SVT

General¶

1) Sinus Node Origin - Sinus Tachycardia (ST) - Inappropriate Sinus Tachycardia (IST) - Sinus Nodal Re-Entry Tachycardia 2) Atrial Origin - Ectopic Atrial Tachycardia (EAT) - Multifocal Atrial Tachycardia (MAT) 3) Junctional (AV) Arrhythmias - Accelerated Junctional Rhythm (ARJ) - Junctional Tachycardia - Non-Re-Entrant Junctional Tachycardia - Ectopic Junctional Tachycardia (JET) - Non-Paroxysmal JT (PJRT) - Re-Entrant Junctional Tachycardias - AVNRT (Typical of Atypical) - AVRT (Accessory Pathway)

2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With SVT
Evaluation and initial treatment of supraventricular tachycardia
Main Point: SVTs originate at or above His-Bundle (excludes AF)
- Originate from or are dependent on conduction through the atrium or AV node to the ventricles
- Any arrythmia initiating in the atria and involving the AV node or an accessory pathway
  - Most common type of SVT is due to AV node reentry (AVNRT)
Usually there are no regular p waves (buried within the QRS), but retrograde P waves can occur
- May be seen in the beginning or the end of a QRS complex when the atria and ventricles are not simultaneous
- Can appear as spikes on QRS complexes or as inverted P waves
Mostly narrow complex tachycardia (QRS <120ms), rate ~160 bpm
- Narrow QRS unless AV nodal dysfunction or pre-excitation
Symptoms
- Sudden onset palpations and dizziness in a young patient, near syncope, lightheadedness, diaphoresis and chest pain
- Symptoms of palpitations: 12 lead ECG

Sinus Nodal Atrial Tachycardias (ST/IST)¶

Sinus Tachycardia (ST)¶

Rate >100 BPM, Regular, rarely exceeds 220
P waves before each QRS, PR interval ≥120ms
Upright P waves in Lead I, II, aVF, V3-V6
Ventricular rate ≥100 bpm - More common than Inappropriate ST - Gradual onset and termination
Slowed by vagal maneuvers, sinus massage - Usually doesn’t exceed maximum for age
(.85) x (220 - patient age) = maximum predicted - Physiologic: Precipitated by exertion, stress, illness (panic attacks), dehydration
Sympathetic stimulation and vagal withdrawal - Pathologic process: Pulmonary Embolism

Inappropriate Sinus Tachycardia (IST)¶

Rate: 100-180 BPM
- Normal P waves, may be an ectopic atrial tachycardia w/focus near the SA node
Dysfunctional Autonomic Regulation
- Tachycardia may continue despite beats that fail to conduct to the ventricles, indicating that the AV node is not participating in the tachycardia circuit
Symptoms
- Fatigue, dizziness ± syncope in 30-40 y/o women
Carotid Massage: Atrial Rate may slow
Treatment if no underlying cause:
- 1) Ivabradine 5mg PO BID (inhibits funny channel responsible for normal Sinus node automaticity, only lowers HR)
- 2) BB, CCBs, Digoxin, or catheter ablation

Sinus Nodal Re-Entry Tachycardia¶

Occurs within the sinus node cluster of cells and is conducted throughout the heart in a normal fashion
- Long RP interval, p waves are identical in axis and morphology as sinus Ps
Vagal maneuvers and adenosine will terminate
Abrupt onset and termination
Treatment
- BB, CCBs, Digoxin

Atrial Tachycardias (EAT/MAT)¶

Most commonly due to enhanced or abnormal atrial automaticity or triggered activity
AV Block: More A’s than V’s

Ectopic (Focal) Atrial Tachycardia (EAT)¶

Rate: 150-250 BPM (slower than Atrial Flutter)
Confined completely to atrial tissue
Regular Atrial Tachycardia with defined p wave (Differs from normal P wave)
- Usually paroxysmal and resolves spontaneously
- Frequent Origins: along valve annuli of LA or RA, pulmonary veins, coronary sinus musculature, SVC
- Abnormal Automaticity, triggered automaticity, a small reentry circuit confined to the atrium or atrial tissue extending into a pulmonary vein, pulmonary sinus, or vena cava
- The closer the ectopic focus is to the SA node, the closer the p-wave resemblance to Sinus Tachycardia, and the narrower the PR interval
- Atrial rate typically increases over initial 10s, then stabilizes to 150-250
Tachycardia may continue despite beats that fail to conduct to the ventricles, indicating that the AV node is not participating in the tachycardia circuit
- 1:1 AV Response
  - AVN Blockade increases AV block with continuation of Atrial Tachycardia, atrial rate unaffected (No termination)
- May terminate tachycardia w/preceding warm up or cold down phase
  - Gradual initiation and gradual termination possible (long RP)
Often seen in CAD, COPD, Alcohol use
Can be Sustained, Non-sustained, Paroxysmal, Incessant
- Sustained and Non-sustained EAT are often a precursor to AF and Aflutter
- Paroxysmal Atrial Tachycardia w/AV block: Digitalis Toxicity
  - Can increase ectopy in atria or ventricles
- Incessant EAT: can cause Tachycardia Induced Cardiomyopathy
- Paroxysmal EAT: may become incessant
Carotid Massage: AV block may increase, doesn’t usually revert, may uncover an ectopic atrial tachycardia
Treatment
- Goal: Slow ventricular rate
- Stable: BB, Diltiazem/Verapamil to decrease HR
  - Refractory/Definitive: Catheter Ablation
- Unstable: Synchronized Cardioversion

Multifocal Atrial Tachycardia (MAT)¶

≥3 different P-wave morphologies prior to QRSs, Irregularly irregular rhythm
- HR typically between 100-150
- Multiple atrial foci (multiple discrete p waves) with increased automaticity irritated by increased atrial pressures or hypoxia
  - AECOPD, Hypokalemia, Catecholamine Surge (Sepsis), PE, Pneumonia, hypomagnesemia
- Clear isoelectric intervals between p waves, and the atrial rate is slower
  - Usually caused by severe pulmonary disease (COPD) or acute illness, pulmonary hypertension, coronary disease, valvular disease, hypomagnesemia, theophylline
Tachycardia may continue despite beats that fail to conduct to the ventricles, indicating that the AV node is not participating in the tachycardia circuit
Symptoms
- Typically asymptomatic
Treatment
- Treat Underlying Condition (generally slower)
  - CCBs/Metoprolol long-term
- Acute Exacerbation: IV Metoprolol/Verapamil (CCBs)
  - Amiodarone/Ablation/Cardioversion do work in MAT

Junctional (AV) Arrhythmias w/o Re-entry (JET/AJR)¶

A rapid, narrow complex arrhythmia arising from the AV junction, including the Bundle of His
VA Block: More V’s than A’s
General Treatment
- Acute: IV BB for symptoms, IV diltiazem, procainamide or verapamil
- Chronic:
  - 1) Oral BB, CCBs
  - 2) Catheter ablation

Accelerated Junctional Rhythm (AJR)¶

Occurs when AV node automaticity rate is faster than SA node or Atrial Foci
Narrow QRS (HR 60-100), retrograde P waves may be visible
- Between 60-100 BPM w/gradual increase in rate (Automatic Focus) or after a PVC (focus of triggered automaticity)
- AV dissociation present
Often caused by digoxin toxicity (assess for upsloping ST throughout and digoxin levels), may be MI also, severe ischemic heart disease, coronary reperfusion

Ectopic Junctional Tachycardia (JET)¶

Due to automaticity within the AV node near the His-Bundle
- Incessant tachycardia in children during perioperative congenital heart surgery, or after cardiac surgery in pts with CHF, Rare in adults
Regular atrial rate, Narrow QRS (120-220) often w/VA block
- Regular rhythm, occasionally irregular
- AV dissociation (due to focus within AV node)
  - Can be seen with Adenosine, but rhythm not terminated
Can be seen after isoproterenol use
Treatment
- Need rate control if symptomatic
- Risk complete AV block due to proximity to AV node if ablation

Junctional (AV) Arrhythmias with Re-entry (AVNRT/AVRT)¶

Atrioventricular Nodal Re-entrant Tachycardia (AVNRT)¶

Most common and regular SVT in adults, more common in women
- Re-entry is the MCC of narrow QRS complex tachycardia
- Slow/Fast pathway + PAC
- MC PSVT (60%), most common paroxysmal sustained tachycardia in young healthy adults, normally structured hearts
Paroxysmal, regular, narrow QRS tachycardia with p waves that may or may not be visible
- HR from 150-250 bpm w/ regular ventricular response of 180-200
- P waves are rarely seen, may be seeing in the terminal aspect if QRS in V1
- RP interval is short, p wave may not be apparent
Uses AV node nodal and perinodal tissue (does not involve atria and ventricles)
Conduction from Atrium into the AV Node that is bidirectional
- Due to the presence of 2 conduction pathways (slow and fast) in the AV node and involving the atrium
- Normally sinus beats pass through the fast pathway and the slow pathway conduction is extinguished due to the refractory period
  - The slow pathway conducts both anterograde to the ventricle and retrograde toward the tricuspid valve (thus simultaneous conduction of atrium and ventricle)
  - The fast pathway does not
- AVNRTs utilize Slow conducting pathway
  - The slow pathway has transitional cells and fibers
  - Usually inferior extension from AV node near His bundle along Tricuspid valve annulus to the coronary sinus floor
  - If a PAC occurs during the refractory period of the fast pathway, it can initiate AVNRT that is then sustained by a reentry mechanism
  - The 2 pathways then form a looped circuit with impulses traveling antegrade through the slow pathway and return through the fast pathway
    - Atria and Ventricles are not a part of circuit
Palpitations > dizziness, dyspnea, chest pain, or SOB
- 1:1 AV response, AVN Blockade terminates Tachycardia
  - Dual electrical pathways within or near the AV node
Vagal Maneuvers (Carotid sinus massage, cold-water immersion or diving reflex, Valsalva, eyeball pressure) increase parasympathetic tone in the heart and slow AV nodal conduction and increase the refractory period (terminating AVNRT)
Treatment
- Acute Stable: Vagal, Valsalva
  - Adenosine 15mg IVx1, 12mg IV q1-2min x1-2 as needed
    - Useful if narrow or wide and regular
  - CCBs, BB
- Chronic: Same as above or flecainide > Ablation of slow pathway
- Acute Unstable: Adenosine/Vagal > Synchronized Cardioversion
  - ± BB or CCB > Flecainide or propafenone if no SHD
  - Amiodarone if SHD
- RF catheter ablation is curative in 95%
  - First line to prevent recurrences
  - Small risk of complete AV block

Atrioventricular Reciprocating Tachycardia (AVRT)¶

General
- Accessory Pathway Rhythms
  - Myocytes spanning between the upper and lower chambers across the AV groove (distinct accessory pathway)
  - Atria and Ventricles are involved in this pathway, Normal AV node (unlike AVNRT)
- Sudden onset, spontaneous termination
- Ventricular Preexcitation
  - Characterized by the Delta Wave
    - Indicates anterograde accessory pathway or bypass tract
    - Conducts impulse from atria to ventricles w/PR <120msec
  - Seen in Ebstein Anomaly
  - Associated with increased risk of sudden death, likely 2ndary to an accessory pathway conducting to the ventricle
    - Can degenerate into VT or VF
    - Lower risk if intermittent loss of preexcitation
- MC in children, 30% of all SVTs
- Caused by a bypass tract from the atrium to the ventricle that extends beyond the tricuspid and mitral valves, which typically block any AV conduction
  - Bypass tract may be anterograde, retrograde, or capable or both
  - Pre-excitation refers to early activation of the ventricles due to impulses bypassing the AV node through this bypass tract
- The accessory pathway may be concealed or manifest
  - A pathway may not be obvious on ECG and only conduct retrograde during an SVT (Concealed)
  - WPW or Ventricular preexcitation are manifest due to the presence of a delta wave
- HR 150-250 with regular ventricular response
- Respond to vagal maneuvers, adenosine, verapamil

Orthodromic AVRT (Retrograde P wave)¶

90-95% of all Accessory Pathway SVTs
Conduction through the AV node, Retrograde conduction back up through the bypass tract
- Uses atrial and ventricular tissue, accessory pathway, AV Node, and His-Purkinje (excitation through the AV node and accessory pathway are required)
- Re-entry through accessory bundle
Paroxysmal sustained tachycardia similar to AVNRT
- Narrow QRS complexes during tachycardia
- 1:1 AV Response, AVN Blockade terminates Tachycardia
Treatment
- Vagal maneuvers
  - Adenosine 15mg IVx1, 12mg IV q1-2min x1-2 as needed
- Acute Unstable: Adenosine/Vagal > Synchronized Cardioversion
  - No Pre-Excitation: CCBs or BBs
  - Catheter Ablation for all AVRT
  - No SHD: Propafenone, flecainide
  - SHD: Amiodarone, sotalol, ibutilide
- Chronic: Oral BB, CCBs if no pre-excitation

Delta Wave Present¶

Delta wave only seen in Anterograde paths (initial slope of QRS)
- Depolarization of the ventricular tissue from conduction of the atrium to the ventricle along the bypass tract
- No delta waves if no anterograde conduction

Wolff Parkinson White Disease (WPW)¶

Accessory pathway conducts depolarization directly from atria to ventricle without traversing AV node
- Characterized by atrial tachyarrhythmia occurring in the presence of an anterograde conducting accessory bypass tract allowing pre-excitation
Features
- Short PR, Delta Wave, Widened QRS complexes
- Ventricular Pre-excitation during Sinus Rhythm Present
  - A-fib in 10-30%, Persistent a-fib can lead to rapid ventricular response (RVR) and eventually VFib
    - Increased risk for A fib and AVRT
    - Can degenerate into VF and cause SCD
WPW Syndrome
- Called WPW Syndrome when symptomatic
  - Pre-existing WPW pattern who develop symptomatic supraventricular arrhythmias involving the accessory pathway
  - No longer pre-exciting the ventricles but instead form a reentrant circuit back to the atria
    - Initial widening of QRS converts to a narrow QRS with tachycardia when symptomatic
      - AVRT is MC, found in up to 80% of syndrome patients
      - 95% of re-entrant tachycardias
      - Afib in 15-30%
        
        Potentially life-threatening
        
        May degenerate into VF if short anterograde refractory period
- Symptoms
  - Palpitations
  - Lightheadedness
  - Presyncope or syncope
  - Chest pain
- Complications
  - SCD (1%)
- WPW and Preexcitation Syndromes
W/U:
- Asymptomatic
  - High Risk for Arrhythmias (Hx of AF or AVRT, Short Refractory Period (<250ms) of the accessory pathway
  - Noninvasive testing (Exercise Treadmill Test or Procainamide Challenge) and/or EPS to identify risk of SCD
    - EPS in high-risk occupations (Truck drivers, pilots, athletes)
    - Intermittent loss of preexcitation w/faster HR (loss of Delta) with the above
      - Suggests longer refractory period that will not be able to conduct often enough during AF to degenerate into VF
      - Low Risk
      - No further Evaluation or treatment
Treatment
- Avoid Amiodarone/AV nodal blocking agents if possible
- BB and Verapamil are CI = cardiac arrest by decreasing the degree of concealed retrograde conduction
- Stable: No therapy
- Stable with Atrial Fibrillation: Procainamide or Ibutilide
  - Do not cause AV block because AV-node blockers promote more conduction through accessory pathway
    - Rapid ventricular response
- Unstable or with Atrial Fibrillation
  - Electrical Synchronized Cardioversion

Delta wave without Tachycardia (Not WPW)¶

High risk for SVTs, short PR, prolonged QRS > 110

Pre-Excitation AVRTs¶

Secondary to pre-excitation along AV accessory pathway
Seen in Ebstein anomaly (up to 20%)
Wide QRS tachycardia with QRS Similar to VT
- Ventricular Pre-excitation during Sinus Rhythm:
  - Absent (Concealed Accessory pathway)
- SVT w/Aberrancy (preexisting or functional BBB)

Antidromic AVRT (Wide QRS)¶

Anterograde conduction down the bypass tract, retrograde conduction back up through the AV node/His-Purkinje System
Wide QRS complex tachycardia with regular rhythm
- Regular paroxysmal tachycardia
  - Occurs in 10% of patients with WPW syndrome with Tachycardia (Least common arrhythmia associated with WPW)
  - Most Common Pre-Excitation Tachycardia
Preexcitation in sinus rhythm

Atrial Fibrillation w/ Preexcitation¶

Irregular wide complex, or intermittently wide complex tachycardia, some >250/min
- Increased risk of SCD
  - Treatment
    - Procainamide of cardioversion
    - No AV blocking agents

Atrial Tachycardia or Flutter w/ Preexcitation¶

Treatment
- Ablation is usually curative

Pre-Excitation AVRTs Treatment¶

Treatment for all:
- No Adenosine (Vfib)
- No CCBS, BBs (hypotension)
- Offer catheter ablation
- Unstable + Wide QRS: Electrical Cardioversion
- Pre-excitation: Procainamide, ibutilide, amiodarone, propafenone