Aortic stenosis

Question 1

What kind of hypertrophy occurs in AS?

Answer 1

Concentric LVH. Defined by thickening in a symmetric fashion without ventricular dilation. Advantage of this? Greater pressure without the increase in wall tension

Question 2

Patients with LVH have decreased O2 delivery. Why? And what makes them prone to ischemia during Anesthesia?

Answer 2

Because LVEDP is increased, which decreases coronary perfusion pressure (CPP=Diastolic aortic pressure-LVEDP). As AS worsens, Diastolic pressure worsens, making matters worse. Isovolumetric relaxation becomes inappropriately long, shortening filling period for diastole. For these reasons, these patients are prone to ischemia during Anesthesia

Question 3

Causes of AS?

Answer 3

Bicuspid
Calcified
Rheumatic

Question 4

Tell me about aortic valve area, peak transvalvukar velocity, and mean transvalvukar gradient as far as how it relates to AS.

Answer 4

Normal valve area: 2.5-3.5 cm
Valve area less than 1=severe
Peak velocity >4
Mean transvalvukar gradient >40=severe

Question 5

Why is it so important to maintain SR in AS?

Answer 5

Because, atrial kick ends up being 40-50% in people with AS. Kick is crucial because passive filling is decreased, owing to no compliant LV

Question 6

Treatment for SVT or Bradyarrythmias in AS?

Answer 6

Cardio version I unstable patients
Stable: Valhalla maneuvers
When underlying rhythm is identified, tx-amiodaronw (prefers for lower EFor CHF or when V tach can’t be ruled out)
Bradyarrhythmias: anticjolinergics, combined aloha or beta agonists, or AV pacing.

Question 7

What happens to left ventricular ESV in AS? What happens to SV? To afterload?

Answer 7

It increases. There’s an increase in afterload, a decrease in SV, and an increase in End systolic volume.

Question 8

What does AS do to the pressure volume loop?

Answer 8

It moves it up and to the right