52 y/o M Chest Pain

It’s around 10 pm on a warm summer evening, and you and your partner have answered a steady stream of non-emergency calls all evening. Falls, small lacerations, and minor illnesses have all seen the attention of your ambulance. None of which, however, required the attention of am emergency room, and were handled by the family by the time you arrived. The next call sounds more serious though.

“… respond to a ten charlie one, 52 year old male with chest pain, at…”

Chest pains usually warrant a transport, and usually get them. With high incidences of cardiac disease, diabetes, obesity, and hypertension in your jurisdiction typically when a chest pain gets sent out, it is guaranteed a trip to the nearest emergency room.

You arrive at a well known regular’s house to find him seated on the couch, huffing and puffing away. He claims a history of COPD, which prompts a quick listen of his lungs. Clear, yet the rate is higher than normal, estimated somewhere in the low thirties just on a quick listen. He says that he has had this pain for several weeks, and states that it is probably related to him hitting his chest when he fell several weeks ago. He is insistent on not going to the hospital. At very least, you convince to come out to the ambulance where you can have some better light and look at him more closely. He complies, gets on the cot, and is moved outside to your waiting unit.

After a quick line of question, you break down his story and he admits that he hasn’t had the pain for a week, it has been closer to an hour. He describes it as “pressure,” localizes it mid-sternal without radiation. He rates that pain as 9/10 on a 0 to 10 scale. He says that he was “out chasing whores” when the pain started (strange, I know) and that he came inside having shortness of breath. He denies nausea or vomiting and has an extensive traumatic injuries and family history of cardiac disease.

His vitals are BP 120/80, HR 82, spO2 100%, RR now 22 and falling. No edema is present. Pt denies alcohol or drug use. No accessory muscle use is noted. Skin is warm and dry without signs of cyanosis. No obvious trauma is present. The pain is not reproducible on palpation, no crepitus is noted on palpation. Barrel chest is noted, confirming patient’s story of COPD history, possibly being emphysema. The abdomen is unremarkable, soft and non-tender to palpation. The patient ambulated with a steady gait and says that sometimes he gets “out of breath” with exertion. Pt denies any previous MI’s.

An initial 12 lead is captured with excellent data quality, showing a normal sinus rhythm and large peaked T-waves in septal and anterior leads. The computerized interpretation comes back as normal sinus rhythm with possible early repolarization.

What are your thoughts?

Do you agree with the computer interpretation? Why or why not?

5 thoughts on “52 y/o M Chest Pain

  1. If you move one of the 12 leads to get a better view of the other side of the heart would that confirm better that possible beginning of some cardiac issue? Either way I would strongly urge this guy to be seen by an ER physician to have blood work drawn to rule out cardiac involvement with his pain. I could then go on to tell him about how my father had the same kind of chest pain with no cardiac history and he ended up having an anterior inferior MI affecting his septal wall. He had no clue he really had an MI. Just thought it was heart burn from stress. Maybe that would further convince this guy to be seen and get checked out so he could live to chase the ladies another day. It’s worth a shot

  2. What the computer can’t tell you is what his electrolytes look like; Could also be hyperkalemia. Without knowing his baseline, I’d err on the side of caution. (my baseline is tattooed around arm).

  3. Most likely early repol. Classic morphology (large, slightly assymetric T, notched J point, minimal STE, mainly precordial), good R waves, QTc not too long. No major reciprocal changes, however clinical picture suggestive and many of the above points are borderline. aVL somewhat suggestive as well. Perhaps NSTEMI. Serial ECGs will help, and push for transport, although would not go nuts with activations and the like.

  4. I would call it a possible evolving MI. STE in V1-V3, T-wave inversion in aVL, and a prolonge QTc. Also the T-waves are hyperacute which helps support that theory. Noted that there are some minor Q-waves in the inferior leads. I couldn’t activate the cath lab but I would trend 12’s and look for any changes

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