Aortic stenosis definitions and phenyl

This is a tough topic and a valvular disease that may cause cardiogenic shock that is very difficult to manage. The last 10 patients I’ve had with severe to critical AS, led to high mortality and morbidity. They declined very rapidly and most were, unfortunately, unsalvageable with medical and interventional therapy.

I can’t find the ACC guidelines for grading severity of AS but here are the ESC criteria that I don’t think would differ that much:

They are defined by peak velocity in m/sec, mean gradient in mmHg, and AVA (aortic valve area in cm2) on TTE

Aortic sclerosis:

• <2.5 cm2
• normal gradients and AVA

Mild AS:

• 2.5–3 cm2
• mean grad <20mmHg
• AVA >1.5 cm2

Moderate AS

• 3–4 cm2 peak velocity
• mean grad 20–40mmHg
• AVA 1–1.5 cm2

Severe AS

• >4 cm2 peak velocity
• mean grad>40 mmHg
• AVA <1 cm2

I use AVA a lot but this is calculated on TTE using LVOT diameter (seen on PLAX), AV TVI (time velocity interval) using apical and PSAX and LVOT TVI. Any of these measurements can effect the calculated AVA.

There exists discordant grading of AS.

Oh I found the ACC criteria for grading which is a lot more involved/in-depth.

• Mild AS with Vmax of 2–3 m/s or mean grad of <20 mmHg
• Moderate AS with Vmax 3–4 m/s with mean grad of 20–40 mmHg
• Severe AS with Vmax>4 m/s or mean grad >40 mmHg *(AVA is not required to define severe AS in this way)
• Very Severe AS with Vmax >5 m/s or mean grad >60 mmHg (typically AVA <1 cm2 but not required)

There are also different staging of AS. Stage A is at risk. Stage B is progressive AS. Stage C is asymptomatic severe AS. Stage D is symptomatic severe AS. To touch upon stage D, these are where you have the sub classes.

Stage D1 — High gradient: severe AS with diastolic dysfunction

Stage D2 — Low flow low gradient: AVA <1 cm2 but with Vmax<4 m/s and mean grad<40 mmHg. Diastolic dysfunction with LVEF <50%. DBA echo stress test shows AVA<1 cm2 with vmax>4 m/s

Stage D3 — low gradient with normal flow or paradoxical low flow AS normal LVEF: AVA<1 cm2 with Vmax <4 m/s and mean grad <40 mmHg AND SVI (stroke volume index) < 35 ml/m2 (restrictive diastolic filling LVEF>50%).

• According to ACC and and study they mentioned, serum BNP is a marker for subclincal HF and LV decompensation and for 5- year risk of AS related events using hazard ratio of BNP>300.

The next question is how to manage cardiogenic shock in the setting of severe AS. What a clinician has to be aware of is what kind of AS: low flow gradient LF-LG AS or paradoxical low flow AS.

To re-iterate, LF-LG AS is defined as AVA <1 cm2 and Vmax <4 m/s or mean grad<40 mmHg with low EF. Paradoxical LF AS or PLF-LG AS is defined as AVA<1 cm2, indexed AVA <0.6 cm2/m2 with mean grad<40 mmHg and SVI < 35 mL/m2 and LVEF >50%.

Ok the initial question is a loaded one. First off, my pressor of choice is phenylephrine, a pure alpha agonist that causes vasoconstriction without the beta adrenergic effects like you get with norepi or epi. I cannot find any RCT or thorough study that tests the mortality or morbidity with patients in cardiogenic shock from severe AS and the usage of neo vs other vasopressors. Most of the “articles” are from EM and anesthesia blogs. But the answer does make sense. If you have severe AS, your LV is already working against a fixed afterload. The LV cannot push blood through the valve any better than the valve allows. So if you have a hypotension patient, it seems like phenyl is a good choice because the vasoconstriction shouldn’t hurt the patient more with afterload because they already have a high afterload. What you get is almost like a IABP sort of effect of coronary and diastolic perfusion. But hmmm is there away to correlate SVR with Vmax? How do you know when your increased SVR > is more than the AV resistance? Theoretically maybe this is when you cap your neo. I don’t know. My echo skills aren’t that good. Maybe its the systemic diastolic pressure that you can utilize as your “gradient” past the aortic valve. If your BP is 90/50 perhaps neo is no good now. Not sure.

Someone with LF-LG with a low LVEF maybe benefit from norepi I guess because they need the contraction. Just need to treat them like any low cardiac output patient. The difficult is how to fix the gradient. That’s when a BAV I guess comes in. But back to my thoughts, most of the patients I’ve had with both paradoxical and regular LF AS were super sick and I don’t think the BAV we did worked because it didn’t change their mortality or morbidity. One of them ended up getting a LVAD.

Let me know what your thoughts are.

Dk