Chest Pain Case

[bakertaylor28]

You are dispatched to a residence for a 31 year old male with chest pain.


Upon arriving, your patient, whom reports no significant past medical history, presents with with complaints of acute upper abdominal heaviness and chest pain of 2 hours’ duration. He reports he was drinking that night at a bar with friends and drank approximately 500ml of vodka. He vomited later while at home. He appears able answer questions. He quantifies his pain as 5/10 in the upper abdominal and precordial regions, dull in nature and improved on forward posture. On further questioning, he related flu-like symptoms a week ago and for the last 2 days he had a sharp chest pain limiting his exertion. A dose of ibuprofen , taken 30 minutes prior to your arival, did alleviate some of his symptoms initially, but the quickly returned.


Initial vitals revealed:

BP of 134/96mmHg, PR 79/minute, respiratory rate of 20/minute with 93% SpO2 on room air.


ECG shows low voltage waves in all leads and P-R depression in lead II. Pupils are slightly dilated but equally reactive, and the Patient is Alert and oriented, though appearing slightly intoxicated. On secondary survey, you hear muffled heart sounds and notice slightly raised veins. Pulsus paradoxus of 18mmHg is also noted.You decide to place the patient on oxygen and have established IV access.

As you begin to prepare for transport, the patient develops 2nd Degree AVB block Type II, his pulse rate drops to 45, with respiration and SPO2 remaining relatively stable. Updated BP is 100 / 82.

What are your next steps in treating this patient?

 

[VentMonkey]

Place pads on him "just in case", low flow O2 @ 2 lpm N/C, grab a BGL (didn't see one above?), place a second lock in this patient.

Ask the patient about his normal alcohol consumption? How often. Work into a more detailed secondary, probably some prophylactic Zofran IVP.

Muffled heart tones and JVD along with pulsus paradoxus could be a working diagnosis of cardiac effusion--->R/O tamponade.

Any recent chest wall trauma? Perhaps an infection within this patients myocardium secondary to prolonged alcohol, and/ or drug abuse (does he use illicit drugs frequently?/ is he forth coming?)

Obviously he should be seen by a cardiologist so this is your transport destination. I am not upgrading unless he becomes an unstable and sustained high degree HB; all I got for now.

 

[bakertaylor28]

Place pads on him "just in case", low flow O2 @ 2 lpm N/C, grab a BGL (didn't see one above?), place a second lock in this patient.

Ask the patient about his normal alcohol consumption? How often. Work into a more detailed secondary, probably some prophylactic Zofran IVP.

Muffled heart tones and JVD along with pulsus paradoxus could be a working diagnosis of cardiac effusion--->R/O tamponade.

Any recent chest wall trauma? Perhaps an infection within this patients myocardium secondary to prolonged alcohol, and/ or drug abuse (does he use illicit drugs frequently?/ is he forth coming?)

Obviously he should be seen by a cardiologist so this is your transport destination. I am not upgrading unless he becomes an unstable and sustained high degree HB; all I got for now.

To clarify, the patient is forthcoming with answers to your questions, and reports that his Alcohol use is relatively normative (i.e. drinks but is not an alcoholic by any means), though he reports a history of the use of marijuana, though says he hasn't used it in the previous 6 months.

There is no Hx of recent trauma, and there is no acute trauma, either.

You get your BGL and it is normal, at 110 mg/dL.

 

[VentMonkey]

To clarify, the patient is forthcoming with answers to your questions, and reports that his Alcohol use is relatively normative (i.e. drinks but is not an alcoholic by any means), though he reports a history of the use of marijuana, though says he hasn't used it in the previous 6 months.

There is no Hx of recent trauma, and there is no acute trauma, either.

You get your BGL and it is normal, at 110 mg/dL.

Fair enough, continue transport as stated above; not much else to do prehospital-wise.

 

[bakertaylor28]

Fair enough, continue transport as stated above; not much else to do prehospital-wise.

Interesting. Any particular reason your not considering atropine per the ACLS guidelines for symptomatic bradycardias ?

 

[VentMonkey]

Interesting. Any particular reason your not considering atropine per the ACLS guidelines for symptomatic bradycardias ?

He's not symptomatic, ACLS guidelines don't dictate my treatment, protocols, or critical thinking skils.

Plus, last time I checked, Atropine is often ineffective in high degree HB's; some say it can even worsen them.

It sounds to me, though by no means am I a physician, as this is some form of myocardial infection be it pericarditis, myocarditis, endocarditis, or any mixture of the three.

If this in fact the case, this patient needs antibiotics, antivirals, antifungals, or whatever treatment would reverse the underlying cause of his arrhythmias.

This is just my thoughts, take them for whatever you wish.

 

[Tigger]

Interesting. Any particular reason your not considering atropine per the ACLS guidelines for symptomatic bradycardias ?

Is there any reason to? His blood pressure is fine and there is no indication of decreasing mentation or an increase/change in chest pain. There is also nothing to say that atropine will benefit a Mobitz II and may cause it to progress to a complete block though I am not sure that is proven.

There is not enough in the initial assessment for me to say that there isn't an ischemic event going on as well.

 

[Summit]

Interesting. Any particular reason your not considering atropine per the ACLS guidelines for symptomatic bradycardias ?

You didn't mention he was symptomatic.

So constrictive pericarditis?

 

[bakertaylor28]

He's not symptomatic, ACLS guidelines don't dictate my treatment, protocols, or critical thinking skils.

Plus, last time I checked, Atropine is often ineffective in high degree HB's; some say it can even worsen them.

It sounds to me, though by no means am I a physician, as this is some form of myocardial infection be it pericarditis, myocarditis, endocarditis, or any mixture of the three.

If this in fact the case, this patient needs antibiotics, antivirals, antifungals, or whatever treatment would reverse the underlying cause of his arrhythmias.

This is just my thoughts, take them for whatever you wish.

Actually you are fairly well on top of it. This one actually came out of the text book, and the case turned out to be a cardiac tamponade.
Its interesting that you didn't pick up the low pulse pressure in the second set of vitals. :-D And correct me if I'm wrong, but do we not treat AVBs to the same basic tune of the other bradys? (thinking along the terms of Atropine, Trans-cutaneous Pacing, High-dose dopamine, and Epinephrine as the basic array of standard treatment options, of a sort?) I've never heard of Atropine having a negative effect with an AVB, and it would seem that we would want to address 2nd Degree Type II BEFORE we end up seeing 3rd degree AVB, or perhaps something more ominous.

 

[bakertaylor28]

Is there any reason to? His blood pressure is fine and there is no indication of decreasing mentation or an increase/change in chest pain. There is also nothing to say that atropine will benefit a Mobitz II and may cause it to progress to a complete block though I am not sure that is proven.

There is not enough in the initial assessment for me to say that there isn't an ischemic event going on as well.

100/82 doesn't ring the bell of a slightly low pulse pressure???

 

[VentMonkey]

Actually you are fairly well on top of it. This one actually came out of the text book, and the case turned out to be a cardiac tamponade.
Its interesting that you didn't pick up the low pulse pressure in the second set of vitals. :-D And correct me if I'm wrong, but do we not treat AVBs to the same basic tune of the other bradys? (thinking along the terms of Atropine, Trans-cutaneous Pacing, High-dose dopamine, and Epinephrine as the basic array of standard treatment options, of a sort?) I've never heard of Atropine having a negative effect with an AVB, and it would seem that we would want to address 2nd Degree Type II BEFORE we end up seeing 3rd degree AVB, or perhaps something more ominous.

All of the above are irrelevant IMO, again, as stated earlier this patient needs definitive care, be it pericardiocentesis, or the proper medication to reverse the underlying cause.

I'm not knocking you for throwing things out there that textbooks present as "classic s/s", just understand real-world medicine calls for a strong clinical base in order to be able to when to with hold, or continue into the next step of proper treatment modalities.

I guess to me the dropping pulse pressure (btw, you gave it away when you mentioned pulsus paradoxus; that is the "drop", so no need to get side tracked with that) isn't going to dictate much more than as previously stated, a judicious fluid bolus for me.

 

[VentMonkey]

Again, aside from my above mentioned treatments, there's no harm in PO ASA, for me, after I have given the Zofran IVP since he's already had N/V; it's the humane thing to do.

You could try a judicious 250 ml fluid challenge, but I'd be hard pressed to go anymore than that.

Op, do you care to share your reasoning for Atropine?...aside from "ACLS guidelines" dictating such therapies?

 

[Summit]

A blind man sees the narrow pulse pressures in the 100/82. Nobody thinks it is worth mentioning because it is so obvious.

In fact 134/96 is slightly suspicious for dehydration or other CV pathologies, except the rest of the presentation points directly towards a degree of tamponade/effusion since you so graciously give us pulsus paradoxus and low voltage.

The reason I said constrictive pericarditis is because you also gave all the other textbook crap: recent illness, now with chest pain, relieved by leaning forward, PR depression, etc etc etc... it is like reading a powerpoint slide about the classic signs of pericarditis.

OP you are asking a fair number of seasoned providers here p-school scenarios and expecting a p-school response but instead you see a bit of scenarioitis. It is to be expected.

 

[Akulahawk]

A blind man sees the narrow pulse pressures in the 100/82. Nobody thinks it is worth mentioning because it is so obvious.

In fact 134/96 is slightly suspicious for dehydration or other CV pathologies, except the rest of the presentation points directly towards a degree of tamponade/effusion since you so graciously give us pulsus paradoxus and low voltage.

The reason I said constrictive pericarditis is because you also gave all the other textbook crap: recent illness, now with chest pain, relieved by leaning forward, PR depression, etc etc etc... it is like reading a powerpoint slide about the classic signs of pericarditis.

OP you are asking a fair number of seasoned providers here p-school scenarios and expecting a p-school response but instead you see a bit of scenarioitis. It is to be expected.

I was initially thinking along the same lines too until I got to the second part of the presentation but tamponade was also high on the list of what was wrong with this patient. Given that the patient developed a 2nd degree, type II AVB, I would probably have foregone anything along the lines of atropine and instead set up for immediate TCP if the patient converted into a 3rd degree or became symptomatic.

OP: I also have to echo Summit here too. While this forum does have a few knuckle dragging paramedics and EMT's, there are only a few here. Most of us are reasonably seasoned, some of us are ICU and ED nurses in addition to having prehospital experience. Then there are those experienced prehospital-only folks that think well beyond the usual p-school level.

 

[bakertaylor28]

My reasoning for atropine is based on the line of reasoning here: https://acls-algorithms.com/rhythms/second-degree-heart-block-type-2/

 

[NomadicMedic]

Redacted to prevent a ban.

 

[bakertaylor28]

A blind man sees the narrow pulse pressures in the 100/82. Nobody thinks it is worth mentioning because it is so obvious.

In fact 134/96 is slightly suspicious for dehydration or other CV pathologies, except the rest of the presentation points directly towards a degree of tamponade/effusion since you so graciously give us pulsus paradoxus and low voltage.

The reason I said constrictive pericarditis is because you also gave all the other textbook crap: recent illness, now with chest pain, relieved by leaning forward, PR depression, etc etc etc... it is like reading a powerpoint slide about the classic signs of pericarditis.

OP you are asking a fair number of seasoned providers here p-school scenarios and expecting a p-school response but instead you see a bit of scenarioitis. It is to be expected.

Yes, but the thing is that it never hurts to re-enforce the basics, regardless of how seasoned one is. Especially given what seems to the tendency not to consider tamponade in the field as a realistic viable cause in non-trauma cases, from what I've been told, anyways.

 

[Akulahawk]

My reasoning for atropine is based on the line of reasoning here: https://acls-algorithms.com/rhythms/second-degree-heart-block-type-2/

Read this very closely from that page:

Second-degree AV block (Type 2) should be treated with immediate transcutaneous pacing or transvenous pacing because there is risk that electrical impulses will not be able to reach the ventricles and produce ventricular contraction. Atropine may be attempted if immediate TCP is not available or time is needed to initiate TCP. Atropine should not be relied upon and in the case of myocardial ischemia it should be avoided.

When I first started working in the field, TCP wasn't universally available. Now, unless you're working for a company that's still stuck in the stone age and can't afford a a now ancient LP-10, all ALS field providers will have TCP available along with atropine. I guarantee that I can rip out, apply, and plug-in TCP pads faster than I can start a line and administer 0.5 mg atropine and I'm no slouch at starting IV lines.

 

[Handsome Robb]

My reasoning for atropine is based on the line of reasoning here: https://acls-algorithms.com/rhythms/second-degree-heart-block-type-2/

Can you explain the mechanism of action of atropine the the pathphysiology behind a second degree Mobitz II block outside of saying "ACLS says so."

Even if this kid was in a CHB I wouldn't pace him. His hemodynamically stable, I'd be setup to pace him if he became unstable but truly he needs an echo, labs, cultures and more than likely a pericardiocentesis. I can do the pericardiocentesis but he'd have to be peri-arrest for me to do it. I could call but no doc is going to give me that order for someone who isn't hemodynamically compromised.


Sent from my iPhone using Tapatalk

 

[bakertaylor28]

I was initially thinking along the same lines too until I got to the second part of the presentation but tamponade was also high on the list of what was wrong with this patient. Given that the patient developed a 2nd degree, type II AVB, I would probably have foregone anything along the lines of atropine and instead set up for immediate TCP if the patient converted into a 3rd degree or became symptomatic.

OP: I also have to echo Summit here too. While this forum does have a few knuckle dragging paramedics and EMT's, there are only a few here. Most of us are reasonably seasoned, some of us are ICU and ED nurses in addition to having prehospital experience. Then there are those experienced prehospital-only folks that think well beyond the usual p-school level.

By the way, HOW IS IT, pray-tell that a patient with significant chest pain and a somewhat low O2 sat with a Mobitz II NOT "symptomatic"?