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Cardiac hyprtrophy and heart failure

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Cardiac hyprtrophy and heart failure

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Cardiac hyprtrophy and heart failure

  1. 1. Cardiac Structure and Specializations  0.4% to 0.5% of body weight  250 to 320 gm in female & 300 to 360 gm in male  wall thickness of right ventricle - 0.3 to 0.5 cm  Wall thickness of left ventricle - 1.3 to 1.5 cm  Hypertrophy= increased weight & thickness  Dilatation = an enlarged chamber size  Cardiomegaly = Increased cardiac weight or size resulting from hypertrophy and/or dilation
  2. 2. OVERVIEW OF HEART DISEASE Cardiovascular dysfunction can be attributed to one (or more) of six principal mechanisms: 1. Failure of the pump 2. Obstruction to flow 3. Regurgitant flow 4. Shunted flow 5. Disorders of cardiac conduction 6. Rupture of the heart or a major vessel
  3. 3. Disruption of any element of the heart can adversely affect pumping efficiency Myocardium Valves conduction system & coronary vasculature
  4. 4. The blood in the heart chambers moves in a carefully prescribed pathway: venous blood from systemic circulation right atrium → right ventricle pulmonary arteries Lungspulmonary veins left atrium → left ventricle aorta → systemic arterial supply
  5. 5. Learning outcomes At the end of this lecture students should be able to 1. Discuss causes and mechanism of cardiac hypertrophy 2. Discuss the consequence of molecular and cellular changes in hypertrophied heart 3. Define congestive heart failure 4. Explain the causes and pathology & clinical feature of left sided heart failure 5. Explain the causes and pathology &clinical features of right sided heart failure
  6. 6. CARDIAC HYPERTROPHY  defined as an increase in size & weight of the myocardium  results from increased mechanical work due to pressure or volume overload  mediated through the activation of β-adrenergic receptors  dependent upon increased protein synthesis, which enables the assembly of additional sarcomeres
  7. 7. CARDIAC HYPERTROPHY Hypertrophic myocytes contain - increased numbers of mitochondria & enlarged nuclei due to increases in DNA ploidy, which result from DNA replication in the absence of cell division Pattern of hypertrophy reflects the nature of the stimulus i. Pressure-overload hypertrophy- concentric hypertrophy ii. Volume-overload hypertrophy- eccentric hypertrophy (ventricular dilatation)
  8. 8. Pressure-overload hypertrophy  in response to increased pressure load -hypertension or aortic stenosis  causes a concentric increase in wall thickness  new sarcomeres are predominantly assembled in parallel to the long axes of cells, expanding the cross-sectional area of myocytes
  9. 9. Volume-overload hypertrophy  is characterized by ventricular dilation  results from increased volume load (valvular incompetence )  new sarcomeres assembled are largely positioned in series with existing sacromeres  heart weight, rather than wall thickness, is the best measure of hypertophy  wall thickness may be increased, normal, or less than normal
  10. 10. Gross Morphology 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 In eccentric hypertrophy the lumen is dilated
  11. 11. Thickness of the left ventricular wall above 15 mm is indicative of significant hypertrophy In concentric hypertrophy, the lumen of the chamber is smaller than usual In eccentric hypertrophy the lumen is dilated Gross Morphology
  12. 12. Microscopic Morphology increase in size of individual muscle fibres
  13. 13. Important changes at the tissue and cell level occur with cardiac hypertrophy.  increase in myocyte size is not accompanied by a proportional increase in capillary numbers  supply of oxygen and nutrients to the hypertrophied heart, is more tenuous than in the normal heart.  oxygen consumption by the hypertrophied heart is elevated due to the increased workload that drives the process  Hypertrophy is also often accompanied by deposition of fibrous tissue  Molecular changes include the expression of immediate-early genes (e.g., c-fos, c-myc, c-jun, and EGR1)
  14. 14. cardiac hypertrophy heightened metabolic demands due to increases in mass, heart rate, & contractility increase cardiac oxygen consumption vulnerable to ischemia-related decompensation cardiac failure and eventually lead to death
  15. 15. CARDIAC HYPERTROPHY can be substantial in clinical heart disease Heart weights of two to three times greater than normal - systemic hypertension - ischemic heart disease - aortic stenosis - mitral regurgitation - dilated cardiomyopathy Heart weights of threefold to fourfold greater than normal - aortic regurgitation -hypertrophic cardiomyopathy
  16. 16. is defined as the pathophysiologic state in which impaired cardiac function is unable to maintain an adequate circulation for the metabolic needs of the tissues of the body HEART FAILURE Definition
  17. 17. HEART FAILURE Heart failure generally is referred to as congestive heart failure (CHF) - is the common end point for many forms of cardiac disease and - typically is a progressive condition that carries an extremely poor prognosis
  18. 18. HEART FAILURE CHF occurs when the heart is - unable to provide adequate perfusion to meet the metabolic requirements of peripheral tissues - inadequate cardiac output is usually accompanied by increased congestion of the venous circulation
  19. 19. HEART FAILURE It can be due to systolic dysfunction or diastolic dysfunction Systolic dysfunction-inadequate myocardial contractile function (cardiac muscle contracts weakly and the chambers cannot empty properly) consequence of - ischemic heart disease - pressure or volume overload (valvular disease ,hypertension & dilated cardiomyopathy )
  20. 20. diastolic dysfunction - inability of the heart to adequately relax and fill (the muscle cannot relax sufficiently to permit ventricular filling) such as in - left ventricular hypertrophy - myocardial fibrosis - amyloid deposition - constrictive pericarditis HEART FAILURE It can be due to systolic dysfunction or diastolic dysfunction
  21. 21. HEART FAILURE It may be Acute or Chronic Chronic CHF  end stage of many forms of chronic heart disease  develops insidiously due to the cumulative effects of chronic work overload such as in - - valve disease - Hypertension - ischemic heart disease - following myocardial infarction with extensive heart damage
  22. 22. HEART FAILURE It may be Acute or Chronic Acute Hear Failure  develops rapidly or suddenly  occur in acute hemodynamic stresses - fluid overload - acute valvular dysfunction - a large myocardial infarction
  23. 23. COMPENSATORY MECHANISMS When cardiac function is impaired or the work load increases, several physiologic mechanisms maintain arterial pressure and perfusion of vital organs Frank-Starling mechanism Myocardial adaptations, including hypertrophy with or without cardiac chamber dilation Activation of neurohumoral systems- release of norepinephrine ,activation of the renin-angiotensin- aldosterone system, & release of atrial natriuretic peptide
  24. 24. CAUSES OF HEAR FAILURE 1. INTRINSIC PUMP FAILURE 2. INCREASED WORKLOAD ON THE HEART 3. IMPAIRED FILLING OF CARDIAC CHAMBER
  25. 25. CAUSES OF HEAR FAILURE INTRINSIC PUMP FAILURE i) Ischemic heart disease ii) Myocarditis iii) Cardiomyopathies iv) Metabolic disorders (beriberi) v) Disorders of the rhythm (atrial fibrillation and flutter)
  26. 26. CAUSES OF HEAR FAILURE INCREASED WORKLOAD ON THE HEART Increased pressure load (pressure overload) - Systemic and pulmonary arterial hypertension - Valvular disease : mitral stenosis, aortic stenosis, pulmonary stenosis - Chronic lung diseases Increased volume load (volume overload)
  27. 27. CAUSES OF HEAR FAILURE INCREASED WORKLOAD ON THE HEART Increased volume load (volume overload) - Valvular insufficiency - Severe anaemia - Thyrotoxicosis - Arteriovenous shunts - Hypoxia due to lung diseases
  28. 28. CAUSES OF HEAR FAILURE IMPAIRED FILLING OF CARDIAC CHAMBER Cardiac failure may result from extra-cardiac causes or defect in filling of the heart: a) Cardiac tamponade - haemopericardium, hydropericardium b) Constrictive pericarditis
  29. 29. LEFT-SIDED HEART FAILURE Causes (1) ischemic heart disease (2) Systemic hypertension (3) aortic and mitral valvular diseases (4) myocardial diseases cardiomyopathies, myocarditis
  30. 30. LEFT-SIDED HEART FAILURE Pathologic changes and clinical effects result from  congestion of the pulmonary circulation  stasis of blood in the left-sided chambers  hypoperfusion of tissues leading to organ dysfunction
  31. 31. LEFT-SIDED HEART FAILURE Morphology Depend on the disease process; - gross structural abnormalities - hypertrophy and dilatation of left ventricle - microscopic changes are non-specific, consisting mainly of myocyte hypertrophy and variable degrees of interstitial fibrosis
  32. 32.  Pulmonary congestion and edema produce heavy, wet lungs  perivascular and interstitial edema, particularly in the interlobular septa  progressive edematous widening of alveolar septa  accumulation of edema fluid in the alveolar spaces  Extravasation of RBCs from the leaky capillaries into alveolar spaces, phagocytosed by macrophages, subsequent breakdown of hemoglobin leads to the appearance of hemosiderin-laden alveolar macrophages called heart failure cells—that reflect previous episodes of pulmonary edema LEFT-SIDED HEART FAILURE Morphology
  33. 33. . Pulmonary edema heart failure cells
  34. 34. Features of pulmonary congestion and edema  Cough  dyspnea with exertion  dyspnea at rest  orthopnea  paroxysmal nocturnal dyspnea  Basal lung crackles  Presence of the third heart sound LEFT-SIDED HEART FAILURE Clinical Features Progressive
  35. 35.  Salt & Fluid retention due to activation of RAAS system  impaired excretion of nitrogenous products may cause azotemia LEFT-SIDED HEART FAILURE Clinical Features
  36. 36. cerebral hypoxia can give rise to hypoxic encephalopathy with irritability, loss of attention span, and restlessness In end-stage CHF, this can even progress to stupor and coma. LEFT-SIDED HEART FAILURE Clinical Features
  37. 37. RIGHT -SIDED HEART FAILURE  As a consequence of left ventricular failure.  Cor pulmonale in which right heart failure occurs due to intrinsic lung diseases  Pulmonary or tricuspid valvular disease  Pulmonary hypertension secondary to pulmonary thromboembolism.  Myocardial disease affecting right heart.  Congenital heart disease with left-to-right shunt
  38. 38. RIGHT -SIDED HEART FAILURE pathologic changes are as under:  Systemic venous congestion in different tissues and organs e.g. subcutaneous oedema on dependent parts, passive congestion of the liver, spleen, and kidneys ascites, hydrothorax, congestion of leg veins and neck veins  Reduced cardiac output resulting in circulatory stagnation causing anoxia, cyanosis and coldness of extremities
  39. 39. RIGHT -SIDED HEART FAILURE  Congested Hepatomegaly- Nutmeg liver - red-brown centrilobular discoloration & pale peripheral regions  Cardiac sclerosis & cirrhosis - Centrilobular necrosis and fibrosis in longstanding severe case  Congested splenomegaly  GI congestion  Subcutaneous edema - dependent portions of the body, especially ankle (pedal) and pretibial edema, is a hallmark of right- sided heart filure, in chronically bedridden patients - presacral edema
  40. 40. RIGHT -SIDED HEART FAILURE Congestion of the kidneys is more marked with right-sided than left-sided heart failure, leading to greater fluid retention and peripheral edema, and more pronounced azotemia Venous congestion and hypoxia of the central nervous system can produce deficits of mental function
  41. 41. FATIGUE “Dependent” edema Hepatomegaly (congestion) ASCITES, PLEURAL EFFUSION Cyanosis Increased peripheral venous pressure (CVP) (nl = 2-6 mm Hg) Increased JVP RIGHT -SIDED HEART FAILURE
  42. 42. Measuring Jugular Venous Pressure
  43. 43. Backward heart failure - increased congestion of the venous circulation Forward heart failure - inadequate cardiac output
  44. 44. Reference 1. Robbins & Cotran Pathologic Basis of Disease, 9th Edition 2. Textbook of Pathology; Mohan Harsh Jaypee Brothers, Medical Publishers Pvt. Limited, 1 Feb 2010

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