Transcript Valvular Heart Disease

VALVULAR HEART DISEASE
AND AUSCULTATION
JAY L. RUBENSTONE, D.O., F.A.C.C
Fall 2012
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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PATHOPHYSIOLOGY
• Pulmonary HTN
• Passive Backward Transmission Of Incr. LA pressure
Pulmonary Arteriolar Constriction Organic Obliterative
Changes in Pulmonary Vascular Bed RV Failure
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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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DIAGNOSIS
• Cardiac Catherization
• Gorlin Equation
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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, TAVR
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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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PHYSICAL EXAMINATION
• Ascultation
• Murmur- mid to late crescendo progressing to holosystolic if
MR becomes severe
• Click and murmur move closer to S1 during strain phase of
valsalva, sudden standing, and Amyl Nitrate
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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 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
• 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 disfunction (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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KEEPSURGERY (VALVE REPLACEMENT)
• Results
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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, Behcets, Psoratic Arthritis, Giant
Cell Arteritis
Degenerative AS-75% w/AR
Infective Endocarditis-Leaflet Distruction
Trauma-ascending aortic tear
Bicuspid aortic valve-prolapse or incomplete
closure
• Myxomatous Degeneration-like MVP
• Appetite suppressant drugs-serotonin related
valve deposits
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ETIOLOGY AND PATHOLOGY
• Aortic Root Disease-More common than primary
valvular. Root Dilatation leads to non-coaptation 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
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CARDIAC
AUSCULTATION
J A Y
L .
R U B E N S T O N E ,
D . O . ,
F . A . C . C .
O C T O B E R
2 0 1 2
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:
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
PROCESS OF ASCULTATION
4.
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
related to LV Volume
• Low Frequency Best Heard
Ventricle (LV)
• 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
• 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
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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
• 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
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
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
• MRRadiates 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
EARLY DIASTOLIC MURMUR
Aortic Regurgitation
• High Pitched, Decrescendo Murmur
• Best heard at
• Left Sternal Boarder with the diaphram 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
• Follows Atrial Systole
• Implies Sinus Rhythm
• Can be present in MS or Complete Heart Block
• 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 MURMURSSYSTOLIC
• 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