Home is where the heart is redux

[Mogollon]

I am running this on another forum; however, I would like people on this site to benefit from a slightly different take on cardiac considerations.

HPI:

54 year old male calls EMS with complaints of generalized malaise. You arrive to a middle class suburb and note a safe, well kept house. Patient is awake and oriented to all spheres, he is without acute distress and appears hygienic and well kept. He complains of malaise and "just not feeling well times several hours."

PMHX:

NKA, Lap-Chole, Appy, HTN

Meds:

Toprol XL 50 mg PO Q Day

VS: 150/100, 60-70 strong reg, 19 unlabored, 37 celsius, 95% R/A, BGL- 220 mg/dl

XII Lead:
http://i82.photobucket.com/albums/j271/chbare/ecg-fig1.jpg


What is your impression?
How are you going to treat?
What about pre-hospital fibrinolytics?

[musicemt]

The first thing that jumps out at me is the symmetrical T-waves all over the ECG. There is definitely some pathology going on.

I also see some ST elevations in V1-V2, sloping upward which indicates some ischemic pathology (rather than strain). Can't see if the elevation is high enough to meet fibrinolytic thresholds, but it's definitely enough to treat as a cardiac call with MONA (at least for me). The septal locale is a heads-up to look at V4R to look for extension to the RV, as well as posterior leads to lok for posterior wall inolvement (the R:S ratio in V1 looks normal, but what the heck, nothing has been what it seems so far, eh?)

There's also a quasi-tombstone looking ST segment in V3. Could be some anterior extension to the suspected AMI; could also be signs of a ventricular aneurysm but since the PMHx doesn't reveal a recent anterior wall MI aneurysm goes down on the list a bit. The other V-leads seem to show reciprocal ST depression.

Bottom line; I'd treat with MONA (caution on the nitro until I've looked at V4R), and call an alert for the receiving hospital, but wouldn't push the TNK just quite yet, at least not without online consultation.

But you're a hell of a lot smarter than me, so.....what am I missing? :)

[Mogollon]

Off to a good start. If I were to say you have the primary category of acute coronary syndromes. Then, I further clarify my statement by saying under the umbrella of ACS exist three different syndromes. Would you have more information to narrow down this patients diagnosis?

[Medic101Charlie]

I would be thinking for differentials:

1) either inferolateral myocardial ischemia/injury Vs. post-nQMI (non-Q wave MI)

2) right atrial enlargement/abnormality

I would want to see what serum markers are at this point, what is the T1, CK and CK-MB

I would also want to see what his H/P is like. Has he had an MI in the past? Does he have a H/O angina? In some cases, flipped T-waves can be present in either prinzmetal or vasospastic angina.

Not all T-waves are currently ischemic. It's the question: cardiac memory or myocardial ischemia? The T-waves show a lengthened time for electricity to pass through the infarcted cardiac muscle. Or it can be indicative of currently inschemia/increased oxygen demand.

The way that I learned it was: non-specific ST-depression >>>flipped/inverted T-waves>>> hyper-acute T-waves >>> ST elevation (concave, as non-concave ST elevation was found to be non-MI related in 30% of cases in a recent major study) >>> Q-wave

The above is for a STEMI.

For NSTEMI or non-Q wave MI, leave the Q-wave off the end.


My opinion and my read anyway.

[Mogollon]

Good going! We are in fact looking at a non ST elevation MI or NSTEMI. Clearly, some of the findings are debatable; however, for the sake of learning let us proceed down the path of NSTEMI. (Non Q Wave MI for you old school providers.)

So, the three types of ACS are:

1) STEMI
2) NSTEMI
3) Unstable Angina (USA)

When we compare NSTEMI and STEMI, are there different treatment modalities? I know people like to say I treat every MI with MONA if indicated. Fair enough; however, lets throw in some critical thinking. Because many medics are working in facilities and providing critical care transport, I think it is important to look outside of the MONA box.

So, are there different modalities? What about fibrinolytics for NSTEMI? What about ACE inhibitors for MI?

[Medic101Charlie]

1) All patients should receive MONA in the face of ischemic chest pain

2) All STEMI or even those with NS ST changes should receive Lopressor 5mg x3, in the absence of uncompensated CHF

3) All patients should have serial cardiac enzymes drawn and serial 12-leads, don't just stop at one in the face of NS ST changes

4) LMWH or another platelet inhibitor such as Aggrastat or Integrillin (increased survival post NSTEMI)

5) in cases where there is moderate to high risk for LV failure, ACE should be given within the first 48 hours

6) fibrinolytics are typically NOT given in UA or NSTEMI

7) in high risk patients, PCI is the preferred treatment

In recent studies, NSTEMI show a HIGHER risk for mortality.

So to sum it up the differences in treatment are:

1) Integrillin/Aggrastat provide higher long-term survival in NSTEMI

2) NSTEMI do NOT receive fibrinolytics

3) UA/NSTEMI at high risk or with associated LV reduction receive PCI

[Mogollon]

Absolutely

+NSTEMI patients actually seem to have increased mortality with fibrinolytics.
+Absolutely agree on glycoprotein inhibitors.
+Absolutely agree that risk stratification based on hemodynamics and plaque stability is in order to help us decide on the proper intervention and time of intervention.
+Absolutely agree on the ACE inhibitor.

So, lets say you are now working in the ER and take over care of this guy. You are holding him until the cat lab takes over care. You only have basic labs and a + troponin at this point. MONA has been given and you are infusing eptifibatide per an appropriate weight based protocol.

The patient reports having "funny" sensations in his chest and you see the following on the monitor:

http://i82.photobucket.com/albums/j271/chbare/ves_interpolated_bigeminy_a.jpg

His vital signs are essentially unchanged. Anything you want to do or look at?

[Medic101Charlie]

Let me also add:

STEMI is usually due to a complete blockage caused by thrombus

NSTEMI is typically associated with unstable plaque 2/2 ASHD, which is why statins, anticoagulants and antiplatelets are administered.

Jim

[wvditchdoc]

I would be thinking for differentials:

1) either inferolateral myocardial ischemia/injury Vs. post-nQMI (non-Q wave MI)

2) right atrial enlargement/abnormality

I would want to see what serum markers are at this point, what is the T1, CK and CK-MB

I would also want to see what his H/P is like. Has he had an MI in the past? Does he have a H/O angina? In some cases, flipped T-waves can be present in either prinzmetal or vasospastic angina.

Not all T-waves are currently ischemic. It's the question: cardiac memory or myocardial ischemia? The T-waves show a lengthened time for electricity to pass through the infarcted cardiac muscle. Or it can be indicative of currently inschemia/increased oxygen demand.

The way that I learned it was: non-specific ST-depression >>>flipped/inverted T-waves>>> hyper-acute T-waves >>> ST elevation (concave, as non-concave ST elevation was found to be non-MI related in 30% of cases in a recent major study) >>> Q-wave

The above is for a STEMI.

For NSTEMI or non-Q wave MI, leave the Q-wave off the end.


My opinion and my read anyway.


At least I was on the right track....I love this guy

[screaming pizza]

Go through his pockets for loose change...

[fishy]

Mona?

[screaming pizza]

Mona?

Morphine
Oxygen
Nitro
ASA

Or a horrible name for a girl with parents that hated her.

[Mogollon]

Mona?

As stated; morphine, oxygen, nitro, ASA.
It has become somewhat of a buzz word taught as an all inclusive way of managing MI patients. However, not all MI's are the same and may need different management. Witholding nitro, or substituting morphine with fentanyl, or plavix instead of ASA for a true contraindication to name a few examples.

This inflexibility and rather linear way of looking at ACS management is one reason I wanted to present this case.

[fishy]

As stated; morphine, oxygen, nitro, ASA.
It has become somewhat of a buzz word taught as an all inclusive way of managing MI patients. However, not all MI's are the same and may need different management. Witholding nitro, or substituting morphine with fentanyl, or plavix instead of ASA for a true contraindication to name a few examples.

This inflexibility and rather linear way of looking at ACS management is one reason I wanted to present this case.

Ah, American Acronym-ism at work. Shoulda thought as much :)
No beta blockers tho?
Thanks for clearing that up for me.

[Mogollon]

No beta blockers; however, I suspect that many EMS providers simply did not have beta blocker protocols, therefore anything beyond MONA was not covered. However, things are changing and MONA is not as applicable as it was in the past.

In fact, even beta blockers are starting to take a back seat to ACE inhibitors in some areas. I know some hospitals no longer have beta blockers among emergency department core measures.

[fishy]

No beta blockers; however, I suspect that many EMS providers simply did not have beta blocker protocols, therefore anything beyond MONA was not covered. However, things are changing and MONA is not as applicable as it was in the past.

In fact, even beta blockers are starting to take a back seat to ACE inhibitors in some areas. I know some hospitals no longer have beta blockers among emergency department core measures.

True, we still run with beta blockers where applicable. No ACE inhibitors on the horizon as of yet.

[FF/EMTP1317]

In MD all we have in our protocols is MONA. STEMI pts are automatically priority 1 pt's requiring consult.

[PSYCtest040]

http://i82.photobucket.com/albums/j271/chbare/ves_interpolated_bigeminy_a.jpg

His vital signs are essentially unchanged. Anything you want to do or look at?

Correct me if I am wrong, I am reading sinus rhythm rate of 58 with 1st deg AV block, BBB and bigeminy PVC's

[Mogollon]

Yeah, you are pretty close. Perhaps I should have chosen a different strip. You can see paper speed differs from the "standard" speed. We typically look at 25 mm per second; however, this is 50. For the sake of discussion, lets say this is a sinus rhythm with ventricular bigeminy. I will throw in multifocal PVC's as well.

What do you think?

[PSYCtest040]

Yeah, you are pretty close. Perhaps I should have chosen a different strip. You can see paper speed differs from the "standard" speed. We typically look at 25 mm per second; however, this is 50. For the sake of discussion, lets say this is a sinus rhythm with ventricular bigeminy. I will throw in multifocal PVC's as well.

What do you think?

Forgive me I'm new at this being a student and all but how will the heart rate interpretation change when it's rolling out at 50mm/sec? Also the QRS's are wide indicating a BBB since they appear to be >200ms I would venture it's a LBBB. The PRI looks to be long in the first and last beat in lead I >320ms that is why I said a 1st degree AV block.

[Mogollon]

Forgive me I'm new at this being a student and all but how will the heart rate interpretation change when it's rolling out at 50mm/sec? Also the QRS's are wide indicating a BBB since they appear to be >200ms I would venture it's a LBBB. The PRI looks to be long in the first and last beat in lead I >320ms that is why I said a 1st degree AV block.

Think about the practical aspect of looking at the waveforms. With a faster paper speed, everything will appear stretched out and widened as opposed to the slower 25 mm/second.

We can still roll with the findings, however. What do you as the ER paramedic want to assess or do for this patient?

[PSYCtest040]

Think about the practical aspect of looking at the waveforms. With a faster paper speed, everything will appear stretched out and widened as opposed to the slower 25 mm/second.

Damn!!!!!!!! Should have been able to figure that one out on my own.


We can still roll with the findings, however. What do you as the ER paramedic want to assess or do for this patient?

ER paramedic??? Let me just get through paramedic first then we'll talk. Were starting advanced cardiology now with 12 lead classes end of October and ACLS starting first week in November.

Lets just say if I were to run across this in the field now, I'd be asking for help from my preceptor.

[PSYCtest040]

Think about the practical aspect of looking at the waveforms. With a faster paper speed, everything will appear stretched out and widened as opposed to the slower 25 mm/second.

So if the speed were 25mm/sec then it would be sinus tach rate of 120 with bigeminy PVC's?

[musicemt]

The bigeminy is concerning, the heart's last-ditch way of boosting cardiac output in the face of a very slow sinus bradycardia. The combination of sinus brady first degree AV block would indicate to me that the sinus node has become ischemic. I believe the RCA is responsible for bloodflow to the SA node in most of the population...therefore a repeat 12-lead, again looking at V4R will be useful to look for any dynamic changes. Also, repeat cardiac enzymes will be helpful to confirm that the ischemia/infarction cycle is progressing.

The clinical question becomes whether or not to treat the bradycardia. You mentioned that the patient's vital signs are unchanged, yet aggressive care would suggest using either TCP or atropine to boost the heart rate and prevent hypotension from the reduced CO before it occurs. On the other hand, AHA guidelines mention only the treatment of sympotmatic bradycardias, with some leeway in what is considered "symptomatic". Also, bradycardias can be cardioprotective in ACS syndromes, a way of decreasing ischemic damage by reducing the overall MVO2. So then, what to do? It'a question I've asked since medic school and never gotten a good answer for.

[Mogollon]

So, let's say he is tachy and starts having runs of non sustained ventricular tachycardia?

As far as the bradycardia, I am not keen on treating bradycardia that is well tolerated without hemodynamic or mental status compromise. Of course, in the hospital, we may look at a TVP or permanent placement if possible. Hope that helps.

[PSYCtest040]

So, let's say he is tachy and starts having runs of non sustained ventricular tachycardia?

As far as the bradycardia, I am not keen on treating bradycardia that is well tolerated without hemodynamic or mental status compromise. Of course, in the hospital, we may look at a TVP or permanent placement if possible. Hope that helps.

Great discussion, you are making me think real hard (which is a good thing) but the neophyte has got nothing. Sorry

[Medic101Charlie]

I agree that treating a well tolerated and compensated bradycardia, in the short term, would not be the best medicine. Sometimes we can do more harm than good.

I think the fact that he developed a BBB with bigeminal escape rhythm would push any physician over the edge if debating whether or not this patient was high risk for future clot.

I would put the pacer pads on and not turn it on. Draw up the sedatives and be prepared to pace but otherwise monitor and see where it foes. A judicious fluid bolus may also be in line.

Judicious fluid bolus 250-500cc may also be in line. Increasing the patient's volume may allow the LV to function a little bid better.

I'm assuming lung-sounds are clear bilaterally, of course.

Would also administer ACEI, if not contraindicated, to inhibit the cardiac/ventricular remodeling.

And make sure the Cath Lab is ready because this one is going.

[Medic101Charlie]

The clinical question becomes whether or not to treat the bradycardia. You mentioned that the patient's vital signs are unchanged, yet aggressive care would suggest using either TCP or atropine to boost the heart rate and prevent hypotension from the reduced CO before it occurs. On the other hand, AHA guidelines mention only the treatment of sympotmatic bradycardias, with some leeway in what is considered "symptomatic". Also, bradycardias can be cardioprotective in ACS syndromes, a way of decreasing ischemic damage by reducing the overall MVO2. So then, what to do? It'a question I've asked since medic school and never gotten a good answer for.

I think cardioprotective would be going a bit far. The bradycardia may be a compensatory mechanism in the face of LV decline/remodeling, most likely due to a reduction in LV pressure, but it is still abnormal.

Even by reducing the MVO2 2/2 the NSTEMI event, there would still be a systemic hypoxia 2/2 to the reduced cardiac output. That the heart is now bradycardiac, rather than tachycardiac (the normal physiologic compensatory action) shows, actually, a sick heart.

In this case, I think the bradycardia with the sudden BBB, shows that the AV node is hypoxic. This can be 2/2 lesion to the Posterior Interventricular Artery, which can be RCA (in right dominant) or LCx in left dominant individuals.

Either way, any cardioprotection would be abnormal to the say the least.


In my opinion anyway, and I am definitely NOT a cardiologist!

[Mogollon]

Now that you are in the ER or CCT, are there any labs that you would want to look at? Can any specific abnormal chemistries be pro-arrhythmic?

[Medic_QT]

Btw, I'm very pissed I didn't see this to begin with. I thought it was some sappy discussion. I didn't see it was in cardiology... D'oh!!! (Btw this is attempt #2, thanks to my computer having a hiccup..)


No beta blockers; however, I suspect that many EMS providers simply did not have beta blocker protocols, therefore anything beyond MONA was not covered. However, things are changing and MONA is not as applicable as it was in the past.

In fact, even beta blockers are starting to take a back seat to ACE inhibitors in some areas. I know some hospitals no longer have beta blockers among emergency department core measures.

My ER still uses Lopressor and MONA. M department is looking into fentanyl for cardiac, (including possibly nebulized fentanyl), and getting rid of our GTN drips and bringing in nitro paste. No beta-blockers in the works, but I have been trying to sneak in some Lopressor.


I agree that treating a well tolerated and compensated bradycardia, in the short term, would not be the best medicine. Sometimes we can do more harm than good.

I think the fact that he developed a BBB with bigeminal escape rhythm would push any physician over the edge if debating whether or not this patient was high risk for future clot.

I would put the pacer pads on and not turn it on. Draw up the sedatives and be prepared to pace but otherwise monitor and see where it foes. A judicious fluid bolus may also be in line.

And make sure the Cath Lab is ready because this one is going.

THANK YOU!!!!!!!!!!!! I GET SOO PISSED OFF WHEN LT'S TELL ME TO PUSH ATROPINE!!! Yes, they MAY be bradycardic, but the heart muscle in injured and compensating. C-O-M-P-E-N-S-A-T-I-N-G. WHY would you mess with that?! A medic or doctor can NEVER do a better job than the body, we can simply stand by and wait for decompensation, then go to work. Let's think now, the muscle is strained, has increased O2 demand, why would you increase that even more for the sake of having a number within certain limits. That makes me so mad. Cookbook medic-- "It says give it for bradycardia-- They're bradycardic." That is probably 70% of my department. That's why I liked my P-School-- They taught theory, thinking for yourself, and pathophysiology, unlike the flowchart medics from some of the area schools.
< /RANT >


I think cardioprotective would be going a bit far. The bradycardia may be a compensatory mechanism in the face of LV decline/remodeling, most likely due to a reduction in LV pressure, but it is still abnormal.

Even by reducing the MVO2 2/2 the NSTEMI event, there would still be a systemic hypoxia 2/2 to the reduced cardiac output. That the heart is now bradycardiac, rather than tachycardiac (the normal physiologic compensatory action) shows, actually, a sick heart.

In this case, I think the bradycardia with the sudden BBB, shows that the AV node is hypoxic. This can be 2/2 lesion to the Posterior Interventricular Artery, which can be RCA (in right dominant) or LCx in left dominant individuals.

Either way, any cardioprotection would be abnormal to the say the least.


In my opinion anyway, and I am definitely NOT a cardiologist!

Wow. VERY impressive! You are my idol. I hope I can learn some of that through some of those classes if I get in there.. I can say some of that in big dummy terms, but just.. wow....


Now that you are in the ER or CCT, are there any labs that you would want to look at? Can any specific abnormal chemistries be pro-arrhythmic?

Look at Troponin (I know you said they were positive already), CK-mB, electrolytes (especially Na+ and K+), lactic, PT, PTT, INR, (clotting tests not for arrhythmia directly, but still look for S&Grins) and sure, why not CBC w/ diff.