Atrioventricular block in the dog and cat

The heart contains a specific system dedicated to the generation of electrical impulses and their conduction to the working myocardium. This system consists of cells able to generate an electrical impulse spontaneously and bundle structures that propagate the impulse to the atria and ventricles. The electrical impulse originates in the sinus node, situated at the junction between the right atrium and cranial vena cava, and propagates via the internodal, interatrial and atrionodal pathways until it reaches the atrioventricular node. The junctional area is the site where the electrical impulse slows most and in normal conditions the impulse takes about 110 msec to cross this area. This slowing of the electrical impulse is necessary in order for ventricular diastole to be effective, and occurs because of the decreased conduction of the junctional area.

Having crossed the junctional area, the electrical impulse travels along the bundle of His, once again at a high velocity. If the impulses arrive at the junctional area at too high a frequency or at too low an intensity, transmission along the conduction system is blocked. This block is particularly important during supraventricular tachycardias, in which the atrioventricular node acts as a filter able to reduce the arrival of high frequency impulses in the ventricles. In pathological conditions, the transmission of the electrical impulse across the junctional area can be stopped, causing the development of an atrioventricular block (AVB).

The atrioventricular blocks can be classified as:

• First-degree AVB;
• Second-degree AVB;
• Third-degree AVB.

FIRST-DEGREE ATRIOVENTRICULAR BLOCK

First-degree AVB is manifested as an abnormally long PQ interval, that is, > 130 msec in the dog and > 90 msec in the cat. Other electrocardiographic findings are P waves with a sinus axis and normal frequency, QRS < 70 msec in the dog and < 40 msec in the cat (Fig. 1).

First-degree AVB can be caused by strong vagal stimulation, degenerative disorders of conduction tissues and iatrogenic factors (β-blockers, calcium antagonists, digitalis drugs) or be secondary to hyperkalaemia. Animals with first-degree AVB do not show any clinical signs of the disorder, either at rest or during effort.

SECOND-DEGREE ATRIOVENTRICULAR BLOCK

In this type of AVB, the interruption of atrioventricular conduction is intermittent and the blocks are classified on the basis of the form of the interruption and the atrioventricular conduction ratio. Second-degree AVB can be a physiological finding in the first few years of life, be secondary to marked vagal stimulation or chronic respiratory diseases, have an iatrogenic cause following the administration of β-blockers, calcium antagonists, digitalis, or opioids, or be secondary to supraventricular tachycardia, stenosis of the bundle of His in pugs or fibrosis of conduction tissue in elderly dogs.

Second-degree atrioventricular blocks are divided into:

• Mobitz I (Wenckebach’s phenomenon);
• Mobitz II;
• Type 2:1 fixed;
• Advanced.

Wenckebach’s (or Mobitz I) AVB

In Wenckebach’s type second-degree AVB the intermittent interruption of atrioventricular conduction is characterized by a PQ interval that is shorter after the block than before it, progressive prolongation of the PQ intervals before the block associated with progressive lengthening of the RR intervals before the block (Fig. 2). The prolongation of the PQ interval is due to an increase in the period of relative refractoriness of the cells of the atrioventricular node. Wenckebach’s type second-degree AVB can be secondary to vagal hyperactivity and typically occurs at end-expiration

Mobitz’s (or Mobitz II) AVB

Mobitz’s second-degree AVB is characterized by an intermittent interruption in atrioventricular conduction with a PQ interval following the block that is the same length as long as the PQ interval preceding the block, no prolongation of the PQ interval or shortening of the RR interval prior to the dropped beat (Fig. 3).

Type 2:1 fixed

Second-degree AVB type 2:1 fixed is characterized by an intermittent interruption in conduction such that only one P wave out of two is transmitted to the ventricles and, therefore, followed by a QRS complex. As a result, the ventricular rate is half that of the atrial rate (Fig. 4).

Advanced type AVB

In second-degree advanced AVB the intermittent interruption of the conduction occurs in such a way that two or more P waves are consecutively blocked giving rise to variable atrioventricular conduction ratios, but always greater than 2:1 (Fig. 5).

Atropine test

The atropine test can be used in animals with first- and second-degree AVB in order to determine whether the block is due to malfunctioning of the atrioventricular node or excessive vagal stimulation.

The test consists in administering 0.04 mg/kg of atropine subcutaneously. After about 15-30 minutes, the block disappears if it is secondary to vagal stimulation. The test can also be performed using sympathomimetic drugs such as isoproterenol 0.02-0.04 μg/kg or dopamine 2-7 μg/kg.

THIRD-DEGREE ATRIOVENTRICULAR BLOCK

Third-degree AVB occurs when atrioventricular conduction is completely interrupted and accessory pacemakers take on the role of the dominant pacemaker. There is dissociation between atrial and ventricular activity; that is, there is a lack of correlation between P waves and QRS complexes. The PP intervals and the RR intervals are, in fact, relatively constant, but not related to each other. The duration of the QRS complexes may be normal, if the ectopic focus is before the bifurcation of the branches, or increased, if the ectopic focus is in the ventricle. The accessory pacemakers that are activated are usually those in the ventricles, which have a very low rate of firing (from 30 to 60 bpm) (Fig. 6). The animal may have clinical signs compatible with severe bradycardia or the prolonged ventricular arrest.

Third-degree AVB may be congenital or secondary to excessive doses of drugs (digoxin, calcium-antagonists, beta-blockers), bacterial endocarditis, myocarditis, degenerative disorders (e.g., atrioventricular dystrophy in Springer spaniels), and hyperkalaemia. The clinical signs include fatigue, exercise intolerance, fainting and syncope. Sudden death or congestive heart failure can occur as a consequence of the reduced cardiac output or the development of bradycardia-dependent ventricular tachyarrhythmias. At physical examination there is variation in the intensity of the first heart sound, the appearance of third and fourth heart sounds and raised jugular venous pressure.

TREATMENT

Implantation of a permanent intracardiac heart stimulator (a pacemaker) is the only effective treatment for fixed type 2:1 and advanced second-degree AVB and for third-degree AVB. A pacemaker is an instrument that can electrically stimulate the contraction of the heart when this stimulus is not provided normally by the cardiac conduction tissue. A pacemaker is formed of a battery, placed in a subcutaneous pocket in the region of the neck, and by one or two electrodes which, introduced through the jugular vein, reach the apex of the right ventricle and right atrial appendage. There are various types of pacemakers, classified on the basis of where the autologous signal is recorded and the chamber(s) stimulated.

Table 1. Classification of atrioventricular blocks, their possible causes, suggested treatment and prognosis.

Suggested readings

1. Santilli RA, Perego M. Elettrocardiografia del cane e del gatto. 2009, Milano, ed. Elsevier, Masson, pp:176-182.
2. Kittleson MD, Kienle RD. Small Animal cardiovascular medicine. 1998, St Louis, MO, ed Mosby, pp: 487-492.
3. Miller MS et al. Electrocardiography. In: Fox PR, Sisson DD, Moise NS. Textbook of canine and feline cardiology. 1999, Philadelphia, PA, ed Saunders Co. pp: 67-105.