Atropine & Bradycardia

[NYCMedic]

What is the opinion of my fellow paramedics on this situation.

So, 45 year old patient. No medical history. No meds. No allergies. Chest pain started 45 minutes earlier while exercising at gym. Continued exercising. Went home and his wife gave him an over the counter nitro-type medication readily available in NYC and then called 911. Pain was a "tightness", 7 of 10, non-radiating, midsternal, constant pain. Reduced to a 3 after taking the medication. No change on palpation, exertion, inspiration. No cough. Denied muscle pull. Never had similar pain. Non-smoker. VS: 118 / 60, HR 48, RR 20, Pale (not normally pale per wife, less pale after taking medication), slightly moist, SaO2 98%. Lungs Clear. 3 Lead Sinus Brady at 48, 12 lead NSR neg ectopy.

Would you give atropine or not? I recognize and subscribe to the theory that atropine is generally for symptomatic bradycardic patients who are hypotensive or ams and that it increases oxygen demand. Would you consider this patient to be symptomatic based on the chest pain? It is an unstable dysrhythmia based on NYC REMSCO GOP guidelines.

Your thoughts?

 

[Shishkabob]

Double post

 

[Shishkabob]

I wouldn't have... Pt wasn't AMS, decent BP, and clear lung sounds, so that would guide me away from atropine. The guy was just at a gym, so does he work out normally? Granted I'm only 21, but my resting HR is 52 and my dad, at 56yo, is in the low 50's as well.


Pain semi-relieved by vasodilators guides me more towards stable angina, but sadly without a pre-dose 12lead it doesn't make our jobs any easier.


Then again I'm the new guy so I'll wait for the more experienced ones.




What's interesting is the adrenergic caused appearance and him being in pain, but the heart rate still being low.

 

[8jimi8]

What is the opinion of my fellow paramedics on this situation.

So, 45 year old patient. No medical history. No meds. No allergies. Chest pain started 45 minutes earlier while exercising at gym. Continued exercising. Went home and his wife gave him an over the counter nitro-type medication readily available in NYC and then called 911. Pain was a "tightness", 7 of 10, non-radiating, midsternal, constant pain. Reduced to a 3 after taking the medication. No change on palpation, exertion, inspiration. No cough. Denied muscle pull. Never had similar pain. Non-smoker. VS: 118 / 60, HR 48, RR 20, Pale (not normally pale per wife, less pale after taking medication), slightly moist, SaO2 98%. Lungs Clear. 3 Lead Sinus Brady at 48, 12 lead NSR neg ectopy.

Would you give atropine or not? I recognize and subscribe to the theory that atropine is generally for symptomatic bradycardic patients who are hypotensive or ams and that it increases oxygen demand. Would you consider this patient to be symptomatic based on the chest pain? It is an unstable dysrhythmia based on NYC REMSCO GOP guidelines.

Your thoughts?

What do you mean by the bolded statement?
I thought the chest pain was exertional?

I would consider the chest pain to be a symptom; however based on the patient's vitals i wouldn't necessarily give the atropine unless the patient's condition further deteriorated. Wouldn't you think that the atropine may increase his myocardial O2 demand?

 

[NYCMedic]

Atropine + Bradycardia

An interesting and legitimate perspective. The patient in question was not an athlete. Would ever so slight initial elevations of less than 1mm in contiguous leads change your perspective one way or the other?

More to be posted later...

 

[rhan101277]

I wouldn't give it. As posted earlier he appears not to be symptomatic now. People that exercise alot, runners, football players etc. usually have normally low heart rates. Their hearts usually have higher stroke volume than folks who don't exercise in a regular regimen.

 

[8jimi8]

An interesting and legitimate perspective. The patient in question was not an athlete. Would ever so slight initial elevations of less than 1mm in contiguous leads change your perspective one way or the other?

More to be posted later...

slight st elevations <1 mm would not change my treatment. If the patient was more symptomatic I would consider the atropine.

*** did you say you only had a 3lead? You didn't have any st depression or inverted t waves?

 

[bstone]

I'd only consider atropine for symptomatic bradycardia.

 

[MrBrown]

No.

 

[EMTinNEPA]

He still appears to be perfusing adequately based on the description you gave. As for the slight ST elevations <1mm, I wouldn't pay it much mind, but I would probably perform serial 12-leads if we had a long transport time. Especially since the 12-lead was negative and the pain was relieved with nitrates, I agree with Linuss in that I'm leaning towards stable angina. Did you by chance get a BGL? Meds, allergies, PMH? Any nausea/vomiting? Was there a positive Levine's sign? No ectopic foci whatsoever?

 

[mgr22]

ASA and NTG, watch the BP, consider a fluid bolus.

 

[Aidey]

Was the pain still going on when EMS showed up or did it go away after he stopped exercising?

 

[Akulahawk]

Atropine? I wouldn't likely administer it immediately. He's conscious, alert, oriented, and appears to have OK circulation. ASA, NTG (depending on what the OTC stuff was), 12-lead, IV TKO or SL. Perhaps check V4R. Consider PE and exercise induced asthma (though that usually clears after a few minutes of exercise). Regardless, I wouldn't consider the CP as "Stable Angina" as he's never had it before...

I'd want to have TCP readily available if it becomes apparent that his problems are rate/non-vagus related. I'd prefer to be able to control the rate and turn off the Tx instantly if something goes sideways. Can't do that with a med you just administered... Of course, our protocols here tell us to use atropine first...:wacko:

A case like this puts me into info gathering mode. If the guy's a non-athlete, a HR of 48 is a bit worrisome... What's the guys's baseline vitals, if known?

Now if I become convinced that at some point during exercise he manage to stimulate his vagus nerve and that's the primary cause of his bradycardia/CP symptoms then I'd consider the atropine to take the proverbial foot off the brake.

 

[Dominion]

Now if I become convinced that at some point during exercise he manage to stimulate his vagus nerve and that's the primary cause of his bradycardia/CP symptoms then I'd consider the atropine to take the proverbial foot off the brake.

Pretty much was thinking this as well. Additionally I would be hesitant to give the Atropine increasing an already annoyed heart. Patient is stable currently, why fix it if it's not broken. On the other side of that though I would get an IV, I would get out my drugs and setup for TCP. In doesn't hurt to be prepared. Serial 12-Leads if able (don't know about your roads but.....) as well I'd probably NTG, ASA, fluid available incase the nitro drops his pressure. I might even consider holding off on the nitro depending on what the OTC stuff was and transport times to consider.

Looking at other options like were mentioned before. PE, exercise asthma, any recent pains when breathing, etc.

For this patient I think your best course of action is to be prepared for the worse but to just perform a good complete history and exam with supportive care.

 

[Melbourne MICA]

Atropine

I subscribe to the idea of the relevance and importance of risk factors for heart disease so I tend to think this patient has a very suggestive story warranting intervention. Looking at the history you have given,

45yo male - puts him a high risk group for MI
Classical description of cardiac pain "tightness" occuring during strenuous exertion, then persisting despite rest with concurrent pallor and diaphoresis. (You excluded pleuritic/musculoskeletal issues) Partial symptomatic relief with a cardiac med - the nitro.

As for his HR and BP. Well despite logic about athletes and low HR's, apparently these CV vitals are insufficient to prevent the pallor and diaphoresis and pain.

PE may be a differential assessment except you haven't indicated any SOB and crappy SPO2's.

Way too many dots for me not to call this ischaemic pain and given his age, unless he has a strong family history of early onset IHD, I would lean towards an infarct.

So I would bolster all the cardivascular obs I can, get a 12lead ASAP and notify the receiving hospital.

Aspirin, IV, O2, rest, fluid, analgesia and yes Atropine.

As for hypotension + brady=Atropine - he's way better off with a better BP and increased HR (from the Atropine and fluid) than waiting till he's hypotensive, his pain increases and he becomes arrhythmic. Any signs of poor perfusion and a bradycardia combined with ischaemic description pain at rest for me at least, means its time to get off my hands and intervene.

Looks like, smells like, tastes like..........treat like.

MM

 

[Aidey]

^^^ The key word is "symptomatic". Chest pain qualifies, so this patient is a candidate for atropine.

The last person I gave atropine to had a pulse of 32, normal BP, no chest pain, and severe SOB. She said it felt like she had been running and couldn't catch her breath. 0.5mg of Atropine later she said she felt normal. The fire paramedic nearly had a stroke, but SOB is symptomatic. The doc was a little irritated until she actually saw the 3 lead with the HR of 32, after that she was fine with it.

 

[Akulahawk]

Don't get me wrong... I'd certainly want to make sure this guy's treated appropriately. Even if he's an athlete, at some point, the HR can become too slow. What *I* want to know is what his baseline is. If he's normally at 48-ish, then I'm not as worried about his HR than if he's normally around 60-80. If his normal baseline HR is a bit higher, I want to go down the path of correcting his rate problem first. That may relieve his CP issue...

Before deciding about which path to take with this guy, I'd want to know more about him and what his wife gave him to provide some relief. For instance, I don't want to give him some NTG if it will dangerously potentiate what he's already been given. The tx can also depend upon local protocols, equipment on hand, and what I'm authorized to provide at the time.

I may be directed, by protocol, to basically sit on my hands with this one... despite what I'd prefer to do.

 

[Melbourne MICA]

Perfusion

Don't get me wrong... I'd certainly want to make sure this guy's treated appropriately. Even if he's an athlete, at some point, the HR can become too slow. What *I* want to know is what his baseline is. If he's normally at 48-ish, then I'm not as worried about his HR than if he's normally around 60-80. If his normal baseline HR is a bit higher, I want to go down the path of correcting his rate problem first. That may relieve his CP issue...

Before deciding about which path to take with this guy, I'd want to know more about him and what his wife gave him to provide some relief. For instance, I don't want to give him some NTG if it will dangerously potentiate what he's already been given. The tx can also depend upon local protocols, equipment on hand, and what I'm authorized to provide at the time.

I may be directed, by protocol, to basically sit on my hands with this one... despite what I'd prefer to do.

We are all expected to follow protocol without a doubt or at the very least to consult a higher authority when moving laterally. But how can you really be sure what his "baseline" is and what relevance to today's event it has or doesn't have? At best information like this is speculative and of little value (if you'll forgive me for saying). It won't manifest a clearer decision pathway for you.

In this I think it's reasonable to draw an initial conclusion and treat. There is sufficient real time evidence (his obs) and sufficient background history and risk factors to produce a trend timeline with ominous overtones.

His overall perfusion state, not his HR in isolation is what matters. His history and symptomology simply provide the clues to implicate the particular system involved in this case the CVS - and heart specifically. His perfusion state provides the impetus to commence treatment - the treatment timeline if you like - and as I said, the history, risk factors symptoms etc guide us us onto which area to attack (or rather support).

In a nutshell he presents as "sick" and it looks like his heart is the problem. So work it.

And because the CVS is central to pretty much everything it is given much more weight in the balance of probabilities. We are much more likely to treat when the CVS is compromised than we might be if other systems are implicated.

So when you combine a relentless and catastrophic process like an MI with a primary system such as the CVS (heart) as its target, its a deadly combination. There is more potential or actual benefit in acting preventatively, that is preemptively (even when unconfirmed) than waiting to see what happens or to get more information.

You have far more dangerous drugs than atropine and few less dangerous events than MI - even if the eventual hospital diagnosis turns out to be something else altogether.

MM

 

[TomB]

^^^ The key word is "symptomatic". Chest pain qualifies, so this patient is a candidate for atropine.

There's a difference between "symptomatic" and "hemodynamically unstable". Chest pain by itself does not qualify (please do not read me the AHA algorithm). The issue is whether or not the chest pain is being caused or aggravated by the bradycardia. What if this patient was having an acute inferior STEMI? Does the mere fact that STEMI is typically accompanied by chest pain qualify the patient for atropine?

Tom

 

[jgmedic]

There's a difference between "symptomatic" and "hemodynamically unstable". Chest pain by itself does not qualify (please do not read me the AHA algorithm). The issue is whether or not the chest pain is being caused or aggravated by the bradycardia. What if this patient was having an acute inferior STEMI? Does the mere fact that STEMI is typically accompanied by chest pain qualify the patient for atropine?

Tom

Agreed, our protocols say "symptomatic" when they should read hemodynamically unstable. Per where I work, this pt would not qualify for atropine, however, if I had an instinct that this might be an MI, I would make base contact and consult with the doc.