First the rhythm – sinus bradycardia at 36/minute

Second – the inferior leads keep catching my eye…no obvious ST-segment elevation, but the T waves look a bit prominent (hyperacute ?), and then there is the T wave inversion in aVL (remember, reciprocal changes in aVL may be the earliest sign of an inferior MI).

Of course, the correct response would be to repeat the EKG. This was done just 10 minutes later:

Now the inferior STEMI is evident! Note the rhythm change – now sinus at 100/minute, and with more prominent P waves. Not having been there, I can only guess – the original rate was likely due to excess vagal tone (common with inferior MI’s – think pale, diaphoretic, nauseous, bradycardic). The subsequent tachycardia might be due to nitroglycerin administration, or just less vagal tone, or maybe they received atropine.

Keep repeating those EKGs when rhythm or rate changes; you could be looking at an early MI

This EKG reveals a regular rhythm at 30/minute. There are no obvious P waves, although there appears to be irregular fine oscillations of the baseline, consistent with fibrillatory waves. Why would atrial fibrillation
present with a slow and regular ventricular response? Perhaps these ventricular beats are escape beats, occurring because the AV node is completely blocked! This is what complete heart block occurring with atrial fibrillation looks like…

If this patient was taking digoxin it would certainly be important to check a level to rule out toxicity. Digoxin toxicity classically causes two important EKG findings: 1) significant AV block (more than 1° AV block), and 2) increased automaticity (often accelerated junctional rhythm or atrial tachycardias). Typically these two EKG findings occur simultaneously – hence the classic dig toxic rhythms (PAT with block or “regularization” of the a fib due to 3° AV block with accelerated junctional escape rhythm).

PAT with 2:1 block (P waves at 150/minute – too slow for flutter waves, so these are discrete P waves and this is atrial tachycardia)

Another PAT (look hard for the P waves at 150/minute) with 2° AV block, type I

“Regularization of atrial fib” – due to accelerated junctional rhythm at 70/minute with 3° heart block of underlying a fib (note fibrillatory waves in V₁)

What looks like simple bigeminy is actually a slightly more interesting diagnosis. Again, calipers are very helpful!

Notice that the ventricular complexes occur at a regular interval, and that the coupling interval (the space between the preceding QRS and the PVC) is not constant, as would happen with bigeminy. This rhythm is an independent ectopic ventricular rhythm, parasystole. Notice that the 6^th complex is a fusion beat (a combination of the sinus beat and the ventricular beat) – a sure indicator of an independent ventricular rhythm.

Traditionally parasystole is felt to represent a “protected” focus that is isolated from, and thus independent of, the electrical activity of the surrounding myocardium.   Parasystole is of no greater clinical import than PVCs of similar frequency or even bigeminy.

Looking at the V1 rhythm strip, the first five beats are an accelerated idioventricular rhythm (no P waves, wide complex, and regular rate of 70/minute). Just before the 6^th beat you can see the “emergence” of a P wave – this particular P wave is very close to the subsequent QRS, and there is slight variation in the QRS morphology. The 6^th QRS represents a fusion beat (a composite between the ventricular beat and a sinus-conducted beat occurring at nearly the same time). The 7^th through 9^th beats appropriately follow P waves and represent sinus conducted beats. This rhythm represents isorhythmic competition between accelerated idioventricular beats and sinus beats occurring at nearly the same rate.

The reason for this rhythm in this patient is apparent from leads V1-3 (the sinus conducted beats, so they can be interpreted) – the patient is having an acute anterior MI. Periods of accelerated idioventricular rhythm are common during acute infarction and especially during reperfusion following thrombolysis.   AIVR has also been termed nonparoxysmal ventricular tachycardia or “slow v. tach”. It usually does not produce any hemodynamic change, and requires no specific treatment.