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Cardiology > Aortic Stenosis > Flashcards

Aortic Stenosis Flashcards

1
Q

What are causes of aortic stenosis?

A

Degenerative = ‘senile’

Bicuspid

Rheumatic (least common often coincides with mitral disease)

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2
Q

What is the most common AS?

A

Calcific Aortic Stenosis (aka senile)

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3
Q

What is Calcific Aortic Stenosis?

A

‘wear and tear’ on normal valve –> fibrosis / calcification of valve leaflets –> stenosis

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4
Q

What are risk factors for senile AS?

A

hypertension, high cholesterol

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5
Q

T or F: it is common for people to end with a bicuspid aortic valve

A

T

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6
Q

What usually is the case in bicuspid aortic valve?

A

usually from congenital fusion of 2 aortic leaflets (usually right and left cusps)

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7
Q

What happens in rheumatic aortic stenosis?

A

fusion of the commissures, some calcification / fibrosis of leaflets (much like mitral valve damage)

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8
Q

What happens to the heart in AS?

A
  • Need markedly –> LV pressures to drive blood flow across stenotic AV
  • Very high pressure gradient from LV to Aorta
  • LV under pressure overload–> CONCENTRIC hypertrophy
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9
Q

What is the benefit of concentric hypertrophy?

A

concentric LVH –> ↓LV radius R + increased LV thickness t

Counterbalances the high LV pressure
so allows LV to empty without increased wall tension (ie. aferload)
= (LVP x R)
/t

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10
Q

What are disadvantages of concentric hypertrophy?

A

increased muscle stiffness –> so increased LAP to ‘drive’ blood into LV (esp. at end-diastole)

increased muscle means more blood supply required

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11
Q

Why does LAP increase in AS?

A

LV less compliant (= increased stiffness)

	- LV pressure rises faster with increased filling
	- reduced LV filling rate 
	- increased LA pressure at end-diastole
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12
Q

Why is atrial kick more important in AS?

A

normally atrial kick only provides <15% LV filling –> >25% with AS

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13
Q

What is end-stage AS?

A

very high LVP (extreme gradients across AV)
–> very high LV wall tension = afterload
–> decreased LV systolic function (eventually)
–> LV unable to empty fully
–> LV starts to enlarge = dilate
–> decompensation
dilation is a very ominous sign in AS, usually associated with heart failure signs

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14
Q

What mediates myofibril thickening?

A

cytokine release

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15
Q

What mediates dilation of heart?

A

fibrosis / apoptosis / MMP activation

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16
Q

T or F: the course of AS is long and asymptomatic

A

T

17
Q

T or F: symptomatic AS is associated with malignancy and poor prognosis

A

T

18
Q

What are symptoms of AS?

A 
S = Syncope
A = Angina
D = Dyspnea
19
Q

Why does syncope happen in AS?

A

Exercise –> body demands an increased cardiac output + decreased vascular resistance

normally, LV able to increase cardiac output

with AS, no major increase output –> reduced BP –> reduced brain perfusion –> SYNCOPE

Reminder: BP = Cardiac output x vascular resistance

20
Q

What can cause syncope in AS?

A

Any stimulus that tends to decrease vascular resistance or decrease LV filling can cause syncope in AS:
Exercise
BP drugs
Severe dehydration / bleeding

21
Q

What does the coronary blood flow depend on?

A

depends on Pressure driving blood from Aorta to inner layer of LV myocardium
Coronary Perfusion Pressure = Aortic P - LV P

Since AP and LVP are the same in systole, coronary flow happens in diastole

22
Q

What is angina a result of?

A

brought on by lack of O2 in cardiac tissue (myocardial ischemia)

23
Q

Why does angina occur in AS?

A

AS –> decreased aortic pressure –> decreased perfusion pressure
AS –> increased LV diastolic pressure bc of myocardium thickening) –> decreased perfusion pressure
AS often associated with coronary disease (coronary blockages)

24
Q

How does dyspnea happen in AS?

A

–> high LV diastolic pressures eventually can lead to:
- high LA pressures
- elevated pulmonary pressures
–> dyspnea
If LV begins to decompensate,
- very high LV diastolic pressures
- very high LA pressures (esp. if Afib)
–> overt HEART FAILURE

25
Q

What symptoms in AS predict prognosis?

A

Angina –> 5 years
Syncope –> 3 years
Heart failure –> 2 years
Atrial fib. –> 0.5 years

Based on 50% mortality

26
Q

What would you find on a phys exam for AS?

A

Vital Signs:
BP usually normal, maybe ↓pulse pressure
HR normal (unless Afib)

Inspection:
LVH [ie. concentric) –> apex usually still in normal position, (unless LV decompensates & dilates –> displaced apex)

27
Q

What is a classic sign of AS?

A

Carotid Pulse [NOT pulse pressure]:

‘low and slow’ pulse (because of low volume going through aorta –> low pressure and slow flow)

28
Q

What would be found palpating the precordium?

A

AS & LVH –> increased LV ejection time
–> sustained apical impulse
(apical impulse lasts > 1/2 of systole)
apex usually normal size and location
may be a palpable S4 or palpable AS murmur (thrill)
when LV fails and dilates –> diffuse, displaced apex

29
Q

What heart sounds will be heard in AS?

A

Aortic part of S2 (A2) may decrease intensity, or even disappear
A2 comes later, even after P2 (pulmonic S2)
= Paradoxical splitting of S2
Atrial kick filling sound can appear = S4

(if LV dilates / fails, very high LAP –> early diastolic filling sound = S3)

30
Q

T or F: there is a murmur in AS

A

True, crescendo-decrescendo, peaks later as AS becomes more severe

31
Q

Where is the murmur loudest in AS?

A

loudest over aortic area (R. upper sternal border)

32
Q

What would you see on ECG for AS?

A

LVH signs common (+/- LA enlargement)

LVH
≥ QRS amplitude (voltage criteria; i.e., tall R-waves in LV leads, deep S-waves in RV leads)

LAH
Notched P wave in limb leads
Terminal P negativity in lead V1

33
Q

What would you see on CXR for AS?

A

not conducted

34
Q

What would you see on cath for AS?

A

can measure both LV and Ao pressures –> estimate severity of AS (can’t get across some tight AS valves)

AV area now usually only done by echo, can be done by cath to resolve discrepant test results

necessary to evaluate coronary artery disease before considering surgery (unless very young)

35
Q

T or F: there are drug to treat AS

A

F

36
Q

How to prevent AS?

A
  1. NO LONGER Antibiotics before dental work (NO endocarditis prophylaxis)
  2. Maintain good dental hygiene ( reducing risk infective endocarditis)
  3. Careful follow-up of asymptomatic patients with AS, counseling about 3 main symptoms
  4. Avoid extreme exertion (to avoid SYNCOPE)
37
Q

What is only surgical option for AS?

A

Only definitive treatment for AS is VALVE REPLACEMENT (tissue or metal valve)

even bad LV’s usually improve after surgery –> IF A.S. WAS THE MAIN CAUSE FOR LV DYSFUNCTION

Good long-term results

Cardiology (29 decks)

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