Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardiology > Aortic Regurgitation > Flashcards

Aortic Regurgitation Flashcards

1
Q

What causes aortic regurgitation?

A

Leaflet problems, or

aortic annulus = Root problems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is primary AR caused by?

A

1° = LEAFLET PROBLEM (reduced / N / ↑ mobility):
leaflets ↓ mobile = scarred, thickened –> improper closing
leaflets normal mobility = perforated / eroded –> leakage
leaflets ↑mobile / flail (partly detached)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What causes secondary AR?

A

2° = AORTIC ROOT PROBLEMS:

support structures of leaflets abnormal = dilated aortic root –> pulls leaflets open

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How can the Aortic valve become sclerotic/scarred?

A

‘wear & tear’ changes

rheumatic sclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What happens in bicuspid aortic valve?

A

Leaflets fail to close / coapt well due to distorted cusps

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

T or F: perforations from endocarditis can lead to AR

A

T:

Perforation due to infective destruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How does a flail aortic leaflet lead to AR?

A

Severe increase in leaflet mobility – severe failure of coaptation –> severe AR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does a dilated aortic root lead to AR?

A

Severe dilation of valve support (root dilation)

  • -> leaflets pulled apart
  • -> leaflets can’t coapt
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What structures are involved in aortic dilation occur?

A

annulus (fibrous skeleton) of aortic valve

ascending aorta –> loss of the ‘waist’ where sinus joins the tubular ascending aorta (sino-tubular junction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are causes of root dilation?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is acute AR?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What causes acute AR?

A

leaflet perforation:
endocarditis

leaflet flail / increased mobility:
trauma
endocarditis
aortic dissection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What happens to pressures in chronic AR?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are symptoms of AR?

A

PALPITATIONS
ANGINA
DYSPNEA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why is there palpitations in chronic AR?

A

common sensation of forceful heart beat

due to increased pulse volume and pulse pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why is there angina in AR?

A

An increase in demand and decrease in supply

17
Q

How is demand increased in AR?

A

AR –> increase in stroke volume

  • -> LV systolic P
  • -> O2 needs

AR –> LV size

  • -> wall tension
  • -> O2 needs

AR –> LVH
–> O2 needs

18
Q

How is supply increased in AR?

A

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)

19
Q

T or F: dyspnea is often a late symptom of chronic AR

A

T

20
Q

How does dyspnea occur in chronic AR?

A

may reflect LV decompensation

	- -> increased LV diastolic pressure 
	- -> increased LAP 
	- -> increased pulmonary venous Pressure 
	- -> increased lung tissue edema  / lung stiffness - -> DYSPNEA
21
Q

What findings would one find in chronic AR with vitals?

A

Hypertension with wide pulse pressure

normal HR

22
Q

What findings would one find in chronic AR with inspection?

A 
visible pulsations (carotids, head bobbing, etc)
apex volume loaded = diffuse / displaced
apex usually hyperdynamic
23
Q

What findings would one find in chronic AR with palpation?

A

wide pulse pressure –> ‘bounding’ pulses
apex diffuse / displaced / hyperdynamic
dilated aorta can cause parasternal lift / heave
rarely can feel aortic regurgitation murmur = ‘thrill’

24
Q

What findings would one find in chronic AR with auscultation over heart?

A

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

25
Q

What findings would one find in chronic AR with auscultation over peripheral arteries?

A

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

26
Q

What would you find on a ECG for chronic AR?

A

may show LVH

27
Q

What would you find on a CXR for chronic AR?

A

enlarged LV
dilated aortic root
may show leaflet calcification
may show heart failure signs (late)

28
Q

What would you find on a Echo for chronic AR?

A

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

29
Q

What would you find on a cath for chronic AR?

A

can (crudely) define severity of AR
can assess LV function and pressures
only way to assess coronaries before surgery

30
Q

How to prevent AR?

A
  1. NO Antibiotics before dental work (NO endocarditis prophylaxis)
  2. Maintain good dental hygiene (increased risk infective endocarditis)
  3. Careful follow-up of asymptomatic patients with AR, counselling about main symptoms
  4. Regular echo exams to assess for LV size & function
31
Q

What is the medical therapy for AR?

A

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

32
Q

What should surgery be sought for AR?

A

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

Cardiology (29 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions