TREATMENT OF CONGESTIVE

HEART FAILURE
 Systole
The contraction of the cardiac muscle
tissue in the ventricles is called systole.
When the ventricles contract, they force
the blood from their chambers into the
arteries leaving the heart.
The left ventricle empties into the aorta
and the right ventricle into the pulmonary
artery.
The increased pressure due to the
contraction of the ventricles is called
systolic pressure.
 Diastole
The relaxation of the cardiac muscle
tissue in the ventricles is called
diastole.
When the ventricles relax, they make
room to accept the blood from the
atria.
The decreased pressure due to the
relaxation of the ventricles is called
diastolic pressure.
Electrical Conduction System

1.Sinoatrial
node (SA
node)
2.Atrioventr
icular node
(AV node)
3. Common
AV Bundle
4. Right &
Left Bundle
Branches
 Congestive Heart Failure
• Condition in which the heart is unable to
pump sufficient blood to meet the needs of
the body.
• Caused by an impaired ability of the cardiac
muscle to contract
• This condition is accompanied by abnormal
increases in blood volume and interstitial
fluid and the heart ,veins and capillaries are
generally dilated with blood.
STAGES OF HEART FAILURE
 Cardiac glycosides
often called digitalis glycosides
cardiac glycosides cause a positive
inotropic effect and
electrophysiologic changes is still not
completely clear.
Several mechanisms have been
proposed, but the most widely
accepted involves the ability of
cardiac glycosides to inhibit the
membrane bound Na+-K+-ATPase
pump responsible for Na+-K+
exchange.
Digoxin
Cardiac glycoside
Inhibits the sodium-potassium ATPase
pump
Positive inotrope—improves the strength
of cardiac contraction
Allows more calcium to be available for
contraction
Used for CHF and atrial dysrhythmias
Monitor potassium levels, drug levels,
and
for toxicity
 Therapeutic uses
Most effective in the treatment of
CHF caused by ishemic or congenital
heart disease.
 Adverse effects
Digitalis toxicity- is one of the most
commonly encountered adverse drug
reactions.
Check potassium levels or if indicated
give potassium supplement.
Adverse effects :Cardiac effects
Severe dysrhythmia moving from
decreased or blocked AV conduction.
Atrial tachycardia
Atrial flutter
Atrial fibrillation
Ventrcular fibrillation
Finally complete heart block-due to
hypokalemia
 Adverse effects :GI effects
Anorexia
Nausea
vomiting
Adverse effects :CNS effects
Headache
Fatigue
Confusion
Blurred vision
 Diuretics
Decrease preload by decreasing
blood volume and venous return
 Beta adrenergic agonist
Dopamine and Dobutamine
+ inotropic effect and vasodilation
MOA: increase in intracellular
cAMP,which result in the activation of
protein kinase thus entry of calcium
ion into the myocardial cells
increases - contraction
Phosphodiesterase inhibitors
Amrinone and milrinone
MOA: increase the intracellular
concentration of cAMP resulting in an
increase intracellular calcium and
therefore cardiac contractility.
Dilatation of venous blood vessels leads
to a decrease in cardiac preload .
Arteriolar dilators reduce TPR and
decrease afterload.
ACE inhibitors –vasodilator of choice for
patients with CHF.