The USMLE Step 1 Will Require You to Connect Ion Channel Physiology with EKG Findings. How Well Can You?

SA node → atrium → AV node → His Purkinje system → ventricle

There is an “accessory pathway” (sometimes called the “Bundle of Kent”) that bypasses the normal conduction pathway through the AV node, allowing conduction directly between the atrium and ventricle.

Purkinje > atria > ventricles > AV node

2.2 m/s (Purkinje)
1.1 m/s (atria)
0.3 m/s (ventricles)
0.03 m/s (AV node)

Note that there is a HUGE difference in conduction speed between Purkinje fibers and ventricles/AV node.

Atrial depolarization

Ventricular depolarization (NOTE: it is technically depolarization, NOT contraction, although contraction happens as a result of this depolarization)

Ventricular repolarization

Since the QRS complex represents ventricular depolarization, the LONGER it takes to get complete depolarization of the entire ventricle, the wider the complex.

In other words, if depolarization moves through the fast His Purkinje system (by first moving through the AV node), it will be narrow-complex.

Instead, if you have conduction between ventricular myocytes (i.e. NOT through the His Purkinje system), it will be wide-complex.

It is wide.

There are two sources of excitation of the ventricles in WPW. One source is the normal source: AV node → His Purkinje → ventricular myocytes. However, the other source actually involves ventricular myocytes in the path of the accessory pathway being excited prior to getting by the His Purkinje system, the so-called “pre-excitation.”

One

Lots (much more than one)

Atrial fibrillation: constant depolarizations of parts of the atrium

In other words, one small fragment of the atrium is depolarizing, while another is repolarizing, while a third has already depolarized, and a fourth is…, etc.

There is not a single wave of depolarization moving from the SA → AV node

During normal cardiac depolarization, it is like having a still pond, and having a single stream of drops, dropping into the same place at a regular rate. That drop will cause ripples throughout the entire rest of the pond.

Using this analogy, the single stream of drops would be like the SA nodal depolarization, while the rippling would be like the wave of depolarization that moves through the atrium.

Atrial fibrillation is like having a rainstorm, whereby LOTS of drops are falling all over the pond, causing mini ripples throughout the pond, but NOT a single ripple that will move through the entire pond.

Continuing with the previous analogy, let’s say that you have a sand castle on the beach (this will be your AV node). Every time one of the ripples hits the sand castle (AV node), it can cause depolarization that will run through the His Purkinje system. Normally, this is in a 1:1 ratio.

HOWEVER, in atrial fibrillation, there are MANY ripples (i.e. waves of depolarization) hitting the sand castle (AV node), constantly, and so the AV node is constantly being depolarized. Each time the AV node is depolarized enough to launch an action potential, the His Purkinje system (and thus the ventricle) will fire.

Each wave of depolarization that hits the AV node will NOT cause ventricular depolarization. This is because you need two things for AV nodal depolarization to conduct through:

1) The AV nodal depolarization must reach conduction (action potential) threshold
2) The AV node must NOT be in an absolute refractory period, and must be able to overcome the relative refractory period

Non-nodal tissue

Non-nodal tissue has a special K+ channel, called IK1. Thus, because a larger proportion of the ion channels open at rest are K+ channels in non-nodal tissue, its resting membrane potential will be much closer to the equilibrium potential of K+.

Sodium

Calcium

In order to activate Na+ channels generally in the heart, you must REMOVE INACTIVATION from them (double-negative, I’m sorry). In order to remove inactivation, you must have a more negative membrane potential. This is ONLY possible in non-nodal tissue, because of the presence of the special K+ channel, called IK1.

In other words, nodal tissues HAS Na+ channels (oddly enough), but it does NOT use them, because the membrane potential does NOT become negative enough to remove inactivation of the Na+ channels.

Ca++ channels do not have this sort of regulation, and thus will be active in nodal tissue.

Slowing down ventricular rate

Slowing conduction through the AV node → more difficult to reach the AV node action potential threshold → fewer depolarizations get through → lower ventricular heart rate

Calcium-channel blockers, β blockers, digoxin – anything that slows AV nodal conduction.

We continue with our previous analogy, where every ripple (atrial depolarization) in our pond that reaches the sand castle (AV node) → AV nodal depolarization → Purkinje depolarization → ventricular depolarization.

A calcium channel blocker makes it HARDER to depolarize the AV node (recall that Ca++, not Na+, is required for AV nodal depolarization), sort of like erecting a small barrier in front of our sand castle, so that only larger ripples (waves of depolarization) can actually reach said sand castle.