I think we all have a good understanding of how to identify AV blocks. In your static cardiology station you probably identified one in something of a “cold read” with a strip of Lead II. As time goes on we learn what we need to put this in clinical context.

When we add 12 leads and clinical presentation, the tracks start to come together. We just need that "aha" moment to make it click ("aha" is meant to be like "ahhhh haaaa" and not like the American Heart Association). For me this came in the form of a Tim Phalen 12 lead course (which I strongly encourage everyone to take). This blog post can barely touch on what he is able to articulate so well. Until you can get into one of his courses, here is a push dose of one of the concepts he covers.

Please imagine a garden variety chest pain patient with a good story and the following EKG:

There are three key features on this 12 lead:

There is a lot going on here - but all of the roads in this case lead to the AV Node.

About 80% of the population is said to be “right dominant”. This means that the right coronary artery (RCA) feeds the inferior wall of the left ventricle. In right dominant patients the AV node is fed by a branch of the RCA called the AV nodal artery (AVna). In most of the remainder of the population the AV node is fed by a branch of the left circumflex (LCx). There is also a small portion of the population (~2%) with “codominance”, where the AV node is fed by branches of the LCx and RCA. We are going to focus on the majority of patients who have “right dominant” vasculature.

It all starts with an occlusion in the RCA proximal or at the AVna. When we localize a STEMI we localize it to the area of the myocardium that is affected. That’s a good start but we can’t ignore the conduction side of the equation. In addition to the muscle cells the RCA is responsible for, it also supplies:

The RCA occlusion in this case also causes ischemia to the AV node and the vagus nerve. Ischemia to the vagus nerve causes it to synapse. Since the AV node is innervated by the vagus nerve on the parasympathetic side, AV node cells act as we would expect when acetylcholine binds to them. This prolongs the refractory period. 

So this leaves us with a question: is the block from ischemia to the node itself, or parasympathetic tone? It’s usually (but not always) parasympathetic tone. 

In this case the prolonged refractory period is what causes the block and bradycardic rate. Here is the normal distribution of the absolute and relative refractory periods:

Absolute: No level of stimulus can depolarize the cell.

Relative: A strong enough stimulus can depolarize the cell.

When a P wave arrives at the AV node it is similar to coming up to a toll plaza.... 

The lane it gets depends on where in the depolarization/repolarization cycle the AV Node is in. Like traffic, it’s more or less chance. 

Remember that in addition to changes in the duration of the absolute and relative refractory periods, the entire refractory period is prolonged. It’s also worth remembering that the patient can cycle through each degree of AV block sequentially. The patient could also spontaneously end up in a second or third degree block. It just depends on the exact ratio of absolute to relative refractory period, and when the P wave arrives.

That’s cool …. but so what?

They key is to focus on the STEMI and the QRS duration, and not so much on what “degree” of a block the patient is in. Since the QRS is narrow- we know that the P waves are conducting normally after the AV Node, we just need for more to get through.

What I am getting at is that in this flavor or ischemia atropine is safe. Atropine shortens the refractory period, the P wave conducts normally, and the block improves or resolves. Subsequently, the ventricular rate increases. Blocks associated with nodal ischemia are usually responsive to atropine. 

As long as we are confident that the ischemia is “nodal”, atropine is safe and usually effective. When acetylcholine from the vagus nerve is blocked the AV node can return to a normal refractory period. 

It has been taught in the past that atropine was inappropriate for all MI patients, and that pacing was the only appropriate therapy for bradycardia. This is by no means a blanket statement about atropine in MI. There are absolutely cases where pacing is the appropriate first-line 

But as always- follow your protocol. 

If you have seen this STEMI presentation I would love to hear about your case.

This is part one of The Block of Knowledge. For that ugly 12 lead with a high degree block, stand by to copy.

Author: Ryan Bolger


Tim Phelan’s Course: The 12 Lead ECG in Acute Coronary Syndromes

Life in the Fast Lane Medical Blog: Inferior STEMI

Radiopedia: Coronary Artery Dominance

 Radiopedia: Right Coronary Artery