Valvular Heart Disease and auscultation. Jay L. Rubenstone, D.O., F.A.C.C

Transcription

1 Valvular Heart Disease and auscultation Jay L. Rubenstone, D.O., F.A.C.C

2 2 Normal Structure Mitral Valve Cross sectional Area 4-6cm2 Anterior and Posterior Leaflets Chordae Tendineae Papillary Muscles

3 3 Mitral Stenosis Etiology & Pathology Rheumatic Fever- 99% Other Congenital Carcinoid Lupus Amyloid Infective Endocarditis Mucopolysaccharide Disease

4 4 Pathophysiology Mild MS- orifice <2 cm2 Critical MS- <1 cm2 A-V pressure gradient >20mmHg Increased LA Pressure Increase Pulmonary Venous + Capillary Pressures Increase Pulmonary Artery Systolic Pressure Decrease RV Function (when PAS>30-60mmHg)

5 5 History Exertional Dyspnea Cough/Wheezing Orthopnea/PND/CHF Hemoptysis-Rupture of Pulm Vein-Brochial Vein Shunts

6 6 History Chest Pain-Increase RV Pressures or Unknown Etiology Systemic Emboli (LA clots) Increased LA size, Decreased C.O., Atrial Fib, IE Significantly decreased w/anticoagulation

7 7 Natural History Asymptomatic for 15-20yrs following Rheumatic Fever Additional 5-10 yrs for progression from mild to severe stenosis Stenosis progression approx..09 cm2/yr

8 8 Natural History Presurgical Survival Rates NYHA Class II 80%-10yrs Class III 38%-10yrs, 62% 5yrs Class IV 15%-5yrs

9 9 Management-Medical Endocarditis Prophylaxis Activity Limitation Diruetics- Decrease Na Intake Heart Rate Control for A-fib or Sinus Rhythm Anticoagulation

10 10 Percutaneous Balloon Angioplasty Moderate-Severe MS Mild MS- if Pulmonary Artery Pressures or Wedge Pressure Elevate with Exercise

11 Valve Replacement Indications Combined MS/MR <1.5 cm2-nyha III or IV <1 cm2 Class II if Pulm Artery Pressure >70mmHg Mortality 3-8% Valve Type-Prosthetic or Bioprosthetic, 11

12 12 Mitral Regurgitation Etiology Rheumatic Heart Disease Infective Endocarditis Collagen Vascular Disease Cardiomyopathy Ischemic Heart Disease Mitral Valve Prolapse-most common cause for valve surgery in US

13 13 Pathophysiology Decreased Impedance to Ventricular Emptying Determinants of Regurgitant Flow Instantaneous Size of MV Orifice Dependent on Preload, Afterload, LV Contractility, LV Size LA-LV Pressure Gradient dependent on Systemic Vascular Resistance, LV Pressure, & LV Size

14 14 Pathophysiology LV Compensation Increased End Diastolic Volume Increased Wall Tension Increased Preload Increased LV Emptying Normal Ejection Fraction should be Super Normal >65% to maintain forward cardiac output and B/P

15 15 Pathophysiology LV Decompensation Increase End Systolic Volume Increased End Diastolic Volume Leads to Annulus Dilatation (MR begets MR) Decreased Ejection Fraction and Stroke Volume

16 16 Pathophysiology Ejection Fraction in Mitral Regurgitation >65% normal in compensated MR 50-65% mild impairment 40-50% moderate-severe impairment <35% advanced impairment As ejection fraction decreases operative risk increases.

17 17 History Shortness of Breath Exertional Dyspnea Congestive Heart Failure RHF Significant symptoms in chronic MR usually do not develop until LV decompensation occurs.

18 18 History Medical Treatment Survival 80% 5yr 60% 10yr 30-45% 5yr if MR severe

19 19 Management of Chronic MR Medical Digoxin Diruetics* Afterload Reduction Anticoagulation in A-fib Endocarditis Prophylaxis

20 20 Management of Chronic MR Surgical Indications Asymptomatic Class I EF < 60% or LV Systolic Diameter >45mm Severe MR Class II, III, or IV generally considered for surgery unless EF <30% Valve Repair vs. Replacement

21 21 Mitral Valve Prolapse Systolic Click-Murmur Syndrome Barlow s Syndrome Billowing Mitral Valve Syndrome Floppy Valve Syndrome Myxomatous Valve Syndrome Parachute Valve

22 22 Mitral Valve Prolapse Over diagnosed 2.4% of population Females>Males 2:1 Severe MR- Elderly Male>Young Female

23 23 MVP Etiology Primary Valvular most frequent Connective Tissue Diseases Hyperthyroidism Myotonic Dystrophy Periarteritis Nodosa Von Willebrands

24 24 MVP Pathology Myxomatous Proliferation and Degeneration of Valve Leaflets Increased Quantity of Acid Mucopolysaccharide in Middle Layer of Valve Tissue

25 25 MVP History Most are asymptomatic throughout life Chest pain, fatigue, anxiety Orthostasis-questionable autonomic dysfunction Arrhythmia-SVT, PACs, PVCs Symptoms of MR if present

26 26 Natural History Progressive MR in 15% over yrs Infective Endocarditis Cerebral Emboli-tearing of endothelial covering of myxomatous valve with platelet activation Sudden Cardiac Death-V fib, increased Q-T interval (not well established)

27 27 MVP Management Endocarditis prophylaxis if MR present Holter monitor-beta blocker for ectopy? Aspirin if focal neurological events present MR-treat like any other MR, valves usually amenable to repair *MVP is usually a benign disease*

28 28 Aortic Valve Normal Structure Valve sits at the base of Aortic Root Three Leaflets (cusps)-non coronary, right coronary, left coronary Cusps give rise to ostea of right coronary artery and left main coronary artery Normal cross-sectional area 3-4cm2

29 29 Aortic Stenosis Etiology and Pathology Valvular Supravalvular Subvalvular Hyperthrophic Cardiomyopathy

30 30 Congenital Aortic Stenosis Unicuspid Presents less than one year of age Bicuspid Adult Presentation Chronic turbulent flow Leads to fibrosis, rigidity, calcification Tricuspid Leaflets of unequal size

31 31 Acquired Aortic Stenosis Rheumatic Rare Usually mitral valve also involved Degenerative or Senile Most common cause of adult AS Most common cause of valve replacement Years of normal mechanical stress leads to calcium deposits on leaflets Inflammatory or Infectious component?? >age 65 2% frank AS, 30% Aortic Sclerosis

32 32 Hemodynamics Severe AS Mean systolic pressure gradient 40mmHg in the presence of normal cardiac output Valve area 1.0cm 2 Moderate AS 1-1.5cm 2 Mild AS 1.5-2cm 2 Aortic Sclerosis

33 33 History Long latent period of increasing obstruction Symptoms usually begin in 5 th or 6 th decade Angina in 2/3 of patients Hyperthrophied myocardium Increased ventricular systolic pressure All of which increase myocardial oxygen consumption Oxygen supply-demand imbalance leads to subendocardial ischemia

34 34 History Syncopy Reduced cerebral perfusion Vasodilation in the presence of fixed cardiac output leads to hypotension Baroreceptor-vasodepression due to high LV systolic pressure Dyspnea (CHF) Particularly with exertion due to fixed cardiac output Pulmonary Venous HTN can lead to CHF

35 35 Natural History Asymptomatic latent period With moderate-severe AS valve area can decrease on average 0.12cm2 per year *Angina, synocopy or CHF Average 1-3 year survival 50% Sudden cardiac death rare

36 36 Surgery (Valve Replacement) Indications Symptomatic Patients -valve area 1.0cm 2 Asymptomatic Patients-progressive LV dysfunction (EF <35%) or hypotensive response to mild exercise Delaying surgery in asymptomatic patients with good exercise tolerance is controversial Valve type Prosthetic, Bioprosthetic or TAVR

37 37 Surgery (Valve Replacement) Results Effective prosthetic valve area not normal Surgery replaces Critical AS with Non-critical AS Symptoms can persist if valve-patient mismatch occurs 10 year survival 85%

38 38 Aortic Regurgitation Etiology and Pathology Valvular Rheumatic-Fibrotic Retraction of Leaflets Ankylosing Spondylitis, Behcet s, Psoriatic Arthritis, Giant Cell Arteritis Degenerative AS-75% w/ar Infective Endocarditis-Leaflet Destruction Trauma-ascending aortic tear Bicuspid aortic valve-prolapse or incomplete closure Myxomatous Degeneration-like MVP

39 39 Etiology and Pathology Aortic Root Disease-More common than primary valvular. Root Dilatation leads to noncoaptation of leaflets. Degenerative-Hypertensive Aortic Dilatation Cystic Medial Necrosis-Classic Marfans Syndrome Aortic Dissection Syphilitic Aortitis Rheumatic Disease-same as valvular

40 40 History Acute AR LV cannot accommodate acute regurgitant volume can lead to cardiovascular collapse Chronic AR Gradual LV enlargement-eccentric hypertrophy Exertional dyspnea, orthopnea, PND, CHF Presents 4 th or 5 th Decade

41 Natural History Acute AR Cardiovascular collapse Inotrophic agents and vasodilators Prompt surgical intervention Chronic AR 75% Five Year Survival 50% Ten Year Survival Progressive downhill course of CHF, Episodic Pulmonary Edema, Sudden Cardiac Death 41

42 42 Medical Treatment Acute AR As above Chronic AR Asymptomatic Mild-Moderate Follow by Echo Yearly Endocarditis Prophalaxis for all AR May not require medical treatment

43 43 Medical Treatment Symptomatic Moderate-Severe AR Limit exertional activity Aggressively treat B/P Diuretics Salt Restriction Digoxin Vasodilators (Nifedipine?)

44 44 Surgical Treatment Indications Defer surgery for chronic severe AR if good exercise tolerance, EF greater than 50%, end systolic diameter < 50 mm, and end diastolic diameter < 70 mm Be aware that progressive decline in LV function or size increases surgical morbidity and mortality

45 45 Surgical Treatment Mortality 3-8% perioperative 5-10% late mortality with significant preop LV dysfunction

46 Cardiac Auscultation Jay L. Rubenstone, D.O., F.A.C.C. October 2012

47 Techniques of Examination Order of Exam Aortic Area Pulmonic Area Tricuspid Area Mitral Area

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49 Process of Auscultation At each auscultatory area: 1. Concentrate on 1st Heart Sound note Intensity and Splitting 2. Concentrate on 2nd Heart Sound note Intensity and Splitting 3. Listen for Extra Sounds in Systole note Timing, Intensity, Pitch

50 Process of Ascultation 4. Listen for Extra Sounds in Diastole note timing, intensity, pitch 5. Listen for Systolic Murmurs* 6. Listen for Diastolic Murmurs* 7. Other Heart Sounds

51 Process of Ascultation *If Systolic or Diastolic Murmur Present, Note: Location Radiation Intensity Pitch Quality

52 Auscultation Timing Systolic Early Mid Late Diastolic Early Mid Late (or Presystolic)

53 Auscultation Location Interspace Centimeters from Midsternal Midclavicular Or Axillary Lines

54 Auscultation Intensity Grade 1 Grade 2 Grade 3 with Grade 4 Grade 5 Grade 6 Very Faint Quiet, but Heard Immediately Moderately Loud, Not Associated a Thrill Loud, May Be Associated with a Thrill Very Loud May be Heard w/stethoscope off chest

55 Auscultation Radiation or Transmission Pitch High, Med, Low Quality Blowing Rumbling Harsh Muscial

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57 COMPONENTS OF S1 Mitral Valve Closure Best Heard: Apex Tricuspid Valve Closure Best heard: Lower Left Sternal Boarder

58 S1 Wide Splitting RBBB PVC from Left Ventricle Single Sound Normal LBBB PVC from Right Ventricle Paced Beats

59 S1 Increased Intensity Short PR Rapid HR Atrial Fibrillation Mitral Stenosis

60 S 1 Decreased Intensity Mitral Stenosis (Immobile Leaflets) Opposite of Causes of Increased Intensity

61 S 2 Two Components Aortic Closure A2 Pulmonic Closure P2 Best Heard at the Base

62 S 2 Normal Splitting Best Heard At 2 nd Left Intercostal Space During Inspiration there is Delayed Pulmonic Valve Closure Due to Increased Capacitance of Pulmonary Bed

63 S 2 Loss of Splitting Inaudible P2- Adults with Increased Chest Diameter Congenital (Tetralogy, Pulmonary Atresia Transposition) Increased Pulmonary Valve Resistance-Pulmonary HTN Eisenmenger s Complex-Equal Pulmonary & Systemic Resistances

64 S 2 Persistent Splitting RBBB Pure MR Healthy Adolescents when in Supine Position Fixed Splitting Atrial Septal Defect- Due to Delayed Closure of Pulmonic Valve from Increased Right-Sided Flow

65 S 2 Paradoxical Splitting- P2 before A2 LBBB Paced Beats Increased Intensity A2 Systemic HTN Dilated Aortic Root P2 Pulmonary HTN Dilated Pulmonary Trunk

66 Early Systolic Sounds Ejection Sound- Usually High Frequency Aortic Valve- Aortic Stenosis, Bicuspid Aortic Valve Pulmonary Valve-Pulmonic Stenosis Vary with Respirations Prosthetic Valves- Mechanical, Not Bioprosthetic

67 Mid-Late Systolic Sounds Click High Frequency Sound Found in Mitral Valve Prolapse Occurs Earlier with Valsalva Maneuver or Squatting to Standing

68 Early Diastolic Sounds Opening Snap of Mitral Stenosis (MS) High Frequency-Left Lateral Decubitus Position, Apex Occurs after S2, before S3 MS More Severe with Short A2-OS Interval Precordial Knock Chronic Constrictive Pericarditis Mitral Regurgitation Atrial Myxoma Older Model Prosthetic Mitral Valve

69 MID DIASTOLIC SOUNDS S3 Occurs During Rapid Filling of Left Ventricle (LV) related to LV Volume Low Frequency Best Heard At the Apex w/bell Pt in Left Lateral Decubitus Position Can Be Normal to Age 40??? Can be Pathognomonic for Congestive Heart Failure

70 Late Diastolic Sounds S4 During Atrial Phase of LV Filling Consequence of Ventricular Stiffness Absent in Atrial Fibrillation or Ventricular Pacing Low Frequency Sound Best Heart At the Apex Pt in Left Lateral Decubitus Position HTN, Aortic Stenosis, Ischemic Heart Disease

71 Diastolic Sounds Right Sided S3, S4 Left Lower Sternal Boarder Intensity Varies with Respiration due to Right Heart Filling (Carvallo s Sign) Summation Gallop Occurrence of an Over Lapping S3 and S4 due to Tachycardia

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75 Systolic Murmurs Obstruction to Ventricular Outflow Dilatation of Aortic Root or Pulmonary Trunk Accelerated Flow into Aorta or Pulmonary Trunk Innocent Murmurs Some Forms of MR (Papillary Muscle Dysfunction)

76 Systolic Murmurs Acute Mitral Regurgitation (MR) or Tricuspid Regurgitation (TR) Mid Frequency Not Classic Murmur Ventricular-Septal Defect (VSD) High Frequency (diaphram) Atrial-Septal Defect (ASD) Pulmonary Outflow Not Defect Murmur

77 Systolic Murmurs Aortic Valve Stenosis Diamond Shaped, Crescendo-Decrescendo Begins After S1 or with Aortic Ejection Sound Ends Before S2 2 nd Right Intercostal Space, Apex, can radiate to Neck High Frequency, Harsh Can be Musical in Quality at the Apex

78 Systolic Murmurs Pulmonic Stenosis Similar to AS Except Relationship to P2 2 nd Left Intercostal Space

79 Systolic Murmurs Mitral Valve Prolapse High Frequency, Sometimes Honking, Crescendo Murmur Usually Extends to S2 Classic Mid-Late Systolic Click Occurs Earlier with Valsalva & Squatting to Standing

80 Systolic Murmurs Holosystolic Begins with S1, Ends at S2 MR- Radiates to Left Sternal Boarder, Base or Neck, More Commonly Apex to Axilla TR- Carvallo s Sign (Inspiratory Variation) VSD-Across Precordium Patent Ductus Arteriosis (PDA)- Aorto-Pulmonary Connection

81 Normal Systolic Murmurs Still s Murmur Medium Frequency, Vibratory, Originating from Leaflets of Pulmonic Valve Rapid Ejection into Aortic Root or Pulmonary Trunk Pregnancy Anemia Fever Thyrotoxicosis

82 Normal Systolic Murmurs Aortic Sclerosis Most Common Innocent Murmur

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84 Early Diastolic Murmur Aortic Regurgitation High Pitched, Decrescendo Murmur Best heard at Left Sternal Boarder with the diaphragm w/patient Leaning Forward at End Expiration Acute, Severe AR Murmur Can be Short, Soft and Med Pitched Chronic, Sever AR- Murmur Usually Long, Loud, Blowing Decrescendo, High Frequency

85 Early Diastolic Murmur Graham Steell Murmur of Pulmonic Regurgitation as a Result of Pulmonary HTN High Freq, Decrescendo Blowing Murmur Heard throughout Diastole

86 Mid Diastolic Murmur Mitral Stenosis (MS) Follows Opening Snap Low Pitch Rumble Best Heard Apex over LV Using Bell of Stethoscope Pt in Left Lateral Decubitus Position

87 Mid Diastolic Murmurs Tricuspid Stenosis Similar to MS, except increases with Respiration (Carvallo s Sign) Best Heard at Left Lower Sternal Edge

88 Mid Diastolic Murmurs Pulmonic Regurgitation Crescendo-Decrescendo Murmur when Primary Valvular Abnormality and Not Associated with Pumonary HTN

89 Diastolic Murmurs Late or Presystolic Austin Flint Murmur of Aortic Regurgitation Bubbling Quality, Short Consequence of Aortic Regurgitation impinging on Mitral Valve

90 Diastolic Murmurs Continuous PDA (AortoPulmonary Connection) Rough Thrill A-V Fistulas Hemodialysis Shunt Aortic Valve Sinus to Right Ventricular Fistula Coronary Artery Fistulas

91 Diastolic Murmurs Venous Hum Rough in quality not actually a hum Hepatic Internal Jugular During Anemia, Fever, Pregnancy and Thyrotoxicosis

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93 Pericardial Friction Rub Three Phases Mid Systolic, Mid Diastolic, Pre Systolic Scratchy, Leathery Best Heard With Diaphragm of Stethoscope Left Sternal Boarder Leaning over at End Expiration Apposition of Abnormal Visceral and Parietal Pericardium Confused with Hamman s Sign in Post Open Heart Surgery (Crunch Sound from Mediastinal Air)

94 Innocent or Normal Murmurs-Systolic Vibratory Systolic Murmur (Still s Murmur) Pulmonic Systolic Murmur (Pulmonary Trunk)* Mammary Soufflé* Peripheral Pulmonic Systolic Murmur (Pulmonary Branches) Supraclavicular or Brachiocephalic Systolic Murmur Aortic Systolic Murmur *common in pregnancy

95 Innocent or Normal Murmurs- Continuous Venous Hum Continuous Mammary Soufflé

96 Conclusions Consistent Approach to Auscultation Knowing What to Look For Follow Through on H&P Confirm or Eliminate Suspicions Knowing How to Find It Proper Utilization of Stethoscope Location and Quality of Heart Sounds & Murmurs

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