Transcript Valvular Heart Disease and Auscultation

Valvular Heart Disease
and auscultation
Jay L. Rubenstone, D.O., F.A.C.C
Fall 2012
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Normal Structure
Mitral Valve
• Cross sectional Area 4-6cm2
• Anterior and Posterior Leaflets
• Chordae Tendineae  Papillary Muscles
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Mitral Stenosis
Etiology & Pathology
• Rheumatic Fever- 99%
• Other
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Congenital
Carcinoid
Lupus
Amyloid
Infective Endocarditis
Mucopolysaccharide Disease
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Pathophysiology
• Mild MS- orifice <2 cm2
• Critical MS- <1 cm2
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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
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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
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Class III 38%-10yrs, 62% 5yrs
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Class IV 15%-5yrs
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Management-Medical
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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
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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
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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
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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
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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 impairment
As ejection fraction decreases operative risk
increases.
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History
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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
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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
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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
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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
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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
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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 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
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Aortic Stenosis Etiology and Pathology
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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
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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 Regurgitation
Etiology and Pathology
• Valvular
• Rheumatic-Fibrotic Retraction of Leaflets
• Ankylosing Spondylitis, Behcet’s, Psoriatic Arthritis, Giant Cell
Arteritis
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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 noncoaptation of leaflets.
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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
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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
Cardiac Auscultation
Jay L. Rubenstone, D.O., F.A.C.C.
October 2012
Techniques of Examination
• Order of Exam
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Aortic Area
Pulmonic Area
Tricuspid Area
Mitral Area
Process of Auscultation
At each auscultatory area:
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Concentrate on 1st Heart Sound
 note Intensity and Splitting
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Concentrate on 2nd Heart Sound
 note Intensity and Splitting
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Listen for Extra Sounds in Systole
 note Timing, Intensity, Pitch
Process of Ascultation
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Listen for Extra Sounds in Diastole
 note timing, intensity, pitch
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Listen for Systolic Murmurs*
Listen for Diastolic Murmurs*
Other Heart Sounds
Process of Ascultation
*If Systolic or Diastolic Murmur Present, Note:
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Location
Radiation
Intensity
Pitch
Quality
Auscultation
Timing
• Systolic
▫ Early
▫ Mid
▫ Late
• Diastolic
▫ Early
▫ Mid
▫ Late (or Presystolic)
Auscultation
Location
• Interspace
• Centimeters from
▫ Midsternal
▫ Midclavicular
▫ Or Axillary Lines
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
Auscultation
• Radiation or Transmission
• Pitch
▫ High, Med, Low
• Quality
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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
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Normal
LBBB
PVC from Right Ventricle
Paced Beats
S1
• Increased Intensity
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Short PR
Rapid HR
Atrial Fibrillation
Mitral Stenosis
S1
• Decreased Intensity
▫ Mitral Stenosis (Immobile Leaflets)
▫ Opposite of Causes of Increased Intensity
S2
• Two Components
▫ Aortic Closure A2
▫ Pulmonic Closure P2
Best Heard at the Base
S2
• Normal Splitting
▫ Best Heard At 2nd Left Intercostal Space
▫ During Inspiration there is Delayed Pulmonic Valve
Closure
 Due to Increased Capacitance of Pulmonary Bed
S2
• 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
S2
• 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
S2
• 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
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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
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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
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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
 TRCarvallo’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
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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
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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
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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 MurmursContinuous
• 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