Tuesday, April 21, 2015

Acute chest pain, bradycardia, and hypotension

A middle-aged male complained of acute onset of chest pain.  He was diaphoretic, weak, lightheaded, but alert.    Blood pressure was 60/palp with a pulse of 40.  was given aspirin and a 500 ml normal saline bolus.

Here is the prehospital 12-lead:
There is bradycardia and some kind of AV block.  P-waves are difficult to discern, so the exact nature of the block is unclear

There is obvious inferior STE.   Reciprocal ST depression in aVL confirms inferior STEMI, and ST depression in lead I is a good indicator that this is an RCA occlusion.

In inferior MI due to RCA occlusion, one should always look to lead V1 for ST elevation indicating right ventricular infarct also.

Here, there is ST depression in V1 and V2, but ST elevation in V3.  This is odd and one must suspect that leads V1 and V3 are reversed.

The ST depression in V2 shows extension to the posterior wall.

The cath lab was activated by the medics.

The patient arrived alert and conversant.   BP was in the 40's to 60's, with pulse in 30s to 40s.

An ECG was recorded 11 minutes after the first:
Now it is clearly 3rd degree AV block.
There is clearly ST elevation in V1 (and now also V2) confirming right ventricular involvement, and confirming that prehospital leads were reversed.  This is such a large RV infarct that the ST elevation extends all the way to V3, which is often called a "Pseudoanteroseptal MI" (See more cases of pseudoanteroseptal MI)

A right sided ECG was immediately recorded (limb leads are not changed):
3rd degree heart block.  There is ST elevation in V2R (identical to V1 on regular 12-lead) extending all the way out to V6R

A bedside echo was done:

There is bradycardia.  The RV is massively dilated due to RV failure from RV infarct.

He was given ticagrelor and heparin.  He was given 25 mg of ketamine and transcutaneous pacing was begun.  Capture was achieved at 114 mA at a rate of 70.  Systolic BP rose to 110.

Capture was verified by bedside echo:

He went for angiogram which showed occlusion of the proximal RCA, proximal to the right ventricular marginal branch to the RV.

It was opened and stented.

The patient did well.

Learning Points

1.  Occlusion of the proximal RCA may result in hemodynamically significant RV MI.
2.  These occlusions also frequently lead to complete AV block because of blood supply to the AV node from the RCA
3.  RV MI can lead to RV failure and dilatation
4.  Fluids are indicated, as cardiogenic shock due to RV failure responds to fluid loading and does NOT result in pulmonary edema
5.  Transcutaneous pacing can be verified with bedside ultrasound.
6.  Rapid reperfusion of RV MI results in a good outcome


  1. - fantastic case !
    - there is all the pathophysiology of RVMI
    - and the echo is extraordinary

    thanks dr Smith


  2. Great case.

    Thoughts about ketamine use in acute cardiac ischemia?

  3. Dr Smith,

    Nice case again.

    Is there an explanation as to why, in the second ECG (With right-sided precordial leads), the upright P-wave is suddenly inverted after the third QRS complex (Lead II long strip) ? At first, one may think it is due to artifact, but looking closely, the P wave is actually inverted. Same observation goes for the 4th P wave which also looks inverted despite the movement artefact.

    That would mean that the P wave is conducted in the opposite direction of lead II - the usual pattern for P wave depolarization - as in a retrograde fashion...


  4. Olivier,
    Nice to hear from you! I see what you're saying, and I am "stumped."
    I also don't know why the sinus rate appears to be slow and irregular
    Fortunately, that does not change the therapy.
    Thanks for your perceptions!

  5. Great case!!
    Great Post and Nice Article.I like it.Thanks for sharing.

  6. Can wrap around LAD occulusions present with similar looking ECG with ST elevations in anterior and inferior leads?

    1. They are quite similar. The main difference is that in RCA, the maximal STE is in V1-V3 vs. V2-V4 for wraparound LAD. One can almost always make the distinction.

  7. Hi Dr. Smith,

    Thank you very much for creating such an informative blog. I find myself finding your blog quite frequently when I am googling questions I have about heart rhythms and EKGs.

    With respect to this patient's rhythm, could the rhythm have been a very long(and variable) first degree heart block as opposed to a 3rd degree heart block, since the P-waves and QRS complexes appear to be close to the same rate and the QRS complex seems a bit narrow?

    Also do you think that atropine could have increased the rate had they not done pacing? Or would the pacemaker/AV node been too hypoxic/damaged to respond to decreased parasympathetic input?


    1. Ben,
      The PR interval varies, there is dissociation because of block.
      Look again.


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