treatment for the brady MI

[Spock]

A topic like this is one of the reasons why I visit the City! This has to be one of the most difficult patients to manage and there are many different approaches. If you suspect a right sided MI (which is probable here) you don't have to take the time to put more leads on. Take your left sided 12 lead and flip it over and read it from the back.

The patient is clearly unstable but is still alert enough that pacing would be painful so I would vote for drugs. Atropine is easy to give but is not precise. Dopamine at low dose may be more beneficial because at 2-5mcg/kg/min a common side effect is increased heart rate which is what this patient needs while also increasing the BP. The chest pain may have decreased with a higher coronary perfusion pressure. Frankly, I would use epi at low doses such as 4-8 mcg boluses but that is only because of my comfort level with epi after doing quite a few CABG's. Early and frequent command consult is mandatory as well as continuous assessment. Walking the tightrope with vasodilators and vasopressors is difficult without an arterial line because you need instant feedback.

A very good heart surgeon I know once said that dobutamine is a great vasopressor when you don't need one!

Live long and prosper.

Spock

[AZCEP]

This is a discussion that needs to happen more and more. Too many providers want to "square-peg, round-hole" this situation and it just won't work.

Increase perfusion pressure. How do we want to do this? Fluids, vasopressors, inotropes, all of the above?

Increase heart rate. Which route do we take? Electricity, anti-cholinergics, sympathomimetics, a combination of all of them.

Decrease myocardial workload. The options abound.

From what I've seen, the only treatments we agree on are oxygen and ASA. Even these have some differences as to how much we should use.

This is the stuff that class just doesn't prepare you for, and we probably should.

[Ace844]

"Fiznat,"

I have some questions but before I ask I am curious as to whether you would be able to answer them as they are HX P/E aand assessment clinical picture types of questions which would effect my Pharm and interventional management of this patient. Do you have that info available or are you aware of it?

Thanks,

ACE844

[fiznat]

"Fiznat,"

I have some questions but before I ask I am curious as to whether you would be able to answer them as they are HX P/E aand assessment clinical picture types of questions which would effect my Pharm and interventional management of this patient. Do you have that info available or are you aware of it?

Thanks,

ACE844

Well like I said I wasnt on the call, but ask away. My partner may have mentioned some details that I forgot to post. ...Even if I dont have the details, we could simply make them up so as to present an educational case study.

[Ace844]

Your patient:

78 y/o female at a skilled nursing facility (SNF) complaining of nausea, weakness, and 8-10 "chest pressure" radiating down the left arm. Tingling in the fingers, skin cool/pale/diaphoretic. Mental status is AOx4, but the nurses on scene say that the patient is "not acting like herself." Blood pressure is 80/40, resps 20, and on the monitor you see a junctional (narrow complex, retrograde P waves) in the low 40's. Pulse ox is 80% on room air, up to 90% with 15lpm o2 via NRB. In the lungs you can hear some light rales in the bases. A 12 lead ECG reveals huge ST elevations in the inferior leads.

I did not have this patient, but my partner did during my day off last week. We were talking about potential treatments for this presentation, and I wanted to hear what you guys think.

There is of course the obvious: IV/Monitor/O2, ASA 324mg PO, 12 lead, transport quickly. The NTG is contraindicated (twice) by the presentation, so what else should we do for this patient? I dont think that there is any question about whether this patient is unstable, so in my medic school sparkyness I suggested pacing. The idea was perhaps we can get a little more perfusion with a better rate, and even though I realise that this does nothing to solve the root of the problem (inferior MI), there is still the hope that we can promote some better perfusion with a quicker, better organised rate. My (paramedic) partner was worried about damaging the already weak heart with the electricity, or perhaps sending the patient into a worse rhythm. Whatcha think about that? What about other treatments (Dopamine? Epi? anything else?) Atropine was most definitely a consideration here, although in my classes I have been consistently told that the unstable patient should get electricity right away, not meds. Why shy away from pacing?

A right sided view was not performed. Truth be told, I cant think of ANY time where my medic partners have taken the time to do extra leads or extra views for a focused, diagnostic ECG. Not that the information wouldnt be valuable, it just seems like this either isnt in the average medic's daily skillset, or lazyness/time constraints get in the way. Another subject for another thread, perhaps. What about epi? Good alpha effect, beta 1 for the rate and pressure (chronotropic/inotropic), beta 2 for perhaps some more effective resps, while at the same time getting that dilation of the coronary arteries.

...Of course you cant have your cake and eat it too-- with epi you're increasing myocardial O2 demand so again you get the balacing act.

Naturally this is what protocols and on-line medical control are for, but still its nice to think about what we *could* do given the tools we have and the permission to use them.

Yes I did read your previous posts and I have some additional questions though.

1.) Does the patient have any Allergies, or did you become aware of any later?

2.) Does the patient take meds/if so which/were you able to find any at the residence-NH?

3.) Any signs of underlying cardiac disease, history, i.e.: body habitus, smoker, htn, substance abuse, etc..?

4.) What other ECG abnormalities were present, i.e.: axis? Other lead elevation, etc… If one had been done or WHEN it was finally done what were the results of the Right sided ECG?

5.) Does the patient have any other abnormal heart sounds besides a gallop?

6.) What about abnormal heart sounds presenting after pharm therepy

7.) Any other PMHX besides that mentioned?

8.) Any arterial/venous bruits noted anywhere during assessment?

9.) Patients loc/orientation/ Mental status?

10.) Does the patient have HJR ( Hepato-Jugular Reflux)?

11.) Does the patient have a + Kussmauls sign?

12.) Any signs of portal HTN/ Varicies?

13.) What was the patients body habitus?

14.) Any recent trauma?

15.) Any signs of etoh abuse/ hepatitis/renal failure

16.) Any caput medusa/spider angioma

17.) Any recent toxic exposures?

18.) Any other noted responses to previous treatments aforementioned?

19.) Any other historians/PHM paperwork present?

20.) Whats your scope of practice?

21.) How far the hosp?

22.) Pt’s Mental status during Tx and treatment as well as MS changes?

23.) Other clinical indicators of change or relief based on aforementioned RX?

24.) If you are going to expand this scenario what labs are available, and what are the values?

25.) What other precipitating history is available?

26.) What is the patients perfusion status and other respiratory P/E findings and complications relevant to this?

27.) Anything else to add?

Thanks,

ACE844

[fiznat]

And just as an FYI, there are medics in your service who have done right sided and even posterior 12-lead EKG's...myself included, but I'm not the only one.

Yeah Shane youre right, there probably are a few who are capable and actually do this for their patients-- I shouldnt speak so generally. Still you have to agree it is pretty rare to see, even in patients for whom it is indicated. Possibly it has to do with our transport times?

1.) Does the patient have any Allergies, or did you become aware of any later?

2.) Does the patient take meds/if so which/were you able to find any at the residence-NH?

3.) Any signs of underlying cardiac disease, history, i.e.: body habitus, smoker, htn, substance abuse, etc..?

4.) What other ECG abnormalities were present, i.e.: axis? Other lead elevation, etc… If one had been done or WHEN it was finally done what were the results of the Right sided ECG?

5.) Does the patient have any other abnormal heart sounds besides a gallop?

6.) What about abnormal heart sounds presenting after pharm therepy

7.) Any other PMHX besides that mentioned?

8.) Any arterial/venous bruits noted anywhere during assessment?

9.) Patients loc/orientation/ Mental status?

10.) Does the patient have HJR ( Hepato-Jugular Reflux)?

11.) Does the patient have a + Kussmauls sign?

12.) Any signs of portal HTN/ Varicies?

13.) What was the patients body habitus?

14.) Any recent trauma?

15.) Any signs of etoh abuse/ hepatitis/renal failure

16.) Any caput medusa/spider angioma

17.) Any recent toxic exposures?

18.) Any other noted responses to previous treatments aforementioned?

19.) Any other historians/PHM paperwork present?

20.) Whats your scope of practice?

21.) How far the hosp?

22.) Pt’s Mental status during Tx and treatment as well as MS changes?

23.) Other clinical indicators of change or relief based on aforementioned RX?

24.) If you are going to expand this scenario what labs are available, and what are the values?

25.) What other precipitating history is available?

26.) What is the patients perfusion status and other respiratory P/E findings and complications relevant to this?

27.) Anything else to add?

Thanks,

ACE844

LOL

alright, haha, I'll run with it:

1. Allergy to PCN

2. Pt takes ASA, an ACE inhibitor, Lasix 40mg, Digoxin, Colace, Ambien, and a MTV

3. hx of HTN and the pt is an ex-smoker (quit 10 yrs ago). There is also a family history ("my father died from a heart attack at age 56")

4. Inferior elevation is all you notice. (I'd like to be able to add more here but I dont have ACLS yet and my 12 lead knowledge is limited)

5. Negative on the abnormal heart sounds

6. Negative again on sounds s/p tx.

7. HTN, A-Fib, CHF

8. None noted, but possible that they are still there.

9. As mentioned, patient is AO to person/place/time/event, but SNF staff say the patient "isnt acting right."

10. Hepato-Jugular Reflux is a little silly to test for given the other S+S of right sided heart failure and the condition of your (unstable) patient, but you decide to to do it anyways cause you are an overachieving showoff and the result is negative. The patient has no JVD before/during/after the test.

11. You notice no JVD at any time, so also negative on the Kussmaul's sign

12. No s+s of any kind of GI dysfunction, the ABD is soft/nontender/no masses, and the patient has no hx of liver disease/failure. From what you see, portal HTN is negative

13. She is a thin, frail old woman.

14. No recent trauma known, no evidence of

15. No signs renal failure/ETOH/hep

16. No caput medusa/spider angioma. I had to look these up, and you already covered this in #12. It was an oppertunity to use an obscure medical term though, jood job.

17. No recent toxic exposures known, no evidence of

18. So far the patient has only recieved the O2 (to which her saturation increased to 90%, negaive MS changes) and the ASA (to which you see no change).

19. No elaborate histories available.

20. You are a paramedic with average protocals. Lets *try* not to get too fancy here, eh?

21. Hospital is just far enough for you to explore a decent amount of treatments. No scoop and run, no 3 hour transport times with crazy drips/med control orders.

22. No MS change so far

23. See #18

24. You ambulance is not equipped with a full lab. Not planning on expanding the scope unless you'd like to copy this thread into some OTHER forum.

25. See #3, #7

26. The patient is unstable in probable cardiogenic shock. The BP/RR/HR are noted. Pt is AOX4 but has a noted MS change by those who are familiar with her baseline.

27. I couldnt possibly

[Ace844]

"Fiznat,"

Ok, thanks for the answers and since we are keeping this at the 'basic general paramedic SOP,' than I would do the following.

Continue previous RX and meds. I agree with what most others would do here as mentioned and will also state this patient is a RX tight rope. Most probably there will be no correct answer.

Treatment:

Initiate a total 4 Large bore IV's with 2 KVO-saline loc'd with the intent for future use at the cath-CABG-hosp.

Since the failure is sub-clinical and it is unknown if this 'frail' 80 yo lady 'slightly wheezes' at baseline, I'm not going to aggressively treat the failure.

Further interventions:

Fluid bolus 250-500 incrementsand re-assess B/P and for signs of progressing failure. kepp the B/p at a clinically acceptable range fro MAP, MS, etc.. with fluids

80mg Lasix IV

4-6 mcgs/kg/min of Dopamine

since she's a 'little old lady,' analgesia-conscious sedation with Etomidate 10 mgs to start than increase as necessary

TCP with monitor, until capture is achieved

Vasopressin drip

when pressure gets to the point where 'protocol' allows titrate NTG drip to effect of keeping B/P, and anginal relief-MIO[sub:c98cde79ed]2[/sub:c98cde79ed] down

Dobutamine drip

Nor-epi drip

Things to consider:

(not sure if you would consider these ALS scope where you are)

Foley

LABS

ACE inhibitors

Plavix

Heprin

2b3a inhibitors

TPA-kinaises

milrone-BNP RX if necessary

Cathlab-cabg capable hosp

depending on HF situation and rate, etc.. may consider B-Blocker as well.

more to follow depending on clinical picture, etc..

out here,

ACE844

[Scaramedic]

I agree with what others have said, this is an excellent discussion. It's refreshing to see the understanding of the various aspects of an MI. Anterior, Inferior, 12 lead, 15 lead, these are all terms that we did not use in the field when I started out. We had 3 leads, 4 if you counted MCL1, and we spent most of our time on lead II. There wasn't a definitive way to know exactly where the MI was and treatment was straightforward, 02, NTG and MS. This thread shows just how far Paramedics and EMS have come in the treatment of AMI.

Thanks to everyone for such informative and well thought out posts.

Rid, you are THE MAN!! :notworthy: I think we should get CME credit for reading your posts.

Peace,

Marty

:joker:

[Just Plain Ruff]

Some useful links regarding AMI Inferior wall MI with extension to right ventricle.

http://heart.bmjjournals.com/cgi/content/abstract/49/4/368

http://content.onlinejacc.org/cgi/content/abstract/24/3/624

http://www.ncbi.nlm.nih.gov/entrez/query.f...p;dopt=Abstract

[AZCEP]

I'm going to disagree with some of Ace's treatment suggestions.

Low blood pressure, slow heart rate, wet lungs-->cardiogenic shock

Milrinone would not be indicated, because it has the potential of vasodilation, and increasing the myocardial workload. It works very well for the CHF patient with an acceptable pressure, but I would stay away from it for this one.

The glycoprotein 2b/3a inhibitors don't play a role in the early treatment of an STEMI. Following the cath lab, they might be considered, but not until then. Same with Plavix, although if there is an allergy to ASA, it would be the drug of choice. An ACE inhibitor isn't recommended for the emergency treatment of STEMI. Leave it for the cardiologist to deal with after we get her to the PCI facility. Tell me you were kidding about the beta blocker for this patient. If the heart rate and blood pressure can tolerate the drop in cardiac output, then fine, but I don't think this patient can. Lasix might be helpful, but again we are going to need to get the blood pressure up first. Dobutamine might make the heart rate increase, but it can also vasodilate, making the pressure worse. I would also be very hesitant to use Levophed, but it might be the only tool to increase rate, and pressure. The risk of expanding the MI is too big to be comfortable with.

I do agree with the Dopamine, TCP, using Etomidate as the sedative (no analgesic properties), Vasopressin drip (a little unusual to be able to use, but why not?), and the consideration of Tridil once the pressure comes up enough.

As I've said before, this is a great discussion topic.