The AV node is unique in the body because electrical conduction is mediated by calcium rather than sodium channels. Atrial tachyarrhythmias in which the atria beat at a very fast rate are a common clinical occurrence. The high atrial rate can cause the ventricles to beat too fast to pump effectively. The ventricular rate can be easily slowed by a class of drugs called calcium antagonists that partially block the L-type calcium channels. These drugs will depress conduction in the AV node to the point at which only a small percentage of the atrial beats is actually conducted to the ventricle.
opens will the cell be receptive to restimulation. This causes an absolute refractory period all through phase 2 and into phase 3, making it impossible to tetanize cardiac muscle. The refractory period ensures that the heart will relax between beats, allowing it to refill with the blood that will be pumped on the next beat. As the inactivation gates begin to open, the heart goes through a relative refractory period late in phase 3 where it can be restimulated but the threshold required for stimulation is elevated. Also an attenuated contraction will result because not all cells have their inactivation gates open yet. In nodal tissue lacking fast sodium channels the L-type calcium channels are also refractory to restimulation well into electrical diastole.
As the wave of excitation finishes traversing the ventricles, the entire heart is in a refractory period, causing the wave to die out and the heart to relax. Sometimes conduction can be slowed in a diseased region to the point where the rest of the heart is out of the refractory period by the time the wave emerges from the depressed segment. When that occurs the heart can be restimulated by this delayed impulse causing a reentrant rhythm, in which the cycle repeats itself over and over. Under those conditions the heart may beat very rapidly or even fibrillate.
Na+ conductance underlies phase 0 and 1 of the action potential. The inactivation gates in the sodium channels spontaneously close within a millisecond or two after activation gate opening. Although the cell remains depolarized, Na+ conductance quickly returns to its resting level.
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