Atropine in the presence of an MI.

[NYMedic828]

So a small debate started over in the BLS section in one of the topics and I thought an ALS section thread couldn't hurt us.

In school we are taught atropine = faster heart-rate = more oxygen demand = bad for infarcting heart.

But at the same time, symptomatic bradycardia can commonly present in conjunction with an MI especially in a more diseased heart. (I have met people who weren't bright enough to perform a 12 lead prior to initiating their treatment, with atropine.)

Now of course we should not be giving atropine to a patient who is otherwise stable. One person stated in the other thread that they recently fired someone at his/her company because they gave atropine to a patient with an inferior wall MI as well as a sinus rate of 45, bp 95/50. Without seeing this patient ourselves, we don't know how stable or unstable they may be. A number is just a general guideline after all not a definitive level for all patients.

Anyway, if you are presented with a patient experiencing an MI as well as symptomatic bradycardia, should we be giving a trial of atropine? Is it truly that detrimental to them or might it potentially help them? Should we be moving right to more aggressive means like fluid boluses, vasopressors, pacing?

 

[Aidey]

Patient condition depending, I would prefer to go straight to pacing, probably after a fluid bolus.

Here is why.

I have no idea what response the patient is going to have to the atropine. I don't know how high it is going to push their heart rate, or how long the effects are going to last. Once the atropine wears off, I will have to give them more, creating a spike and crash effect.

With pacing I can control exactly how high the heart rate goes, and aim for a heart rate high enough to stabilize the patient without creating excessive workload on the heart. The patient is likely going to get paced in the hospital until they can get definitive treatment. I firmly believe that if you putz around too long waiting to pace it will decrease the chance of being able to successfully pace.

In the case of bradycardia in the presence of an AMI we have a pretty good idea of why the patient is bradycardic, and there are two definitive treatments, pacing and PCI. We know atropine isn't going to 'fix' the patient, so I think it is better to use a treatment that is going to provide the best 'fix' possible until the pt gets to surgery.

 

[Christopher]

In school we are taught atropine = faster heart-rate = more oxygen demand = bad for infarcting heart.

Pacing = faster heart-rate = more oxygen demand = wait... good for the heart?!

But you just said faster heart rates is bad for the heart

I don't think the atropine is bad because it increases myocardial oxygen demand argument holds any water. Neither does the literature:

Atropine has also been suggested to potentially worsen the ischemic situation in patients who are in the midst of an acute coronary ischemic event. Although we did not search for such a response in our retrospective survey, we did not uncover any instance in which acute coronary ischemia was intensified or aggravated. Acute Myocardial Infarction Complicated by Hemodynamically Unstable Bradyarrhythmia: Prehospital and ED Treatment with Atropine (PubMed)

This retrospective study even showed a clinically significant (albeit not statistically significant) trend towards the restoration of a normal sinus rhythm with atropine in AMI patients (40% AMI vs 18% non-AMI).

The only patients who had an adverse reaction with an AMI and atropine were those with wide complex 3AVB. I do believe that using atropine in the face of dueling atrial and ventricular pacemakers will increase dyssynchrony, which would definitely cause a problem.

Anyway, if you are presented with a patient experiencing an MI as well as symptomatic bradycardia, should we be giving a trial of atropine? Is it truly that detrimental to them or might it potentially help them? Should we be moving right to more aggressive means like fluid boluses, vasopressors, pacing?

I look at the utility of atropine as based on the likelihood of a vagal cause of the patient's bradyarrhythmia.

2AVB or 3AVB with a wide complex rhythm? Atropine isn't going to help as these are probably not vagally mediated bradyarrhythmias.

2AVB or 3AVB with a narrow complex rhythm in the face of an IWMI? Bezold-Jarisch reflex with a high vagal tone is a likely cause and is a prime candidate for fluid, antiemetics, and atropine! Get a demand pacer ready as the atropine is only a temporizing measure if the AVN problems are ischemic in nature.

Pacing, dope, epi, isuprel, atropine...none of these are substitutes for lytics and/or PCI in the face of a myocardial infarction. But we shouldn't forget about atropine because of a myth about myocardial oxygen demand.

 

[Christopher]

...there are two definitive treatments, pacing and PCI.

Most of the literature around transcutaneous pacing have not found it to be "better". Often, prehospital pacing is inappropriately deemed to have been successful when in fact only pseudo-capture or false-capture is present. We see a lot of that at the EMS 12-Lead Blog.

Pharmacologic means of fixing bradycardia are coming back into favor and have demonstrated near equal efficacy as far as studies have gone (PrePACE study comes to mind). Regardless, atropine/pacing/dopamine/whatever are all temporizing measures.

Thrombolytics and/or PCI are the definitive treatments for AMI.

 

[NYMedic828]

As a newer medic, I have only used atropine one time and we only did a 0.5mg trial does which quite honestly had no effect. Pacing and fluids was the answer in this particular case and it did end up being an MI, I do not recall the location of the infarction though.

My program mostly advocated that the 0.5mg trial of atropine was mostly in place as a potentially beneficial treatment while your partner is setting up to pace the patient.

Pacing = faster heart-rate = more oxygen demand = wait... good for the heart?!

But you just said faster heart rates is bad for the heart

I don't think the atropine is bad because it increases myocardial oxygen demand argument holds any water. Neither does the literature:

See, thats what I never understood. How can they advocate in various classes that increasing heart rate, hence increasing oxygen demand and overall workload is bad, when the current situation the heart is in is obviously not working. Sure a vessel may be compromised, but if the heart is ultimately failing why shouldn't we jump start the remaining healthy portion to compensate, if only for a little while.

Also, as you stated pacing obviously increases workload via heart rate.

Furthermore, as a last resort over here we have standing orders for dopamine drips up to 20mcg/kg. Talk about increasing the workload of the heart, though it is a last ditch effort.

2AVB or 3AVB with a narrow complex rhythm in the face of an IWMI? Bezold-Jarisch reflex with a high vagal tone is a likely cause and is a prime candidate for fluid, antiemetics, and atropine! Get a demand pacer ready as the atropine is only a temporizing measure if the AVN problems are ischemic in nature.

I can't say I am familiar with the Bezold-Jarisch reflex. I tried looking it up and didn't find a very definitive explanation. Would you happen to know any resources or care to briefly explain?

 

[Christopher]

As a newer medic, I have only used atropine one time and we only did a 0.5mg trial does which quite honestly had no effect. Pacing and fluids was the answer in this particular case and it did end up being an MI, I do not recall the location of the infarction though.

Inferior MI's with bradyarrhythmias (nb. those amenable to atropine administration) will respond about half the time to atropine. The other half are thought to be adenosine-mediated and some literature supports the administration of aminophylline (an adenosine antagonist) to reverse these.

Anterior MI's with bradycardia are usually due to hypovolemia and do not respond favorably to atropine. Those patients need pressors.

My program mostly advocated that the 0.5mg trial of atropine was mostly in place as a potentially beneficial treatment while your partner is setting up to pace the patient.

0.5mg increments are a good way to go.

See, thats what I never understood. How can they advocate in various classes that increasing heart rate, hence increasing oxygen demand and overall workload is bad, when the current situation the heart is in is obviously not working. Sure a vessel may be compromised, but if the heart is ultimately failing why shouldn't we jump start the remaining healthy portion to compensate, if only for a little while.

Also, as you stated pacing obviously increases workload via heart rate.

Furthermore, as a last resort over here we have standing orders for dopamine drips up to 20mcg/kg. Talk about increasing the workload of the heart, though it is a last ditch effort.

I was in the same boat you were...I accepted it at first, but after talking with some of the cardiologists and reading the literature it seemed I was simply mistaken in my "knowledge" that atropine was bad.

I can't say I am familiar with the Bezold-Jarisch reflex. I tried looking it up and didn't find a very definitive explanation. Would you happen to know any resources or care to briefly explain?

Sure, it is basically a high vagal tone resulting in bradycardia and hypotension. It is most often seen post-lysis/PCI, but similar effects are seen pre-lysis/PCI. The studies on the cardiodepressor effects of the BJR are mostly from CCU's, and they've shown it responds well to positioning, fluids, and atropine.

It may be a bit of a misnomer on my part to attribute high vagal tone in IWMI to the BJR, but it is certainly one of the better studied causes of the parasympathetic response.

 

[Shishkabob]

Risk vs reward.


Sure, if an MI is the cause of the bradycardia, increasing oxygen demand isn't the best of ideas, but if the bradycardia is causing AMS, SOB, CP and other things due to a crappy BP, you need to fix the rate. If their BP is 60/30, altered mental status, with a rate of 30, you bet your butt I'm going think about making that heart beat faster. Some of their heart producing a good BP is better than the whole heart not producing a good BP.

Just like a patient with stroke like symptoms, who has a history of strokes and diabetes. Just because the BGL is 40 doesn't mean they aren't having a stroke too, and fixing the low BGL with D50(25/10/etc) can end up making things worse. But you still have to go for it.


My partner and I were talking last night and have come to a conclusion: Sometimes we in EMS are just put in to a no-win situation where all choices suck. You just have to pick what you think is best for the patient at that time.

 

[RocketMedic]

A question- would it be appropriate to put a timeframe to atropine administration? Something along the lines of "symptoms times x hours= atropine initial bradycardia control measure, vs symptoms times y hours contraindicate atropine?

I was thinking that "severely" ischemic hearts might be excluded this way, but as y'all pointed out, it seems that the overall patient mentation and presentation is the most important thing.

 

[systemet]

In school we are taught atropine = faster heart-rate = more oxygen demand = bad for infarcting heart.

The first part of this is true. The major determinants of cardiac oxygen demand are wall tension, contractility and heart rate. The second part, i.e. whether atropine is "bad" per se, is a little more difficult.

But at the same time, symptomatic bradycardia can commonly present in conjunction with an MI especially in a more diseased heart.

Or they can have acute SA or AV nodal dysfunction due to ischemia from the MI.

Anyway, if you are presented with a patient experiencing an MI as well as symptomatic bradycardia, should we be giving a trial of atropine?

Probably not, under most circumstances, because the bradycardia may be protective, and by increasing heart rate we increase oxygen demand.

[This is similar to the justification for giving nitroglycerin, we reduce preload, thus reducing the wall tension and demand].

But, there's also the issue that the coronary perfusion pressure = MAP - RAP, and if you have no blood pressure, your coronary perfusion will decrease. So there's a point at which it may be necessary to increase the heart rate to preserve arterial pressure and oxygen supply.

Is it truly that detrimental to them or might it potentially help them?

This is a judgment call based on their presentation, how timely reperfusion therapy can be provided (which should be the primary focus), and how hypotensive they are.

Should we be moving right to more aggressive means like fluid boluses, vasopressors, pacing?

For an RVI, fluid boluses are a good idea to optimise preload. We may be able to increase cardiac output through filling the right atrium better. If the preload is borderline low, increasing the rate isn't going to help, because the stroke volume is already poor, and is going to get worse.

I don't personally see pressors as being a better option to atropine. More likely to work in some circumstances, e.g. infranodal AV block. But they are going to increase afterload, which will increase heart rate. And, as said earlier, many of the patients with bradycardia are RVIs (SA node is supplied by the right coronary distribution in 90% of people). These people probably will benefit more from increased preload than from chronotropy.

 

[Doczilla]

The small boluses are not only good from a preload standpoint, but they also activate stretch receptors in the ventricles that will increase heart rate.

It's a slippery slope using atropine--- but severe bradycadria might cause global ischemia, which is much worse than exascerbating a local infarction. But that's where you'll see injury patterns without a clear guess as to where it is, because its everywhere.

You might actually see severe bradycadria with a-fib in these cases, its pretty trippy when you do see it, but it does happen. But that's where cardiologists make their money.

First dose of atropine rarely works for me, usually when I get over 1mg total do I see results. If the dose of atropine too low, there might be a paradoxical vagal response which further supresses the SA node.

 

[18G]

Atropine was originally intended to be used in MI according to Dr. Cory Slovis. At the JEMS conference this topic was talked about and it is perfectly okay to use atropine in the setting of MI.

 

[Doczilla]

That's really interesting. When you think about it, you're bot directly stimulating the heart with atropine. You're just removing inhibitory signals from the vagus nerve. It's restoring automacity.

That's not bad compared to going the B-1 route, where you Jack up cellular metabolism right along with the heart rate. I think it goes without saying that this might spread an infarction; but like I mentioned before global ischemia from bad CO is worse.

 

[TatuICU]

Often, prehospital pacing is inappropriately deemed to have been successful when in fact only pseudo-capture or false-capture is present. We see a lot of that at the EMS 12-Lead Blog.
.

How is that? Are people not checking pulses while pacing or just not being taught about refractory periods

 

[abckidsmom]

That's really interesting. When you think about it, you're bot directly stimulating the heart with atropine. You're just removing inhibitory signals from the vagus nerve. It's restoring automacity.

That's not bad compared to going the B-1 route, where you Jack up cellular metabolism right along with the heart rate. I think it goes without saying that this might spread an infarction; but like I mentioned before global ischemia from bad CO is worse.

For this reason, I use atropine when there is a vagal problem. I learned this lesson clearly when we had a burn patient who would brady down whenever we turned him to change his bed. We would premedicate him for turns with a mg of atropine. The first couple of times he was very vigorous in his attempts to stop his heart beating.

 

[Christopher]

How is that? Are people not checking pulses while pacing or just not being taught about refractory periods

A lot of the time they see pacer artifact and it looks a lot like a QRS complex, coupled with an increase in mentation and pulse rate.

Usually they're just getting coordinated electroshock therapy at that point.

 

[NYMedic828]

It takes a real special individual to not realize they have matching electrical and mechanical capture...

If you can't check a pulse while looking at the monitor you should be stripped of your certification and sent back to elementary school.

 

[Christopher]

It takes a real special individual to not realize they have matching electrical and mechanical capture...

If you can't check a pulse while looking at the monitor you should be stripped of your certification and sent back to elementary school.

It is usually not that simple, from the archives of the EMS 12-Lead Blog:

At this point, the paramedic reported radial pulses that corresponded to the pacer and an improved level of consciousness. The rate was changed from 60 to 70 PPM.

Those phantom QRS complexes look pretty convincing. Especially when you get pseudo-fusion of a real complex and a paced complex!

 

[NYMedic828]

It is usually not that simple, from the archives of the EMS 12-Lead Blog:

Those phantom QRS complexes look pretty convincing. Especially when you get pseudo-fusion of a real complex and a paced complex!

Good read, thanks for that.

But essentially it is still saying the fault lies on the provider not properly assessing pulse rate.

Unless I misinterpreted something, the article states that in one particular case a paramedic had what he thought to be capture on the monitor at 70bpm but the pulse-oximeter only read 40. Had he had true capture, the pulse-oximeter should be nearly identical to the electrical rate. This would imply that the medic did not properly assess for true mechanical capture.

If the monitor reads 60bpm and I feel 60bpm, either the patient returned to a normal rhythm or I do in fact have capture.

One thing the article mentioned which is certainly true is that we may think we feel a pulse mentally just by looking at a pacer spike. Easy way to combat this is to feel a pulse without looking at the monitor at first and if you have 1 beat every second or more, than you are at 60-70bpm, then you can match it with the monitor to be completely certain the rhythm is coming from you and not the patient.

 

[TatuICU]

Good read, thanks for that.

But essentially it is still saying the fault lies on the provider not properly assessing pulse rate.

Unless I misinterpreted something, the article states that in one particular case a paramedic had what he thought to be capture on the monitor at 70bpm but the pulse-oximeter only read 40. Had he had true capture, the pulse-oximeter should be nearly identical to the electrical rate. This would imply that the medic did not properly assess for true mechanical capture.

If the monitor reads 60bpm and I feel 60bpm, either the patient returned to a normal rhythm or I do in fact have capture.

One thing the article mentioned which is certainly true is that we may think we feel a pulse mentally just by looking at a pacer spike. Easy way to combat this is to feel a pulse without looking at the monitor at first and if you have 1 beat every second or more, than you are at 60-70bpm, then you can match it with the monitor to be completely certain the rhythm is coming from you and not the patient.

HAd a nurse in a unit one time decide to mentally check a pt's pulse for some time after he had been complaining of SOB, feeling of impending doom, etc s/p craniotomy. Screen said sinus at 82 and then he went from that to asystole. She printed all the EKG paper off to show us all how she did an awesome job and started CPR immediately after the family complained that she didn't "do enough to help him while he was struggling". What she forgot was that there was an art line waveform underneath the EKG on the paper that looked like this _____________________________________
for about 4 minutes prior to him going asystole. oops

 

[Doczilla]

On the plus side, asystole is the most stable rhythm.