Bradycardic STEMI

[miamiheatrn]

Had a pt like last night and the MD who just came off residency was very passive in the treatment to the point where the pts HR went from 50 to 40 to 30 and then into vfib. It was a complete disaster. We ended up treating the VFIB per acls protocol. But i think the pt would have had a better outcome had he not stalled for almost 10 minutes.

Now I ask you ER or experienced nurses, the pt's BP was 40/26 and HR 46, symptomatic and ekg confirmed a RV MI , how should this situation have been handled? Fluids? dopamine? atropine? levophed? These seem to the be the hardest MI's to treat

[Cowboyardee]

In isolated RV failure, the resultant septal shifting (ballooning I mentioned earlier) into the LV/LA is what causes the hypotension (LV outflow is obstructed). Dopamine can worsen this outflow obstruction, where Dobutamine does not. The variable reduction in MAP from Dobutamine would be more than overcome by the increased CO, Dobutamine's vasodilatory effects are also somewhat rate-dependent, so the 7-10 mcgs I would start on this pt would be closer to the point where the little alpha mediated vasoconstriction it has overshadows the vasodilation. The neat thing about the RV vs the LV, is that it's much thinner wall thickness allows for biphasic coronary artery perfusion vs the diastolic phase only perfusion in the LV. This helps to slightly negate the very high increased O2 demand that the Dobut is sure to cause. Again, unique to isolated RV failure.

If the increased HR from the pacer and little beta-1 from the Dobut along with the improved CO don't get the MAP> 60, and the cath lab team is still minutes out, consider adding a little Levo instead of using that as another means to justify Dopa.

Thanks for the explanation. You seem to know this situation pretty well. If you don't mind me picking your brain a bit, I have a few more questions:

You said that dopamine can worsen septal shifting in RV failure, while dobutamine does not. Is this directly because of dobutamine's tendency to lower SVR compared to dopamine or is some other mechanism at play?

Also, why do you suggest adding levo rather than dopa if pacing and dobut don't achieve a decent MAP? Just for more tightening of the vasculature? If so, any reason why levo is preferred over other pressors?

[Wile E Coyote, ASN, RN]

Thanks for the explanation. You seem to know this situation pretty well. If you don't mind me picking your brain a bit, I have a few more questions:

You said that dopamine can worsen septal shifting in RV failure, while dobutamine does not. Is this directly because of dobutamine's tendency to lower SVR compared to dopamine or is some other mechanism at play?

Also, why do you suggest adding levo rather than dopa if pacing and dobut don't achieve a decent MAP? Just for more tightening of the vasculature? If so, any reason why levo is preferred over other pressors?

Great guess. Yes, the increased afterload from the Dopamine further restricts LV emptying aka CO vs the mildly lowered SVR from Dobut which works WITH its inotropic effects to reduce the ballooned RV quickly. Since the loss of ventricular interdependence from RV infarction is so acute, and the 'fix' from dobutamine is likewise so acute, the effects on afterload from later on adding Levo to get MAP > 60 or 65 no longer are negative and are instead beneficial like we would normally expect. I avoid adding dopa since dopa plus dobut is more arrythmogenic than dobut plus Levo. Neo (phenylephrine) can worsen the bradycardia we just worked hard to reverse. Epi wont give the same inotropic oomph that Dobut will at doses low enoigh to avoid tachycardia and has the same effect on SVR that we wanted to avoid with dopa. Lastly, Epi stimulates production of lactate, which is no bueno in this super-sick pt. I again must emphasis that this is all specific to isolated RV infarction.