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HEART FAILURE

Learn about factors affecting cardiac output, pathophysiology, clinical manifestations, and pharmacological treatment of heart failure. Explore intrinsic and extrinsic changes, classification, and clinical uses of drugs.

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HEART FAILURE

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  1. HEART FAILURE BY Prof. Azza El-medany

  2. Heart failure • Results 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 needs at rest or during exercise.

  3. Low out put failure

  4. Factors affecting cardiac output • Intrinsic factors which regulate myocardial contractility . • Extrinsic factors including contractile state of arterioles & veins.

  5. Pathophysiology of cardiac performance in heart failure - Intrinsic changes . • Extrinsic changes. • Intrinsic changes: • Myocardial hypertrophy to maintain cardiac performance in the face of adverse effects as decrease in myocardial contractility.

  6. Continue • Extrinsic changes: • Decrease in cardiac outputrenal blood flow renin release , angiotensin 11 • in after load, preload ,sympathetic dischargecardiac output • Remodeling: Proliferation of connective tissue cells, abnormal myocardial cells.

  7. Clinical manifestations of heart failure • Tachycardia, decreased exercise tolerance with rapid muscular fatigue, dyspnea ( pulmonary congestion) peripheral edema, cardiomegaly.

  8. Classification of Low out put Failure • Left Heart Failure :Most common due to L.V.S . Dysfunction • Right Heart Failure : In Pulmonary hypertension

  9. Classification of Heart Failure • According to NYHA • Class 1: No limitations on ordinary activities and symptoms occur only with greater than ordinary exercise. • Class11: Slight limitation of ordinary activities , that result in fatigue & palpitation

  10. Continue • Class 111: No symptoms at rest, fatigue occur with less than ordinary physical activity • Class 1V : Is associated with symptoms even at rest

  11. High output failure • Even though there is an increase in cardiac output; still not enough to meet all the body needs as in hyperthyroidism, anemia.

  12. Drugs used in treatment of heart failure • Drugs with positive inotropic effect as : • Cardiac glycosides • Phosphodiesterase inhibitors • β- adrenoceptor agonist

  13. Drugs without positive inotropic effect • Diuretics • Aldosterone antagonist • ACEI & Angiotensin receptor blockers • Vasodilators • β- adrenoceptor blockers

  14. Vasodilators • The chose of vasodilators according to signs and 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

  15. Clinical uses of vasodilators • Acute heart failure • Chronic heart failure Long-term use of hydralazine & isosorbide dinitrate can reduce remodeling of heart

  16. ACEI & Angiotensin11 receptor blockers •  afterload • preload • sympathetic activity • remodelingmortality rate

  17. β-adrenoceptor blockers • Antagonism the enhancing action of sympathetic overactivity . • Reduce mortality ( reduce the remodeling changes through inhibition the mitogenic activity of catecholamines. • Inhibit renin release • Some of them have antioxident activity • E.g. carvedilol & metoprolol

  18. Diuretics • Reduce salt and water retentionventricular preload . • Reduction of edema and its symptoms • Reduction of cardiac size improve cardiac performance • Spironolactone has two benefits:potassium sparing effect & inhibit the action of aldosterone .

  19. β-agonist • Dopamine :acts on α ,β1 and dopamine receptors. • Dobutamine :selective β1- agonist. • Both of them are given intravenously & used in acute cardiac emergencies. • Dopamine is effective in patients with impaired renal function.

  20. Adverse effects • Tachycardia • Angina • Tachyphylaxis

  21. Phosphodiesterase inhibitors • Bipyridines : (Amrinone ,Milrinone ) • They are given only intravenously. • Half-life 3-6hrs. • 10-40% excreted in urine.

  22. Mechanism of action • Inhibit phosphodiesterase enzyme (isozyme 3) in both cardiac & smooth muscles resulting an ↑ in cAMP leading to: - Positive inotropism . - Dilation in both resistance & capacitance vessels (reduction in after load & preload.)

  23. Therapeutic uses • Used only for acute heart failure ( Short term use )

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

  25. Digitalis (cardiac glycosides ) • Origin • Chemistry • Preparations

  26. Structure o of cardiac glycoside

  27. Pharmacokinetics • Oral availability • Ouabain Digoxin Digitoxin • 0 75 > 90 • Half- life • 21 40 168 • Plasma protein binding • 0 20-40 > 90 • Percentage metabolized • 0 < 40 > 80

  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. (A) MECHANICAL EFFECT Increase in myocardial contractility

  31. (B) ELECTRICAL EFFECTS

  32. At Therapeutic Doses A) • Slow conduction through S.A.N. & A.V.N.  prolong conduction time between atrium and ventricles ( prolong P-R interval in ECG.) . B) • Short duration of action potential & refractoryperiods of both atrium & ventricles(Short in QT interval ).

  33. At Toxic Doses •  in automaticity of ectopic focus All forms of arrhythmias can be detected : - - Second-degree of A-V block. - In Purkinje conducting system leading bigeminy rhythm.

  34. Extra cardiac effects • GIT:Anorexia, nausea,vomiting, diarrhea. • C.N.S. :Disorientation,hallucination,visual disturbances, agitation, convulsions. • Gynecomastia • Kidney : Diuretic effect • Improve renal function . • Inhibit Na+ reabsorption from P.C.T.

  35. Adverse effects • Heart All forms of cardiac arrhythmias • GIT • C.N.S. • Skin : rash • Gynecomastia

  36. Contraindications • Toxic myocarditis • Constrictive pericarditis • Cardioversion • Digitalis are effective in H.F. due to hypertension, atherosclerosis or ischemic heart diseases.

  37. Factors increase digitalis toxicity • SmallLean body mass • Renal disease • Hypothyroidism • Hypokalemia • Hypomagnesemia • Hypercalemia

  38. Treatment of digitalis toxicity • Stop drug • Potassium therapy • Cholestyramine • Atropine • Lidocaine • Fab antibodies in life-threating or severe cases.

  39. Clinical uses • Heart failure ( LVSD) • 2-Atrial flutter or fibrillation

  40. Drug interactions • Diuretics hypokalemia (arrhythmia) • Quinidine : plasma level of digitalis through (1) displaces from protein binding sites (2) renal clearance. • Antibiotics that alter intestinal flora digoxin bioavailability • Agents that release catecholamines sensitize myocardium to digitalis to induce arrhythmias.

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

  42. Cont. • Digitalis • β- blockers ( class II-IV stable HF) • Vasodilators

  43. Management of acute heartfailure • Volume replacement • Diuretics • Positive inotropic drugs • Vasodilators

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