Transcript Valvular heart disease aortic valve disease

Valvular heart disease
Aortic Valve Diseases
Dr. Hussam Al-Faleh
Med 341 course
Lecture outline
 General
principles :
 Pressure overload and volume overload
 Heart murmurs
 Aortic valve disease
 Mitral valve disease
VALVULAR STENOSIS
Pressure in upstream chamber IS HIGHER than
Pressure in downstream chamber during time of flow
(when valve is normally open).
Hemodynamic abnormality = "PRESSURE GRADIENT"
Upstream
Down stream
High pressure
low pressure
VALVULAR REGURGITATION
Retrograde flow of blood "upstream" during time when
valve is normally closed.
Hemodynamic abnormality = "VOLUME OVERLOAD"
Upstream
Volume overload
Down stream
Left Ventricular Hypertrophy
“Pressure and Volume overload”
Vena
Cava
RA
Pulm
Vein
LA
LV
RV
Pulm
Artery
Aorta
Aortic stenosis
Normal
RA
RA
LV
RV
LV
Vena
Cava
RA
Pulm
Vein
LA
LV
RV
Pulm
Artery
Aorta
Aortic
Insufficiency
Example: Aortic regurgitation
RA
RA
↑↑LV
RV
LV
AI
AS
Heart murmurs
 Produced
by turbulent blood flow
 Turbulence is mainly determined by
velocity of blood flow across a structure
 Timing of murmurs (either systolic, or
diastolic) can give helpful information
regarding the valve lesion
Common Murmurs and
Timing
Systolic Murmurs
 Aortic stenosis
 Mitral insufficiency
 Mitral valve prolapse
 Tricuspid insufficiency
Diastolic Murmurs
 Aortic insufficiency
 Mitral stenosis
S1
S2
S1
Outline for every valve lesion
 Etiology
 Pathphysiology
 Symptoms
and signs
 Natural history
 Investigations
 Management
Aortic stenosis
Etiology
 Supra-Valvular
 Valvular
- Congenital
- Acquired
Sub-Valvular
- Discreet
- Tubular
Etiology
 Valvular
Congenital
1. Uni-cusped - Rare
- Ages affected 2-30yrs
2. Bi-cusped - 2% of the population
- More common in males
- Associated with coarctation
in 6% of patients
- Ages affected 40-50yrs
Etiology

Acquired
1. Rheumatic
- Adhesion and fusion of valve commissures leads to
stiffening of the free borders as well as calcification
2. Degenerative (senile)
- Results from mechanical stress
- Associated with traditional risk factors for
CAD such as HTN, Dyslipidemia and smoking
A. Normal Trileaflet AV
B. Congenital AS
C. Rheumatic AS
D. Calcific AS
E. Degenerative AS
Pathphysiology
Symptoms
 Cardinal
symptoms:
1. Chest pain
- Occurs due to ↑ O2 demand
(LV hypertrophy) and ↓ O2 delivery
- Is often related to concomitant CAD.
2. Presyncope/Syncope
- Caused by transient ↓ cerebral blood flow
- May also be related transients VF or AF
3. Dyspnea
- Late manifestation of severe AS
Signs

Central Pulse :
- Slow rising , low volume ( Pulsus Parvus et tardus)
- Coarse systolic vibrations at Carotid artery (Carotid
Shudder)

JVP:
- Prominent a wave

Apex:
- Sustained
- Systolic thrill
- Displaced (late with LV failure)
Aortic pulse
Slow rising pulse
Signs ( Auscultation)
 S2
may be soft and single
 Paradoxical splitting of S2 in severe AS
S1
S2
Inspiration
Expiration
Signs (Auscultation)
 Aortic
ejection sound with Bicuspid AV
 S4
Ejection
S1 Click
S4 S1
S2
S2
Auscultation
S1
S2
Mild-Moderate
S1
S2
Severe
Natural history
Investigations
 ECG
- LAD
- LVH
Investigations

CXR
- Aortic Calcification
- Post stenotic dilation of Ascending Aorta

Echocardiography
- Routinely used to diagnose and estimate the severity of
AS
- Peak and mean gradients are measured
- Valve area is measured
Mild AS (area >1.5 cm2)
Moderate (area >1.0 to 1.5 cm2)
Severe (area <1.0 cm2)
Management
 No
place for medical therapy if severe AS
is associated with symptoms.
 Surgery is the treatment of choice.
 Generally speaking ,if the patient has
symptoms with severe AS Surgery is
indicated.
Aortic Regurgitation
Etiology
Etiology (chronic AR)
 Two major causes:
A. Intrinsic structural valve problem
1. Congenital : Bicuspid valve
2. Acquired : - Inflammatory (Rheumatic,
Connective tissue diseases)
- Infectious (IE)
- Degenerative
Etiology( chronic AR)
B. Abnormality of the Ascending Aorta
1. Congenital : Marfans disease
2. Infectious : Syphilis (15-25yr after infection)
3. Inflammatory : Connective tissue diseases
(RA, AS, GCA)
4. Idiopathic : progressive dilation (cystic medial
necrosis)
Etiology (Acute AR)
 Trauma
 Aortic
dissection
 Infective endocarditis
Aortic regurgitation
↓ effective Stroke volume
Excess volume to the LV
↑LV end diastolic pressure
↓ Myocardial O2 supply
Stretching of Myocardium
LV failure
↑ wall stress
Eccentric LV hypertrophy
(Ischemia)
↑ Myocardial O2 demand
(Ischemia)
Symptoms
 Gradual
development of Dyspnea ,
Orthopnea, and PND
 Angina
 Palpitations
 With Acute AR , abrupt development of
dyspnea.
Signs of Chronic AR
 Peripheral
signs
- De Musset sign (head movment with pulse)
- Water hammer pulse (abrupt distention and
quick collapse)
- Duroziez sign
- Muller’s sign (systolic pulsation of Uvula)
- Pistol shot/ Traube sign
- Quincke sign
- Hill’s sign (Popliteal pressure at least 20 mmHg
higher than brachial pressure
Signs of chronic AR
 Wide
pulse pressure
 Central pulse:
- Large volume pulse
- Bisferines pulse
- Corrigan pulse
 JVP may be normal or elevated
 Displaced and hyperdynamic apex
Auscultation
 S2
may be soft or accentuated
 S3 indicates severe AI
 Ejection click
 High pitched, blowing, decrescendo
diastolic murmur at LSB, best heard at
end-expiration & leaning forward
Auscultation
S1
S2
S1


Length of murmur correlates with severity.
In Acute AR diastolic murmur is low pitched and
short.
 Austin-Flint murmur indicates severity (mid to late
diastolic murmur)

Systolic murmur related to high flow state
Investigations
– LVH, LAD
 CXR- may show ↑cardiothoracic ratio, and
dilated aorta
 ECG
Investigations
 Angiography:
- Would aid in diagnosis and grading of
severity
 Echocardiography:
- The easiest and fastest way of diagnosing
and grading the severity of AR.
- Detection of the underlying mechanism of
AR.
Natural history
Asymptomatic
%/Y
Normal LV function (~good prognosis)
Progression to symptoms or LV dysfunction
Progression to asymptomatic LV dysfunction
Sudden death
<6
< 3.5
< 0.2
Abnormal LV function
Progression to cardiac symptoms
> 25
Symptomatic (Poor prognosis)
Mortality
> 10
Management
 Any
patient with severe AR and any of the
following should have aortic valve
replacement:
1. Symptomatic patients
2. Patients without symptoms, but with
LV systolic dysfunction (EF<50%), or
marked dilation of the LV.
Management
 Vasodilator
therapy ( ACE I, or CCB’s) for:
1. Patients not candidates for surgery
2. Short term to Improve hemodynamics
3. Treatment of hypertension