Supraventricular arrhythmias are tachyarrhythmias with a rate over 90 beats per minute that are usually associated with symptoms. They are classified as narrow or wide complex tachycardias based on the width of the QRS complex on ECG. Narrow complex tachycardias (NCTs) require rapid activation of the ventricles through the His-Purkinje system and depend on AV node conduction. The most common types of NCTs are atrioventricular nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), and atrial tachycardia. Initial management of stable NCTs involves

1. Supraventricular
Arrhythmias
An overview of the approach to SVTs

2. What we’re going to discuss today
▪ Brief introduction to tachyarrhythmias in general
▪ What are Narrow ComplexTachycardias (NCTs)?
▪ Brief approach to diagnosis of NCTs
▪ Initial Management
– ClinicalConsiderations
– Emergency Management
– Long-term Management
▪ FAQs

3. Introduction to
Tachyarrhythmias

4. Tachyarrhythmias
▪ Rate > 90 beats per min (bpm)
▪ Usually associated with symptoms
– Either symptoms due to the aetiology (dig deep)
– Symptoms due to the arrhythmia itself
▪ Classified as
– Narrow ComplexTachycardia (≤120 ms)
– Wide ComplexTachycardia (>120 ms)
Based on the width of the QRS (widest) seen on the ECG

5. Wide vs. Narrow Complex Tachycardias
▪ Management is grossly different
▪ Most (not all) Wide complex tachycardias areVT (80%)
▪ Aetiologies are different (further management also changes)

6. What determines width of QRS on ECG
▪ Narrow QRS complex requires
rapid highly synchronous electrical activation of the
RV & LV myocardium
▪ Only possible through the
specialized, rapidly conducting His-Purkinje system (HPS)
▪ Wide QRS complex means less synchronous ventricular activation of
longer duration
– can be due to IVCDs, or
– activation not mediated by His bundle (HB) eg: bypass tract (BT; preexcitation)
or a site within a ventricle (ventricular arrhythmias)

7. What does this say about NCTs
▪ This implies that the NCT necessarily is dependent on the AV Node
conduction
▪ Regardless of where it originates, the ventricles are activated
through the His Purkinje system
▪ Vulnerable point for us to terminate the arrhythmia or at least slow
down it’s conduction to the ventricles

8. Approach to Diagnosis of NCTs

9. Narrow Complex Tachycardia
▪ Based on whether the arrhythmia needs the AV node for initiation
and maintenance, they can be classified into
– Requiring onlyAtrialTissue
▪ AtrialTachycardia
▪ Atrial Fibrillation
▪ Atrial Flutter
– Requiring AV junction
▪ JunctionalTachycardia
▪ AVNRT
▪ AVRT

10. Narrow Complex Tachycardia
▪ The term ”Paroxysmal SupraventricularTachycardia (PSVT)” usually
refers to intermittent SVT other than AF, AFl or MAT
▪ Major causes of PSVT are
AVNRT (50-60%)
AVRT (30%) or
AT(10%)

13. Steps in Assessing the Rhythm
▪ Confirm QRS width
▪ Regularity of QRS complexes
▪ Identifiable P waves?
▪ P wave : QRS wave
▪ RP interval to PR Interval

15. Varying R-R Interval,
Irregularly Irregular
No Definite P wave
Atrial Fibrillation
Narrow QRS < 120 ms or <3 small blocks
5 Big Blocks = 1 Second, 30 Big Blocks = 6 Seconds

17. Narrow QRS < 120 ms or <3 small blocks
Regular R-R Interval
Pseudo S
Pseudo R’
Typical AVNRT
Short RP (<70 ms,Very Short RP)

19. Narrow QRS < 120 ms or <3 small blocks
Regular R-R Interval

20. Initial Management of PSVTs

21. Acute Management
▪ Most episodes of PSVT require 1:1 AVN conduction for continuation
(AVN-dependent)
▪ AVN conduction and refractoriness can be modified by vagal
manoeuvres and pharmacological (weak links)
▪ Termination of a sustained episode of SVT usually done by producing
transient block in the AVN

22. Vagal Manoeuvres
▪ Simple, Non invasive
– Carotid Sinus Massage
– Valsalva Manoeuvre +/- suddenTrendelenburg
– Dive reflex
▪ Work better soon after onset
▪ 6-22% successful termination

23. Pharmacological Treatment
▪ Achieved with antiarrhythmic drugs that
– increaseAVN refractoriness
– decrease AVN conduction
– or both
▪ Drug of choice is usually adenosine or verapamil

24. Adenosine
▪ 6 – 12 mg
▪ MUST be given via RAPID IV BOLUS
▪ Sequential dosing can be given at 60-second intervals
▪ Termination is caused by block in the anterograde slow pathway
▪ If re-initiation occurs after successful termination, can repeat
Adenosine or substitute with CCB

25. Adenosine
▪ Caution needed in patients with suspected AVRT
▪ Adenosine may induce AF
▪ If patients have a bypass tract they may progress toVF:
Be prepared forVT/Vfib and cardioversion

26. Verapamil/ Diltiazem
▪ Verapamil
– 5 mg intravenously over 2 minutes
– followed in 5 to 10 minutes by a second 5- to 7.5-mg dose
▪ Diltiazem
– 20 mg intravenously
– Followed if necessary, by a second dose of 25 to 35 mg
▪ Hypotension can occur with CCBs
▪ Risk of atrial/ ventricular ectopy exists, prepare forVT/Vfib

27. Intravenous Beta Blockers
▪ Propranolol (1 to 3 mg)
▪ Metoprolol (5 mg)
▪ Esmolol (500 µg/kg over 1 minute and a 50-µg/kg/min infusion)
▪ If all 3 groups contra-indicated, can try IV Digoxin (0.5-1.0 mg), but
least efficacious for termination of PSVT

28. Procainamide
▪ Can be used as second-line for patients with suspected AVRT and narrow
complex tachycardia
▪ Also can be used if AF develops and patient has pre-excitation
▪ Hypotension may occur
▪ Up to 17 mg/kg at a rate of 20 to 50 mg/minute or
100 mg every 5 minutes;
▪ Administer until
– Arrhythmia is controlled or
– Hypotension occurs or
– QRS complex widens by 50% of its original width

29. Hemodynamically unstable patient
▪ If the patient has
– a SBP <90 mm of hg
– signs of systemic hypoperfusion (cool extremities, altered sensorium)
▪ Patient may be cardioverted
– 100-150 J for biphasic defibrillators
– Synchronised to the R wave

31. Chronic Management

32. General Principles
▪ Major reason for treatment is to alleviate symptoms
▪ Initiation of therapy
Oral antiarrhythmic vs. catheter ablation
depends on
frequency and duration of the arrhythmia
severity of symptoms
patient preference, occupation, tolerance to drugs etc

33. Long-term therapy in AVNRT
▪ Catheter ablation can be recommended as first-line treatment for AVNRT
– 95% efficacy
– Low rate of complications (<1% risk of need for permanent pacemaker)
▪ CCBs –Verapamil, Diltiazem
▪ Beta Blockers
▪ If no response, class IC and III drugs can be considered
– Flecainide and propafenone affect the AVN and BTs and reduce SVT frequency
– Sotalol, dofetilide, and amiodarone are other second-line agents
– Concomitant therapy with a beta blocker can improve efficacy
▪ Pill in the pocket ?
– Propranolol orVerapamil
– Should exclude LV dysfunction, Bradycardia, Pre-excitation

34. Long Term Management of AVRT/ Pre-
excitation
▪ Catheter ablation is first-line therapy (class I) for
WPW syndrome
– manifest preexcitation
– Symptoms
▪ For patients with pre-excitation on ECG but no symptoms
– sodium or potassium channel blockers
– ? Long term betablocker therapy
– AvoidVerapamil, diltiazem, digoxin

35. Frequently Asked Questions

36. FAQs
▪ Patient comes in with a tachycardia and is in shock, but I’m not sure
that it’s sinus tachycardia on the ECG.What do I do?
▪ Patient has repeated symptoms of fast palpitations at home, but the
ECG shows a normal sinus rhythm. What next?
▪ Patient has an ECG suggestive ofAVNRT, but adenosine is unable to
terminate the tachycardia.What to do?
▪ AVNRT terminated after adenosine, but AF developed. What to do?

37. ▪ Reveal the P wave by repeating the ECG while
– Try vagal manoeuvres; slows down, may reveal hidden P wave
– Run Rhythm strip at 50 mm/sec
– Adenosine bolus
▪ Regular vs. Irregular
– Card test (Most useful)
– Pulse rate by monitor (fluctuating versus steady)
– Canon “a”Waves of JVP
▪ Frog sign (AVNRT rather than AVRT)
Tricks to unmask the rhythm

42. Summary
▪ NCT vs. WCT – treatment is different
▪ Most PSVTs depend onAV conduction
▪ Adenosine is ideal forAVNRT, but causes AF, caution if possible AVRT
▪ Diltiazem,Verapamil probably better forAVRT
▪ Catheter ablation can be first-line treatment after stabilization
▪ Synchronized cardioversion in case of hemodynamic instability

43. Thanks for listening