accompanied by an increase activation of sympathetic
nervous system.
Beta blockers binds to B1 receptors in the heart and block Nor
adrenaline and it will cause decrease heart rate and
contractility which in turns reduces cardiac output and blood
pressure. Decrease heart rate allows more diastolic filling time. So
stroke volume is not reduced.
Side effects:
Bradycardia
Hypotension
Worsening of CHF Symptoms

13. ACE Inhibitors:
Drugs Inhibits ACE which in turns reduces angiotensin-II
production and its effects on vasoconstriction as well as
ADH aldosterone secretion.
Inhibition of ACE increases levels of a potent
Vasoactive peptide called bradykinin.
Unlike angitensin-II which is a vasoconstrictor so
bradykinin is endogenous vasodilators which is
normally degraded by ACE.
So decrease ACE, Decreases Angiotensin and
increases bradykinin as a result blood vessels get dilated,
total peripheral resistance is reduces, and it causes
decrease blood pressure, thereby reducing the efforts
needed to pump blood around the body.

14. Side effects-Hypotension, renal insufficiency, Dizziness, dry cough,
blurred vision

15. Angiotensin Receptors Blockers
ARBs bind to AT1 receptors located on vascular smooth muscles as well
as other tissues such as heart and directly blocking the actions of
angiotensin-II,
As a result the effects are similar to ACE inhibitors that is less
vasoconstriction and less ADH and aldosterone secretion
which decreases blood pressure and ultimately prevents
damage to the heart and kidneys.
Also because ARBs do not inhibit ACE they do not cause bradykinin
levels to rise. This makes ARBs a good alternative to ACE as more
bradykinin not only contributes to the vasodilation but also contributes to
some of the side effects of ACE inhibitors such as cough and angioedema
e.g. Condesartan, losartan, Telmisartan

16. Side effects:
Hypotension
Impairment of renal Functioning

17. Aldosterone Antagonist
Aldosterone causes fibrosis of myocardium and cardiac remodeling.
To prevent this we can give aldosterone antagonist
e.g Spironolactone
The beneficial effects of spironolactone derive from direct and
competitive blockade of aldosterone receptor.

18. Vasodilators
It directly relaxes the arterioles and arteries reducing the peripheral vascular
resistance and preload. Used specially in patients who cannot tolerate ACE
inhibitors
Nitroglycerine is denitrated by glutathione S-Transferase in smooth
muscle
Free Nitrite ion is released, which is converted to Nitric oxide
Activation of Guanyl cyclase Enzyme
Increase in cGMP
Dephosphorylation of myosin light chain,preventing the interaction
of myosin with actin(myosin light chain kinase responsible for
Smooth muscle contraction)
Results in Vasodilation

19. Side effects:
Nausea
Palpitation
Tachycardia
Salt and water retention on prolong
therapy

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