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Valvular Heart Disease

Reading. Klabunde, Cardiovascular Physiology ConceptsCD ROM material on Valve Disease. Overview of Valves. Major Factors That Affect Flow Across Any Valvular Lesion . The valve areaThe square root of the hydrostatic pressure gradient across the valveThe time duration of transvalvular flow (applies to both systole and diastole).

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Valvular Heart Disease

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    1. Valvular Heart Disease

    2. Reading Klabunde, Cardiovascular Physiology Concepts CD ROM material on Valve Disease

    3. Overview of Valves

    4. Major Factors That Affect Flow Across Any Valvular Lesion The valve area The square root of the hydrostatic pressure gradient across the valve The time duration of transvalvular flow (applies to both systole and diastole)

    5. Valvular Heart Disease Increasing any of the major factors that affect flow across the valve increases transvalvular flow. Conversely, decreasing any of these major factors decreases transvalvular flow.

    6. Goals in Management of Various Valvular Lesions Regurgitant Lesions Reduce or minimize regurgitant flow across the mitral or aortic valve. Stenotic Lesions Maximize and enhance stenotic flow across the mitral or aortic valve

    7. Goals in Management of Various Valvular Lesions The valve area in regurgitant lesions can respond to changes in loading conditions (preload, afterload) The valve area with stenotic lesions is generally fixed

    8. Adult Valvular Heart Disease Aortic Stenosis Aortic Regurgitaiton Mitral Stenosis Mitral Regurgitation Hypertrophic Obstructive Cardiomyopathy

    9. Aortic Stenosis

    10. Aortic Stenosis Normal AVA = 2.6 3.5 cm2 Idiopathic Calcific Degeneration Congenital Bicuspid Endocarditis Other Pagets Disease Systemic Lupus Erythematosus

    11. Aortic Stenosis

    13. Aortic Stenosis: Senile

    15. Natural History of AS May be a long asymptomatic period Symptomatic Usually have severe AS with AVA of 0.9 cm2 or less Presenting symptoms: Angina Syncope CHF

    16. Natural History of AS Symptomatic patients without surgery show the following average life spans: Angina = 5 years Syncope = 3 years CHF = 2 years AS is considered an independent risk factor for perioperative morbidity

    17. Survival of Patients with Valvular Heart Disease Treated Medically

    18. Pathophysiology of Aortic Stenosis

    19. Myocardial Function Develop left ventricular hypertrophy as an adaptation LVH reduces wall stress T =(Pr)/h LVH causes increased diastolic stiffness

    20. Ischemia in AS Hypertrophied LV muscle mass Increased systolic pressure Prolongation of ejection Shortened diastolic time Relative decrease in myocardial capillary density High incidence of concomitant coronary artery disease

    21. Aortic Stenosis

    22. Measuring the Valve Gradient in AS Mean gradient Peak-to-peak gradient Peak instantaneous gradient

    23. Degree of Stenosis Critical AS Peak systolic pressure gradient > 50 mmHg AVA < 0.9 cm2 Moderate AS 1.0 1.4 cm2 Mild AS 1.5 2.0 cm2

    24. Aortic Stenosis

    25. AORTIC STENOSIS: HEMODYNAMIC GOALS

    26. Aortic Regurgitation

    27. Aortic Regurgitation (Insufficiency) Rheumatic heart disease Endocarditis Aortic root dissection Trauma Connective tissue disorders Dexfenfluramine (appetite suppressant)

    28. Aortic Regurgitation

    29. Natural History Long asymptomatic period during which the LV undergoes progressive eccentric hypertrophy CHF Angina

    30. Aortic Regurgitation

    31. Pathophysiology of Aortic Regurgitation

    32. Pathophysiology LV overloading Increased diastolic wall-tension produces eccentric hypertrophy (increase both in chamber size and wall thickness) Reduced diastolic compliance (Acute AI) Very high diastolic compliance (Chronic AI)

    33. Eccentric Hypertrophy

    34. Pathophysiology Baseline myocardial oxygen demand higher than normal because of increased LV mass Reduced coronary perfusion pressure Lower diastolic pressure Increased LVEDP

    35. Pathophysiology Myocardial contractility is usually preserved until late in course of the disease Late in disease there is progression to irreversible contractile impairment

    36. Aortic Regurgitation

    37. AORTIC REGURGITATION: HEMODYNAMIC GOALS

    39. Normal MVA = 4 6 cm2

    40. Mitral Stenosis Causes: Rheumatic Women 4x > Men Congenital Rheumatoid arthritis Systemic Lupus Erythematosus Carcinoid Syndrome Asymptomatic for approximately 20 years Presenting symptoms: CHF (50%) Atrial fibrillation

    41. Mitral Stenosis

    42. Pathophysiology of Mitral Stenosis

    43. Mitral Stenosis

    44. Pathophysiology Chronic obstruction to left atrial emptying during diastole LV chronically volume-underloaded Chronic volume and pressure over-loading of the left atrium and structures behind it

    45. Pressure Gradient across the Mitral Valve Pressure Gradient CO = Cardiac Output DFP = Diastolic Filling Period

    46. Pathophysiology: LV LV function is usually normal Decreased LVEF in about 1/3 of MS patients: Rheumatic carditis Chronic volume underloading Concomitant CAD Septal hypertrophy in patients with pulmonary hypertension (PHT)

    47. Pathophysiology: RV RV function is normal in absence of pulmonary hypertension (PHT) Severe pulmonary hypertension will result in RV failure and secondary abnormalities of LV function

    48. Mitral Stenosis

    49. MITRAL STENOSIS: HEMODYNAMIC GOALS

    51. Mitral Regurgitation (Insufficiency) Valve leaflets Chordae tendineae Papillary muscles

    52. Mitral Regurgitation (Insufficiency) Rheumatic disease Endocarditis Mitral valve prolapse Mitral annular enlargement Ischemia Myocardial infarction Trauma Fenfluramine diet suppressants

    53. Prolapsed Mitral Valve Leaflet

    54. Mitral Regurgitation

    55. Pathophysiology of Mitral Regurgitation

    56. Pathophysiology LV unloads itself into left atrium Chronic left atrial overload Chronic overload on left ventricle Volume of regurgitant flow determined by: Ventriculo-atrial gradient Diastolic time Size of the regurgitant orifice Measurements of LV function tend to be slightly elevated Moderately depressed ejection fraction in a patient with MR may be indicative of a severely depressed inotropic state

    57. Natural History Chronic MR (variable course) Chronic MR may be protected from pulmonary congestion by dilated, highly compliant left atrium Acute MR usually with fulminant pulmonary edema

    58. Mitral Regurgitation

    59. MITRAL REGURGITATION: HEMODYNAMIC GOALS

    60. Hypertrophic Cardiomyopathy

    61. Hypertrophic Cardiomyopathy Primary disease of cardiac muscle Histologic evidence of myocardial cellular disarray Characteristics LVH (often marked in the septum) Reduced diastolic compliance Subvalvular pressure gradient Ventricular arrhythmias May have Systolic Anterior Motion (SAM) of the mitral valve Blood is ejected into the LV outflow tract at high velocity which creates Venturi effect. This pulls the anterior leaflet of the mitral valve toward the septum during systole. This creates dynamic outflow tract obstruction and mitral regurgitation.

    63. Hypertrophic Cardiomyopathy Management Avoid anything that causes reduction in left ventricular volume Decreased preload Increased contractility Decreased afterload Reduce determinants of myocardial oxygen consumption as thickened myocardium is predisposed to ischemia.

    64. HYPERTROPHIC CARDIOMYOPATHY : HEMODYNAMIC GOALS

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