Aortic Regurgitation Flashcards
What causes aortic regurgitation?
Leaflet problems, or
aortic annulus = Root problems
What is primary AR caused by?
1° = LEAFLET PROBLEM (reduced / N / ↑ mobility):
leaflets ↓ mobile = scarred, thickened –> improper closing
leaflets normal mobility = perforated / eroded –> leakage
leaflets ↑mobile / flail (partly detached)
What causes secondary AR?
2° = AORTIC ROOT PROBLEMS:
support structures of leaflets abnormal = dilated aortic root –> pulls leaflets open
How can the Aortic valve become sclerotic/scarred?
‘wear & tear’ changes
rheumatic sclerosis
What happens in bicuspid aortic valve?
Leaflets fail to close / coapt well due to distorted cusps
T or F: perforations from endocarditis can lead to AR
T:
Perforation due to infective destruction
How does a flail aortic leaflet lead to AR?
Severe increase in leaflet mobility – severe failure of coaptation –> severe AR
How does a dilated aortic root lead to AR?
Severe dilation of valve support (root dilation)
- -> leaflets pulled apart
- -> leaflets can’t coapt
What structures are involved in aortic dilation occur?
annulus (fibrous skeleton) of aortic valve
ascending aorta –> loss of the ‘waist’ where sinus joins the tubular ascending aorta (sino-tubular junction)
What are causes of root dilation?
hypertension (chronic high pressures in root)
genetic defects –> weak fibrous tissue in aorta:
Marfan’s syndrome (think Abe Lincoln)
others (Ehlers-Danlos syndrome)
bicuspid aortic valve (‘annulo-aortic ectasia’) = weakening of root fibrous tissue, similar to Marfan’s, but not necessarily genetic, common in bicuspid aortic valves
syphilis infecting the aortic walls
What is acute AR?
no time for LV to dilate to accommodate volume load
LV non-compliant, can’t dilate–> very high LV diastolic P
very high LV diastolic P –> very high LA pressure –> high pulmonary P –> severe pulmonary edema / shock
may get early MV closure
What causes acute AR?
leaflet perforation:
endocarditis
leaflet flail / increased mobility:
trauma
endocarditis
aortic dissection
What happens to pressures in chronic AR?
LV has time to dilate to accommodate volume load
LV compliant –> slight increase LV diastolic P
Increased flow ejected needs increased LV systolic P –> pressure load
long-standing LV volume / pressure load –> slow decrease LV systolic function
long-standing LV volume & pressure load –> increased wall tension –> compensatory eccentric hypertrophy
Severe AR can have 80% back-leak!! –>
Still need to deliver normal cardiac output to tissues –> 5-fold ↑↑↑ cardiac output out of LV to maintain normal net cardiac output to tissues
What are symptoms of AR?
PALPITATIONS
ANGINA
DYSPNEA
Why is there palpitations in chronic AR?
common sensation of forceful heart beat
due to increased pulse volume and pulse pressure
Why is there angina in AR?
An increase in demand and decrease in supply
How is demand increased in AR?
AR –> increase in stroke volume
- -> LV systolic P
- -> O2 needs
AR –> LV size
- -> wall tension
- -> O2 needs
AR –> LVH
–> O2 needs
How is supply increased in AR?
AR –> drastic decrease in diastolic aortic root pressure –> reduced perfusion pressure
AR –> high LV diastolic pressure –> reduced perfusion pressure
often associated with increased age –> coronary disease (coronary blockages)
T or F: dyspnea is often a late symptom of chronic AR
T
How does dyspnea occur in chronic AR?
may reflect LV decompensation
- -> increased LV diastolic pressure - -> increased LAP - -> increased pulmonary venous Pressure - -> increased lung tissue edema / lung stiffness - -> DYSPNEA
What findings would one find in chronic AR with vitals?
Hypertension with wide pulse pressure
normal HR
What findings would one find in chronic AR with inspection?
visible pulsations (carotids, head bobbing, etc) apex volume loaded = diffuse / displaced apex usually hyperdynamic
What findings would one find in chronic AR with palpation?
wide pulse pressure –> ‘bounding’ pulses
apex diffuse / displaced / hyperdynamic
dilated aorta can cause parasternal lift / heave
rarely can feel aortic regurgitation murmur = ‘thrill’
What findings would one find in chronic AR with auscultation over heart?
S3 = sign of LV volume loading
S4 = sign of high end-diastolic LV pressure, atrial ‘kick’ emptying into LV
aortic outflow murmur (increased stroke volume) –> early to mid-peaking ‘diamond-shaped’
AR murmur = blowing, diastolic, decrescendo
AR may hit anterior mitral leaflet –> partially close the MV –> functional mitral stenosis
= Austin-Flint murmur
What findings would one find in chronic AR with auscultation over peripheral arteries?
wide pulse pressure –> high pulses –> ‘pistol shot’ = systolic flow sound over femoral arteries
can sometimes hear regurgitant flow going back towards heart inside the femoral arteries = Duroziez’s sign
What would you find on a ECG for chronic AR?
may show LVH
What would you find on a CXR for chronic AR?
enlarged LV
dilated aortic root
may show leaflet calcification
may show heart failure signs (late)
What would you find on a Echo for chronic AR?
can define leaflet and root anatomy
can assess severity of AR (+ other valve lesions)
can assess LV size, LVH, LV function
test of choice to assess suspected AR
What would you find on a cath for chronic AR?
can (crudely) define severity of AR
can assess LV function and pressures
only way to assess coronaries before surgery
How to prevent AR?
- NO Antibiotics before dental work (NO endocarditis prophylaxis)
- Maintain good dental hygiene (increased risk infective endocarditis)
- Careful follow-up of asymptomatic patients with AR, counselling about main symptoms
- Regular echo exams to assess for LV size & function
What is the medical therapy for AR?
Blood Pressure Drugs:
lower BP –> lowered aortic root diastolic pressure
–> lowered aortic regurgitation
especially vaso-dilating calcium channel blocker (Nifedipine) –> decreases the need for surgery
avoid drugs that decrease heart rate –> increase diastolic time for more leakage
Diuretics and nitrates:
may help alleviate heart failure symptoms from excessive LV volume loading
What should surgery be sought for AR?
Once significant symptoms (heart failure, angina) develop
When asymptomatic patients with progressive bad LV dilation or dysfunction should have surgery (before irreversible LV dysfunction occurs)
need to also fix co-existent coronary disease at time of operation
