Valvular Heart Diseaseand auscultation

Jay L. Rubenstone, D.O., F.A.C.C

Normal StructureMitral Valve

• Cross sectional Area 4-6cm2• Anterior and Posterior Leaflets• Chordae Tendineae Papillary Muscles

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Mitral StenosisEtiology & Pathology• Rheumatic Fever- 99% • Other▫ Congenital ▫ Carcinoid▫ Lupus▫ Amyloid▫ Infective Endocarditis▫ Mucopolysaccharide Disease

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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)

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History

• Exertional Dyspnea• Cough/Wheezing• Orthopnea/PND/CHF• Hemoptysis-Rupture of Pulm Vein-Brochial

Vein Shunts

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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

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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

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Natural History

• Presurgical Survival Rates▫ NYHA Class II 80%-10yrs▫ Class III 38%-10yrs, 62% 5yrs▫ Class IV 15%-5yrs

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Management-Medical

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

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Percutaneous Balloon Angioplasty

• Moderate-Severe MS• Mild MS- if Pulmonary Artery Pressures or

Wedge Pressure Elevate with Exercise

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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,

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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

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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

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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

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Pathophysiology

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

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Pathophysiology

• Ejection Fraction in Mitral Regurgitation▫ >65% normal in compensated MR▫ 50-65% mild impairment▫ 40-50% moderate-severe impairment▫ <35% advanced impairmentAs ejection fraction decreases operative risk

increases.

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History

• Shortness of Breath• Exertional Dyspnea• Congestive Heart Failure• RHF• Significant symptoms in chronic MR usually do

not develop until LV decompensation occurs.

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History

• Medical Treatment Survival▫ 80% 5yr▫ 60% 10yr▫ 30-45% 5yr if MR severe

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Management of Chronic MR

• Medical▫ Digoxin▫ Diruetics*▫ Afterload Reduction▫ Anticoagulation in A-fib▫ Endocarditis Prophylaxis

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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

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Mitral Valve Prolapse

• Systolic Click-Murmur Syndrome• Barlow’s Syndrome• Billowing Mitral Valve Syndrome• Floppy Valve Syndrome• Myxomatous Valve Syndrome• Parachute Valve

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Mitral Valve Prolapse

• Over diagnosed▫ 2.4% of population▫ Females>Males 2:1▫ Severe MR- Elderly Male>Young Female

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MVP Etiology

• Primary Valvular most frequent• Connective Tissue Diseases• Hyperthyroidism• Myotonic Dystrophy• Periarteritis Nodosa• Von Willebrands

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MVP Pathology

• Myxomatous Proliferation and Degeneration of Valve Leaflets

• Increased Quantity of Acid Mucopolysaccharide in Middle Layer of Valve Tissue

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MVP History

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

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Natural History

• Progressive MR in 15% over 10-15 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)

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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*

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Aortic ValveNormal 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

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Aortic Stenosis Etiology and Pathology

• Valvular• Supravalvular• Subvalvular• Hyperthrophic Cardiomyopathy

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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

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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

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Hemodynamics• Severe AS▫ Mean systolic pressure gradient ≥ 40mmHg in the

presence of normal cardiac output▫ Valve area ≤ 1.0cm2

• Moderate AS▫ 1-1.5cm2

• Mild AS▫ 1.5-2cm2

• Aortic Sclerosis

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History

• Long latent period of increasing obstruction• Symptoms usually begin in 5th or 6th 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

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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

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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

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Surgery (Valve Replacement)

• Indications▫ Symptomatic Patients -valve area ≤ 1.0cm2

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

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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%

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Aortic RegurgitationEtiology 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

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Etiology and Pathology• Aortic Root Disease-More common than

primary valvular. Root Dilatation leads to non-coaptation of leaflets.▫ Degenerative-Hypertensive Aortic Dilatation▫ Cystic Medial Necrosis-Classic Marfans Syndrome▫ Aortic Dissection▫ Syphilitic Aortitis▫ Rheumatic Disease-same as valvular

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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 4th or 5th Decade

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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

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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

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Medical Treatment

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

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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

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Surgical Treatment

• Mortality▫ 3-8% perioperative▫ 5-10% late mortality with significant preop LV

dysfunction

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Cardiac AuscultationJay L. Rubenstone, D.O., F.A.C.C.

October 2012

Techniques of Examination

• Order of Exam▫ Aortic Area▫ Pulmonic Area▫ Tricuspid Area▫ Mitral Area

Process of Auscultation

At each auscultatory area:1. Concentrate on 1st Heart Sound

note Intensity and Splitting2. Concentrate on 2nd Heart Sound

note Intensity and Splitting3. Listen for Extra Sounds in Systole

note Timing, Intensity, Pitch

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

Process of Ascultation

*If Systolic or Diastolic Murmur Present, Note:▫ Location▫ Radiation▫ Intensity▫ Pitch▫ Quality

AuscultationTiming• Systolic▫ Early▫ Mid ▫ Late

• Diastolic▫ Early▫ Mid▫ Late (or Presystolic)

AuscultationLocation• Interspace

• Centimeters from ▫ Midsternal▫ Midclavicular▫ Or Axillary Lines

AuscultationIntensity• Grade 1 Very Faint• Grade 2 Quiet, but Heard Immediately• Grade 3 Moderately Loud, Not Associated

with a Thrill• Grade 4 Loud, May Be Associated with a

Thrill• Grade 5 Very Loud• Grade 6 May be Heard w/stethoscope

off chest

Auscultation

• Radiation or Transmission• Pitch▫ High, Med, Low

• Quality▫ Blowing▫ Rumbling▫ Harsh▫ Muscial

COMPONENTS OF S1

• Mitral Valve Closure▫ Best Heard: Apex

• Tricuspid Valve Closure▫ Best heard: Lower Left Sternal Boarder

S1

• Wide Splitting▫ RBBB▫ PVC from Left Ventricle

• Single Sound▫ Normal▫ LBBB▫ PVC from Right Ventricle▫ Paced Beats

S1

• Increased Intensity▫ Short PR▫ Rapid HR▫ Atrial Fibrillation▫ Mitral Stenosis

S 1

• Decreased Intensity▫ Mitral Stenosis (Immobile Leaflets)▫ Opposite of Causes of Increased Intensity

S 2

• Two Components▫ Aortic Closure A2▫ Pulmonic Closure P2

Best Heard at the Base

S 2

• Normal Splitting▫ Best Heard At 2nd Left Intercostal Space▫ During Inspiration there is Delayed Pulmonic Valve

Closure Due to Increased Capacitance of Pulmonary Bed

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

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

S 2

• Paradoxical Splitting- P2 before A2▫ LBBB▫ Paced Beats

• Increased Intensity▫ A2 Systemic HTN

Dilated Aortic Root▫ P2 Pulmonary HTN

Dilated Pulmonary Trunk

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

Mid-Late Systolic Sounds

• Click ▫ High Frequency Sound Found in Mitral Valve

Prolapse ▫ Occurs Earlier with Valsalva Maneuver or Squatting

to Standing

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

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

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

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

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)

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

Systolic Murmurs

• Aortic Valve Stenosis▫ Diamond Shaped, Crescendo-Decrescendo ▫ Begins After S1 or with Aortic Ejection Sound▫ Ends Before S2▫ 2nd Right Intercostal Space, Apex, can radiate to

Neck▫ High Frequency, Harsh ▫ Can be Musical in Quality at the Apex

Systolic Murmurs

• Pulmonic Stenosis▫ Similar to AS Except Relationship to P2▫ 2nd Left Intercostal Space

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

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

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

Normal Systolic Murmurs

• Aortic Sclerosis▫ Most Common Innocent Murmur

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

Early Diastolic Murmur▫ Graham Steell – Murmur of Pulmonic Regurgitation as a Result of

Pulmonary HTN High Freq, Decrescendo Blowing Murmur Heard

throughout Diastole

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

Mid Diastolic Murmurs

• Tricuspid Stenosis▫ Similar to MS, except increases with Respiration

(Carvallo’s Sign)▫ Best Heard at Left Lower Sternal Edge

Mid Diastolic Murmurs

• Pulmonic Regurgitation▫ Crescendo-Decrescendo Murmur when Primary

Valvular Abnormality and Not Associated with Pumonary HTN

Diastolic Murmurs

• Late or Presystolic▫ Austin Flint Murmur of Aortic Regurgitation Bubbling Quality, Short Consequence of Aortic Regurgitation impinging on

Mitral Valve

Diastolic Murmurs

• Continuous▫ PDA (AortoPulmonary Connection) Rough Thrill

▫ A-V Fistulas Hemodialysis Shunt Aortic Valve Sinus to Right Ventricular Fistula Coronary Artery Fistulas

Diastolic Murmurs

• Venous Hum▫ Rough in quality not actually a hum▫ Hepatic▫ Internal Jugular▫ During Anemia, Fever, Pregnancy and Thyrotoxicosis

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)

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

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

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