Teach me everything about psvt according to harrison and braunwald

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paroxysmal supraventricular tachycardia PSVT classification mechanisms pathophysiology

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PSVT SVT ECG diagnosis treatment management adenosine ablation

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AV nodal reentrant tachycardia AVNRT mechanism dual pathway ECG features

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AVRT accessory pathway WPW Wolff-Parkinson-White orthodromic antidromic tachycardia

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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

TypeMechanismFrequency
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:
TypeDirectionQRSNotes
Orthodromic AVRTAnterograde via AV node, retrograde via APNarrow (normal AV conduction)~95% of AVRT
Antidromic AVRTAnterograde via AP, retrograde via AV nodeWide (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

FeatureDescription
SymptomsPalpitations (abrupt onset/termination), lightheadedness, dyspnea, chest discomfort, near-syncope
SyncopeUncommon, 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
PolyuriaPost-tachycardia polyuria from ANP release
AgeAVNRT: 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:

FeatureAVNRT (typical)Orthodromic AVRTAtrial Tachycardia
Rate150–250 bpm150–250 bpm100–250 bpm
QRSNarrowNarrowNarrow
P waveBuried/pseudo-r' V1, pseudo-S II,III,aVFRetrograde, after QRS (RP 70–150 ms)Abnormal morphology, before QRS
RP intervalVery short (<80 ms)Short–intermediateLong (>50% RR)
OnsetPAC-inducedPAC-inducedGradual "warm-up" (automaticity)
Delta wave (sinus)AbsentMay 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:

  1. 12-lead ECG during tachycardia — most critical
  2. 12-lead ECG in sinus — look for pre-excitation (delta wave, short PR)
  3. Holter/event monitor — if paroxysmal and not captured in office
  4. Echocardiogram — rule out structural disease, especially with AVRT
  5. 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:
TypeTargetSuccess RateRecurrenceRisk
AVNRTSlow 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 TachycardiaFocal ectopic site85–95%VariesLow
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 ClassExamplesUse
Non-DHP CCBsVerapamil, DiltiazemAVNRT, AVRT (without pre-excitation)
Beta-BlockersMetoprolol, AtenololAVNRT, AVRT
Class ICFlecainide, PropafenoneAtrial tachycardia, some AVRT
Class IIISotalol, DofetilideRefractory cases
AmiodaroneAmiodaroneLast 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

PopulationConsiderations
PregnancyAdenosine safe; avoid CCBs in first trimester; ablation deferred if possible
Heart transplantUse adenosine 3 mg (exquisitely sensitive)
Theophylline useHigher adenosine doses needed; consider CCBs instead
AsthmaAdenosine is relatively contraindicated (bronchoconstriction); use CCBs or beta-1 selective BBs with caution
WPW + AFAvoid AV nodal blockers; use procainamide or DC cardioversion
ElderlyCCBs 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

AVNRTOrthodromic AVRTAtrial Tachycardia
MechanismDual AV nodal pathwaysAV node + accessory pathwayFocal/micro-reentry
Frequency60%30%10%
Delta waveNoPossible (WPW)No
P wave locationBuried/pseudo-r'Short RPLong RP
Vagal maneuversTerminatesTerminatesSlows
AdenosineTerminatesTerminatesSlows/reveals
Ablation targetSlow pathwayAccessory pathwayEctopic 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.
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