Shannon Blog For Students at Rush University

I’ve been asked quite a bit about the effect of class I anti-arrhythmic drugs.  The three subclasses of these drugs have different effects but they share one thing in common:  they block Na channels.

Na channels in ventricular and atrial cells much are like the Na channels in nerve and skeletal muscle.  They media rapid depolarization once threshold is attained.  Decreasing the number of available Na channels – in this case by blocking them – decreases action potential conduction velocity just like it did in these other tissues when we studied them previously.

Consider the situation illustrated above.  The unidirectional block is in the beta branch of the pathway (top figure).  The action potential travels down the alpha branch (which is normal) and back up the beta branch (bottom figure).  Note that though conduction is still allowed up the beta branch in a retrograde fashion, these cells are still abnormal and conduction may be slowed (bottom figure, squiggly line).  If the action potential goes up the beta branch and reaches the alpha branch after the alpha branch has exited its refractory period, a re-entrant arrhythmia results.

With all of the class I anti-arrhythmic subclasses, the hope is that you will slow the conduction down in the already diseased beta branch enough to where it just completely stops and never gets back up to propagate back down the alpha branch.  Some of the subclasses are more effective than others in this regard.  And, of course, they all have different effects in addition to this.  But they all do the above to at least some extent.

I’m getting this one a lot:

I have a question regarding #28 on one of your old exams: “If the AV node is destroyed then it is expected that…”

I understand that “b) the ventricles will beat at a slower rate than normal” because their pace will be set by the purkinje fibers. But would “d) the atria will beat at the normal rate” not also be true because their contraction is dictated by the SA node and depolarization occurs independent and before the AV node?

Third degree heart block is, of course, what you get when the AV node can’t conduct action potentials to the ventricles.

Propagation of the action potential around the heart. The numbers are the time in seconds that it takes for the action potential to reach each region as it propagates away from the SA node.

Physiologically, the SA node, the AV node and some Purkinje fibers all will spontaneously depolarize. In this case, the action potentials aren’t getting to the ventricle. Without action potentials from the the SA node, the AV node takes over first and if that can’t take over due to disease, the Purkinje fibers do. The SA node set the pace when healthy because it depolarizeS fastest during phase 4. The action potential propagates away and stimulates the AV node and Purkinje fibers before they have has a chance to spontaneously throw an action potential on their own.

Therefore you may conclude that the SA node sets the pace at a higher rate than the AV node or Purkinje fibers would.  If the SA node action potentials aren’t making it through, the AV node sets the pace at its own rate, which is slower or, if that’s not possible, the Purkinje fibers set an even slower rate.

Therefore:

I’ve been asked several times about question 27 on page 46 of the week 4 course notes.  The question asks about the steady state MAP during vigorous exercise.  The answer is that MAP is increased.

The problem is that, as most of you will recall, in the lecture I did in the Human Simulation Laboratory I said that the MAP wouldn’t change or might decline a little bit with an initial drop followed by a reflexive increase that wouldn’t quite get back up to the starting point.

In fact, if you look at the real data in the figure in that lecture, the MAP increases just slightly in this figure.  I don’t emphasize this in class because its due to a little understood central mechanism and the effect is very slight.

I’ve been asked several times about this because I put a question on the practice exam related to it.

In retrospect, I wish that I hadn’t used the class IB as the example on this question and I will change it next year.  However, for the record, all of the class I anti-arrhythmics block Na channels and blocking Na channels slows the action potential propagation.  I admit that the effect is nowhere near as strong with the IB as it is in the IC and IA because the IB are open channel blockers that aren’t as effective during the rapid upstroke.  Nevertheless, it will always happen to some extent and it is an effect which you may see particularly in diseased tissue.