1. Supraventricular tachycardia (SVT) refers to a group of tachyarrhythmias originating above the ventricles. Paroxysmal SVT is characterized by episodes of tachycardia with abrupt onset and termination. 2. The main types of PSVT are atrioventricular nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), and focal atrial tachycardia. They have different mechanisms and ECG patterns that can help determine the underlying rhythm. 3. Acute management involves vagal maneuvers, medications like adenosine or beta blockers, or cardio

1. Supraventricular Tachycardia

2. OUTLINE
• Introduction
• Epidemiology
• Pathophysiology
• Classification
• Clinical Features
• Investigations
• Management
• Specific SVTs
• Conclusion

3. INTRODUCTION
A tachycardia originating in the following
• Sinus node
• AV node
• Atrial myocardium
• Bundle of His above the bifurcation
Presents with a characteristic narrow QRS complex on ECG with few
exceptions(pre-excitation or aberrant conduction)

4. • PSVT is characterized by episodes of tachycardia which occur with
abrupt onset & termination
• A subset of SVT
• Includes AVRT, AVNRT & AT(occasionally)
Paroxysmal Supraventricular Tachycardia

5. EPIDEMIOLOGY
Prevalence of SVT: ~ 2.3 per 1000
Incidence of PSVT: 36 per 100,000 per year
F : M(2:1)
More common in people with underlying structural heart disease,
family history of SVT or Sudden Cardiac death

6. PATHOPHYSIOLOGY

7. Normal Physiology

8. Tachyarrhythmias occur as a result of 3 main mechanisms:
 Reentry
 Automaticity
 Enhanced
 Abnormal
 Triggered activity; due to
 Early Afterdepolarizations(EADs)
 Delayed Afterdepolarizations(DADs)

9. REENTRY(Reentrant Arrhythmia)
Requires 2 pathways which form a circuit
Can be within the AV node or between the AV node & an
Accessory pathway

10. Automaticity
• Repetitive firing from a single focus, which may either be
ectopic or originate from the SA node
• Enhanced Automaticity: originates in the SAN or other
subsidiary pacemakers
• Abnormal Automaticity; Scar tissue forms foci for ectopic
impulse generation

11. Triggered Activity
These arrhythmias are produced by early or delayed
afterdepolarizations depending on the timing of the first depolarization
relative to the preceding action potential
EAD - occurs before full repolarization
- Affects patients with Heart failure, prolonged QT syndrome
DAD - Occurs after full repolarization
-Typically in states of high intracellular calcium(digitalis toxicity
Hyperkalemia, Hypercalcemia)

12. CLASSIFICATION

13. BASED ON MECHANISM
BASED ON LOCATION

14. CLINICAL FEATURES

15. • May be asymptomatic
• Palpitations
• Chest pain or discomfort
• Dyspnea
• Diaphoresis
• Dizziness or presyncope
• Syncope
• Feeling of neck pounding/shirt flapping
• Urinary urgency & Polyuria
• May be agitated or calm
• Tachycardia
• If unstable, may be;
Hypotensive
Acute Pulmonary oedema
Altered mental status
Usually similar in all forms of SVT

16. INVESTIGATIONS

17. Initial Investigations
• ECG
• Must be performed for all suspected SVT
• May be regular or irregular with rates >100/min(typically >150/min
• Usually Narrow QRS complex
• LAB STUDIES
• FBC
• TFT
• EUCR
• Transthoracic Echocardiography

18. Additional Investigations
• Prolonged ECG
• 24 hour ambulatory ECG
• Event or Implantable loop recorders
• Electrophysiological study(Gold standard)
• Exercise Tolerance testing; Indicated in pre-excitation
• Cardiac stress testing: Indicated in patients with ASCVD risk factors

19. MANAGEMENT

20. PRINCIPLES
1. Stabilize patient & restore sinus rhythm
2. Identify SVT & treat underlying precipitant(if present)
3. Terminate SVT
4. Long term Control
5. Prevention of complications

21. ACUTE MANAGEMENT
Unstable patients
• Synchronized electrical Cardioversion
• May be ineffective for Multifocal AT & Junctional Tachycardia
Stable Patients
• Perform vagal maneuvers
• Reassess Rhythm, then pharmacotherapy
• Irregular(Aflut, AFIB, MAT); Rate or rhythm control
• Regular; Administer IV Adenosine
If still resistant, then administer AV nodal blockers(nDHP CCBs OR BB)
Anti-arrhythmics if still unresponsive
Synchronized Electrical Cardioversion as last resort

22. VAGAL MANEUVRES
Set of actions which slow conduction through the AV node and may
terminate the arrhythmia
Diagnostic & may be therapeutic and includes
• Valsalva Maneuvre
• Modified Valsalva
• Carotid Sinus Massage(avoid in patients with carotid bruit)
• Diving reflex

23. VAGAL MANEUVRES

25. LONG TERM MANAGEMENT
Catheter Ablation(first line)
• Curative in PSVTs
• Symptomatic patients who want to avoid long-term drug therapy(especially
younger patients)
• Asymptomatic patients with special lifestyle considerations(.eg Pilots,
Athletes)
Pharmacotherapy
• Depends on the SVT;
• AV nodal Blocking Agents(nDHP CCBs or BB)
• Antiarrhythmics

26. Atrioventricular Nodal Reentrant Tachycardia(AVNRT)
AV node contains 2 pathway, one slow and one fast Impulses circle around the AV
node within both pathways a continuous circuit is formed Tachyarrhythmia
Antegrade conduction across the slow pathway & retrograde conduction across the fast
pathway occurs in over 90% of cases(although the reverse is possible)
ECG findings; May be normal between episodes of tachycardia
• Rate; 150-220/min
• Regular rhythm
• Narrow QRS complex(<120ms)
• P wave typically not visible(buried in QRS complex) or may be seen after QRS complex
as retrograde P waves(pseudo S or R waves)

28. 12-lead ECG (paper speed: 25
mm/s)
– Regular rhythm; heart rate
∼190/min.
– Normal cardiac axis
– Narrow QRS complexes
– No visible P waves (they are
buried in the QRS complexes)
– Widespread ST segment
depression, prominent in V3–V5
– QRS alternans
.
A regular, narrow-complex tachycardia without visible P-
waves is characteristic of AVNRT

29. 12-lead ECG (paper speed: 25
mm/s)
– Regular rhythm; heart rate
approx. 188/min
– Normal cardiac axis
– Narrow QRS complexes
– P waves are largely buried,
occasional retrograde P waves
can be seen after the QRS
complexes. e.g., in III, aVF
– ST depression in V5, V6
– QRS alternans: QRS
amplitude is normal
throughout but oscillates (best
seen in rhythm strip at bottom
of image

30. 6-lead ECG (paper speed 25
mm/s) showing AVNRT being
terminated with adenosine
Left of dashed line: AVNRT
before onset of adenosine effect
(typical slow-fast subtype)
– Heart rate approx. 160/min
– Regular rhythm (regular RR
intervals)
– Narrow QRS complexes
– P waves are visible after the
QRS complexes (examples
indicated by arrows and “P”)
Right of dashed line: transient
irregular rhythm following
termination of AVNRT by
adenosine

33. Atrioventricular Reciprocating Tachycardia(AVRT)

34. A tachyarrhythmia caused by an accessary pathway that creates a
reentrant circuit with the AV node
May be Orthodromic or Antidromic AVRT
Orthodromic AVRT(most common; 90-95%)
• Antegrade conduction through AV node; retrograde conduction
through accessory pathway
• Narrow QRS
Antidromic AVRT(rare; 5-10%)
• Antegrade conduction through accessory pathway; retrograde
through AV node
• Wide QRS complex

37. -Rate > 250bpm
-Regular rhythm
-Narrow QRS complex
-Retrograde P waves in
V1 (notch just
preceding T wave)with
long RP interval> 70ms
Regular, narrow complex tachycardia with retrograde P waves
and long RP interval suggestive of Orthodromic AVRT

38. Antridromic AVRT
Regular wide QRS complexes

39. Acute Management
DC cardioversion, if unstable
Stable orthodromic AVRT
• First step: Vagal maneuvers
• If it persists; IV medical therapy(AV nodal blocking agents);
• Adenosine(first line(if no contraindications)
• Other options; nDHP CCBs(verapamil, diltiazem) or beta blocker(.e.g metoprolol)
Stable Antridromic AVRT
• Established diagnosis of AVRT: Antiarrhythmics( Procainamide, Ibutilide)
• Uncertain diagnosis: Avoid AV nodal blocking agents

40. Long-term Management
First-line: Catheter ablation
Pharmacotherapy
• Pre-excitation pattern visible- Antiarrhythmics
• Known Heart disease: Sotalol, Doferilide
• No known Heart disease; Flecainide, Propafenone
• Pre-excitation pattern not visible- AV nodal blockade
• nDHP CCBs
• Beta blockers
• Consider Amiodarone if above are ineffective or contraindicated

42. Wolff-Parkinson White Syndrome

43. • A congenital condition characterized by intermittent tachycardias and
signs of ventricular preexcitation on ECG, both of which arise from
an accessory pathway known as the bundle of Kent
• Abnormal connection between atria and ventricles leading
to ventricular preexcitation
• May be associated with structural abnormalities(e.g Ebstein anomaly)
• May be asymptomatic (WPW pattern) or associated
with arrhythmias (WPW syndrome), including:
• AVRT(most common; 80%)
• Atrial fibrillation(15–35%; incidence increases with age)
• Atrial flutter (5%)
• Others (rare): MAT, focal atrial tachycardia, VFIB

44. •While in sinus rhythm, a preexcitation
pattern may be present
• Short PR interval
• ECG delta wave: a slurred upstroke at the
start of the QRS complex
• Widened QRS
•Can show any of
the arrhythmias associated with WPW
ECG FINDINGS

46.  Unstable Patient: DC Cardioversion
 Stable: Assess underlying rhythm.
• Regular NCT (i.e. orthodromic AVRT): vagal maneuvers, Adenosine
• WCT: irregular (e.g., underlying Afib or multifocal AT) OR regular
(underlying Aflut or focal AT)
• Avoid AV nodal blocking agents and vagal maneuvers (may
precipitate Vtach or Vfib)
• Rhythm control measures (i.e., cardioversion or IV procainamide are the safest
treatment option.
Acute Episodes

47. Long-term Management
Risk stratify based on clinical features, dynamic ECG testing and
Electrophysiologic studies
Catheter ablation(first line)
Pharmacotherapy
• No associated heart disease: Class 1C antiarrhythmic(Flecainide,
Propafenone)
• Known structural heart disease: nDHP CCBs, BBs or Class III
antiarrhythmics(Amiodarone, sotalol)

48. Focal Atrial Tachycardia

49. • A supraventricular tachycardia that arises from a localized atrial focus
outside of the SA node
• May be Idiopathic(most common), due to Chronic
conditions(hypertension, cardiomyopathy), Acute conditions(MI,
sepsis) or Drug toxicity(.e.g. Digoxin, Theophylline, Cocaine)
• Different mechanisms including triggered activity, micro-reentry or
enhanced automaticity
• Abrupt in onset and worsened by adrenergic activity

50. ECG findings
• Heart rate 100–250/minute
• Regular rhythm
• May be 1:1 or 2:1 AV conduction
• P wave
• Typically visible in 2:1 AT
• May be hidden by the QRS complex or T wave in 1:1 AT
• Morphology depends on the site of origin but remains constant.
• An isoelectric baseline is present between P waves
• QRS complex: morphology does not vary
• Narrow complex: most common
• Wide QRS complex may be present in SVT with aberrant conduction

51. Nonsustained focal atrial
tachycardia
12-lead ECG (paper speed: 25
mm/s)
- Two periods of sinus rhythm
(varying between 79–85/min)
alternating with two periods of
tachycardia (∼ 137/min)
- P-wave morphology during
tachycardia different from those
during sinus rhythm but remain
constant indicating a single
ectopic focus.
- 1:1 AV conduction
- Normal QRS
- An isoelectric baseline is
present.
These features are suggestive of
focal atrial tachycardia.

52. TREATMENT
• Usually self-limiting and asymptomatic
• Treatment same as for other SVTs, although may not be as effective
• Ensure to rule out Pre-excited Focal AT
• Identify & treat reversible underlying conditions in all patients

54. Multifocal Atrial Tachycardia

55. An irregular SVT featuring ≥ 3 morphologies of P waves due to
multifocal origins of pacemaker activity
Etiology
• Severe underlying conditions (e.g., heart failure and pulmonary
diseases, such as COPD or pneumonia)
• Drugs (e.g., theophylline, isoproterenol) [52]
• Electrolyte abnormalities (e.g., hypokalemia, hypomagnesemia)
• Others: hypoxia, hypercapnia, acidosis

56. ECG findings
Heart rate 100–200/minute
Irregularly irregular rhythm
P waves
Three or more varying morphologies
Separated by an isoelectric baseline
Variable PR interval
QRS complex: morphology does not vary
Narrow QRS complex: most common
Wide QRS complex may be present in aberrant conduction
May progress to atrial fibrillation

57. -Irregularly irregular tachycardia
with both atrial and ventricular
rates of approx. 120–200/min
-Left axis deviation
-P waves with different
morphologies (including normal,
biphasic, and inverted waves) in
the same lead. P waves return to the
isoelectric line (thus there is no
atrial flutter/fibrillation).
-Normal QRS
-In summary: Irregularly irregular
tachycardia with variable P-wave
morphology, consistent with the
diagnosis of multifocal atrial
tachycardia.

58. Treatment
Very challenging. Rhythm control and electrical cardioversion are not
effective.
First-line treatment: management of underlying causes
• Manage exacerbations of chronic diseases
• Correct reversible conditions, e.g., hypoxemia, acidosis, electrolyte abnormalities,
discontinue offending medications
• IV magnesium may be helpful even in patients with normal magnesium levels.
Rate control
• Beta blockers: e.g., metoprolol
• Calcium channel blockers : verapamil
AV node radiofrequency ablation: Consider in refractory MAT

60. Junctional Tachycardia

61. A tachyarrhythmia caused by ectopic focus of abnormal automaticity
of myocytes in the AV node and bundle of His
There are two possible presentations
• Paroxysmal junctional tachycardia (PJT): sudden onset, rapid
tachycardia (heart rate > 100/minute)
• Accelerated AV junctional rhythm (nonparoxysmal junctional
tachycardia): gradual onset (and termination) rhythm, which can cause
a mild tachycardia (heart rate ∼ 60–100/minute)

62.  PJT
• Infants with congenital heart
disease(most common)
• Post-myocardial infarction
• Transiently during slow pathway
ablation in AVNRT
 Accelerated AV Junctional Rhythm
• Digoxin toxicity
• Catecholamine use
• COPD
• Hypokalemia
Etiology
ECG appearance similar in both types
.Heart rate
• PJT: > 100/minute
• Accelerated AV junctional rhythm:
60–100/minute
 Narrow QRS complex
• Regular (occasionally may be
irregular)
 Inverted P waves in lead II and can be:
• Hidden within the QRS complex
• Immediately before QRS complex
• Immediately after QRS complex
 Short PR interval
ECG findings

63. -Regular rhythm
-Heart rate: ~ 130/min
-P waves immediately
follow the QRS complexes
(examples indicated with
green arrowheads) and
are inverted in I, I, aVF,
and V4-V6 (retrograde P
waves; examples indicated
with red arrowheads)
-Cardiac axis borderline
normal/right axis deviation
(isoelectric in I, R > S in
aVF)
-Narrow QRS complexes
(-80 ms)
-A regular, narrow complex
tachycardia with
retrograde P waves is
suggestive of junctional
tachycardia.

64. Treatment
Acute episodes
• Intravenous pharmacotherapy
• Beta blockers or nDHP CCBs
Long-term management
• Accelerated AV junctional rhythm: Identify and treat the underlying
cause (e.g., digoxin toxicity).
• Paroxysmal junctional tachycardia: medical therapy with AV nodal
blocking agents or Class 1C antiarrhythmics
• Catheter ablation: Consider in selected patients with PJT.

65. Thank you