As we saw, the atrial rate is actually somewhere between 400 and 600 BPM. If the ventricles responded on a 1:1 conduction (as can occur in someone with an accessory pathway), the result would be catastrophic. Luckily, the atrioventricular (AV) node cannot respond in a 1:1 conduction to the constant barrage of impulses hitting it from the atrial wavelets. Figure 20-3 showed a small section of atrial tissue with various wavelets competing for control. In this example, the red wavelet is able to weave its way through the quagmire of refractory tissue and eventually reaches the AV node. That red depolarization wave, however, may not be the lucky one that triggers the ventricular depolarization. Can you figure out why?
Each depolarization wavelet that manages to survive has to compete for control over the AV node (Figure 20-4). Remember, there can be any number of depolarization wavelets hitting the AV node at any one time. When these wavelets reach the AV node, they will depolarize a small area of AV nodal tissue, causing their own little refractory sections. Eventually, one wavelet will manage to weave its way through and reach the main area of the AV node. Then, and only then, will the AV node fire and trigger off a ventricular response. This process is variable, and which wavelet will eventually reach the main area of the AV node will be completely random. This randomness reflects exactly how the ventricular response will occur—completely at random.
Figure 20-4 This diagram shows five depolarization waves headed toward the AV node at the same time. Each of the waves enters the AV node and begins to depolarize the node. The blue, pink, green, and yellow waves cancel each other out. They cancel each other out because they hit a “wall” of refractory tissue caused by one of the other waves. The red wave hits the AV node, and is able to weave its way through the refractory tissue and effectively depolarizes the distal node. The impulse is then conducted through the rest of the electrical conduction system as usual, leading to a normal-width QRS complex.
Other factors also affect the conduction of the impulse through the AV node. The most common problem is intrinsic disease of the AV node itself or the electrical conduction system. Almost all patients with atrial fibrillation have some form of structural heart disease. Age and time-related wear and tear on the heart are the most common precipitating factors in the arrhythmia. Left atrial enlargement is another major precipitating factor in the formation and stability of the arrhythmia.
The state of the autonomic nervous system will also greatly affect conduction rates and the irritability of the AV node. Sympathetic stimulation increases the ventricular response, and parasympathetic stimulation slows the ventricular response. Finally, drugs can greatly affect conduction through the AV node. Amiodarone, digitalis, beta-blockers, and calcium channel blockers all slow the ventricular response to atrial fibrillation.
On average, the ventricular response in many untreated patients is between 100 and 160 BPM. The term uncontrolled or decompensated atrial fibrillation is commonly used to describe patients with rates above 100 BPM, to differentiate this state from the controlled state. Ventricular responses that are at or below 100 BPM are referred to as controlled. Treatment, advanced AV nodal disease, and the chronic state of the arrhythmia all help to slow down ventricular response to the clinically preferred controlled rates.
