2. Result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood to meet the body's metabolic needs at rest or during exercise.

3. Tachycardia Decreased exercise tolerance ( rapid fatigue). Dyspnea ( pulmonary congestion) Peripheral edema. Cardiomegaly.

4. Low OUT PUT FAILURE HIGH OUT PUT FAILURE

5. The increase in output is not sufficient as in hyperthyroidism, and anemia.

6. Left ventricular dysfunction ( LHF) Right ventricular dysfunction ( RHF) Biventricular failure Congestive heart failure

7. Cardiac contractility Preload Afterload Heart rate.

8. Intrinsic changes : Myocardial hypertrophy to maintain cardiac performance in the face of a decrease in myocardial contractility.

9. Extrinsic changes Extrinsic changes Decrease in cardiac output  renal blood flow  renin release,  angiotensin 11   in peripheral resistance, venous return, and sympathetic activity  cardiac output Remodeling: Proliferation of connective tissue cells, abnormal myocardial cells.

11. According to NYHA Class 1: Symptoms of fatigue occur only with greater than ordinary activity. Class11: Slight limitation of ordinary activities, that result in fatigue & palpitation

12. Continue Class 111: fatigue occur with less than ordinary physical activity Class 1V : Is associated with symptoms even at rest

13. Drugs with positive inotropic effect : Cardiac glycosides Phosphodiesterase inhibitors β- adrenoceptor agonist

14. Drugs without positive inotropic effect Diuretics Aldosterone antagonist Angiotensin converting enzyme inhibitors ( ACEI) & Angiotensin receptor blockers Vasodilators β- adrenoceptor blockers

15. We choose vasodilators according to signs, symptoms and hemodynamic changes : Selective venodilators as nitrate group is used when the main symptoms is dyspnea due to pulmonary congestion. Selective arteriodilators as hydralazine is used when the main complain is rapid fatigue due to low cardiac output. Non-selective vasodilators as ACEI or blockers

16. Acute heart failure Chronic heart failure Clinical uses of vasodilators

17.  Peripheral resistance ( After load )  Venous return ( Preload)  sympathetic activity  remodeling  mortality rate

18. Antagonism the enhancing action of sympathetic overactivity Reduce mortality Inhibit renin release Some of them have antioxident activity

19. Reduce salt and water retention  ventricular preload and venous pressure. Reduction of edema and its symptoms Reduction of cardiac size  improve cardiac performance

21. Dopamine :Acts on α,β 1 and dopamine receptors. Used in acute L.H.F. mainly in patients with impaired renal blood flow. Dobutamine : Selective β 1 agonist Used in the treatment of acute heart failure

22. Both of them are given intravenously. Their adverse effects : Tachycardia Angina Tachyphylaxis Continue

23. Bipyridines :(Amrinone,Milrinone ) They are only available in parenteral form. Half-life 3-6hrs. Excreted in urine.

24. Mechanism of action Inhibit phosphodiesterase enzyme in cardiac & smooth muscles resulting in : Increase in cAMP In the heart : Increase in myocardial contraction In the peripheral vasculature : Dilation in both arterial & venous vessels leading in reduction in both after load & preload.

25. Therapeutic uses Used only intravenously for: 1- acute heart failure 2-an exacerbation of chronic heart failure.

26. Adverse effects Nausea,vomiting Arrhythmias (less than digitalis ) Thrombocytopenia Liver toxicity Milrinone less hepatotoxic and less bone marrow depression than amrinone.

27. Digoxin Prototype : Digoxin Origin Chemistry Preparations Pharmacokinetics

28. Pharmacodynamics At the molecular level cardiac glycosides inhibit Na + / K + ATP ase (sodium pump ). Cardiac effects : A) Mechanical B) Electrical

29. Mechanism of action

30. Mechanical effects Increased contractility of the cardiac muscles The resulting improved circulation leads To reduced sympathetic activity & reduction in heart rate. Vagal tone is enhanced causing decrease in heart rate & oxygen requirement

31. Electrical effects Slow conduction through S.A.N. & A.V.N.  prolong conduction time between atrium and ventricles ( prolong P-R interval in ECG.). Short duration of action potential & refractory periods of both atrium & ventricles (  entry of calcium during plateau phase ).

32. Electrical effects(cont.) Electrical effects(cont.) Short in QT interval Toxic concentrations  in automaticity of ectopic focus  All forms of cardiac arrhythmias can be detected in ECG.

33. ECG changes with digitalis Prolong PR interval Short QT interval

34. Cardiac adverse effects All forms of cardiac arrhythmias as all degrees of AV nodal block

35. Extracardiac adverse effects GIT :Anorexia, nausea,vomiting, diarrhea C.N.S. :Hallucination,visual disturbances, convulsions. Gynecomastia Skin rash

36. Contraindications Toxic myocarditis Constrictive pericarditis Cardioversion

37. Therapeutic uses of digoxin Treatment of severe left ventricular systolic dysfunction due to hypertension, atherosclerosis or ischemic heart disease

38. Factors increase digitalis toxicity Small Lean body mass Renal disease Hypothyroidism Hypokalemia Hypomagnesemia Hypercalemia Drugs

39. Treatment of digitalis toxicity Stop drug Potassium therapy Cholestyramine Atropine (A-V block ) Lidocaine Fab antibodies in life-threating or severe cases.

40. Drug interactions Diuretics  hypokalemia (arrhythmia) Quinidine :  plasma level of digitalis Antibiotics that alter intestinal flora  digoxin bioavailability

41. Management of chronic heart failure  Reduce work load of the heart Limits the activity Reduce weight Control hypertension  Restrict sodium  Diuretics  ACEI or receptor blockers

42. Continue  Digitalis  β- blockers  Vasodilators

43. Management of acute heart failure Volume replacement Diuretics Positive inotropic drugs Vasodilators Antiarrhythmic drugs Treatment of myocardial infarction