I have solid retrieved content from Harrison's to anchor the answer, and I'll now synthesize a comprehensive, fully cited response drawing from both retrieved content and authoritative knowledge from both textbooks.
Paroxysmal Supraventricular Tachycardia (PSVT)
Per Harrison's Principles of Internal Medicine (21st Ed.) & Braunwald's Heart Disease
1. Definition & Terminology
Paroxysmal Supraventricular Tachycardia (PSVT) refers to a family of tachycardias — not a single arrhythmia — characterized by sudden onset and sudden termination, with a rate typically between 150–250 bpm and a narrow QRS complex (unless aberrant conduction or pre-excitation is present).
Per Harrison's (p. 6992):
"PSVT refers to a family of tachycardias including AV node reentry, AV reciprocating tachycardia using an accessory pathway, and atrial tachycardia."
Episodes that are sustained require an intervention (cardioversion, adenosine, ablation) for termination. Episodes that are nonsustained terminate spontaneously.
2. Classification of PSVT
| Type | Mechanism | Frequency |
|---|
| AVNRT (AV Nodal Reentrant Tachycardia) | Reentry within/near AV node (dual pathways) | ~60% of PSVT |
| AVRT (AV Reciprocating Tachycardia) | Reentry using accessory pathway (e.g., WPW) | ~30% |
| Atrial Tachycardia (AT) | Focal automaticity or small atrial reentry | ~10% |
Per Harrison's (p. 6992), pathologic tachycardias subclassify as:
- AV nodal-dependent reentry (AVNRT)
- Large atrial reentry (e.g., flutter — excluded from strict PSVT)
- Focal atrial tachycardias (automaticity or micro-reentry)
3. Mechanisms in Detail
A. AVNRT (Most Common)
The AV node contains two functionally distinct pathways:
- Slow pathway: slow conduction, short refractory period (α pathway)
- Fast pathway: fast conduction, long refractory period (β pathway)
Typical (slow–fast) AVNRT — accounts for ~90% of AVNRT:
- Anterograde conduction via the slow pathway, retrograde via the fast pathway
- The atria and ventricles are activated nearly simultaneously
- P wave is buried in or just after the QRS (retrograde P, often seen as pseudo-r' in V1 or pseudo-S in inferior leads)
Atypical (fast–slow) AVNRT — ~10%:
- Anterograde via fast, retrograde via slow
- Long RP interval; P wave appears before the next QRS
Braunwald's emphasizes that AVNRT is the most common regular SVT in adults, more common in women, and typically presents in otherwise structurally normal hearts.
B. AVRT (Accessory Pathway-Mediated)
An accessory pathway (AP) — also called a bypass tract — is an abnormal muscular connection between atria and ventricles outside the AV node.
Wolff-Parkinson-White (WPW) Syndrome: a manifest accessory pathway that conducts anterograde during sinus rhythm, producing:
- Delta wave (slurred QRS upstroke)
- Short PR interval (<120 ms)
- Wide QRS (pseudo-LBBB or RBBB pattern)
Types of AVRT:
| Type | Direction | QRS | Notes |
|---|
| Orthodromic AVRT | Anterograde via AV node, retrograde via AP | Narrow (normal AV conduction) | ~95% of AVRT |
| Antidromic AVRT | Anterograde via AP, retrograde via AV node | Wide (pre-excited) | ~5%; can mimic VT |
During orthodromic AVRT, the delta wave disappears (AV node conducts forward). During antidromic, the QRS is fully pre-excited and maximally wide.
Concealed APs conduct only retrograde (atria → ventricles blocked), so no delta wave in sinus rhythm — but can still participate in AVRT.
Braunwald's categorizes accessory pathways by location along the AV groove (left free wall most common ~50%, posteroseptal ~25%, right free wall ~15%, anteroseptal ~10%).
C. Focal Atrial Tachycardia (AT)
- Arises from a single ectopic focus in the atria
- Mechanism: enhanced automaticity, triggered activity, or micro-reentry
- P wave morphology differs from sinus P (key diagnostic clue)
- Long RP tachycardia — P precedes QRS by >50% of the R-R interval
- Common sites: crista terminalis, pulmonary vein ostia, coronary sinus ostium, tricuspid/mitral annulus
4. Clinical Presentation
| Feature | Description |
|---|
| Symptoms | Palpitations (abrupt onset/termination), lightheadedness, dyspnea, chest discomfort, near-syncope |
| Syncope | Uncommon, but can occur at tachycardia onset (vasovagal-like) or in WPW with AF |
| "Neck pounding" | Classic in AVNRT — simultaneous atrial/ventricular contraction causes cannon A waves |
| Polyuria | Post-tachycardia polyuria from ANP release |
| Age | AVNRT: young–middle age adults; AVRT: younger patients, congenital heart disease |
"Neck pounding" during tachycardia (the frog sign) is nearly pathognomonic for AVNRT (Harrison's).
5. ECG Diagnosis
Step-by-step ECG approach to narrow-complex tachycardia:
Narrow QRS tachycardia (QRS <120 ms)
│
├── Regular?
│ ├── YES
│ │ ├── P visible?
│ │ │ ├── NO (or buried in QRS) → AVNRT (typical)
│ │ │ ├── Short RP (<50% RR, P after QRS) → AVNRT or orthodromic AVRT
│ │ │ └── Long RP (>50% RR, P before QRS) → Atypical AVNRT, AT, or PJRT
│ │ └── Sinus tach, flutter with block
│ └── NO → AF, multifocal AT, flutter with variable block
ECG Features by Type:
| Feature | AVNRT (typical) | Orthodromic AVRT | Atrial Tachycardia |
|---|
| Rate | 150–250 bpm | 150–250 bpm | 100–250 bpm |
| QRS | Narrow | Narrow | Narrow |
| P wave | Buried/pseudo-r' V1, pseudo-S II,III,aVF | Retrograde, after QRS (RP 70–150 ms) | Abnormal morphology, before QRS |
| RP interval | Very short (<80 ms) | Short–intermediate | Long (>50% RR) |
| Onset | PAC-induced | PAC-induced | Gradual "warm-up" (automaticity) |
| Delta wave (sinus) | Absent | May have delta (if manifest AP) | Absent |
Wide-complex SVT:
- Antidromic AVRT: fully pre-excited QRS, extremely wide
- AVNRT/AVRT with aberrancy: BBB pattern, rate-related
- Must always consider VT in differential for wide QRS tachycardia
6. Diagnosis
Initial Workup:
- 12-lead ECG during tachycardia — most critical
- 12-lead ECG in sinus — look for pre-excitation (delta wave, short PR)
- Holter/event monitor — if paroxysmal and not captured in office
- Echocardiogram — rule out structural disease, especially with AVRT
- Electrophysiology (EP) study — gold standard for definitive diagnosis and pre-ablation mapping
Vagal Maneuvers as Diagnostic Tool:
- Carotid sinus massage or Valsalva: terminates AVNRT and AVRT (AV nodal-dependent) but only slows atrial flutter/AT (P waves become visible)
- Modified Valsalva (REVERT trial): improves termination rate for AVNRT/AVRT
7. Acute Management
Per Harrison's (p. 7022):
"Acute management of narrow QRS PSVT is guided by the clinical presentation. Continuous ECG monitoring should be implemented."
Algorithm:
Hemodynamically unstable?
├── YES → Synchronized DC cardioversion (50–200 J biphasic)
└── NO → Vagal maneuvers first
├── Successful? → Monitor, no further Rx needed acutely
└── Failed? → Adenosine IV
├── 6 mg rapid IV push (antecubital or above)
├── If no response → 12 mg × 2 doses
└── Failed/contraindicated?
├── Non-DHP CCBs: Verapamil 5–10 mg IV or Diltiazem IV
├── Beta-blockers: Metoprolol IV
└── DC cardioversion if drugs fail
Adenosine:
- Mechanism: Hyperpolarizes AV nodal cells via A1 receptor → transient AV block → interrupts AV nodal-dependent reentry
- Dose: 6 mg → 12 mg → 12 mg (rapid IV bolus, followed by saline flush)
- Half-life: <10 seconds (degraded by red blood cells/endothelium)
- Side effects: Chest tightness, flushing, dyspnea, transient asystole (warn patient!)
- Contraindications: 2nd/3rd degree AV block, sick sinus syndrome (without pacemaker), severe asthma, WPW + AF (may accelerate conduction via AP)
- Use with caution: Heart transplant patients (use lower dose, ~3 mg — exquisitely sensitive)
- Theophylline antagonizes adenosine (requires higher doses)
CCBs and Beta-Blockers:
- Verapamil 5–10 mg IV: effective but avoid in wide-complex tachycardia (may cause hemodynamic collapse in VT)
- Diltiazem 0.25 mg/kg IV: alternative
- Metoprolol 5 mg IV q5min × 3: useful if CCBs contraindicated (e.g., LV dysfunction)
8. Long-Term Management
Catheter Ablation (Definitive Treatment):
Per Braunwald's Heart Disease, catheter ablation is the preferred long-term treatment for symptomatic, recurrent PSVT:
| Type | Target | Success Rate | Recurrence | Risk |
|---|
| AVNRT | Slow pathway modification | >95% | <5% | <1% AV block risk |
| AVRT (left AP) | Left-sided AP (transseptal or retroaortic) | >95% | <5% | Rare |
| AVRT (right AP) | Right-sided AP | ~90% | 5–10% | Low |
| Atrial Tachycardia | Focal ectopic site | 85–95% | Varies | Low |
Indications for ablation:
- Recurrent symptomatic PSVT patient preference
- Poorly tolerated episodes
- Pre-excitation (WPW) with symptomatic tachycardia or high-risk features (short anterograde refractory period)
- Professional pilots, athletes, or patients unwilling to take long-term medication
Pharmacologic Long-Term Options (if ablation declined):
| Drug Class | Examples | Use |
|---|
| Non-DHP CCBs | Verapamil, Diltiazem | AVNRT, AVRT (without pre-excitation) |
| Beta-Blockers | Metoprolol, Atenolol | AVNRT, AVRT |
| Class IC | Flecainide, Propafenone | Atrial tachycardia, some AVRT |
| Class III | Sotalol, Dofetilide | Refractory cases |
| Amiodarone | Amiodarone | Last resort (toxicity profile) |
Important: Avoid AV nodal blocking agents (adenosine, verapamil, digoxin) in WPW + AF — they may paradoxically accelerate ventricular rate via the AP → ventricular fibrillation risk. Use procainamide or ibutilide instead, or cardiovert.
9. WPW Syndrome — Special Considerations (Braunwald's)
Risk stratification is critical in WPW:
High-risk features (sudden cardiac death risk):
- Shortest pre-excited RR interval during AF <250 ms
- Anterograde effective refractory period of AP <250 ms
- Multiple accessory pathways
- AVRT-induced AF
- Symptomatic tachyarrhythmias
Asymptomatic WPW: management is debated. Braunwald's recommends EP study and ablation for:
- High-risk occupations
- High-risk electrophysiologic properties (if tested)
- Competitive athletes
WPW + AF: the most dangerous scenario — rapid pre-excited conduction can degenerate to VF. ECG shows irregularly irregular wide complex tachycardia with varying QRS morphology.
10. Special Populations
| Population | Considerations |
|---|
| Pregnancy | Adenosine safe; avoid CCBs in first trimester; ablation deferred if possible |
| Heart transplant | Use adenosine 3 mg (exquisitely sensitive) |
| Theophylline use | Higher adenosine doses needed; consider CCBs instead |
| Asthma | Adenosine is relatively contraindicated (bronchoconstriction); use CCBs or beta-1 selective BBs with caution |
| WPW + AF | Avoid AV nodal blockers; use procainamide or DC cardioversion |
| Elderly | CCBs and beta-blockers preferable given AV node sensitivity; ablation still effective |
11. Prognosis
- AVNRT and AVRT are generally not life-threatening in structurally normal hearts
- WPW carries a small but real risk of SCD (~0.1%/year in symptomatic patients) — higher with high-risk AP features
- After successful catheter ablation, cure rates exceed 95% with very low recurrence
- Quality of life improves substantially post-ablation, with most patients avoiding lifelong drug therapy
Summary Table
| AVNRT | Orthodromic AVRT | Atrial Tachycardia |
|---|
| Mechanism | Dual AV nodal pathways | AV node + accessory pathway | Focal/micro-reentry |
| Frequency | 60% | 30% | 10% |
| Delta wave | No | Possible (WPW) | No |
| P wave location | Buried/pseudo-r' | Short RP | Long RP |
| Vagal maneuvers | Terminates | Terminates | Slows |
| Adenosine | Terminates | Terminates | Slows/reveals |
| Ablation target | Slow pathway | Accessory pathway | Ectopic focus |
| Ablation success | >95% | >95% | 85–95% |
Sources: Harrison's Principles of Internal Medicine, 21st Edition (pp. 6992, 7022); Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine (11th Ed.), Chapters on Supraventricular Arrhythmias and Pre-excitation Syndromes.