68 Year Old Male: Chest Burning – Part 2

This is the second installment in a multi-part case study; you may want to review the initial description of the patient’s presentation in Part 1. We’re going to save dissection of the ECGs for the next post and continue with his case…

Here’s the patient’s initial ECG again:

You start by administering 324mg of aspirin PO, chewed well. Recognizing that the patient is in rapid atrial fibrillation at about 125 bpm and that his fast heart-rate could be contributing to his symptoms, you start to draw up a loading dose of diltiazem. However, before you can administer the medication, you notice a change on the monitor and shoot a 12-lead.

You shoot a posterior ECG with posterior leads V7-V9 for good measure.

Aside from an obvious decrease in the patient’s heart rate, his vitals are unchanged. You question him closely about his symptoms and they are still exactly the same. He still feels a “burning” in his chest that he rates as a 6 out of 10, but it’s no different from when he first presented.

You start to think that maybe it wasn’t the rapid a-fib causing his chest pain…

You administer 0.4 mg of nitro SL, reassess his pain as being mildly reduced to a 5/10, and run another 12-lead.

You administer a second dose of 0.4 mg nitro SL, his pain drops to 3/10, and you run fifth 12-lead.

You administer a third dose of 0.4 mg nitro SL and the patient tells you that his pain is nearly gone. “Nearly? Not entirely?” you ask. He admits that there is still a little discomfort. “It’s a 1/10.” You print yet another 12-lead.

The patient seems to be responding well to nitro but at this point you’ve reached your ceiling—not due to some arbitrary number of doses but because of the patient’s BP. You would like to keep going but his pressure is now 94/52 mmHg and it’s not within your training, protocols, or comfort level to take him any lower.

His skin is still warm, pink and dry, his radial pulse is strong, and he looks great. In-fact, he feels much better. He’s even questioning why he called the ambulance in the first place and looks forward to getting home to catch a football game later that evening.


What are your next considerations in the care of this patient?

Is this patient a candidate for immediate cardiac catheterization or thrombolysis?


For the conclusion of this case, check out Part 3 (coming soon!).

created 2013.12.31  last modified 2017.08.25


  • MedicSBK says:

    Next considerations – Continue with the serial 12 leads.  Consult with medical control for possibly some Fentanyl since it is not as bad hemodynamically with the goal of making the patient complaint free. 

    ED Handoff – I actually had a case just like this a few months ago.. didnt meet our stemi protocols etc.. my partner called it in as a "strongly suspiscious EKG" and they had the STEMI alert button "half pressed."  Our patient was still largely symptomatic when we arrived though, being the major difference.  I would show the EKGs to the resident/attending and convey the fact that we were suspecting a subendocartal MI on this patient.

    Concern – I am still concerned that there is some blockage even though the patient's symptoms have improved.  He needs continued monitoring etc.. by us and the ER.

  • Dane Friley says:

    I am still pretty concerned about pt after all he is still have discomfort although minimal after all the nitro. He still has diffuse ischemia. Posterior leads negative. He will not be going directly to cath lab. Troponins will guide tx at hospital. Continue to monitor vs for remainder of trip. You could think about a bolus if his pressure drops anymore and he still has good lung sounds and sat. I would be ok with pressure in the 90's. You could think about fentanyl for pain, but pain is down to 1/10 and you are 10 minutes away. I may just leave well enough alone and continue to assess pt vs, 12 lead and pain closely for rest of trip! Very anxious to hear results!

  • Chee Yong Chuan says:

    Interesting follow up. With the second tracing, the changes that I could observe

    1) Rhythm changed back into sinus. Distinct P waves can be seen, most obvious in lead V1 preceding each QRS complexes. PR interval is normal. 
    2) Rate decreases significantly. RR is about 80 beats per minute. I think patient went out of Atrial fibrillation with RVR
    3) STE in aVR remains so as the diffuse widespread ST segment depression inferolaterally. There is subtle decrease in the amount of ST depression seen
    4) New ST depression seen in V1
    5) R wave progression remains poor

    Posterior leads did not show ST in V7-V9, making posterior infarction(in isolation) very unlikely. Posterior infarction accompanies inferior STEMI most of the time. 

    After administration of 3rd dose of S/L GTN, and with the resolution of chest discomfort, the ECG changes are indeed obvious. The rhythm is still sinus but the amount of STE in aVR and widespread STD had decreased quite a fair bit. Dynamic changes with administration of S/L GTN points towards ischemia. One can also argue that the amount of STE and STD decreased quite a bit because the rate has slowed down, and the fact that the patient went out of atrial fibrillation. What we are seeing could be rate related or due to demand ischemia. 

    However, with documented history of ischemic heart disease, coronary and vascular(DVT) heart disease and new onset chest discomfort, he needs to be admitted and investigated further. It is also likely that he experienced all the symptoms due to a tight,stenosed LAD/Left main that was unable to supply adequate perfusion to the rest of the myocardium during AF with RVR(Demand ischemia). 

    Impression: For medical stabilization in a PCI capable centre. Thrombolysis not indicated. Will require EARLY PCI to confirm left main disease and proceed. I personally will keep PE(History of DVT) at the back of my mind. But saturation under room air is still acceptable. 

  • John says:

    Possible dissecting aortic arch 

  • J.Ruble says:

    Several things come to my mind when I look at this. The diffuse depression could be ischemia secondary to a subendocardial MI.  Simple blood work can confirm this and a trip to the PCI center.  However, I suspect something far graver than the simple subendocardial or ischemia secondary to whatever may cause oxygen depletion, such as an aortic dissection.  There are several suggestions, most of which will be found out upon catheterization, such as triple vessel disease, LAD occlusion, or LMCA occlusion, with all being fatal if not recognized. There is an 80% specificity if the elevation in aVR is greater than V1 to suggest LMCA occlusion, and if there is greater than .5mm of elevation in aVR there is an 86% specificity of triple vessel disease. I would treat as such and defiantly alert the PCI center that I was coming and my EKG findings. aVR is such an important lead that tells us a lot and should be taught more, rather than discarded.


  • Ernie :) says:

    This is a LMCA occlusion.,  aVR elevation with depressions in the lateral leads is the is the give away here.  There is likely triple vessel dieses here, I bet he gets a cabg This is a LMCA occlusion.,  aVR elevation with depressions in the lateral leads is the  is the give away here.  I bet this guy has a CABG.  aVR has historically been the "red headed" step child of monitoring leads… No so much anymore.  🙂  Pay attention to this aVR.  This is still some debate in my area about aVR and it is not currently “PCI activation criteria”This is a LMCA occlusion.,  aVR elevation with depressions in the lateral leads is the is the give away here.  There is likely triple vessel dieses here, I bet he gets a cabg This is a LMCA occlusion.,  aVR elivation with depressions in the lateral leads is the  is the give away here.  I bet this guy has a CABG.  AVR has historically been the "red headded" step child of monitoring leads… No so much anymore.  🙂

  • Renee says:

    I agree with J. Ruble. aVR has my attention, big-time. Aortic dissection and possibly even a DVT/PE… even though it isn't presenting as such, are in the back of my head, along with the LMCA being occluded (possibly by a DVT???). Each EKG I saw led me right to aVR after review. I like that the posteriors were done. I would continue to the PCI center, use fentanyl for any re-entrant pain, continue serial EKGs until arrival.

  • Nick Adams says:

    This is a very good example of a "not so obvious" LMCA occlusion.  Chee Yong Chuan……you are the man.  Your explainations are spot on.  One thing that you mentioned is that you mostly see an inferior involvement also.  This is true in a right dominant pt……..approximately 80% of all pts are right dominant.  Is it safe to say that this pt is left dominant?  And this is the reasont the pt has no inferior wall involvement?  I'm not 100% sure.  J. Ruble.  Does an aortic disection effect the LMCA?  I was under the immpression that an aortic dissection can effect the right main coronary artery.  Can it occlude the LMCA too?  Renee- I'm not exactly sure how you can get an occlusion from a DVT.  How can a clot in the leg and travel through the right side of the heart, imto the pulmonary capillary system, back to the left heart to occlude the LMCA?  I'm just a paramedic, and love to learn.  I'm not challenging anyone, I just don't know.  No disrespect to anyone.  If i'm wrong, please let me know.

  • Nick Adams says:

    Hahaha………I was wrong by saying that this pt is left dominant.  He must be right dominant to not involve the inferior wall.  Sorry folks

3 Trackbacks

Leave a Reply

Your email address will not be published. Required fields are marked *