Bradycardic STEMI

Esme12, ASN, BSN, RN · Sep 13, 2016

It is good to learn which coronary arteries supply which area of the heart and the symptoms that accompany each MI.

THINK about your cardiac anatomy and what an interruption of the blood flow means to that area of the heart.

[TABLE]

[TR]

[TD]Wall[/TD]

[TD] Artery Lead[/TD]

[TD] Reciprocal Wall[/TD]

[TD] Reciprocal Leads[/TD]

[/TR]

[TR]

[TD] Inferior

[/TD]

[TD] RCA II, III, aVF[/TD]

[TD] Lateral[/TD]

[TD] I, aVL[/TD]

[/TR]

[TR]

[TD] Anterior[/TD]

[TD] LAD V3, V4[/TD]

[TD] Inferior[/TD]

[TD] II, III, aVF[/TD]

[/TR]

[TR]

[TD] Lateral[/TD]

[TD] Cx I, aVL, V5, V6[/TD]

[TD] Inferior[/TD]

[TD] II, III, aVF[/TD]

[/TR]

[/TABLE]

Cowboyardee · Sep 13, 2016

A moderate fluid bolus followed by dobutamine gtt and transvenous pacing while waiting on cath lab. Avoid larger fluid challenges, as a hyperdilated RV will cause septal "bowing" or ballooning into LV, reducing overall cardiac output. Never seen this in ED, but iNO2 (inhaled nitric oxide) can really help lower PVR and reduce RV overload.

Take a second look at the BP. Dobutamine is dilates blood vessels (which is good for coronary arteries in an MI) but presents a double edged sword when it comes to cardiogenic shock. The BP is already dangerously low, and you don't want dobutamine making it any lower.

I would go with a dopamine gtt, pacing if that doesn't produce the desired response, and getting the pt into the cath lab ASAP.

If anyone has a strong argument for why you wouldn't use dopamine in this situation, I'm all ears.

Esme12, ASN, BSN, RN · Sep 13, 2016

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

Is this MD the only MD in the department? I would have gotten the other MD...if there was one.

As an experienced ED nurse I would treat this as a medical emergency. This patient is in immediate danger of coding.

Not knowing the whole scenario and patient history this is a code/critical situation. If the ST was elevated in the inferior leads we know that is the inferior part of the heart and the blood supply is the right coronary artery. What else do we know. In a majority of the population the SA node is supplied by the RCA. With the blood supply being affected bradycardia is the expected arrhythmia. The RCA supplies the Right ventricle. If the right ventricle isn't pumping effectively....the blood pressure will decrease. Another EKG needs to be done to look for a true posterior MI.

Activate the bradycardia ACLS algorithm

ACLS Bradycardia Algorithm

Lev, MSN, RN, NP · Sep 13, 2016

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

Fluids and pacing to start and see what that does...

With a right sided MI, you don't want to fluid overload them. If they don't respond to a liter then there is no need to keep pushing fluids.

They need the cath lab ASAP if this is a true STEMI case.

(What about TPA?)

Wile E Coyote, ASN, RN · Sep 14, 2016

Take a second look at the BP. Dobutamine is dilates blood vessels (which is good for coronary arteries in an MI) but presents a double edged sword when it comes to cardiogenic shock. The BP is already dangerously low, and you don't want dobutamine making it any lower.
I would go with a dopamine gtt, pacing if that doesn't produce the desired response, and getting the pt into the cath lab ASAP.
If anyone has a strong argument for why you wouldn't use dopamine in this situation, I'm all ears.

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.

KatieMI, BSN, MSN, RN · Sep 14, 2016

In this situation (unstable patient BECAUSE of low heart rate), the problem is NOT the AMI itself, but rather what it does (it effectively kills heart's command center, that is to say, and without it HR depends on Purkinje fibers with their inner rate of max 40 impulses/min, which is not enough to sustain coronary flow and global BP). Oxygen delivery, etc. will be easier to improve and manage as soon as the left ventricle actually contracts with acceptable rate and stroke volume. Coronary flow is from the uppermost part of aorta - if LV stays idle, there will not be any flow in them, and the myocardial ischemia will increase, inflammatory mediators will release, slow flow will potentially produce more thrombosis, etc.

The patient as he is, cannot go to the cath lab. All other things put aside for a sec, how you're going to see contrast flowing into coronary arteries if there is practically no flow in these arteries because the LV doesn't generate enough output to fill them in the first place? If nothing else, doing so will catastrophically increase ischemia (contrast carries no oxygen, and the life of the patient during the procedure actually depends on the speed with which contrast is flushed outta there by incoming blood).

Dobutamine is a good choice of pressor because of its powerful inotropic action while, due to his direct b1 stimulating action, it also has chronotropic and dromotropic effects (making those impulses which are still there more frequent and better running). Its classic side effect is tachycardia/tachyarrythmia, which is basically what we want to see instead of ventricular-generated heart rate. Dopamine is a preferred agent for hypotension with cardiogenic shock but in this particular case blood pressure is be low in the first place because of low contractility due to, that is to say, no work command for LV. Once such command is delivered, one way or another, the HR will rise and, hopefully, AD will follow - if patient would not come to full-blown cardiogenic shock at that point.

The patient needs to be put on external pacer as it only take a second to do, then taken out of ER and into cardiac ICU where he could be stabilized before any intervention might be performed. tPA really depends on how much time passed from the point of thrombosis (first symptoms) to the patient being seen. To tPA or not, to attempt PTCA or "acute" pacer, and what kind of it, is up to the physicians (hopefully, cardiologist, although ER docs as well as intensivists are trained in "dropping" transvenous pacers and "pacing" Swans through IJ. It is not much more than putting a central line in through the same access, way more manageable and way less painful for the poor soul, who probably cannot be sedated due to low BP). From the nursing standpoint, patient should have external pads or LifeVest slapped on him and kept there and connected at all times (so that some genius of customer service would not remove it due to the need to give patient admission bed bath "as per policy" - I'd seen it done), and not being left even for a second without them on, ECG monitor on and a crash cart accessible. Not for atropine - as I wrote, it is probably won't work anyway, - but for possible PEA, VF or flat line arrest, and everything that follows. Also, it would be cool if some would ask family, if they are there, if the guy was taking a pill ending with "OL" (b-blocker) and, if so, when did it happen last time. If it still in the system, the heart may not react on anything at all save for pacer till the drug is washed out, and the half-life will be probably prolonged somewhat (due to some degree of renal/hepatic/enteric shutdown caused by hypotension). Any intensivist would love forever a nurse who would let him know that piece of H&P. And it would be cool as well if someone would watch for an order of b-blocker "as per policy" or "cardiology admission protocol" and take care to ask the doc to remove it.

Wile E Coyote, ASN, RN · Sep 14, 2016

. Also, it would be cool if some would ask family, if they are there, if the guy was taking a pill ending with "OL" (b-blocker) and, if so, when did it happen last time. If it still in the system, the heart may not react on anything at all save for pacer till the drug is washed out, and the half-life will be probably prolonged somewhat (due to some degree of renal/hepatic/enteric shutdown caused by hypotension). Any intensivist would love forever a nurse who would let him know that piece of H&P. And it would be cool as well if someone would watch for an order of b-blocker "as per policy" or "cardiology admission protocol" and take care to ask the doc to remove it.

In cases of chronic Beta-blockade, think of substituting Dobut or Dopa for a PDE inhibitor like Milrinone.

KatieMI, BSN, MSN, RN · Sep 14, 2016

In cases of chronic Beta-blockade, think of substituting Dobut or Dopa for a PDE inhibitor like Milrinone.

Oh, yeah. But someone still needs to ask about it. And I bet that the ER doctor who did not yelled "pacer and crash cart here now!" in the first place omitted that question as well

My forever nightmare: septic/overdialyzed/hypotensive for any other reason/etc., patient on Levophed/Dopamine/etc., dutifully given his due evening dose of metoprolol because it was still in EMR. And then I call intensivist to plead him to please for the love of God delete that order because whoever put it there is as elusive as a bigfoot. And then someone from QA comes with all godspeed because of patient with h/o CAD/AMI/etc. has no order for b-blocker and "we have strict policy about that".

:madface:

Wile E Coyote, ASN, RN · Sep 14, 2016

Oh, yeah. But someone still needs to ask about it. And I bet that the ER doctor who did not yelled "pacer and crash cart here now!" in the first place omitted that question as well
My forever nightmare: septic/overdialyzed/hypotensive for any other reason/etc., patient on Levophed/Dopamine/etc., dutifully given his due evening dose of metoprolol because it was still in EMR. And then I call intensivist to plead him to please for the love of God delete that order because whoever put it there is as elusive as a bigfoot. And then someone from QA comes with all godspeed because of patient with h/o CAD/AMI/etc. has no order for b-blocker and "we have strict policy about that".

Cold-turkey withdrawal of chronic beta blockers can be bad juju for a really sick patient. A better approach is continuing with a reduced dose. Yes, even when the Dobutamine or Dopamine gtts are running.

miamiheatrn, BSN · Sep 14, 2016

I work in a small ER just 16 beds so we only have a PA and an MD. This pt is still intubated in the ICU with cariogenic shock and low prognosis. Currently on levophed drip. Had this been a LV MI and pt was hypertensive could beta blockers/ ACE inhibitors been used along with ntg or morphine?

Lev, MSN, RN, NP · Sep 14, 2016

Take a second look at the BP. Dobutamine is dilates blood vessels (which is good for coronary arteries in an MI) but presents a double edged sword when it comes to cardiogenic shock. The BP is already dangerously low, and you don't want dobutamine making it any lower.
I would go with a dopamine gtt, pacing if that doesn't produce the desired response, and getting the pt into the cath lab ASAP.
If anyone has a strong argument for why you wouldn't use dopamine in this situation, I'm all ears.

I agree. Given this patient's BP dopamine or levophed is probably the better choice. Dobutamine decreases the SVR and can decrease the BP. Dopamine (at doses >10mcg/kg/hr) increases the SVR. In cardiogenic shock, SVR is increased to attempt to maintain BP.

Lev, MSN, RN, NP · Sep 14, 2016

I work in a small ER just 16 beds so we only have a PA and an MD. This pt is still intubated in the ICU with cariogenic shock and low prognosis. Currently on levophed drip. Had this been a LV MI and pt was hypertensive could beta blockers/ ACE inhibitors been used along with ntg or morphine?

Given the bradycardia, I don't think a beta blocker would be ok in this situation. If the patient was hypertensive and not bradycardic then a beta blocker would be a good choice because it would also decrease the myocardial oxygen consumption.

Typically, nitro/morphine is given first for the chest pain. See how BP responds and then if still hypertensive after nitro - move on to beta blocker. If patient responds to nitro, they may get a tridil drip which will decrease BP. We will also give fentanyl for pain. Sometimes the cardiologist is unsure if the patient needs to go to the cath lab stat and thinks they may be able to wait til the next morning. These cases are decided sometimes based on whether we can get the chest pain under control. Sometimes it takes a dose of fentanyl.