What are the differences between paroxysmal supraventricular tachycardia (PSVT) and ventricular tachycardia (VT)?

Distinguishing PSVT from VT

PSVT and VT are fundamentally different arrhythmias: PSVT originates from tissue at or above the His bundle with narrow QRS complexes (<120 ms) and rates of 150-250 bpm, while VT originates from the ventricles with wide QRS complexes (≥120 ms) and carries significantly higher mortality risk. 1, 2, 3

Origin and Mechanism

PSVT (Paroxysmal Supraventricular Tachycardia):

• Originates at or above the atrioventricular node, involving atrial or AV nodal tissue from the His bundle or above 4, 2
• Caused by re-entry mechanisms, most commonly atrioventricular nodal reentrant tachycardia (AVNRT) or atrioventricular reciprocating tachycardia (AVRT) involving accessory pathways 1, 5
• Characterized by sudden, abrupt onset and termination—not gradual like sinus tachycardia 2, 6

Ventricular Tachycardia:

• Originates from ventricular tissue below the His bundle 3
• Results from abnormal automaticity, triggered activity, or re-entry within ventricular myocardium 3
• Associated with structural heart disease, prior myocardial infarction, or cardiomyopathy in most cases 3

ECG Characteristics

PSVT Features:

• QRS duration <120 ms (narrow complex) in the absence of pre-existing bundle branch block 1, 2
• Heart rate typically 150-250 bpm with extreme regularity after the first 10-20 beats—"like a metronome" 2, 7
• P waves are hidden within or immediately after the QRS complex in approximately 60% of cases 2, 5
• In AVNRT, P waves create pseudo S-waves in inferior leads (II, III, aVF) and pseudo R' waves in V1 7
• RP interval <70 ms in typical AVNRT; RP interval 70-100 ms or longer in AVRT 7, 5

VT Features:

• QRS duration ≥120 ms (wide complex) 1, 3
• Presence of AV dissociation (ventricular rate faster than atrial rate) or fusion complexes strongly indicates VT 1
• R-S interval >100 ms in any precordial lead suggests VT 1
• Initial R wave in aVR or initial R/Q wave >40 ms in aVR indicates VT 1
• QRS concordance (all positive or all negative) in precordial leads V1-V6 suggests VT 1
• Notch on descending limb of predominantly negative QRS in aVR indicates VT 1

Clinical Presentation

PSVT:

• Palpitations (86%), chest discomfort (47%), dyspnea (38%), lightheadedness, or fatigue 1, 6
• Syncope occurs in approximately 15% of patients, usually at tachycardia onset or after abrupt termination 1, 2
• Polyuria may occur due to atrial natriuretic peptide release 1
• Generally benign in structurally normal hearts, though prolonged episodes can cause tachycardia-mediated cardiomyopathy 1, 6

VT:

• Carries significantly higher risk of hemodynamic collapse, syncope, and sudden cardiac death 3
• More likely to present with severe symptoms requiring immediate intervention 3
• Frequently associated with underlying structural heart disease 3

Acute Management Differences

PSVT Management (Hemodynamically Stable):

• Vagal maneuvers first-line (modified Valsalva maneuver 43% effective) 1, 6
• IV adenosine second-line (91% effective) if vagal maneuvers fail 1, 6
• Beta-blockers or calcium channel blockers (diltiazem, verapamil) as alternatives 6, 8
• Synchronized cardioversion only if hemodynamically unstable 1, 6

VT Management:

• Immediate synchronized cardioversion for hemodynamically unstable patients 1
• Antiarrhythmic medications (amiodarone, lidocaine) for stable monomorphic VT 3
• Never use adenosine, calcium channel blockers, or beta-blockers as first-line for wide-complex tachycardia of uncertain origin—these can be dangerous if the rhythm is VT 1

Critical Diagnostic Pitfalls

The most dangerous error is misdiagnosing VT as PSVT with aberrancy:

• When confronted with wide-complex tachycardia (QRS ≥120 ms), assume VT until proven otherwise 1, 3
• Wide-complex tachycardia can represent: VT, SVT with pre-existing bundle branch block, SVT with aberrant conduction, SVT with accessory pathway conduction (pre-excitation), or paced rhythm 1
• Only 31% of physicians correctly identify atrial fibrillation with prominent atrial activity, frequently misdiagnosing it as atrial flutter 7
• If AV dissociation or fusion complexes are present, the diagnosis is VT 1, 7

Long-Term Management

PSVT:

• Catheter ablation is first-line therapy for recurrent symptomatic PSVT with success rates of 94.3-98.5% 1, 6
• Low threshold for cardiology referral for electrophysiologic study 1, 9
• Pharmacologic suppression with beta-blockers or calcium channel blockers is less effective than ablation 6

VT:

• Requires comprehensive evaluation for structural heart disease and ischemia 3
• Implantable cardioverter-defibrillator (ICD) consideration for secondary prevention 3
• Catheter ablation for recurrent VT in selected patients 3
• Antiarrhythmic drug therapy as adjunct to device therapy 3