Atrioventricular Node Block Is a Common Cause of Cardiac Arrhythmias
Whereas sick sinus syndrome exemplifies a dysfunction of action potential formation, AV node block is a common dysfunction of action potential conduction. If damage to the AV node prevents (blocks) conduction of atrial action potentials into the ventricles, the atria continue to beat at a rate determined by the SA node pacemaker cells.
The ventricles also continue to beat, but at a much lower rate. In such a case the ventricular action potentials and contractions are being initiated by auxiliary pacemaker cells low in the AV node (i.e., below the level of the block). Because the AV node pacemaker cells depolarize more slowly than the SA node pacemaker cells, the ventricles in a resting dog with AV node block typically beat at only 30 to 40 beats/min. Furthermore, these ventricular beats are not synchronized with the atrial contractions.I hree degrees of severity of AV node block are recognized. Complete block of the AV node, in which no atrial action potentials are conducted to the ventricles, is called third- degree AV node block. If action potentials are conducted sporadically from the atria to the ventricles, so that the AV node transmits some atrial action potentials but not all of them, the condition is called second-degree AV node block. In a patient with second-degree block, some atrial contractions are followed by ventricular contractions, and others are not. Strong parasympathetic activity can create or exaggerate second-degree AV node block because parasympathetic activity increases the refractory period of the AV node cells. For example, in quietly resting horses, parasympathetic activity is often so strong, and the AV node refractory period so long, that some atrial beats are not conducted to the ventricles. Therefore, if the pulse of a relaxed, resting horse is palpated, some “missing” ventricular contractions are likely to be noticed.
During exercise the same horse does not show AV node block because parasympathetic activity has been decreased and sympathetic activity increased. Both these changes shorten the refractory period of the AV node and make it much more certain that every atrial action potential will be conducted to the ventricles.Second-degree or third-degree AV node block often involves the electrical phenomenon known as decremental conduction. As mentioned, AV node cells have “slow” action potentials, characterized by a less rapid upstroke, a lower voltage amplitude, and a slower velocity of conduction than the action potentials in regular atrial or ventricular cells. All these differences make conduction of the action potential from cell to cell less reliable in the AV node than in regular atrial or ventricular tissue. When the AV node cells are in an electrically depressed state» an atrial action potential may simply die out within the AV node and may not be conducted to the ventricles. This fading and eventual stoppage of a cardiac action potential in a slowly conducting region is called decremental conduction.
The mildest degree of AV node block is first-degree block, in which every atrial action potential is transmitted to the ventricles, but the action potential propagates even more slowly than normal through the AV node. Therefore, in first-degree block, the delay between atrial contraction and ventricular contraction is abnormally long. Because the AV node conduction velocity can be slowed by parasympathetic activity and sped by sympathetic activity, the behavioral stale of the patient characteristically influences the severity of first-degree block.
AV node block can be caused by cardiac trauma, toxins, viral or bacterial infections, ischemia, congenital heart defects, or cardiac fibrosis. AV node block is sometimes caused by inadvertent damage of AV node tissue during a surgical repair of a ventricular septal defect.
AV node block must be treated if the resulting ventricular rate is too low to maintain adequate blood flow to the body. Drugs that block parasympathetic actions on the heart (muscarinic cholinergic antagonists such as atropine) might reduce the AV node refractory period and decremental conduction sufficiently to overcome a blocked state. The same effect might be achieved with a drug that mimics the effect of sympathetic nerves by activating β-adrenergic receptors (e.g., isoproterenol) (see Table 19-2). If drug treatment fails to correct AV node block, an artificial pacemaker is needed. In the case of AV node block, the pacemaker needs to be applied to the ventricles; pacing the atria would not be beneficial because atrial action potentials would not be conducted to the ventricles.