Transcript Drug acting on the Heart

Drug acting on the Heart
Heart failure
Lecture objectives
At the end of the this lecture, the student will able to:
• Describe basic anatomy of the heart.
• List determinants factor of cardiac out put.
• Describe main approach to the treatment of
heart failure.
• List the names of drug used to treat heart
failure and hypertension
• A state in which the heart cannot provide
sufficient cardiac output to satisfy the
metabolic needs of the body.
• It is commonly termed congestive heart
failure (CHF) since symptoms of increase
venous pressure are often prominent
Cardiac Physiology
(remember this?)
CO = SV x HR
• HR: parasympathetic and sympathetic tone
• SV: preload, afterload, contractility
Cardiac Output
• Volume of blood ejected per minute
• Averages between 4-6L/min
• CO = Stroke volume X heart rate
=70 ml X 60 beats/min
=4,200 ml/min
70
ml
Preload
• Degree of stretch of myocardial fibers
• Determined by the volume of blood in left
ventricle (LV) at end of diastole
• Increased volume –> increased preload->
increased cardiac output (CO)
• Decreased volume –> decreased preload
–> decreased cardiac output (CO)
• Compliance of myocardial cells also
affects preload
Factors on Cardiac Output
More out
1) Preload:
 Preload   cardiac output
(Starling-Frank Mechanism)
More in
Factors Which Increase Preload
1. IV fluids
2. Blood
3. Vasoconstriction
Factors Which Decrease Preload
1. Diuretics
2. Dehydration
3. Hemorrhage
4. Vasodilation
Factors on Cardiac Output Afterload
1) Preload:
2) Afterload:
 afterload   CO
R
Afterload
• Related to arterial pressure or diameter of
arteries
• As pressure increases, resistance
increases, afterload increases
• As pressure decreases, resistance
decreases, afterload decreases
Contractility
• Force generated by the myocardium when
it contracts – inotropic property
• Ejection fraction (EF) - percentage of LV
end-diastolic volume that is ejected with
each contraction
• EF - normally approximately 50-55%
Factors on Cardiac Output
1) Preload:
2) Afterload:
3) Contractility:
 contractility   CO
Left versus Right Failure
• Left Heart Failure
- Dyspnea
- Dec. exercise tolerance
- Cough
- Orthopnea
- Pink, frothy sputum
Right Heart Failure
- Dec. exercise
tolerance
- Edema
- JVD
- Hepatomegaly
- Ascites
Five main drugs are used
1.
2.
3.
4.
5.
Diuretics
ACE inhibitors
Positive isotropic drugs
Vasodilator
ß blockers
1) Diuretics
• Drugs that accelerate the rate of urine
formation.
• Result: removal of sodium and water
• They relive distention of the heart by
reducing blood volume
• Side Effects
– Pre-renal azotemia
– Skin rashes
– Neutropenia
– Thrombocytopenia
– Hyperglycemia
– ↑ Uric Acid
– Hepatic dysfunction
• More severe heart failure →
loop diuretics
– Lasix (20 – 320 mg QD), Furosemide
– Bumex (Bumetanide 1-8mg)
– Torsemide (20-200mg)
2) Inhibitors of renin-angiotensinaldosterone system
– Renin-angiotensin-aldosterone system is
activation early in the course of heart
failure and plays an important role in the
progression of the syndrome
– Angiotensin converting enzyme inhibitors
– Angiotensin receptors blockers
– Spironolactone
Angiotensin Converting Enzyme Inhibitors
• They block the R-A-A system by
inhibiting the conversion of angiotensin
I to angiotensin II → vasodilation and ↓
Na retention
Side effects of ACE
inhibitors
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Angioedema
Hypotension
Renal insuffiency
Rash
cough
3)Digitalis Glycosides
(Digoxin, Digitoxin)
• The role of digitalis has declined
somewhat because of safety concern
• Recent studies have shown that digitals
does not affect mortality in CHF patients
but causes significant
– Reduction in hospitalization
– Reduction in symptoms of HF
Digitalis (cont.)
Mechanism of Action
• +ve inotropic effect by ↑ intracellular Ca
& enhancing actin-myosin cross bride
formation (binds to the Na-K ATPase →
inhibits Na pump → ↑ intracellular Na →
↑ Na-Ca exchange
• Arrhythmogenic effect
Digitalis Toxicity
• Narrow therapeutic to toxic ratio
• Non and cardiac manifestations
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Anorexia,
Nausea, vomiting,
Headache,
Disorientation
Sinus bradycardia and arrest
A/V block (usually 2nd degree)
Atrial tachycardia with A/V Block
Development of junctional rhythm in patients with a fib
4) β Blockers
• Has been traditionally contraindicated in pts
with CHF
• Now they are the main stay in treatment on
CHF & may be the only medication that
shows substantial improvement in LV function
• In addition to improved LV function multiple
studies show improved survival
Subdivisions of ANS
• Parasympathetic – acetylcholine produces
inhibitory response
• Sympathetic – catecholamines stimulate
– Increase heart rate – Beta 1 receptors
– Dilate smooth muscles – Beta 2 receptors
– Vasoconstrict vessels – Alpha receptors
5) Vasodilators
• Reduction of afterload by arteriolar
vasodilatation (hydralazin)  reduce LVEDP,
O2 consumption,improve myocardial
perfusion,  stroke volume and COP
• Reduction of preload By venous dilation
• ( Nitrate)  ↓ the venous return ↓ the
load on both ventricles.
• Usually the maximum benefit is achieved by
using agents with both action.
Positive inotropic agents
• These are the drugs that improve myocardial contractility
(β adrenergic agonists, dopaminergic agents,
phosphodiesterase inhibitors),
•
dopamine, dobutamine, milrinone, amrinone
• Several studies showed ↑ mortality with oral inotropic
agents
• So the only use for them now is in acute sittings as
cardiogenic shock
Home work?
1. Write the nursing implication to the drug that treat HF?
2. Write two examples to each group of medication?
thank you for listening