1. Supraventricular arrhythmias
Jerry John
July 29, 2009

2. Objectives Supraventricular Arrhythmias
How do supraventricular arrhythmias manifest?
What are the common supraventricular arrhythmias?
What is the mechanism of atrioventricular arrhythmias?
Which drugs are used in the management of supraventricular arrhythmias?
Which patients should be offered catheter ablation?
Atrial Fibrillation and Atrial Flutter
What are the incidence and prevalence of atrial fibrillation?
What are the major sequelae of atrial fibrillation?
What are the risk factors for stroke in atrial fibrillation?
What are the treatment options for patients with atrial fibrillation?

3. History F > M (2:1) – AVNRT M >F AVRT Posture Menses
3rd trimester pregnancy
Neck pulsations (“Frog sign”)
Age of onset (10 year difference AVNRT(39) vs. AVRT (26)
Thyroid symptoms
Acute precipiants (post op, PE, drug withdrawal, ischemia)
Age of onset (10 year difference AVNRT(39) vs. AVRT (26) in the absence of pre-excitation on ECG
JACC 2009; 53:

4. EKG AV node dependent (Y/N) Re-entrant circuit (Y/N) P wave
Circuit (Macro/Micro)
Anatomic (e.g. previous ASD repair, CVTI)
Accessory pathway ( WPW, Mahaim, etc. )
P wave
Rate
Morphology (Sinus/Retrograde/abnormal): look at the T waves and the psuedo R (V1) and psedo S (inferior leads)
Conduction (2:1; 3:1, etc.)
Response to AV Block
VA conduction (i.e. R-P relationship): (short/long)
Initiation (PAC or PVC) & Termination (P wave or QRS)

7. Anatomy & Physiology SA node AV node His-Purkinje Accessory pathways
1 mm subendocardial near RSPV
AV node
Decremental conduction properties
His-Purkinje
Accessory pathways
No decremental conduction
AV conduction ms
The central fibrous body (annulus fibrosus) partitions the atria and ventricle and electrically isolates the chambers

8. ORT
AVNRT
Non paraoxysmal junctional tach
Atach (reentry or automaticity)

9. AV Node Depdendence (Y/N)
AV nodal dependent arrhythmias
AVNRT (micro-reentrant circuit)
AVRT (macro-reentrant circuit): anti/orthodromic
JET (junctional ectopic tachycardia) - childhood and associated with congenital heart disease
AV nodal independent arrhythmias
Atrial tachycardia
Inappropriate Sinus Tachycardia
Sinus Node Reentrant Tachycardia
Atrial flutter
Atrial fibrillation

10. RP relationship Short “RP” Tachycardias: Typical AVNRT AVRT
Long “RP” Tachycardias:
Atrial Tachycardia
Atypical AVNRT
AVRT with long retrograde conduction
PJRT

11. Where’s the P wave Valsalva Carotid sinus massage Adenosine
Slows SA nodal; and/or AV nodal conduction
Adenosine
Slows sinus rate
Increases AV nodal conduction delay
T ½ 5 seconds
6 or 12 mg bolus
Effect blocked by theophylline, methylxanthines (caffeine); and potentiated by dipyridamole

13. P waves Rate Morphology (Sinus/Retrograde/abnormal)
Conduction (2:1; 3:1, etc.)
Response to AV Block
VA conduction (i.e. R-P relationship): (short/long)

14. AVRT; AVNRT; ATach; Aflutter
Each panel shows the tracings for surface electrocardiographic lead II and an intracardiac bipolar high right atrial electrogram (AEG)
that shows the position of the P waves. Retrograde P waves and QRS complexes are registered simultaneously during atrioventricular
nodal reentrant tachycardia, whereas retrograde P waves are registered shortly after each QRS during atrioventricular reentrant tachycardia
but with RP
PR. In both atrioventricular reentrant tachycardia and atrioventricular nodal reentrant tachycardia, adenosine
blocks anterograde conduction in the atrioventricular node, causing termination of the tachycardia after a retrograde P wave. During
atrial tachycardia, the RP interval is greater than the PR interval. Adenosine causes transient 2:1 atrioventricular conduction without
affecting the atrial rate or interrupting the tachycardia, thus ruling out an accessory pathway as part of the mechanism of the tachycardia.
During atrial flutter there is 2:1 atrioventricular conduction, but only alternate P waves are visible on the surface electrocardiogram,
with the RP interval apparently greater than the PR interval. Adenosine causes transient atrioventricular block, revealing typical
flutter waves.

15. P waves
(-) Inferior leads atrial activation from low to high: AVNRT, atypical AVNRT; AVRT
Right atrial focus:
1) (-/+) in aVL right atrium activated first and then left atrium)
2) (-) or biphasic in V1
Left atrial focus:
1) (-) or isoelectric in aVL
2) (+) V1 suggests back to front

16. Tachycardia onset Most SVTs triggered by a PAC
If the PAC conducts with a long PR, dual AV nodal physiology is suggested with the conduction being through the slow pathway
If a PVC initiates SVT, it is likely to be AV node dependent

17. Tachycardia termination
Ends with a P wave: suggests an AV nodal dependent arrhythmia because the generation of the P wave without a QRS suggests block in the AV node… this is more likely to be AVNRT or AVRT
AVNRT p waves however can be buried in the QRS if VA conduction is very short
Ends with a QRS : almost always atrial tachycardia (some rare AV node dependent tachycardias can terminate in this manner)

18. AVNRT Most common cause of a regular narrow complex tachycardia
Involves a slow and a fast pathway in the region of the AV node
Turn around point appears above the bundle of His
bpm but may exceed 200 bpm
Slow-fast form accounts for 90% of AVNRT
Fast-slow or slow-slow AVNRT accounts for 10%
Pseudo r’ in V1, pseudo S wave in 2,3,avf, and p wave absence help distinguish AVNRT from AVRT and atrial tachycardia

19. AVNRT
Initiation and termination by APDs, VPDs or atrial pacing during AVW
Dual AVN physiology
Initiation depends on critical A-H delay
Concentric retrograde atrial activation(V-A -42 to 70 msec)
Retrograde P wave within QRS with distortion of terminal portion of the QRS
Atrium, His bundle and ventricle not required , vagal maneuvers slow and then terminate SVT

21. Atypical AVNRT
Initiation and termination by APDs, VPDs, or ventricular pacing during retrograde AVW
Dual retrograde AVN physiology
Initiation dependent on critical H-A delay
Earliest retrograde activation at CS os
Retrograde P wave with long R-P interval
Atrium, His bundle, and ventricle not required, vagal , maneuvers slow and then terminate SVT, always in the retrograde slow pathway

22. AVNRT Treatment
Low threshold for catheter ablation given long term success rate > 90% and low risk of complications
AV nodal blocking agents (diagnosis/treatment)
Adenosine
BB/CCB
Digoxin
Anti-arrhythmics (third choice)
Procainamide
Amiodarone
Disopyramide
Flecainide/Propafenone

23. AVRT
Activation sequence is ventricle via atria; therefore P wave often in the ST or T
Left lateral AP: (+) Delta V1; (-) Delta I
Right sided AP: (-) Delta V1 {QS pattern}; (+) Delta I
Concealed AP implies only retrograde conduction; i.e. no pre-excitation and only orthodromic AVRT.
Rapidly conducted Afib occurs may occur for 2 reasons: 1) AP may have a short refractory period ; 2) AP does not exhibit decremental conduction properties like the AV node
Flecainide and Propafenone preferred as they prolong the effective refractory period

24. BBB on tachycardia
Interval development of BBB and increased tachycardia cycle length suggests contralateral AVRT
Pre-existing BBB
Rate related BBB: will look like a conventional BBB
Accessory pathway

25. LBBB morphology and the cycle length slows suggesting a right sided accessory pathway.

26. Fig lead electrocardiogram showing conversion of a narrow QRS tachycardia into a sinus rhythm without wave. During the tachycardia, the visible retrograde P wave (arrows) after the QRS complex suggests that this is an AV reentrant tachycardia caused by a concealed accessory pathway

27. AVRT Use of Adenosine or Verapamil
There is a small risk (3-5%) of preferential conduction down the accessory pathway, and ibutilide or procainamide, or electric cardioversion should be immediately available

28. Afib and WPW

29. Asymptomatic WPW 165 children (5-12 years) screened
60 randomized, 3 withdrew: 20 ablation and 27 no ablation
1 child in ablation group had arrhythmia (5%) and 12 of 27 in control group ( 44% )
2 children in control group had VF and one died
Pappone et al; NEJM 2004;351:

30. AVRT Treatment
Low threshold for catheter ablation given long term success rate > 90% and low risk of complications
Posteroseptal pathways have less success rates
L sided
AV nodal blocking agents (diagnosis/treatment)
Adenosine
BB orCCB in conjunction with Flecainide or Propafenone

31. Atrial tachycardia
Older patients - related to atrial stretch or scarring
If conduction to the ventricle via the AV node, variable AV block may occur
A bystander (accessory) pathway may be used to conduct antegrade to the ventricles; i.e. the accessory pathway is not what is causing the atria to beat so fast
Tachycardia may be incessant: “the ventricle is a slave to the atrium”
Procainamide may be considered to achieve immediate control
AV nodal blocking agents and sotalol may be considered for chronic treatment

32. Irregular SVT AV block Multifocal atrial tachycardia (MAT)
Wenckebach
Variable block (e.g. atrial tachycardias)
2:1 with typical flutter; odd multiples with atypical flutter
Multifocal atrial tachycardia (MAT)
Atrial Fibrillation (with or w/o pre-excitation)

33. Focal Atrial Tachycardia
Incessant or paroxysmal atrial rhythms bpm
Demographic profile similar to reentrant AT, but less likely to have cardiac surgery
Typically 1:1 conduction
P wave morphology different from sinus
Typically terminate or transiently suppress with adenosine
Centrifugal activation
Cannot be entrained

34. Focal Atrial Tachycardia
Three Subgroups:
Cristal Tachycardia
- Initiated and terminated with PES
- Arise along crista
- P wave similar to NSR
- Terminates with adenosine
Repetitive monomorphic AT
- Repetitive runs of nonsustained AT
- Suppress with adenosine
- Variable locations
Automatic AT
- Incessant AT
- Transient suppression with adenosine

35. Atrial tach
Variable conduction

36. Macroentrant Atrial Tachycardia
Incessant or Paroxysmal atrial rhythms bpm
Demographic similar to focal atrial tach but more likely to have had cardiac surgery
P wave morphology usually differs from sinus
Typically are insensitive to adenosine
Demonstrate features specific for reentry
- concealed or manifest entrainment
- fractionated mid diastolic EGM’s
- concealed activation during diastole

38. Junctional Tachycardia
Nonparoxysmal Junctional Tachycardia
Junctional Ectopic Tachycardia
Congenital Automatic Junctional Tachycardia

39. Nonparoxysmal Junctional Tachycardia
bpm
Generally regular with VA conduction
Seen with dig toxicity, ischemia, COPD, metabolic disturbances, carditis and after cardiac surgery
Mechanism is triggered activity due to DADs

40. Junctional Ectopic Tachycardia (JET)
Following surgery for congenital heart disease
3% of VSD repairs, 10% of TGV, 7% of TOF and 2% of Fontan
Perinodal trauma
Procainamide and cooling, amiodarone

41. Congenital Automatic Junctional Tachycardia
< 1% of pediatric SVTs
Average HR 230 bpm ( )
Infants < 6 months old
High mortality. Less malignant older the child is
Triggered activity, enhanced automaticity
Amiodarone, ablation with PM

42. PJRT Orthodromic reciprocating tachycardia
Earliest retrograde activation in proximal CS
Tachycardia terminates with adenosine with retrograde AP block
HIS refractory PVC advances atrial activation

44. Atrial Flutter Typical or type I atrial flutter:
Counter clockwise atrial activation manifested as - P waves in II,III,avf and + in VI with transition to - P in V6
Clockwise with reverse activation
Atypical or type II atrial flutter
Also called as fib flutter
In the absence of AFib symptomatic Aflutter is often amenable to ablation (success rates >90%)

46. Type I typical flutter

47. Clockwise flutter

48. Afib What are the incidence and prevalence of atrial fibrillation?
What are the major sequelae of atrial fibrillation?
What are the risk factors for stroke in atrial fibrillation?
What are the treatment options for patients with atrial fibrillation?

49. Afib epidemiology
Age adjusted incidence has been increasing from 1980 to 2000: 3.2 million in 1980; 5.1 million in 2000
The detection of Afib requires symptoms and asymptomatic PAF may go undetected.. Current estimates at the Mayo Clinic would suggest 2.3 million Americans.
Afib prevalence increases with age: 0.1% <55 years; at 9% in octogenerians.
At younger ages (<70), Afib has a greater prevalence among males (5.8%) than females (2.8%) based on data from CHS
The lifetime risk based on the Framingham cohort is 23-26% among 40 year olds.
Circulation 2006; 114(2): ;Am J Cardiol 1994; 74: ).; JAMA 2004; 292: ; JACC 2007; 49: ).

50. Afib epidemiology
Age alone does not explain the increased incidence: an increase in obesity accounted for 60% of the age adjusted increase in AF incidence
HTN and Diastolic dysfunction
Obesity has been associated with new onset Afib in the Framingham and other cohorts
OSA, Etoh, Anger, ethnicity, and genetic influences have been reported to be associated with incident Afib.
Appropriately treated OSA reduces AFib recurrence after cardioversion
AA race is associated with less Afib than whites.
Afib and CAD are co-existent
Rheumatic heart disease and valvular heart disease
Circulation 2006; 114(2): ;Am J Cardiol 1994; 74: ).; JAMA 2004; 292: ; JACC 2007; 49: ; Circ 2003; 107: ).

51. Afib categories
Lone atrial fibrillation: no structural heart disease (usually <60 years)
Paroxysmal : terminate spontaneously <7 days
Persistent: fails to self-terminate within 7 days. Episodes may eventually terminate spontaneously, or they can be terminated by cardioversion.
Permanent : > 1 year and CV not attempted or failed.
** Episodes > 30 seconds unrelated to a reversible cause (cardiac surgery, pericarditis, MI, hyperthyroidism, PE)

52. What are the major sequelae of atrial fibrillation?
Worsened heart failure
Afib begets afib leading to electrical and structural remodeling
Tachycardia induced cardiomyopathies
Stroke
Decreased quality of life and exercise tolerance
Acute hemodynamic compromise

53. CHADS2
. Risk of Stroke: (CHAD score ranges from 0-6; 2 points for prior TIA or stroke, 1 for HTN, CHF, DM, Age>75, JAMA 2001; 285: ). Annual risk of stroke: (non-rheumatic Afib)
0=1.9%
1=2.8%
2=4.0%
3=5.9%
4=8.5%
5=12.5%
6=18.2%

54. Afib treatment options
Rate control
AV nodal agents
AV node ablation and pacemaker
Rhythm control
Cardioversion: chemical or electrical; +/- TEE
Anti-arrhythmics
Catheter Ablation
MAZE
Anticoagulation
ASA
ASA + clopidogrel
Warfarin

55. Irregularly irregular rhythms
MAT
Afib
ATach with variable conduction

56. Pregnancy and SVTs 50% have SV ectopics
Sustained arrhythmia rare (2-3/1000)
Symptomatic increase in 20%
Risk to mother and fetus
No controlled study and there would be none
AA drugs toxic and should be reserved for only highly symptomatic patients
Role of RF ablation

57. Antiarrhythmic drugs in Pregnancy

58. Radiofrequency Catheter Ablation
Who should be referred?
What arryhthmias should be referred for ablation?
What are the success rates?
What are the risks of ablation?

59. Who should be referred? Symptomatic patients
AVNRT (>90% succes rates)
WPW and symptomatic AVRT (CCB ; BB and Dig not appropriate as sole therapy) (>90%)
Aflutter(>90%)
AFib (40-70%)
High risk for sudden death
AFib with WPW and cycle length <250 ms
Not amenable to catheter ablation
MAT
Reversible causes (thryotoxicosis; PE; post-op)

60. Question 1
A 35-year old woman with unrepaired Ebstein's anomaly is evaluated in the emergency department for recurrent tachycardia episodes. Several episodes occur while she is being evaluated. She notes that she feels somewhat lightheaded.
The patient's blood pressure is 110/60 mm Hg. She is acyanotic and afebrile. Cardiac examination demonstrates a brief systolic murmur along the lower left sternal border, which increases with inspiration. The jugular venous pressure is elevated.
The electrocardiogram shows a short PR interval, an abnormal initial portion of the QRS complex, and right bundle branch block. The tachycardia is wide-complex and regular at a rate of 190/min.
What is the most appropriate acute treatment of choice?
A Adenosine
B Procainamide
C Digoxin
D Direct-current cardioversion

62. Question 2
A 26-year-old nurse is evaluated in the emergency department after an episode of syncope. While working in the intensive care unit, she developed tachycardia and then lost consciousness. She admits to having a stressful day and having had more caffeine than normal. She has had brief episodes of tachypalpitations in the past but no prior syncope.
Physical examination is unremarkable and the patient is in sinus rhythm. The chest radiograph is unremarkable. The electrocardiogram initially demonstrates sinus rhythm and is unremarkable. Ten minutes later, the patient develops an episode of brief tachycardia. Shortly after the tachycardia episode, a repeat electrocardiogram is performed and is shown (Figure 122).
What is the most likely diagnosis in this patient?
A Atrioventricular nodal reentrant tachycardia
B Accelerated idioventricular tachycardia
C Atrioventricular reentrant tachycardia
D Multifocal atrial tachycardia

64. Question 3
A 68-year-old woman comes to the emergency department because of a racing heart for the past 2 hours. She reports a 2-year history of similar episodes, for which her physician instructed her to cough or strain. The episodes usually terminate after a few minutes of following her physician's instructions, but the current episode is persisting. She does not have chest pain, and she has no other cardiac history.
The physical examination demonstrates a blood pressure of 110/60 mm Hg, heart rate of 165/min, respiratory rate of 20/min, clear lungs, and no murmurs or gallop. After the carotids are auscultated and the presence of bruit excluded, carotid sinus massage is attempted, but the tachycardia persists. The electrocardiogram obtained in the emergency department is shown .
Which is the drug of choice for terminating this patient's arrhythmia?
A Metoprolol
B Verapamil
C Adenosine
D Digoxin
Adenosine

66. References www.blaufuss.org
Cardiac Arrhythmias by Eric N. Prystowsky and George J. Klein

67. Toothbrush arryhthmia