Hold on, wait a second. I?m confused. I have never heard of this ?repolarization from apex to base? business as a separate process from the endo-epi repolarization. I have not seen the evidence for this, could anyone point me to where this is shown? I will be the first to admit that I have much to learn, but I don?t think these are separate things.
Here?s how I understand it, it may not conflict much with those posted before me, but apparently I think of it a little differently.
If we put a set of leads on a single muscle cell, and introduced an action potential on the side of the negative lead (such that the AP, which is a negatively charged wave front, would propagate from negative lead to positive lead) the trace would deflect in the positive direction until exactly half of the membrane was depolarized (negatively charged) and half was not yet depolarized (positively charged). It is at this point that there is maximal potential difference, and hence, the peak of the ?spike? on the tracing. As the negative wave front continues across the cell, the potential difference decreases, and the trace reverses direction returning to the baseline. The channels are now inactivated (refractory) and the membrane is in an isoelectric state.
If this were a normal, non-cardiac cell, the first portion to depolarize would be the first portion to repolarize. Now with a positive wave front, the polarity is reversed and there is a very small positive charge at the negative lead that will grow (in terms of potential difference) as it propagates toward the positive lead side (which is at this point negative) and thus is manifested as negative trace deflection from baseline. The trace will continue downward until exactly half of the cell is positive and half negative on the outside, which is the greatest measured potential difference, and then will travel back positively until base line as the cell is repolarized.
In the ventricle, however, the cells in the endocardium depolarize first, but then repolarize last (Some say they repolarized late because they are cooled more by the passing blood, but that is for another discussion).
The depolarization of the ventricles is registered positively in most of the leads (depending on the axis, being seen best in lead II) because the action potential originates from the midpoint of the interventricular septum on the left side, travels down the septum and out across the walls of the ventricles. This is a huge peak (QRS) because of the large net dipole (particularly from traveling down the septum). The axis of lead II is approximately in line with the septum, so the deflection is greatest here, and it is positive because the positive lead is closest to the apex. After full depolarization, we are now back at baseline, and the cells of the heart are now relatively negative. Now if the septum repolarized first, the tracing would go down, but it doesn?t. The epicardial cells repolarize first. What is the charge state of the cells and their relation to the leads at this point? The positive charges are once again at the positive lead, the negative charges are at the negative lead, just as it was in depolarization, thus, a positive deflection.
So you need to ask: where is the positive lead, and what is the charge state of the outside of the membrane by that lead? If it is positive relative to parts by the negative lead, then it will register as activity above the baseline, if it is negative it will register as activity below it (provided these events have a vector component parallel to the axis of the leads).
Now this is where I am confused about the base-to-apex, apex-to-base business. Since the AP travels from the left, mid-septum out to the apex, (in addition to the just previous atrial contraction) I can see where one would say that there is base-to-apex depolarization. But I don?t understand the apex-to-base repolarization business. If this were truly the case, lead II would show a huge dipole just like the QRS complex (and hence a large deflection of the trace) as the repolarization wave traveled back up the septum to the base but it doesn?t. I thought that the net dipole of repolarization (and as a result, the shape and direction of the wave) could be explained adequately by the endo-epi repolarization direction switch and the heart simply not being symmetrical (the dipole created by the wall of the left ventricle pretty much overpowers and cancels out the wall of the right as far as the meter is concerned).
Now are we all even more confused?
