Download Valvular Heart Disease - South Jersey Heart Group

Valvular Heart Disease
Jay L. Rubenstone, D.O., F.A.C.C
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Normal Structure
Mitral Valve
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Cross sectional Area 4-6cm²
Anterior and Posterior Leaflets
Chordae Tendineae  Papillary Muscles
Mitral Stenosis
Etiology & Pathology
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Rheumatic Fever- 99%
Other
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Congenital
Carcinoid
Lupus
Amyloid
Infective Endocarditis
Mucopolysaccharide Disease
Stenotic Pathology
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Etiology & Pathology
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Commissural
Cuspal
Chordal
Mixed
30%
15%
10%
Remaining
Valve becomes funnel shaped or “fish mouthed”
Thickened immobile leaflets or chordal structures
Stenotic Pathology
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Debate:
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Smoldering rheumatic process or
Constant blood flow trauma leading to valve fibrosis
and thickening
Pathophysiology
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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)
Pathophysiology
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Pulmonary HTN
–
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Passive Backward Transmission Of Incr. LA
pressure Pulmonary Arteriolar Constriction
Organic Obliterative Changes in Pulmonary
Vascular Bed RV Failure
History
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Exertional Dyspnea
Cough/Wheezing
Orthopnea/PND/CHF
Hemoptysis-Rupture of Pulmonary VeinBronchial Vein Shunts
History
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Chest Pain-Increase RV Pressures or
Unknown Etiology
Systemic Emboli (LA clots)
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Increased LA size, Decreased C.O., Atrial Fib, IE
Significantly decreased w/anticoagulation
Physical Exam
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Auscultation
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O.S.
Diastolic Rumble
Assoc Murmur of MR
Loud S1-thickened leaflets
Increased P2-pulmonary hypertension
Decreased B/P if C.O. decreased
Prominent a wave if sinus rhythm present
Physical Exam
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Mitral Facies-pink, purple facial patches due to
decrease CO and systemic vasoconstriction
Hepatomegally
Edema
Ascites
Hydrothorax With Right Heart Failure
Diagnosis
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ECG
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Left Atrial Abnormality
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P wave becomes bifid and greater than 0.12 sec in
duration in V1 and Lead II
RVH- right axis deviation
R wave > S wave in V1
Diagnosis
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Chest X-ray
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Echo- Cornerstone of Diagnosis
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Dilated LA, RA, RV
Elevated Left Main stem Bronchus
Interstitial Edema
Thickened Calcified Leaflets
Doming of Leaflets on Opening
Bernoulli equation
Diagnosis
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Cardiac Catherization
 Gorlin
14
Equation
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Natural History
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Asymptomatic for 15-20yrs following
Rheumatic Fever
Additional 5-10 yrs for progression from mild to
severe stenosis
Stenosis progression approximately .09 cm²/yr
Natural History
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Presurgical Survival Rates
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NYHA Class II 80%-10yrs
Class III 38%-10yrs, 62% 5yrs
Class IV 15%-5yrs
Management-Medical
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Endocarditis Prophylaxis
Activity Limitation
Diuretics- Decrease Na Intake
Heart Rate Control for A-fib or Sinus Rhythm
Anticoagulation
Percutaneous Balloon Angioplasty
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Moderate-Severe MS
Mild MS- if Pulmonary Artery Pressures or
Wedge Pressure Elevate with Exercise
Valve Replacement
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Indications
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Mortality
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Combined MS/MR
<1.5 cm²-NYHA III or IV
<1 cm²
Class II if Pulmonary Artery Pressure >70mmHg
3-8%
Valve Type-Prosthetic or Bioprosthetic
Mitral Regurgitation
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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
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Decreased Impedance to Ventricular Emptying
Determinants of Regurgitant Flow
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Instantaneous Size of MV Orifice
Dependent on Preload, After load, LV Contractility,
LV Size
LA-LV Pressure Gradient dependent on Systemic
Vascular Resistance, LV Pressure, & LV Size
Pathophysiology
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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
Pathophysiology
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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
Pathophysiology
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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
Right Heart Failure
Significant symptoms in chronic MR usually do
not develop until LV decompensation occurs.
History
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Medical Treatment Survival
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80% 5yr
60% 10yr
30-45% 5yr if MR severe
Diagnosis
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Physical Exam
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ECG
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LA abnormality
LVH
RVH
Chest X-ray
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Holosystolic Murmur
Increase Carotid Impulse
Increase LA, LV, RV, Interstitial Edema
Diagnosis
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Echo
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Transesophageal superior to transthoracic
Evaluation of Chamber Sizes, Regurgitant Jet,
Leaflets
Management of Acute MR
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Medical
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After load Reduction (Nitropresside & Intra aortic
balloon pump)
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Decrease impedance to LV ejection
Decrease regurgitant volume into left atrium
Inotropic Support (Dobutamine)-if LV function
reduced
Management of Acute MR
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Surgical Intervention
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Progressive LV Failure or Hemodynamic
Deterioration
CHF
Hypertension
Valve Disruption
Management of Chronic MR
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Medical
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Digoxin
Diuretics*
After load Reduction
Anticoagulation in A-fib
Endocarditis Prophylaxis
Management of Chronic MR
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Surgical
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Indications
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Asymptomatic Class I
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Severe MR Class II, III, or IV
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EF < 60% or LV Systolic Diameter >45mm
generally considered for surgery unless EF <30%
Valve Repair vs. Replacement
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
Mitral Valve Prolapse
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Over diagnosed
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2.4% of population
Females>Males 2:1
Severe MR- Elderly Male>Young Female
MVP Etiology
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Primary Valvular most frequent
Connective Tissue Diseases
Hyperthyroidism
Myotonic Dystrophy
Periarteritis Nodosa
Von Willebrands
MVP Pathology
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Myxomatous Proliferation and Degeneration of
Valve Leaflets
Increased Quantity of Acid
Mucopolysaccharide in Middle Layer of Valve
Tissue
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
Physical Examination
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Body type
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Auscultation
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Asthenic, low weight body habitus, straight back
syndrome
Systolic click- multiple, non-ejection (after carotid
upstroke) due to tensing of elongated chordae and
prolapsing valve
Physical Examination
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Auscultation
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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
Diagnosis
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ECG and Chest X-ray
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Echo
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Normally unremarkable
Billowing of one or both leaflets into the left atrium
during systole at least 2mm
Parasternal long axis view for diagnosis
Associated MR
Leaflet thickness
Natural History
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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)
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*
Aortic Valve
Normal Structure
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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
Aortic Stenosis Etiology and
Pathology
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Valvular
Supravalvular
Subvalvular
Hyperthrophic Cardiomyopathy
Congenital Aortic Stenosis
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Unicuspid
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Bicuspid
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Adult Presentation
Chronic turbulent flow
Leads to fibrosis, rigidity, calcification
Tricuspid
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Presents less than one year of age
Leaflets of unequal size
Acquired Aortic Stenosis
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Rheumatic
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Degenerative or Senile
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Rare
Usually mitral valve also involved
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
Is this atherosclerotic disease?
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Degenerative A.S. accelerated in diabetes and
hyperlipidemia.
Associated with tobacco use and HTN.
Potentially treated with HMGcoA agents?
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Hemodynamics
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Critical (Surgical) AS
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Moderate AS
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1-1.5cm²
Mild AS
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Peak systolic pressure gradient > 50mmHg in the
presence of normal cardiac output
Valve area <0.7-0.8cm²
1.5-2cm²
Aortic Sclerosis
History
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Long latent period of increasing obstruction
Symptoms usually begin in 5th or 6th decade
Angina in 2/3 of patients
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Hypertrophied myocardium
Increased ventricular systolic pressure
All of which increase myocardial oxygen
consumption
Oxygen supply-demand imbalance leads to
subendocardial ischemia
History
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Syncope
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Dyspnea (CHF)
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Reduced cerebral perfusion
Vasodilatation in the presence of fixed cardiac
output leads to hypotension
Baroreceptor-vasodepression due to high LV
systolic pressure
Particularly with exertion due to fixed cardiac output
Pulmonary Venous HTN can lead to CHF
Diagnosis
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Physical Examination
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Systolic Murmur
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Pulses Parvus
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Diamond-Shaped, harsh, left sternal boarder to right
intercostal spaces, neck and apex
Late peak, obliteration of S2, consistent with bedside Dx of
Critical AS
Delayed and Prolonged Carotid Impulse
Diagnosis
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ECG
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Chest X-ray
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Concentric LVH
Calcification of Aortic Valve
Echo
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Classic LVH
Bernoulli (continuity) equation-calculation of LVAortic pressure gradient and valve area
Diagnosis
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Cardiac Catherization
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Gorlin Equation
Natural History
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Asymptomatic latent period
With moderate-severe AS valve area can
decrease on average 0.12cm² per year
*Angina, syncope or CHF
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Average 1-3 year survival 50%
Sudden cardiac death rare
Medical Management
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Endocarditis Prophylaxis
Limit Physical Activity
Watch Beta Blockers and Diuretics
*Treatment of Critical AS in viable candidates
is surgery
Surgery (Valve Replacement)
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Indications
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Symptomatic Patients -valve area 0.7-0.8cm² or less
Asymptomatic Patients-progressive LV dysfunction
(EF <35%) or hypotensive response to mild
exercise
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Delaying surgery in asymptomatic patients with good
exercise tolerance is controversial
Surgery (Valve Replacement)
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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%
Aortic Regurgitation
Etiology and Pathology
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Valvular
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Rheumatic-Fibrotic Retraction of Leaflets
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Ankylosing Spondylitis, Behcets, 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
Appetite suppressant drugs-serotonin related valve
deposits
Etiology and Pathology
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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
History
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Acute AR
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Chronic AR
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LV cannot accommodate acute regurgitant volume
can lead to cardiovascular collapse
Gradual LV enlargement-eccentric hypertrophy
Exertional dyspnea, orthopnea, PND, CHF
Presents 4th or 5th Decade
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Physical Examination
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Diastolic Murmur
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Left sternal boarder
Decrescendo, high pitched
Best heard Sitting Up, End Expiration
Longer murmur equals worse AR
Physical Examination
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de Mussett’s Sign (head bobbing)
Corrigan’s Pulse “water hammer”
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Bisferiens-pulse
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Pistol shot sounds over femoral pulse
Duroziez’s Sign
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2 peaks
Traube’s Sign
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Abrupt Distention with Quick Collapse
Murmur over femoral pulse with compression
Physical Examination
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Quinckes Sign
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Muller’s Sign
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Systolic pulsations of uvula
Hill’s Sign
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Capillary pulsations
Popliteal pulse exceed brachial pulse by >
60mmHg
Physical Examination
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Korotkoff Sounds
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Can persist to 0mmHg
Wide Pulse pressure
Diagnosis
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ECG
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Chest X-ray
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Cardiomegaly predominantly inferior and leftward
Echo
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LVH
Can aid in detecting etiology, quantifying degree of
regurgitation, and assessing LV size and function
Cardiac Catheterization
Natural History
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Acute AR
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Chronic AR
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Cardiovascular collapse
Inotrophic agents and vasodilators
Prompt surgical intervention
75% Five Year Survival
50% Ten Year Survival
Progressive downhill course of CHF, Episodic
Pulmonary Edema, Sudden Cardiac Death
Medical Treatment
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Acute AR
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As above
Chronic AR
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Asymptomatic Mild-Moderate
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70
Follow by Echo Yearly
Endocarditis Prophylaxis for all AR
May not require medical treatment
Medical Treatment
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Symptomatic Moderate-Severe AR
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Limit exertional activity
Aggressively treat B/P
Diuretics
Salt Restriction
Digoxin
Vasodilators (Nifedipine?)
Surgical Treatment

Indications
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Defer surgery for chronic severe AR if good
exercise tolerance, EF greater than 50%, end
systolic diameter < 50 mmHg, and end diastolic
diameter < 70 mmHg
Be aware that progressive decline in LV function or
size increases surgical morbidity and mortality
Surgical Treatment

Mortality
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3-8% perioperative
5-10% late mortality with significant preop LV
dysfunction