36 YOM with Chest Pressure: Reperfusion AIVR

This the case of a 36 year old, black male, complaining of chest pressure 8/10 pain scale, for 1 week.

The patient was born with unknown cardiac complications, which led to multiple near death arrhythmias, which is why the patient has an on demand pacemaker/defibrillator in place. He also has a history of Hypertension (HTN), which he takes Lisinopril and Carvedilol for.

EMS was activated by his physician after he presented with chest pressure, no longer able to tolerate it. A 12 lead ECG was obtained approximately 1 1/2 hours prior requesting EMS.

This was their ECG:



This is an Accelerated Idioventricular Rhythm (AIVR) at a rate of approximately 50 beats/min suggestive of reperfusion post Myocardial Infarction. AIVR is one of the most common rhythm post cardiac arrest and reperfusion, following resolution of infarct, commonly seen in the cath lab setting following PCI.

  •  P waves? (the long Lead II strip which may appear to have P waves not correlating to every QRS, i.e. AV Dissociation)
  • Regular rhythm with wide complex QRS > 200 ms (extremely wide and not consistent with a typical Bundle Branch Block)
  • There are Primary changes seen as ST elevation in leads I, aVL and V6 with marked pathological Q waves (a Q wave > 1/3 of the R wave or > .04 s wide) and Hyperacute T waves in the precordial leads, marked in V2-4
  • There is no pacemaker function as the rate is not below the pacemaker’s threshold

(If you do not remember my last post, Primary ST segment changes is due to ischemia or infarction, while Secondary ST changes are due to repolarization abnormalities)

  • Reciprocity in the opposing leads, III and aVR
  • Pathologic Rightward Frontal axis (limb leads), or Right Axis Deviation (RAD)

Note that, the computer interpretation suggests Junctional rhythm or AIVR. As opposed to what many believe, a junctional rhythm should have a narrow complex, since the AV junction is located above the Bundle of His, unless there is a preexisting Bundle Branch Block.

Also notice that although, the QRS complexes may have similarity to a LBBB, these complexes are extremely wide, and there is RAD, also not present during a normal LBBB as these vectors towards the Left Ventricle (LV) are stronger than the Right Ventricle (RV), which is why a LBBB often presents with physiologic and pathologic Left Axis Deviation (LAD).

The physician had administered a total of .8 NTG sublingual prior EMS arrival, and 325 mg ASA.

Baseline vital sings:

BP: 120/90 mmHg
HR: 54 beats/min regular
RR: 16 breaths/min
SpO2: 100 % RA

This is the 12 lead ECG  obtained by EMS upon their arrival and patient contact, approximately 1 hour and 2 minutes after the initial ECG.

LBBB coleman

Now we have a sinus rhythm with a LBBB. Now that we can compare tracings, we can safely conclude the initial rhythm was AIVR.

Although there is no Sgarbossa or Dr. Smith’s Modified Sgarbossa criterion met here, there are positive T waves present in Lead II, V4-6. Remember, a normal LBBB has Discordant T waves (the opposite direction of the QRS).

There is no presence of Cabrera’s Sign, which is a notch of the S wave upstroke in V3, which is very specific for prior or acute MI in a LBBB, or Chapman’s Sign, which is a notch in the upslope of the R wave in Lead I, aVL and/or V6, which also support prior or current MI.


For more on Sgarbossa’s Criteria, click HERE

For more on Dr. Smith’s Modified Sgarbossa Rule, click HERE

This patient had a prior LBBB confirmed by a previous ECG found in the Emergency Department’s database, which we were not able to obtain, however, it was verified. The only thing that was different from this LBBB was the appropriate T wave discordance present before, which differs here with Inappropriate concordance.

Cardiac Troponin I was .02 ng/mL with all other cardiac enzymes and electrolytes within normal limits. This may be due to normalization of myocardial function, especially after 1 week of the event. The patient was admitted for further observation and we were not able to follow up with the patient.


AIVR is one of the most common rhythms post reperfusion, and although we can’t fully compare QRS morphology and ST segments from AIVR and LBBB, primary ST-T changes can still be found in both ECG patterns with proper ECG evaluation.



  • Brent D says:

    Thanks for the interesting article / ECG III & aVR seem similar rather than reciprocal?

    The the ECG criteria. Along with the duration of pain suggest a spontaneous reperfusion or post intervention?

    Has time meant no PCI or don’t prisoners get them?

    • Ivan Rios says:

      Lead III and aVR look similar as the vectors move away from the left, towards the right. They are reciprocal to the lateral leads (I and aVL), which is why when you see elevation in aVL, you will have depression in lead III and vise versa. This is because these leads are pretty much 180 degrees from each other.

      They did not do PCI because of the length of the event.

  • Babs says:

    Prisoners do get PCI, unless they refuse it. If this person didn’t present himself to the sickbay then they wouldn’t have had reason to do an EKG on him or give him ntg.
    Thank you for this cool case! I am a nurse and cardiac is not my strongest suit!!! You make this interesting!

  • This struck me as an incorrect interpretation of Chapman’s sign, which is a notch on the ascending limb of the R-wave in I, aVL, or V6. This V6 looks like a normal variant of LBBB V6 to me. So I looked up Chapman’s original paper from 1957 (it is full text online!) , and it does NOT include this morphology as a sign of MI. It is a fascinating paper, and contradicts the old dogma that you can’t use Q-waves to diagnose old MI in the presence of LBBB. It states how that notion only applies to the free wall, but not to any infarct that involves the septum.
    Here is the link: http://circ.ahajournals.org/content/16/4/558.full.pdf

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