What are the causes and treatment options for supraventricular tachycardia (SVT) in patients with a history of cardiac issues, such as Wolff-Parkinson-White syndrome or thyroid disease?

Causes of Supraventricular Tachycardia

SVT arises from reentry mechanisms or abnormal automaticity at or above the atrioventricular node, with specific etiologies including intrinsic cardiac conduction abnormalities, accessory pathways, and secondary triggers that must be systematically excluded. 1

Primary Mechanisms and Intrinsic Causes

Reentrant Arrhythmias (Most Common)

• Atrioventricular nodal reentrant tachycardia (AVNRT) accounts for the majority of SVT cases, caused by dual AV nodal pathways creating a reentry circuit within the AV node itself 1, 2
• Atrioventricular reciprocating tachycardia (AVRT) results from accessory pathways connecting atria to ventricles, bypassing the normal conduction system—this includes Wolff-Parkinson-White syndrome where the accessory pathway (Bundle of Kent) is capable of antegrade conduction 1
• Concealed accessory pathways conduct only retrograde (ventricle to atrium), causing AVRT without visible pre-excitation on resting ECG 1

Automatic/Focal Mechanisms

• Focal atrial tachycardia originates from abnormal automaticity or triggered activity in atrial tissue, often from the crista terminalis or pulmonary vein ostia 1
• Sinus node reentrant tachycardia involves reentry within or near the sinus node 1
• Junctional tachycardia arises from the AV junction with abnormal automaticity 1

Macroreentrant Atrial Tachycardias

• Typical atrial flutter (cavotricuspid isthmus-dependent) creates a macroreentrant circuit in the right atrium 1
• Atypical atrial flutter involves left atrial circuits (mitral isthmus-dependent) or other non-CTI-dependent right atrial circuits 1

Secondary Causes and Triggers (Critical to Exclude)

Metabolic and Endocrine

• Hyperthyroidism is a critical secondary cause that must be excluded, as thyroid hormone excess increases automaticity and triggers SVT 1
• Electrolyte abnormalities including hypokalemia, hypomagnesemia, and hypocalcemia can precipitate arrhythmias 1

Exogenous Substances

• Caffeine and energy drinks are well-established triggers for tachyarrhythmias, particularly in young adults, and should be completely eliminated 3
• Drugs of abuse including cocaine, amphetamines, and other sympathomimetics 1
• Medications that prolong QT interval or increase sympathetic tone 1

Physiological States

• Anxiety and emotional stress trigger physiological sinus tachycardia through appropriate autonomic responses, which differs mechanistically from true SVT but must be distinguished 1, 4
• Dehydration, anemia, pain, and fever cause secondary sinus tachycardia that resolves with correction of the underlying condition 1, 4
• Pregnancy increases SVT risk due to hemodynamic and hormonal changes 1

Cardiac Structural Abnormalities

• Congenital heart disease significantly increases SVT risk and is associated with worse outcomes including heart failure, stroke, and sudden cardiac death 1
• Cardiomyopathies must be excluded, though SVT rarely causes structural heart disease itself 1
• Valvular heart disease can predispose to atrial arrhythmias 1

Special Populations and Contexts

Wolff-Parkinson-White Syndrome

• Pre-excitation on ECG (delta waves, short PR interval) indicates an accessory pathway capable of rapid antegrade conduction 1, 3
• This carries risk of sudden death if atrial fibrillation develops and conducts rapidly to ventricles, requiring immediate electrophysiology referral 3, 5

Inappropriate Sinus Tachycardia (IST)

• IST is a diagnosis of exclusion after ruling out all secondary causes including thyroid disease, anemia, dehydration, anxiety, and structural heart disease 1
• Mechanisms include dysautonomia, neurohormonal dysregulation, and intrinsic sinus node hyperactivity 1
• Must be distinguished from postural orthostatic tachycardia syndrome (POTS), where symptoms relate to postural changes 1

Perioperative SVT

• Sympathetic hyperactivity is the primary mechanism in the perioperative setting 1
• Aggravating factors include respiratory failure, electrolyte imbalance, and high adrenergic states 1

Critical Diagnostic Distinctions

Capturing a 12-lead ECG during tachycardia is essential before any treatment decisions, as the mechanism cannot be reliably determined from symptoms alone 3. The resting ECG must be examined for pre-excitation (delta waves), which mandates immediate specialist referral due to sudden death risk 3.

The prevalence of SVT is 0.2% in the general population, increasing five-fold in those aged ≥65 years, with women having twice the risk of men 1. Unlike ventricular tachycardia, SVT is rarely life-threatening but can cause heart failure, pulmonary edema, and myocardial ischemia if untreated due to sustained rapid rates 1.