1. Drug acting on the Heart
Heart failure

2. Lecture objectives Describe basic anatomy of the heart.
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

3. 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

5. Cardiac Physiology (remember this?)
CO = SV x HR
HR: parasympathetic and sympathetic tone
SV: preload, afterload, contractility

6. 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
75 beat/min ml

7. 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

8. Factors on Cardiac Output
More in
More out
Factors on Cardiac Output
Preload:
 Preload   cardiac output
(Starling-Frank Mechanism)

9. Factors Which Increase Preload
IV fluids
Blood
Vasoconstriction
Factors Which Decrease Preload
Diuretics
Dehydration
Hemorrhage
Vasodilation

10. Factors on Cardiac Output Afterload
Preload:
2) Afterload:  
 afterload   CO R

11. Afterload Related to arterial pressure or diameter of arteries
As pressure increases, resistance increases, afterload increases
As pressure decreases, resistance decreases, afterload decreases

12. 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%

13. Factors on Cardiac Output
Preload:
2) Afterload:  
3) Contractility:
 contractility   CO

14. 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

16. Five main drugs are used
Diuretics
ACE inhibitors
Positive isotropic drugs
Vasodilator
ß blockers

17. 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

18. Side Effects Pre-renal azotemia Skin rashes Neutropenia
Thrombocytopenia
Hyperglycemia
↑ Uric Acid
Hepatic dysfunction

19. More severe heart failure → loop diuretics
Lasix (20 – 320 mg QD), Furosemide
Bumex (Bumetanide 1-8mg)
Torsemide (20-200mg)

20. 2) Inhibitors of renin-angiotensin- aldosterone 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

21. 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

23. Side effects of ACE inhibitors
Angioedema
Hypotension
Renal insuffiency
Rash
cough

24. 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

25. 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

26. Digitalis Toxicity Narrow therapeutic to toxic ratio
Non and cardiac manifestations
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

27. 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

28. 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

29. 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.

30. 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

31. thank you for listening
Home work?
Write the nursing implication to the drug that treat HF?
Write two examples to each group of medication?
thank you for listening