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BY:

Dr. Muhammad Alauddin Sarwar


(MBBS)
Sindh Government Qatar Hospital,
Karachi, Pakistan.
• Introduction.
• AS causes progressive
obstruction of the left ventricular
(LV) out flow tract.
• Normal aortic valve area is 3 -4
cm2 and is reduced to less then
one 1 cm2 in severe AS
 Types
1.Valvular ( most common).
2. Sub valvular ( below the valve).
3. Supra valvular ( above the valve).
 Etiology

1) Valvular has several causes including


congenital, rheumatic, bicuspid and age
related calcific degeneration.
2)Sub valvular AS is a congenital
condition in which a fibro muscular
membrane is present in the LVOT below the
aortic valve.
3)Supra valvular is uncommon it may
occur as part of a congenital syndrome such
as William’s syndrome.
 Patho physiology
Pressure over load : It causes
concentric LV hypertrophy.
Diastolic Dysfunction: Because of
LVH compliance of LV reduces
which reduces the early passive
filling of LV.
Supply Demand Mismatch:
increase demand b/c of LVH &
reduced supply b/c of AS.
Clinical Manifestation:
1. Angina.
2.Syncope.
3. Heart failure.
NOTE: AS patients wit Angina have 50% per
5 yrs survival rate.
AS patients wit syncope have 50% per
3 yrs survival rate.
AS patients wit HF have 50% per 2 yrs
survival rate.
 Physical Findings:
1. Diminished and delayed carotid
upstroke.( pulsus parvus et
tardus)
2. Non displaced, diffused and
sustained apical impulse.
3. Systolic ejection murmur at
upper right sternal border
radiating to the neck.
 Diagnostic Testing:
1. ECG: showed LVH.
2. X-Ray Chest: May be normal or
become boot shaped b/c of LVH.
3. Echocardiography: It is the
method of choice to Diagnose,
to determine the cause and to
assess the severity of AS.
4. Cardiac catheterization: only for
those patients who are older
than 50 yrs or having angina or
patients with significant risks
factors for CAD.
Therapy
B)MEDICAL:
Alone medical therapy is
ineffective for AS.
Antibiotic prophylaxis for Infective
Endocarditits must be given to all.
Medical therapy for associated
CAD or HF may be needed.
B) Percutaneous aortic balloon valvoplasty
(PABV)
Safe & effective for pediatric patients
with congenital non calcific AS, But in adults
it is not an effective long term therapy.
C) Surgical Therapy:
AVR is the surgical treatment of choice.
It is preferred over repair.
Surgical options: include
1. Ross Procedure: Pulmonary valve
autograft. Best suited for pediatric and
adolescent patients.
2. Bioprostheses: Porcine heterografts and
bovine pericardial prostheses. Mostly for
patients older than 60 yrs.
3. Mechanical Valves: Most commonly used
are St.Jude, Medtronic-Hall and
CarboMedics prostheses. All need
anticoagulation therapy after wards.
INTRODUCTION
◦ Back or retrograde blood flow
through incompetent aortic valve.
◦ Can be divided into
a) Chronic AR and
b)Acute AR.
ETIOLOGY
Chronic AR: The most common causes of
leaflet and aortic root abnormalities that
lead to the AR.are

Leaflet Abnormalities Aortic root or Ascending


aorta Abnormalities
Rheumatic fever Age-related aortic
Infective endocarditis dilatation.
Trauma Annuloaortic ectasia.
Leaflet Abnormalities Aortic root or Ascending
aorta Abnormalities
Bicuspid aortic valve Cystic medial necrosis
Myxomatous of the aorta.
degeneration HTN
Congenital aortic Aortitis ( Syphilis etc)
degeneration Reiter syndrome
SLE Behcet syndrome
Rheumatoid arthritis Psoriatic arthritis
2) Acute AR: its causes are

Leaflet Abnormalities Aortic root or Ascending


aorta Abnormalities
Traumatic rupture Acute aortic dissection
Ac.infective endocarditis Perivalvular leak or
Acute prosthetic valve dehiscence of prosthetic
dysfunction valves.
Post aortic balloon
valvoplasty.
PATHOPHYSIOLOGY
2) Chronic AR:
AR increase end diastolic volume
increase in wall tensionLVH after
certain time progressive interstitial fibrosis
occurs decrease in LV compliance
dilated heart & decreased cardiac out put.
2) Acute AR:
◦ It’s a hemodynamic emergency.
◦ LV does not have sufficient time to
adopt to rapid increase in LV
volume.
◦ Effective cardiac out put fall
acutely, potentially resulting in
hypotension and cardiogenic shock.
Clinical Presentation
2) Chronic AR:
Asymptomatic for a long time.
After LV dysfunction develops
patient gradually develop
exertional dyspnea, orthopnea
& PND, Angina my be there as
well.
1) Acute AR:
Sudden hemodynamic
deterioration.
weakness, altered mental
status severe shortness of
breath or syncope.
PHYSICAL FINDINGS
2) Chronic AR:
a) Peripheral Pulse Examination:

Physical Sign Description


Water-hammer Rapid upstroke followed by
pulse. quick collapse.
DeMusset’s Head bob with each heart beat
sign
Physical Sign Description

Traube’s sign Pistol shot sound heard over the


femoral arteries in both systole &
diastole.
Muller’s sign Systolic pulsation of the uvula.
Duroziez’s sign Systolic murmur over the femoral
artery when compressed
proximally and diastolic murmur
when compressed distally.
Physical Sign Description
Quincke’s sign Capillary pulsation visible in the
lunula of the nail bed
Hill’s sign Popliteal cuff systolic pressure
exceeding brachial cuff systolic
pressure by > 60 mmHg.
Becker’s sign Arterial pulsation visible in the
retinal arteries and pupils.
b) Auscultation:
S1 may be diminished, S2 may be
soft, S4 is often present.
Blowing Diastolic murmur at left
upper sternal border best heard
when patient sitting or leaning
forward.
A second diastolic murmur may
be present at the apex in severe
AR. The Austin Flint murmur.
1) Acute AR:
Physical examination may be most
notable for signs of hemodynamic
compromise, such as Hypotension,
tachycardia, pallor, cyanosis, diaphoresis,
cool extremities & pulmonary congestion.
a) Peripheral Pulse pressure may be
normal or slightly widened.
b) Heart sounds: S1 may be
diminished, P2 loud due to PH, S3 is
often there as well.
c) Murmurs: early diastolic murmur ,
shorter and low in pitch. In severe
acute AR the murmur may not be audible.
DIAGNOSTIC TESTINGS
1) ECG:
In Chronic AR it shows LVH, Left
axis deviation and left atrial
abnormality.
In acute AR it is notable only for
nonspecific ST-T wave
abnormalities.
2) X-Ray Chest:
In chronic AR it may show
cardiomegaly, dilatation of the
aortic knob and root.
In acute AR chest radiograph is
notable for sign for pulmonary
congestion.
1) Echocardiography:
Different modes of echo cardiography are
now essential & method of choice for
evaluating the cause and severity of AR.
3) Cardiac catheterization:
All patients older than 50 yrs with severe
AR should undergo coronary angio. To
exclude any CAD.
THERAPY
B) Medical b) Percutaneous c)
Surgical
A) Medical Therapy:
a) Chronic AR:
1) Antibiotic Prophylaxis must be given.
2) Vasodilators, ACE inhibitors and
Calcium channel blockers form the
mainstay of pharmacological therapy of
chronic AR.
b) Acute AR:
The goal of medical therapy is
hemodynamic stabilization before
proceeding with surgical correction.

I/V vasodilators or I/V ionotropic support


may be needed.
A) Percutaneous Therapy:
Not really suitable for both chronic
moderate to severe and acute AR.
C) Surgical Therapy:
Aortic Valve Replacement (AVR) indicated
almost for all symptomatic AR patients.
Indication for AVR in asymptomatic
patients remain controversial.
alauddinsarwar@gmail.com
doctoralauddin@yahoo.co.in