Approach to svt

1. SUPRVENTRICULAR
TACHYARRHYTHMIAS
Mohammad Hassan Khedr
MD Cardiology

2. Case #1
Q. A 32 year old female is treated in the
emergency room for palpitations. The first
ECG is tachycardia and the second is
after adensosine.What is the arrhythmia?
 A. AVNRT
 B. ORT
 C. Atrial tachycardia
 D. Atrial fibrillation

5. Answer: AVNRT (A)
 A small R’ is seen is lead V1 with pseudo-S
waves in the inferior leads that are absent
after termination of the arrhythmia. These
represent retrograde atrial activation with a
very short RP interval.

6. Q. A 42 year old smoker presents to the ED
with palpitations. His blood pressure is
110/60. The following rhythm strip is
obtained . What is the next appropriate
step?
 Emergent cardioversion for polymorphic VT.
 B. I.V. procainamide
 C. I.V. lidocaine
 D. diltiazem drip to obtain rate control.

10. Approach to classification of
SVT
1) Clinical behavior (ie. Paroxysmal, persistent,
permanent, incessant, sustained,
nonsustained, chronic, and repetitive)
2) Mechanism (ie, ectopic, automatic,
reenterant, orthodromic, antidromic)
3) ECG appearance (narrow or wide)
4) Location (sinus, atrial, AV nodal/ juntional)

11. Mechanism
All cardiac tachyarrhythmias are produced by
one or more mechanisms including:
1) Disorders of impulse initiation
2) Abnormalities of impulse conduction.

12. Mechanisms of Arrhythmia
 Abnormal automaticity
 automatic impulse generation from unusual site
or overtakes sinus node
 Triggered activity
 secondary depolarization during or after
repolarization
 Dig toxicity, Torsades de Pointes
 Reentry
 90 % of arrhythmiasythmias

13. Hypothermia decrease, hyperthermia increase phase
4 slope
Hypoxia & hypercapnia both increase phase 4 slope
Cardiac dilation increases phase 4 slope
Local areas of ischemia or necrosis increases
automaticity of neighboring cells
Hypokalemia increases phase 4 slope, increases
ectopics, prolongs repolarization
Hyperkalemia decreases phase 4 slope; slow
conduction, blocks
Altered Automaticity

14. Reentry
 Most common
mechanism
 Requires two
separate paths of
conduction
 Requires an area of
slow conduction
 Requires
unidirectional block

15. Symptoms
 palpitations
 fatigue
 lightheadedness
 Chest discomfort
 dyspnea
 Presyncope
 Polyurea (release of atrial natriuretic peptide in
response to increased atrial pressures from
contraction of atria against a closed AV valve)
 Syncope (rare)

16. Clues from Symptoms
 Regular vs. Irregular
 Premature depolarizations,
AF, MAT
 AVNRT, AVRT
 Sudden onset and offset
 No clear precipitating
factor
 AT
 Gradual onset of
symptoms and get
more rapid over time
(warm-up)
 Particular maneuver
or position provokes
the syndrome

17. Supraventricular Tachycardias
Diagnosis
 ECG is cornerstone
 Observe zones of transition for clues as to
mechanism:
 onset
 termination
 slowing, AV nodal block
 bundle branch block

18. Regular SVT in adults
 90% reentrant 10 % not reentrant
 60% AV nodal reentrant tachycardia (AVNRT)
 30% orthodromic reciprocating tachycardia
(ORT)
 10% Atrial tachycardia
 2 to 5% involve WPW syndrome

21. Differential Dx of Regular SVT
 Short RP
tachycardia
 AV nodal reentrant
tachycardia
 ORT( Orthodromic
reciprocating
tachycardia)
 Atrial tachycardia
when associated with
slow AV nodal
conduction (rare)
Short RP interval

22. Differential Dx of Regular SVT
 Long RP tachycardia
 Atrial tachycardia
 Sinus node reentry
 Sinus tachycardia
 Atypical AV nodal
reentrant tachycardia
Long RP interval

26. Sinus Tachycardia
 Appropriate
physiological
stimulus (eg,
exercise) or to an
excessive stimulus
(eg,
hyperthyroidism).
 Pyrexia
 Hypovolemia
 Anemia
 Drugs
 caffeine, alcohol, nicotine
 Prescribed compounds
(eg, salbutamol,
aminophylline, atropine,
catecholamines)
 Recreational/illicit drugs
(eg, amphetamines,
cocaine, “ecstasy,”
Physiological Stimulus Pathological Causes

27. Management
 Treat underlying mechanism
 Beta blockade for physiological symptomatic
sinus tachycardia triggered by emotional
stress and other anxiety related disorders

28. Other Long RP tachycardias
 Sinus node reentrant
 abrupt onset and
offset
 P wave complex
same as sinus
 Amenable to calcium
channel blockers,
much less responsive
to beta blockers
 Amenable to catheter
ablation
 Syndrome of
inappropriate sinus
tachycardia
 typical sinus
tachycardia with
lowest rate on Holter
of 130 bpm
 Treated with high dose
beta blockers
 Poor results with
catheter ablation

30. AV Nodal Reentrant
Tachycardia
 2 pathways within or
limited to perinodal
tissue
 anterograde
conduction down fast
pathway blocks with
conduction down slow
pathway, with
retrograde conduction
up fast pathway.
Slow pathway
Fast pathway

31. Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
Premature Beat Impulse
Cardiac
Conduction
Tissue
1. An arrhythmia is triggered by a premature beat
2. The beat cannot gain entry into the fast conducting pathway
because of its long refractory period and therefore travels down
the slow conducting pathway only
Repolarizing Tissue
(long refractory period)
The “Re-Entry” Mechanism of Ectopic Beats &
Rhythms.

32. 3. The wave of excitation from the premature beat arrives
at the distal end of the fast conducting pathway, which has
now recovered and therefore travels retrogradely
(backwards) up the fast pathway
Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
Cardiac
Conduction
Tissue
The “Re-Entry” Mechanism of Ectopic Beats &
Rhythms.

33. 4. On arriving at the top of the fast pathway it finds the slow
pathway has recovered and therefore the wave of excitation ‘re-
enters’ the pathway and continues in a ‘circular’ movement.
This creates the re-entry circuit
Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
Cardiac
Conduction
Tissue
The “Re-Entry” Mechanism of Ectopic Beats &
Rhythms.

34. Initiation of AV Nodal Reentrant
Tachycardia
PAC = premature atrial
complex (beat)
PAC
PAC

35. Sustainment of AV Nodal Reentrant Tachycardia
Rate 150-250
beats per min
P waves
generated
retrogradely
(AV node
→ atria) and
fall within or
at tail of QRS

36.  May have very short
RP interval with
retrograde P wave
visible as an R’ in
lead V1 or psuedo-S
wave in inferior leads
in 1/3 of cases .
 No p wave seen in
2/3

38. Tachycardia Algorithm (1 of 2)
38

39. Tachycardia Algorithm (2 of 2)
39

40. Narrow QRS Tachycardia
40

41. AV Nodal Reentrant
Tachycardia
 Responds to vagal
maneuvers in 1/3 cases
 Very responsive to AV
nodal blocking agents
such as beta blockers, Ca
channel blockers,
adenosine.
 Recurrences are the
norm on medical therapy
 Catheter ablation 95%
successful with 1% major
complication rate

42. Determining AV Nodal Participation in SVT by
Transiently Depressing AV Nodal Conduction
 Vagotonic Maneuvers
 Carotid sinus massage
 Valsalva maneuver (bearing down)
 Facial ice pack (“diving reflex;” for kids)
 Adenosine (6-12 mg I.V.)
 If SVT “breaks,” a reentrant mechanism
involving the AV node is likely
 If atrial rate unchanged, but ventricular rate
slows (#P’s > #QRS’s), SVT is atrial in origin

43. Carotid Sinus Massage
Stimulation of
carotid sinus
triggers
baroreceptor
reflex and
increased vagal
tone, affecting
SA and AV
nodes

44. Termination of SVT by
Vagotonic Maneuver (Carotid Sinus
Massage)

45. SVT
Carotid Sinus Massage

51. Junctional Tachycardias
1) Focal Junctional Tachycardia (automatic or
paroxysmal junctional tachycardia)
2) Non paroxysmal Junctional Tachycardia

52. Focal Junctional Tachycardia
- Uncommon
- Pediatrics or post-
op
The ECG features:
 HR 110 to 250 bpm
 A narrow complex or
typical BBB
conduction pattern
 Atrioventricular
dissociation is often
present

53. Nonparoxysmal Junctional
Tachycardia
 Narrow complex
tachycardia with rates of
70 to 120 bpm
 A typical “warm-up” and
“cool-down” pattern
 The arrhythmia
mechanism
 enhanced automaticity
arising from a high
junctional focus or
 in response to a
triggered mechanism
 it may be a marker
for a serious
underlying condition,
such as digitalis
toxicity, postcardiac
surgery,
hypokalemia, or
myocardial ischemia

57. Ex. RT. Ante ro se ptalAP

59. AVRT
 Orthodromic
tachycardia- 95%
 ORT with a
concealed
accessory pathway
(retrograde only
conducting
pathway)
 Antidromic
tachycardia- 5%

61. Sustainment of Orthodromic
AV Reciprocating Tachycardia
Atria
AP
AVN
Ventricles
Retrograde P’s fall
in the ST segment
with fixed, short RP
Rate 150-250
beats per min

62. Accessory Pathway with
Ventricular Preexcitation
(Wolff-Parkinson-White
Syndrome)
“Delta” Wave
AP
PR < .12 s
QRS ≥ .12 s
Sinus
beat
Hybrid
QRS shape
In sinus rhythm, every ventricular activation is a fusion
between accessory pathway and AV nodal conduction

63. Varying Degrees of
Ventricular Preexcitation

64. ORT
 Amenable to AV nodal
blocking agents in
absence of
anterograde
conduction of pathway
 Amenable to catheter
ablation with 95%
success and 1% rate
major complication
Conduction down
AVnode
Up
accessory
pathway

65. WPW syndrome
 The diagnosis of WPW
syndrome is reserved for
patients who have both
pre-excitation and
tachyarrhythmias
 AVRT is the most
common arrhythmia,
accounting for 95% of
re-entrant tachycardias
that occur in patients
with an accessory
pathway
Louis Wolff, Sir John Parkinson and Paul Dudley

66. Classic ECG pattern
 Accelerated AV conduction PR <120
msec
 Prolonged QRS > 120 msec
 Abnormal slurred upstroke of QRS ( delta
wave)
 Abnormal depolarization and
repolarization may lead to
pseudoinfarction pattern

67. WPW epidemiology
 Present in 0.3% of the
population
 Risk of sudden death
0.15% to 0.39% over 3- to
10-year follow-up
 Sudden death due to
atrial fibrillation with rapid
ventricular conduction
 Atrial fibrillation often
induced from rapid ORT
ORT(orthodromic
reciprocating tachycardia

68.  Markers associated with increased sudded
cardiac death
1) a shortest pre-excited R-R interval less than
250 ms during spontaneous or induced AF
2) a history of symptomatic tachycardia
3) multiple accessory pathways
4) Ebstein’s anomaly

69.  The detection of intermittent preexcitation,
which is characterized by an abrupt loss of the
delta wave and normalization of the QRS
complex, is evidence that an accessory
pathway has a relatively long refractory period
and is unlikely to precipitate VF.
 The loss of pre-excitation after administration
of the antiarrhythmic drug procainamide has
also been used to indicate a low-risk
subgroup.

70.  Antiarrhythmic drugs that primarily modify conduction
through the AV node include:
 digoxin, verapamil, beta blockers, adenosine, and diltiazem
 Antiarrhythmic drugs that depress conduction across the
accessory pathway include:
 Class I drugs, such as procainamide, disopyramide,
propafenone, and flecainide, as well as class III
antiarrhythmicdrugs, such as ibutilide, sotalol, and
amiodarone.

71. Atrial Fibrillation and WPW
 Atrial fibrillation is a potentially life-threatening
arrhythmia in patients with WPW syndrome.
 If an accessory pathway has a short
anterograde refractory period, then rapid
repetitive conduction to the ventricles during
AF can result in a rapid ventricular response
with subsequent degeneration to VF.

72. Atrial Fibrillation and WPW
 AV nodal blocking
agents may
paradoxically increase
conduction over
accessory pathway by
removing concealed
retrograde penetration
into accessory
pathway. Concealed penetration into the
pathway causes intermittent block
of pathway conduction

73. Management of Atrial Fibrillation
with WPW
 Avoid AV nodal blockers
 IV procainamide to slow accessory pathway
conduction
 Amiodarone if decreased LVEF
 DC cardioversion if symptomatic with
hypotension

74. Management of Patients with
WPW
 All patients with symptomatic AF & WPW
should be evaluated with EPS
 Accessory pathways capable of conducting
faster than 240 BPM should be ablated
 Patients with inducible arrhythmias involving
pathway should be ablated
 WPW patients in high risk professions should
be ablated.

77. Atrial Tachycardia
 Atrial rate between 100 and 250 bpm
 Does not require AV nodal or infranodal
conduction
 P wave morphology different than sinus
 P-R interval > 120 msec differentiating from
junctional tachycardia

78. Atrial tachycardia
 P wave upright lead V1 and negative in aVL
consistent with left atrial focus.
 P wave negative in V1 and upright in aVL
consistent with right atrial focus.
 Adenosine may help with diagnosis if AV block
occurs and continued arrhythmia likely atrial
tachycardia

79. Atrial Tachycardia
 Most are due to
abnormal automaticity
and have right atrial
focus
 May be reentry
particularly in patients
with previous atriotomy
scar, such as CABG or
congenital repair
patients
 it is often
 associated with