Third-Degree Atrioventricular Block

History. A 5-year-old male English bulldog has fainted several times during the past 3 weeks. On each occasion he collapses, is apparently unconscious for a few seconds, and then slowly recovers.

Clinical Examination. The dog is moderately obese. There are no obvious neurological deficits. His mucous mem­branes appear normal; they are pink, and the capillary refill time is normal (1.5 seconds). Auscultation of the chest reveals a slow, regular heart rate of 45 beats/min. The femoral pulse rate is also 45 beats/min and strong. Thoracic radiography reveals a mildly enlarged heart, but the radiographs are otherwise within normal limits.

The electrocardiogram (ECG) reveals a disparity between the atrial rate (atrial depolarizations occurring regularly, 140 times/min) and the ventricular rate (ventricular depolar­izations occurring regularly, 45 times/min). There is no con­sistent time interval between the atrial and ventricular depolarizations.

Comment. Voltage fluctuations are produced at the body sur­face by atrial and ventricular depolarizations (see Chapter 20). Electrocardiography detects these voltage fluctuations and produces a graph of voltage as a function of time. I he ECG of this dog shows a complete dissociation between atrial and ventricular depolarizations, which provides definitive diag­nostic evidence of complete (third-degree) AV node block. The dog’s atria are depolarizing 140 times/min in response to action potentials being initiated in the normal manner by pacemaker cells of the SA node. However, the atrial action potentials are not being conducted through the AV node. Ventricular action potentials are being initiated, at the slow rate of 45∕min, by auxiliary pacemaker cells located below the blocked region of the AV node.

The low ventricular rate in this dog allows a longer-than- normal time for ventricular filling between beats. Therefore the volume of blood ejected with each beat (the stroke vol­ume) is greater than normal. The increased stroke volume causes the femoral pulse to be very strong.

In a normal dog, sympathetic and parasympathetic nerves acting on the SA node pacemaker cells adjust the heart rate so that cardiac output is matched to the metabolic requirements of the body. In a dog with complete AV block, the ventricles do not respond to these autonomically mediated changes in SA node pacemaker rate. Typically, the rate of ventricular con­tractions is low at rest and cannot increase much during exer­cise. Therefore, cardiac output does not increase enough during exertion to meet the increased metabolic needs of exercising skeletal muscle. As a consequence, arterial blood pressure decreases. The decreased arterial pressure during exercise causes brain blood flow to fall below the level needed to sustain consciousness. The dog faints.

Treatment. Drug therapy for AV node block involves either blocking the effects of parasympathetic nerves on the AV node (with a muscarinic cholinergic antagonist drug such as atro­pine) or mimicking the effects of sympathetic activation (with cautious use of a β-adrenergic agonist such as isoproterenol or dopamine). The rationale for these treatments is based on the following physiology: AV node block occurs because atrial action potentials “die out” in the AV node (decremental con­duction). Parasympathetic activation increases the tendency for decremental conduction because parasympathetic nerves act on AV node cells to increase their refractory period and to decrease the velocity with which action potentials spread from cell to cell. Therefore, blocking parasympathetic effects some­times (but rather rarely) reverses AV node block. Sympathetic nerves decrease the refractory period of AV node cells and increase their conduction velocity. Therefore, sympathetic activation decreases the tendency for decremental conduc­tion; a sympathomimetic drug (one that mimics the effects of sympathetic activation) has the same effect. In addition, sympathetic nerves act directly on the ventricular auxiliary pacemaker cells to increase their rate. Therefore, even if a sym­pathomimetic drug does not unblock the AV node, it increases somewhat the ventricular rate.

Many cases of third-degree AV block cannot be managed effectively with drugs, so an artificial ventricular pacemaker must be installed. The procedure is straightforward; pace­maker electrodes can be inserted into the right ventricle through a systemic vein (e.g., external jugular) with only sedation and local anesthesia. The electrode wires are attached to a battery- powered pacemaker unit that is then implanted under the skin.