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heartfailure.pptx
- 1. 2 Heart Failure a. Introduction b. Etiology c. Classification d. Pathogenesis e. Stages f. Pathology g. complications
- 2. Heart Failure (HF): Definition A state in which the heart is unable to pump sufficiently to maintain blood flow to meet the body’s needs. Signs and symptoms- shortness of breath, excessive tiredness, etc. 6
- 4. 7 Contractility Afterload Preload Factors Affecting Cardiac Output Stroke Volume Heart rate Cardiac output
- 5. Preload: Ventricular end-diastolic volume. Afterload: Aortic or pulmonary pressure. Preload vs. Afterload
- 6. 9 Impaired systolic and/or diastolic function of theheart Decreasedcardiac output (absolute or relative) Inability to meet themetabolic requirements Heart failure
- 7. 1. Cardiacoverload Preload ↑ Interatrial septal defect Interventricular septaldefect Chronic anemia I. Causes Afterload ↑ Hypertension Stenosis of aortic valve Corpulmonale Pulmonary embolism 11
- 8. Primary Primary change of myocardial function 2. Myocardial Injury Myocardial infarction Myocarditis Cardiomyopathy Myocardial toxicosis Coronary atherosclerosis Anemia Respiratory failure Deficiency of VitB1 Diabetes Secondary Myocardial function affected through decreased blood, oxygen, or energy metabolism
- 9. 3. Disorder of Ventricular Filling Stenosis of atrioventricularvalves Fibrosis Pericarditis Cardiac tamponade (stuffing) 16
- 10. 17 Systemic Infection Acid-base & electrolyte disturbance Arrhythmia Pregnancy & child birth Infusion too fast Emotion Exercise Climate change II. Precipitating Factors
- 11. Infection Fever Metabolic rate ↑ →Cardiac load ↑ Infection T oxin HR→Oxygenconsumption ↑ Myocardial function ↓ Lungvesselresistance ↑
- 12. Pregnancy and Child Birth During pregnancy, blood volume ↑ →Cardiac load ↑ During birth, uterine contraction→ Sympathetic excitement →Venousreturn ↑ →Peripheral resistance ↑
- 13. Classification Course Output Function Severity L e f t h e a r t Ri ght hear t Whole heart Acute Chronic LowCO High CO Systolic Diastolic Mixed C l a s s I ClassII Class III ClassIV According to: Location 21
- 14. New York Heart Association (NYHA) Classification Class % of Patients Symptoms I 35% II 35% III 25% IV 5% No symptoms or limitations duringordinary activity. Mild symptoms and slight limitationsduring ordinary activity. Marked limitations even duringminimal activity. Comfortable only atrest. Severelimitations. Showsymptoms even at rest. 28
- 15. 30 Responses of the Body Neurohormonal compensation Cardiac compensation Systemic compensation
- 16. Changes S ympathetic activity Favorable effect HR,contractility, vasoconst. V return, filling Salt & water retention Vreturn Renin-Angiotensin- Aldosterone System Vasopressin Sameeffect ILs&TNF Endothelin Myocardial hypertrophy Vasoconstriction V return Unfavor. effect Arteriolar constriction Afterload Vasoconstriction Afterload Sameeffect Apoptosis Afterload 31 (1) Neurohormonal Changes
- 17. Theheart tries to compensate forthe lossin pumping function by: (2) Compensation by the Heart Functional change Pumping faster Enlarging Developing more musclemass (hypertrophy) Structural change 32
- 18. 33 Normal Concentric Ecentric (2) Cardiac Compensation (Myocardial hypertrophy) T ype Cause Thickness of ventricularwall Volumeof ventricle Concentric Pressure Nor hypertrophy Eccentric hypertrophy overload Volume overload
- 19. Redistribution of bloodflow Increasein blood volume Increaseof red bloodcells Increasedability of tissues toutilize O2 34 (3) Systemic Compensation
- 20. 1) Redistribution of blood flow 35 Cardiac output ↓ Sympathetic nerve activity ↓ Catecholamines ↓ Contraction of the renal,muscular, skin arteries (more α-receptor) ↓ More blood supply toheart and brain
- 21. 2) Increase in blood volume 36 Cardiac output ↓ sympathetic activity ↓ ↓ Reducedrenal blood flow ↓ ADH& ADS↑ ↓ Reabsorption of H2O& Na+
- 22. 3) Increase of Red Blood Cells 38 Cardiac output ↓ Renalblood flow ↓ Synthesisand release of erythropoietin (EPO) ↓ Production of red blood cells ↓ Oxygensupply to the tissues
- 23. 4) Ability of tissues to utilize O2 ↑ HF→chronic hypoxia→ • Quantity of mitochondria and their surface area↑ • Quantity and activities of enzymesinthe respiratory chain ↑ →ATP↑ 39
- 24. a. Lossof cardiomyocytes b. Metabolic dysfunction c. Disorder of excitation-contractioncoupling d. Reducedventricular compliance Pathogenesis of Heart Failure
- 25. Loss of cardiomyocytes Myocardial infarction Myocarditis Cardiomyopathy Myocardial toxicosis Necrosis and/or apoptosis
- 26. Disorder of Myocardial Energy Metabolism Impaired energy production TCAcycledysfunction Decreased generation of AcetylCoA (Vit B1deficiency, diabetes) Reducedenergy storage Impaired energy utilization Hydrolysis of ATP↓
- 27. 56 (A) ↓ uptake, storage and release of Ca2+ by SR. (B) ↓ influx of extracellular Ca2+. (C) Dysfunction of Ca2+ binding to troponin. Dysfunction in Excitation-Contraction Coupling
- 28. Ventricular Compliance ↓ in HF Patients 60 Causes Fibrosis Hypertrophy … Consequences Ventricular filling ↓ Blood flow to coronary artery↓
- 29. 1. Venous Congestion of Systemic Circulation - Right Heart Failure 1. Liver enlargement 2. Ascites 3. Gastrointestinal tract congestion 4. Engorgement of jugularveins 5. Edemaof lower limbs 67
- 30. 68
- 31. 2. Congestion of Pulmonary Circulation - Left Heart Failure Pulmonary congestion and edema →Dyspnea 69
- 34. Microscopically • There is increase in size of individual muscle fibres. There may be multiple minute foci of degenerative changes and necrosis in the hypertrophied myocardium. • These changes appear to arise as a result of relative hypoxia of the hypertrophied muscle as the blood supply is inadequate to meet the demands of the increased fibre size. • Ventricular hypertrophy renders the inner part of the myocardium more liable to ischaemia.
- 35. Pathology transverse section through the ventricles with left ventricular hypertrophy (concentric and eccentric)
- 37. Hypertrophy of the myocardium without dilatation is referred to as concentric, and when associated with dilatation is called eccentric. Gross • Thickness of the left ventricular wall (excluding trabeculae carneae and papillary muscles) above 15 mm is indicative of significant hypertrophy. • In concentric hypertrophy, the lumen of the chamber is smaller than usual, while in eccentric hypertrophy the lumen is dilated. • In pure hypertrophy, the papillary muscles and trabeculae carneae are rounded and enlarged, while in hypertrophy with dilatation these are flattened.
- 38. pathophysiology of compensatory mechanisms in cardiac failure
Editor's Notes
- A, Concentric cardiac hypertrophy. Weight of the heart is increased. The chambers opened up at the apex show concentric thickening of left ventricular wall (white arrow) with obliterated lumen (hypertrophy without dilatation). B, Eccentic cardiac hypertrophy. The heart is heavier. The free left ventricular wall is thickened (black arrow) while the lumen is dilated (white arrow) (hypertrophy with dilatation).