This week I went to the ER. While there, things sped up and slowed down constantly, making for a very different pace than at the CCU. Every spare second, doctors were doing a ton of documentation and paperwork. It was most interesting to see the docs interview patients that had just been sent from triage. One woman was refusing further treatment and I acted as a witness.
Surgical VSD closure
I also got myself back into the OR for a pediatric CT procedure. This patient, age 18, had a congenital VSD, which is unusual since these are normally fixed early in life. The VSD was appreciated on TEE to be about 2.5cm, quite a large hole, at the base of his heart. There was also a piece of muscular tissue that had grown between the right side of his septum and his RV wall which was probably messing with hemodynamic flows out of his tricuspid and through his PA.
The most interesting part was the behavior of the ventricles after the surgery.
The VSD was causing a L to R shunt, causing oxygenated blood to return back to the right side of the heart.
You’d be tempted to think that the LV has been working harder to accommodate this inefficiency, but the contrary is actually true. The shunt acted like a pressure relief valve such that the LV never had to work very hard to contract. In other words, there’s a healthy EF (ejection fraction) with less work from the heart, but some percentage is leaking back across the heart. The patient has been able to live normally but did not exercise, which wasn’t a surprise. To my understanding, this is the same way a patient with mitral regurgitation would present, in which case the MV is the pressure release valve.
The RV on the other hand has been working exceptionally hard to push blood not only across the PA but also against the L to R shunt. There was also a low to mild grade tricuspid regurgitation which you might attribute to this extra RV function (in this case a healthy TV will function as a pressure release valve but only at abnormally high pressures).
After sealing the shunt, EF dropped from around 70% to around 25%, which implies a very weak LV. As the fellow said “the LV is squeezing and then it realizes ****, why is it so hard to pump now?” in case you needed another reiteration. Meanwhile the RV was strong. I don’t remember if the TR was gone, but it was more important to get the LV pumping harder. To encourage the LV to pump, the patient was given epinephrine and probably some dobutamine. His LV function improved but was still terrible. It’s weird to see (on TEE as always) an 18yo with the same LV as you’d find in an elderly patient pre CABG. His LV will probably make a full recovery with time. On the same note, his heart was unusually fatty for such a young patient.
The RV on the other hand has been working exceptionally hard to push blood not only across the PA but also against the L to R shunt. There was also a low to mild grade tricuspid regurgitation which you might attribute to this extra RV function (in this case a healthy TV will function as a pressure release valve but only at abnormally high pressures).
After sealing the shunt, EF dropped from around 70% to around 25%, which implies a very weak LV. As the fellow said “the LV is squeezing and then it realizes ****, why is it so hard to pump now?” in case you needed another reiteration. Meanwhile the RV was strong. I don’t remember if the TR was gone, but it was more important to get the LV pumping harder. To encourage the LV to pump, the patient was given epinephrine and probably some dobutamine. His LV function improved but was still terrible. It’s weird to see (on TEE as always) an 18yo with the same LV as you’d find in an elderly patient pre CABG. His LV will probably make a full recovery with time. On the same note, his heart was unusually fatty for such a young patient.
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