Supraventricular Tachyarrhythmias

Perhaps the most common supraventricular tachyarrhythmia is atrial fibrillation, although it is uncertain how often dogs faint from this rhythm disturbance. Atrial fibrillation usually is associated with advanced heart disease that has produced severe atrial dilation, generally affecting the left atrium. If the condition is untreated, the ventricular response rate in the hospital setting usually is 200 to 250 beats/min. New-onset atrial fibrillation can cause episodic weakness, collapse, or syncope. The loss of the atrial boost to left ventricular filling as well as rapid and particularly irregular diastolic filling durations, coupled with the underlying disorder, produce a marked drop in cardiac output.

Other causes of SVT include nodal tachycardia, AV reciprocating tachycardia, atrial flutter, and atrial tachycardia. Some of these SVTs can be associated with ventricular rates that exceed 300 beats/min and can be as high as 400 beats/min, especially with reciprocating tachycardias using an accessory pathway. The ventricular response rate to atrial flutter and some ectopic atrial tachycardias is quite variable because these often are associated with physiologic AV block that may control the ventricular rate response, sometimes to less than 200 beats/min. However, if AV nodal conduction is rapid, ventricular rates of 300 beats/min or higher can be seen. Rapid SVT is less likely to induce syncope because the rhythm is regular and the sequence of ventricular activation is normal, but collapse or loss of consciousness has been observed in some dogs. Many SVTs are not associated with overt structural heart disease, and structural changes may be due to the presence of tachycardia-induced cardiomyopathy. Of note is the SVT caused by AV reciprocating tachycardia (accessory pathway mediated) in the Labrador retriever.

Ventricular Tachycardia

One of the most common causes of syncope is rapid VT, especially in boxers with arrhythmic right ventricular cardiomyopathy (see Chapter 179) and Doberman pinschers with dilated cardiomyopathy (see Chapter 178). An inherited VT also occurs in certain families of young German shepherd dogs. Cardiac output and blood pressure can fall precipitously with rapid VT related to shortened diastole, AV dissociation, and aberrant sequence of ventricular activation. All dogs with dilated cardiomyopathy are at increased risk of VT, and sustained rates above 300 beats/min likely will degenerate into ventricular fibrillation and death. Boxers with arrhythmic right ventricular cardiomyopathy without myocardial failure often experience rapid VT and faint. However, as long as left ventricular function is normal, sudden death is unusual, even when VT is sustained. VT in animals with hypertrophic cardiomyopathy or subaortic stenosis can cause syncope and death at rates as slow as 180 beats/min.

In both VT and SVT, it has been shown in humans and experimental studies that the drop in blood pressure at the onset can be transient, and after several seconds the blood pressure can rise and syncope can resolve despite continued tachycardia. This stabilization results from reflex vasoconstriction and elevation of catecholamine levels.

Neurally Mediated Syncope

Neurally mediated (reflex) syncope probably is the most common bradycardia-associated syncope (Web Figure 67-1). Neurocardiogenic syncope is triggered by fight, flight, or fright scenarios and can occur in apparently healthy individuals or those predisposed by high preload, genetics (boxer), or dilated cardiomyopathy. The diagnosis often is presumptive.