Aortic valve replacement

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Gross pathology of rheumatic heart disease: ao...
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As people get older, there’s a tendency for their valves to become calcified.  The calcifications cause narrowing of the main valve for blood flow out of the heart to the rest of the body.

We took care of a patient the other day that had a very, very stenotic aortic valve.  The transthoracic echo stated an ejection fraction of 10% with global hypokinesis and estimated aortic valve area of 0.6.  (I can’t remember the peak/mean of aortic valve gradient…with an EF10%, I’m not sure that it’ll be that impressive).  The cath report stated an aortic valve area of 0.3!  Additionally, systolic PA pressures were 50s-60s with a mean in the 40s.

That information alone is enough to be a scary anesthesia candidate!  On arrival to the OR, the patient was tough in just about every way (except his demeanor; he was a total sweetheart).  IV placement was difficult, arterial line was difficult (even with U/S).  Prior to induction we were finally able to obtain 18g PIV and 20g brachial a-line…with a little help of our friend midazolam.

Induction: 4mg midazolam worked in…  phenylephrine running at 40mcg/min peripherally prior to induction meds.  The patient’s poor EF was pretty evident based on his poor radial pulses and scarily low BP (90s/60s).  Prior to pushing the induction agents, I administered roughly 200mcg of phenylephrine (in 50mcg increments)… then 250 mcg fentanyl… then 10mg etomidate… then 250mcg fentanyl… then 10 mg etomidate.  Yes, small…slow… careful induction.  This was one of the times that I definitely wanted the surgeon in the room ready to go prior to induction.  The patient was rock-solid stable, despite my internal anxiety of what may have transpired if the induction had gone awry.  After the resident was able to easily mask the patient, I pushed 100mg of rocuronium.  He secured the ETT and I breathed a huge sigh of relief.  This was definitely my scariest induction – but with appropriate planning and setup, I was thrilled that everything occurred by the book.

By TEE, I calculated a AVA of 0.8 under anesthesia via planimetry and continuity equation.  I reported an annulus size of 27mm… the surgeon ended up going with a 25.  The LV was globally hypokinetic – it was just a poor functioning chamber.  It almost appeared as just a “quiver” of tissue.  (My thoughts for coming off CPB: “this guy needs squeeze – must grab epi!).  The RV appeared to be moving ok (not hypertrophic or dilated; mild hypokinesis; no tricuspid annular dilation) and PA looked okay (not dilated).  In retrospect, I probably should’ve used Bernoulli’s equation to calculate pressure gradient for the R heart.

Upon re-warming, I decided to start an epinephrine infusion.  This just made sense to me.  He needed as much beta activity to get his heart going!  Sure, we had dopamine, but I wanted him to FLY off CPB!  So, I started him on just baby epi to see how his heart would respond:  Epi 2mcg/min.  I think his heart was so happy that the obstruction (stenotic aortic valve) was opened he really took off and was able to generate the afterload for pressure.  Also, I was concerned about his pulmonary hypertension, which seemed to be attributed mainly to the decreased forward flow from the stenotic aortic valve causing left heart failure.  His pulmonary pressures decreased after the new valve was placed.  My main concern was to make sure he had the contractility (the squeeze) to maintain a decent forward flow (cardiac output).  I’m really glad we didnt’ go the IABP route.

Postop, the patient was doing well.  The surgeon had him on both dopamine and epinephrine (I’m still trying to figure out that one).  Post-op day #1, the patient was extubated and had been weaned off epinephrine, but was still on dopamine.  My guess is that the surgical team is more comfortable managing dopamine in the ICU.

Any thoughts?  What would you do differently?

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