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VALVULAR

HEART DISEASE

Valvular Heart Disease


Structural and functional abnormalities of the
valves
Stenosis
Regurgitation
(insufficiency)

Prevents efficient blood flow through the heart

Heart Valves

AV valves:

Mitral valve
Tricuspid valve
OPEN during DIASTOLE
CLOSE during SYSTOLE

Semilunar valves

Aortic valve
Pulmonic valve
OPEN during SYSTOLE
CLOSE during DIASTOLE

Heart Valves
Normal Heart Sound
S1:
Caused by the closure of mitral valve and tricuspid
valve
the beginning of the systole

S2:
Caused by the closure of aortic valve and pulmonic
valve
the end of the diastole

Mitral Stenosis

Pathophysiology
normal 4-6 cm2
Mild MS- orifice <2 cm2
Elevated left A-V pressure gradient

Severe MS- <1 cm2


Increased LA Pressure
Increase Pulmonary Venous + Capillary
Pressures
Increase Pulmonary Artery Systolic Pressure

History
Exertional Dyspnea
Cough/Wheezing
Orthopnea/PND/CHF
Hemoptysis
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

Pulmonary infections
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auscultation
Rumbling apical diastolic murmur
After S2

ECG:
AF

Management
Problem/Symptom

Management

Prevention

Prevention of rheumatic fever


occurrence (Penicillin G)
against group A -hemolytic
Streptococci
Activity limitation
Oxygen

Dyspnea, Orthopnea
Pulmonary Congestion

Diuretics
Low Na diet
Nitrates

Atrial Fibrillation (RVR and


emboli)

CCB
Coumadin

Impaired contractility

Digoxin

Ineffective valve

Surgery (repair/replace)

Mitral Regurgitation

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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
Increased
Increased
Increased

End Diastolic Volume


Wall Tension
Preload
LV Emptying

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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 impairment
As ejection fraction decreases operative risk
increases.

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History
Fatigue
Exertional Dyspnea
Orthopnea
Palpitations
RHF
Auscultation:
High-pitched, apical systolic, blowing murmur
Between S1 and S2
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Diagnosis
Eletrocardiography
Mitral valve normal size = 4-5 cm2
Regurgitation: Displacement >2 cm2

ECG:
Atrial fibrillation
Left ventricular Hypertrophy

Management
Problem/Symptom

Management

Prevention

Prevention of rheumatic
fever occurrence (Penicillin
G) against group A hemolytic Streptococci
Oxygen

Dyspnea, Orthopnea
Pulmonary Congestion

Atrial Fibrillation (RVR and


emboli)
Impaired contractility

Diuretics
Low Na diet
Nitrates
CCB
Coumadin
Digoxin

Ineffective valve

Surgery (repair/replace)

Mitral Valve Prolapse


Systolic Click-Murmur Syndrome
Barlows Syndrome
Billowing Mitral Valve Syndrome
Floppy Valve Syndrome
Myxomatous Valve Syndrome
Parachute Valve

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MVP Etiology
Unknown
Connective Tissue Diseases

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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
Palpitations, lightheadedness, syncope
Arrhythmia-SVT, PACs, PVCs

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MVP Management
Infective endocarditis prophylaxis
Beta blockers
Mitral valve repair or replacement
Antiplatelet agents or anticoagulants

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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

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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
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subendocardial ischemia

Symptoms
Cardinal symptoms:
1. Chest pain
- Occurs due to O2 demand
(LV hypertrophy) and O2 delivery
- Is often related to concomitant CAD

2. Syncope
- Caused by transient cerebral blood flow
- May also be related transients VF or AF

3. Dyspnea
- Late manifestation of severe AS

Auscultation:
Harsh systolic crescendo=decrescendo murmur
Between S1 and S2

Diagnosis
Echocardiogram
Normal size >2 cm2
Mild stenosis
Size: 1.5-2 cm2
Mean gradient pressure: difference in pressure
between LV and aorta
Degree of
Mean Gradient Aortic Stenosis
Aortic Stenosis Pressure
Area
Mild
<25 mmHg
>1.5 cm2
Moderate
25-40 mmHg
>1.0-1.5 cm2
Severe
>40 mmHg
<1.0 cm2
Critical
>70 mmHg
<0.5 cm2

Management
Problem/Symptom
Prevention

Heart Failure symptoms

Atrial Fibrillation (RVR and


emboli)
Ineffective valve
Angina
If replacement surgery is not
possible

Management
Prevention of rheumatic fever
re occurrence (Penicillin G)
against group A -hemolytic
Streptococci
Diuretics
Low Na diet
Nitrates
CCB
Coumadin
Surgery (the only definitive
treatment)
MONA
Percutaneous balloon
valvuloplasty

Aortic Regurgitation

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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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Auscultation:
Blowing decrescendo diastolic murmur
Between S2 and S1

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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