Diagnosis and Management of Supraventricular Tachycardias

Supraventricular tachycardias (SVTs) are rhythm disturbances arising above the bundle of His and include arrhythmias originating from the sinus node, atrial tissue, or atrioventricular node. They are characterised by narrow QRS complexes and rapid heart rates on electrocardiography (ECG).

SVTs may develop because of abnormalities in impulse formation or impulse conduction. Mechanisms include increased automaticity of pacemaker tissue, triggered activity, re-entry circuits, fibrosis, myocardial stretch, ischaemia, or accessory pathways.

SVTs commonly occur in animals with structural heart disease, systemic illness, metabolic abnormalities, endocrinopathies, or electrolyte disturbances, although idiopathic cases also occur. Clinical signs range from asymptomatic disease to panting, exercise intolerance, congestive heart failure, haemodynamic instability, and tachycardia-induced cardiomyopathy.

Holter monitoring is highlighted as an important diagnostic tool because it allows assessment of rhythm disturbances over 24–48 hours, facilitates identification of intermittent arrhythmias, and helps assess treatment response.

Sinus tachycardia is described as an increase in sinus node discharge caused by physiological or pathological stimuli such as exercise, congestive heart failure, hypoxia, anaemia, pain, or hypotension. ECG findings include normal P waves, normal PQ intervals, narrow QRS complexes, and gradual onset and offset of tachycardia.

Atrial fibrillation (AF) is one of the most common arrhythmias in veterinary medicine and is characterised by rapid, disorganised atrial electrical activity, loss of coordinated atrial contraction, and irregular ventricular rhythm. Most affected dogs and cats have structural heart disease and atrial enlargement, although lone AF may occur in large breed dogs.

Electrocardiographic findings in AF include absence of identifiable P waves, fibrillatory “f” waves, irregular R-R intervals, and narrow QRS complexes. Some dogs may show aberrant conduction producing wide QRS complexes resembling ventricular tachycardia. Echocardiography is recommended to assess chamber enlargement and congestive heart failure. Treatment usually focuses on ventricular rate control using medications such as diltiazem and digoxin.

Atrial flutter is described as a rapid but organised arrhythmia caused by a macro re-entrant circuit, usually within the right atrium. ECG findings include characteristic “sawtooth” flutter waves with atrial rates between 200–450 bpm. Ventricular response depends on atrioventricular conduction ratio and may be regular or irregular. Radiocatheter ablation is discussed as a definitive treatment option.

Focal atrial tachycardia (FAT) originates from an ectopic atrial focus and may occur with congenital heart disease, myocarditis, neoplasia, hyperthyroidism, or digoxin toxicity. ECG findings include narrow QRS complexes, rapid ventricular rates, ectopic P′ waves, and long RP′ intervals. Dogs refractory to medical treatment may undergo electrophysiological mapping and radiofrequency ablation.

Multifocal atrial tachycardia (MAT) is associated with severe atrial disease, electrolyte abnormalities, and digitalis toxicity. ECG findings include multiple P′ wave morphologies, variable P′Q intervals, irregular R-R intervals, and narrow QRS complexes.

Focal junctional tachycardia (FJT) is caused by rapidly discharging foci near the atrioventricular junction and is reported commonly in Labrador Retrievers. ECG findings include narrow QRS complexes, ventricular rates of 100–160 bpm, and atrioventricular dissociation with variable PR intervals.

Accessory atrioventricular pathways are congenital muscular connections between atria and ventricles that bypass the atrioventricular node. Labrador Retrievers and Boxers are overrepresented. Antegrade conduction produces ventricular pre-excitation with short PR intervals, wide QRS complexes, and delta waves.

Orthodromic atrioventricular reciprocating tachycardia (OAVRT) occurs when impulses travel normally through the AV node and return retrogradely through an accessory pathway. ECG findings include narrow QRS complexes, regular tachycardia, retrograde P′ waves, short RP′ intervals, and electrical alternans.

The paper presents a stepwise ECG approach to diagnosis of SVTs based on QRS width, rhythm regularity, ventricular rate, P wave identification, RP′ relationships, atrioventricular block, electrical alternans, and ventricular pre-excitation.

Diagnosis of SVTs may require Holter monitoring, vagal manoeuvres, drug trials, echocardiography, or intracardiac electrophysiological studies. Persistent tachycardia can lead to tachycardia-induced cardiomyopathy, making early referral and accurate diagnosis important.

The paper concludes that SVTs represent a diverse group of tachyarrhythmias with overlapping ECG features, and that systematic ECG interpretation combined with ambulatory monitoring can improve diagnostic accuracy and management.