Cells of the Atrioventricular Node Act as Auxiliary Pacemakers and Also Protect the Ventricles from Beating Too Fast

As with SA node cells, the cells of the AV node normally exhibit pacemaker activity and slow action potentials. As shown in Figure l9-lθ, the AV^r node cells spontaneously depolarize toward threshold, but much more slowly than do the SA node cells.

Under certain abnormal conditions, AV node pacemaker function becomes critical for survival. For example, if the SA node is damaged and does not depolarize to threshold, the spontaneous depolarization of the AV node pacemaker cells initiates action potentials and therefore cardiac contractions. If not for this auxiliary pacemaker function of AV node cells, the heart with a damaged SA node would not beat at all. The heart rate is characteristically very low when the AV node cells are initiating the heartbeats. Because the AV node pacemaker cells depolarize more slowly than normal SA node cells, the heart rate resulting from AV node pacemakers is very low, about 30 to 40 beats/min in a resting dog, compared with 80 to 90 beats/min when the SA node cells are the pacemakers. Nevertheless, if the SA node fails as a pacemaker, enough heartbeats are initiated by the AV node to sustain life tem­porarily. Thus, AV node cells are sometimes called the heart’s emergency pacemakers.

Another important feature of the AV node cells is that they have much longer refractory periods than do normal atrial cells. The long refractory period of AV node cells helps protect the ventricles from being stimulated to contract at rates that are too rapid for efficient pumping. This protective function of the AV node is critical to an animal's survival when atrial action potentials are extremely frequent (see later discussion of atrial HutterZfibrilIation). The long refractory period of the AV node cells plays an important role, even in a normal heart. Once a normal action potential reaches the ventricles, it is prevented from “circling back” (and reactivating the atria) by the prolonged refractory state of the AV node cells.

Table 19-2 summarizes the four important electrical charac­teristics of the AV node previously discussed. Note that three of these characteristics are influenced by the nervous system. As indicated in the table, sympathetic activity increases the conduction velocity of the AV node cells, shortens their refrac­tory period, and speeds their auxiliary pacemaker activity. Parasympathetic activation has the opposite effects. These sym­pathetic and parasympathetic effects are appropriate for dif­ferent heart rates. For example, when sympathetic activity is high and the SA node pacemakers are initiating heartbeats frequently, the whole process of cardiac contraction and relaxation must be sped up. Thus it is appropriate that sym­pathetic action also increases the velocity of action potential conduction through the AV node, which shortens AV delay. In addition, sympathetic activation shortens the AV node refractory period, which allows each of the frequent atrial action potentials to be conducted to the ventricles. Finally, sym­pathetic activation enhances AV node auxiliary pacemaker activity, which provides the animal with a high enough ven­tricular rate to cope with some stress, even if the SA node pacemaker has failed. Conversely, when parasympathetic activation causes the SA node pacemakers to decrease the heart rate, all aspects of cardiac contraction and relaxation can proceed at a more leisurely pace.

Table 19-2

•Through activation of β-adrenergic receptors. ^tThrough activation of muscarinic cholinergic receptors.