76 year old male with chest pain and “peanut allergy” that turns out to be STEMI

EMS is dispatched to the residence of a 76 year old white male with a chief complaint of chest pain.

Upon patient contact the patient is found sitting on his couch, alert and oriented to person, place, time and event with GCS of 15.

The patient appears to be in no distress, advising he believes he is having an allergic reaction to peanuts since he has been eating a lot of peanuts for the last hour.

Primary assessment:

  • Patent airway with no audible stridor or upper airway swelling
  • Adequate ventilation with proper tidal volume, non-labored, bilateral chest expansion and clear lung sounds. No urticaria, mottled skin or signs of allergic reaction
  • Strong, regular radial pulses with skin pink, warm, dry
  • No signs of bleeding and capillary refill <2 seconds

History and events:

  • Sudden onset while sitting on the couch eating peanuts
  • Denies any provocation
  • Complaining of chest tightness
  • Denies radiation
  • 4/10 discomfort level
  • Chest tightness started approximately 5 minutes before calling 911


  • Sings and Symptoms: Chest tightness
  • Allergies: Denies any allergies (although he believed to be having an allergic reaction to peanuts)
  • Medications: Atorvastatin (Lipitor) and Lisinopril
  • Past Medical History: Hypertension (HTN) and Hypierlipidemia (High Cholesterol)
  • Last Oral Intake: Peanuts for the past hour
  • Events: Sitting on the couch while eating peanuts

Vital Signs:

  • Initial Blood Pressure: 142/87 mmHg (MAP: 119)
  • Heart Rate: 94 beats/min and slightly irregular
  • Respiratory Rate: 16 breaths/min
  • SpO2: 100% on Room Air
  • Blood Glucose Level: 107 mg/dL

The patient was placed on cardiac monitoring (LIFEPAK 15), and the following strip was obtained:

inferior strip ems

The strip is a bit dirty to determine an exact rhythm etiology, however, it appears slightly irregular and there are obvious ST segment changes which warrant further and immediate assessment, so, the crew obtained a 12 lead ECG, shown below:



original inferior ems



As we suspected:

We have a sinus arrhythmia, with Inferior STEMI… But there is more!

Lets break it down a bit more:

  • ST segment elevation in leads II, III and aVF
  • Reciprocity in Leads I and aVL
  • Slight depression in V1 with marked depression in V2


 As many have heard before, when one encounters an Inferior Wall MI (IWMI), one should also suspect Right Ventricular Involvement (RVI). But, why suspect? There are a few tricks that can assist us in determining RVI.

  • ST segment elevation in lead III (3.5 mm) > Lead II (1.5 mm) and aVF (3mm)
  • Reciprocity (depression) in aVL (2 mm) > Lead I (1.5 mm)


 Remember the Hexaxial Reference System and Einthoven’s Triangle? If not, click on this link for further review of axis determination, which will help you understand what we will discuss momentarily.


Why Lead III and aVL?

 Remember, out of all the Limb leads which provide a Frontal Plane view, Lead III is the most rightward lead, meaning, it looks at the RV more than any other of the limb leads.

 aVL looks almost directly away from Lead III, therefore, elevation in Lead III will cause a mirror vector in aVL…


the higher the elevation in Lead III, the deeper the reciprocal change in aVL.

v4-6r ems


 Based on these findings, RV view was obtained, moving V4-6 to the right chest wall, known as V4-6R. As expected, there is RV Involvement.


What about V1-2?

 Sometimes during IWMI with RVI, V1 may present with ST segment elevation or isoelectric, while V2 may be slightly depressed. But, here we have a small difference. V1 is slightly depressed and V2 is has obvious depression. This suggests something else.


What would that be?

 If you thought about Posterior Involvement, you deserve a big ol’ pepperoni with bacon pizza slice with extra parmesan cheese!!!


A posterior ECG was obtained, moving V4-6 to become V7-9.


v7-9 ems


Again, as suspected, there is Posterior Involvement, not as marked as the inferior wall of the LV or RV, but enough to create ST segment deviation.



At this point, the patient is already packaged and ready for transport.

2 large bore peripheral IVs were established and now the big question came up.


To give or not to give Nitroglycerin (NTG)?



 This is a hot topic which calls for an overall patient presentation and hemodynamic status, some will agree, while others might disagree with the administration of NTG (for a similar case click here). For example, the American Heart Association (AHA) does not recommend the use of any vasodilators in the presence of Right Ventricular Infarction, while some prehospital guidelines advise to “Use With Caution“.


 Based on the fact that the patient had no prior history of Coronary Artery Disease (CAD), currently hypertensive, no signs of AV Nodal conduction delays or signs of hypoperfusion and no medication to potentiate its use, the crew elected to give a trial of .4 mg of NTG sublingual, after a 250 ml fluid bolus, in anticipation of any blood pressure reduction.


 With no dramatic drop in blood pressure and improved symptoms, the crews administered a total of 500 ml of fluids, .8 mg NTG and 324 mg ASA.

 Keep in mind that, while our RV receives Venous Blood Flow, an injured RV may not be working as expected, especially with prior CAD, hypotension (SBP <90 mmHg), bradycardia or with high degree AVBs. Therefore, a patient presenting with these findings or overall hypoperfusion appearance, should not receive sublingual or transdermal NTG pre-hospitally, since titration is not predictable or controllable compared intravenous NTG infusion.

Last pre-hospital set of vital signs:

  • Blood Pressure: 144/87 mmHg (MAP: 113)
  • Heart Rate: 93 beats/min with sinus arrhythmia
  • Respiratory Rate: 16 breaths/min
  • SpO2: 98 at 3lpm
  • Chest tightness: 1/10

Transport to PCI facility was approximately 35 minutes long.

Upon arrival to the receiving Emergency Department, the following ECG was obtained.

inferior ed



 Now, in case you didn’t notice, there is an obvious inferior STEMI. Just kidding, but seriously, yes. As Dr. Ken Grauer mentioned, looking back closely to the previous ECGs, V1 and V2 appeared to be swapped, otherwise, there is a clear progression of myocardial injury. There is also, an unusual lateral (precordial) ST segment morphology with symmetric T wave inversion, suggesting the lateral wall of the LV might be starting to get affected, which was already present during the first ECG, but unchanged.




Door to Balloon time was <35 min, revealing a 100% occluded Right Coronary Artery.


  • Nice case Ivan. I have to comment that the last ECG (done @ 8:48:31) looks like leads V1,V2 are switched compared to the earlier ECG done @8:08:04 – rather than “progression of the posterior infarction”. The sequence of R wave progression in this last ECG (@ 8:48) just looks “off”. Otherwise – EXCELLENT case! – 🙂

    • Ivan Rios says:

      Thank you Ken… I do agree, they definitely appear to be swapped based on the lack of prominent R wave and isoelectric segment which we usually see in V1, which is now in V2, like on the initial 12 lead ECG. Lead misplacement sounds convincing!

  • Jeremy Smith says:

    Good case, very informative.

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