treatment for the brady MI

[Ace844]

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.

In short, note that I wrote, these therepies under THINGS TO CONSIDER.... Menaing that I may not necessarily use this meds, and it would depend on what I 'see' clinically in an evolving situation.I think in a situation such as this so much depends on actaully being able to 'see' the patient in real time. That being said, I will say the following. B-Blockers although contraindicated in occult failure also have many properties which MAY be beneficial in this pateint. Also you should note that I used a multifacted approach. For example, a vasopressin drip in combination with another pressor in critical patients has shown to have the following beneficial effects. Up regualte vasopressing receptors in the periphery having the benefit of better glucose-sugar metabolisim in diabetics as well as increasing SVR. Next, it will also potentiate the effect of another differnt MOA pressor and augment it's effectiveness, as well as performing many other functions. So as I have mentioned previously many individual independently liscenced clinicians will often use meds which have undesirable side effect profiles in the long term for their short term benefits. A prime practice is some ED docs using Albuterol in acute presentation CHF-Dyspnia with lasix and other therepies. The evidence and efficacy is there, it is just more a matter of the individual clinicians comfort and knowledge as well as training and opinions on which therepies and the level of aggression they would use in a particular case with a particular pt's clinical presentation.

At the end of the day, if you sit down and think abit 'out side' the protocol box, there are many benefits and interventions which one could provide here with various end points of sucess. Still, I acknowledge not every provider is comfortable enough in their knowledge, skills, abilities, etc... to step up and 'take that chance'. Hence my aforementioned statements where if you obsserve emergent and acute care MD practice you will see this variation between theses indivuals practice preferences.

Out Here,

ACE844

[AZCEP]

And some of those points are very good ones, I would have a hard time justifying some of the suggestions in my own mind, but I'd probably be willing to give them a go after some significant time to consider them.

Thinking "outside the box" presumes that you have an intimate knowledge of what is inside said box.

I don't recall seeing it mentioned, but wouldn't CPAP also be beneficial to this patient? Just another thought to further muddy the field.

[Ace844]

And some of those points are very good ones, I would have a hard time justifying some of the suggestions in my own mind, but I'd probably be willing to give them a go after some significant time to consider them.

Thinking "outside the box" presumes that you have an intimate knowledge of what is inside said box.

I don't recall seeing it mentioned, but wouldn't CPAP also be beneficial to this patient? Just another thought to further muddy the field.

"Brother AZCEP,"

I brought alittle something for ya... I'm only on my 2nd cup so bear with me as my logic maybe alittle hazy here. I am quite comfortable with my abilityt to read and know the what the box contains, both inside and out. :wink: :shock: 8) The reason I didn't mention RSI, or CPAP-BIPaP, is that clinically this patient didn't warrant it with their spo2, and degree of distress noted. I do think that if at some point that the patient developed occult or worsening CHF these are definately among the additional modialities to consider. But without further information or a 'changing' accurate clinical picture being posted on these matters I think it's too early to say. The end point here is truely the cath lab and or CABG.

Out here,

ACE844

[Spock]

I think as long as the patient is ventilating adequately you should keep them doing so. Positive pressure ventilation would drop the BP even further because of the drugs used and increased intrathoacic pressure. I'm curious about the use of etomidate for sedation. This patient has no reserves left and 10mg of etomidate would put her out and you would need to tube her. I routinely use 10-12 mg of etomidate as a "stun dose" to tube patients in severe resp distress.

So many modalities to choose from but the most important one would be rapid transport to a facility with a cath lab because the patient needs reperfusion and probably a balloon pump.

Live long and prosper.

Spock

[Ace844]

I think as long as the patient is ventilating adequately you should keep them doing so. Positive pressure ventilation would drop the BP even further because of the drugs used and increased intrathoacic pressure. I'm curious about the use of etomidate for sedation. This patient has no reserves left and 10mg of etomidate would put her out and you would need to tube her. I routinely use 10-12 mg of etomidate as a "stun dose" to tube patients in severe resp distress.

So many modalities to choose from but the most important one would be rapid transport to a facility with a cath lab because the patient needs reperfusion and probably a balloon pump.

Live long and prosper.

Spock

"spock,"

Just curious where you got the thought that the patient has no reserves left? As for the etomidate it is being used 2nd to TCP, and to be augmented with fentanyl as needed. These 2 agents were chosen because of their cardio-resp protective properties...

Out Here,

ACE844

[Spock]

BP 80/40, junctional rate of 40 and room air sat of 80% suggest the patient is circling the drain and will arrest very soon without significant interventions. Hence my comment of no reserves left. Etomidate and fentanyl for this patient would result in intubation which may not be a bad thing. She was still awake so that was why I suggested medications prior to TCP. I realize AHA ACLS guidelines call for TCP in unstable bradycardia but sometimes you have to be more aggressive than ACLS. There are many ways to treat this patient all of which have been covered here. A good discussion overall.

Live long and prosper.

Spock

[Ace844]

Here's soemthing to add to this subject "Fiznat," which dove tails nicely with your scenario....

This should make for some interesting discussion at your clinical site.

HTH,

ACE844

(The American Journal of Emergency Medicine

Volume 24 @ Issue 4 , July 2006, Page 512

doi:10.1016/j.ajem.2005.12.001

Copyright © 2006 Elsevier Inc. All rights reserved.

Correspondence

Does aging influence quality of care for acute myocardial infarction in the prehospital setting?

Elderly patients with acute myocardial infarction

F.X. Duchateau MDa, , A. Ricard-Hibon MDa, M.L. Devaud MDa, A. Burnod MDa and J. Mantz MD, PhDa

aDepartment of Anaesthesiology and Intensive Care, Beaujon University Hospital, 92110 Clichy, France

Available online 17 June 2006.)

The primary goal of prehospital management in acute myocardial infarction (AMI) is to reduce the delay of reperfusion therapy. Quality of care of AMI is known to be lower for elderly patients, particularly because of disparities in the access to acute reperfusion therapy and the lower proportion of patients receiving adjunctive treatments [1] and [2]. A recent trial showed that this nonoptimal therapy for patients aged 80 years and older is already present in the ED [3]. The aim of this study was to evaluate whether our quality of care in elderly people with AMI was altered or not during the prehospital setting.

This prospective, observational study was conducted in our Emergency Medical Service department, covering an area of 290 172 inhabitants during a period of 3 years. The survey was part of the regional AMI registry, supported by the Regional Medical Board, which originates from the Ministry of Health. Mobile Intensive Care Units (MICU) are physician staffed (French EMS system SAMU), who provide on-scene diagnosis of AMI and initiate reperfusion therapies. Patients were enrolled by the physician of the MICU when diagnosis of AMI was established. Inclusion criteria for reperfusion strategy were the presence of a typical chest pain associated with ST elevation in 2 contiguous leads or a new left bundle branch blockade on the electrocardiogram. Reperfusion strategy consisted of prehospital thrombolysis or primary angioplasty. The following data were collected: demographic characteristics, reperfusion strategy, adjunctive treatment, and different time intervals. Results are reported as mean values ± SD and percentages. Statistical analysis was performed using an analysis of variance for quantitative data and a Yates-corrected χ2 test for qualitative data. A P value of less than .05 was considered the threshold for significance.

Of the 149 patients included, 18 (12 %) were aged 80 years or older. All patients aged less than 80 years had reperfusion therapy, whereas this was the case in 72% (n = 13) of patients aged 80 or older (P < .001). There was no significant difference in the proportion of patients receiving aspirin (95% vs 94%) or intravenous analgesics (60% vs 39%) in the 2 groups. For patients undergoing primary angioplasty, time from arrival of MCIU to hospital admission (64 ± 19 vs 67 ± 14 minutes), time from arrival of MCIU to arterial puncture (96 ± 49 vs 98 ± 26 minutes), and time from arrival of MICU to balloon inflation (105 ± 26 vs 106 ± 22 minutes) were similar in both groups (young vs elderly, respectively).

These results confirm and extend those of previous studies, which show that patients aged more than 80 years are proposed for reperfusion therapy less frequently than those aged less than 80 years. Possible explanations have been suggested: fear of increased risk of therapy-related side effects or therapeutic nihilism toward older patients [3]. Nevertheless, adjunctive therapies were not observed to be less used, and when a reperfusion therapy was decided, quick admission in catheter laboratory was not delayed.

References

[1] K. Barakat, P. Wilkinson and A. Deaner et al., How should age affect management of acute myocardial infarction?, Lancet 353 (1999), pp. 955–959. SummaryPlus | Full Text + Links | PDF (132 K)

[2] S.S. Rathore, R.H. Mehta and Y. Wang et al., Effects of age on the quality of care provided to older patients with acute myocardial infarction, Am J Med 114 (2003), pp. 307–315. SummaryPlus | Full Text + Links | PDF (91 K)

[3] D.J. Magid, F.A. Masoudi and D.R. Vinson et al., Older emergency department patients with acute myocardial infarction receive lower quality of care than younger patients, Ann Emerg Med 46 (2005), pp. 14–21. SummaryPlus | Full Text + Links | PDF (212 K)

[ukcanuck]

Have to admit this is the type of call that makes you think at two in the morning

Over this side of the pond we would give atropine, r/o contras for pre hospital thrombolysis, assess the effect of atropine and then give tenectaplase with heparin. I would be expecting some arrythmias and BP fluctuations with the TNK but most pts stay the way you found them with TNK.

I would also consider small doses of NS to help with pre load. Would also try legs up but would watch his breathing effort carefully.

NTG is contra'd several times and is not good for inferiors and our MD would want to have a one way and only he gets a cup of coffee type chat with you. I would titrate the morphine in due to BP.

I would disagree with TCP as even etomidate has some effect on BP at these low levels and even the most burnt paramedic does want to cause pain and suffering. Solve the MI and you should solve the brady and hypotension.

I think doing 12 leads for RVI and post MI are great but would you really want to be shifting this particular pt just to do a 12 to prove that he is having an MI. With the inf lead st elevation you can look for st depression in V1-3 with large r waves and the post is almost a cetainity. Statistically it is almost a dead certainty.

Really enjoyed watching this thread. Thanks [/font:1aa72e5e7f]

[AZCEP]

You bring some interesting points up.

NTG contraindicated for inferior wall MI? RVI sure, but careful administration with inferior wall MI might respond favorably.

No NTG, but okay to use Morphine? They will both have similar actions on the RVI. Morphine is easier to titrate, so you will have fewer negative effects, but you still have to be careful.

Prehospital fibrinolysis isn't widely used in the States, but for those that are able, it might be a good consideration. Depending on how long it will take to get this patient to a PCI facility.

Atropine would be a consideration, as mentioned previously, but I would shy away from it. The lower doses of Etomidate may very well reduce blood pressure, but if we can get the rate up with TCP, the situation resolves itself, right?

The right sided leads would be considered after treatment has begun, only as additional confirmation.

Good points, and glad to hear from someone not held to the same standards. These are the situations that we can all learn from.

[FL_Medic]

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?)

This has the huge possibility of being R sided failier caused by a R sided inferior MI. Nitrates are contraindicated in this type of MI simply because of the pressure.

Tx.- R sided 12-lead (which isn't done enough w/ inferior presentation) C-Pap/Bi-Pap would really help. Deffinatley did the right thing with the ASA. Now EPI and or Atropine would give you your rate and pressure but you gotta remember that you don't want to increase O2 demand because heart tissue is priceless. Maybe a slow dopamine drip and if your rales don't clear up a moderate dose of lasix. If you decide at this time to give NTG than make sure you have a thousand bag hanging with a nice gauge to get it through preferably in an AC. A fluid challenge is proven to be successfull in a rapid drop of the BP with a R-sided MI. Or skip the nitro and use morphine to decrease the O2 demand and afterload. Now a simple BLS measure like trendelenberg could be done as well to assist you in managing the BP. I think the rate will fix itself if you treat the pressure and rales.

The brady rythym could be occuring in response to a couple of things. This patient could very probably be in cardiogenic shock and it's decompansating. So if you fix your perfussion problems with the pressure the rate should come up. Or the pt. could have some serious heart tissue damage impeding electrical impulses which I doubt because of the narrow complex.

If the brady is still present I would sedate and pace. Reason being that this pt. is having an MI and any sympathomimetic or parasympathetilytic is going to make the heart work harder especially since we are allready doing that with the dopamine. Pacing will get your rate up if it hasn't gone up after the tx. of the pressure.