SVT Types and discussion, self assessment

1. NARROW QRS
TACHYARRHYTHMIA
NARROW QRS TACHYARRHYTHMIA

3. CONDUCTION SYSTEM

4. THE NORMAL SINUS IMPULSE

5. ACTIVATION OF THE ATRIA – P wave

6. ACTIVATION OF AV NODE & HIS-
PURKINJE SYSTEM

7. ACTIVATION OF THE VENTRICLES- QRS
COMPLEX

8. REPOLARIZATION OF THE VENTRICLES

9. The PR Interval, QRS Complex, and
QT Interval

10. CLASSIFICATION OF TACHYARRYTHMIAS

11. SINUS TACHYCARDIA

13. • ECG Findings
1. Sinus P waves are present with a
rate >100 bpm.
2. The sinus P waves precede each QRS
complex with a PR interval 0.12
seconds.
3. The morphology of the P wave
should be upright in leads I, II, and

14. • TYPES:
1. Physiologic
2. Pathologic:
-Inappropriate sinus tachycardia
-Postural orthostatic tachycardia
syndrome
-Sinoatrial reentry tachycardia

15. TREATMENT
• Treat the underlying cause
• INAPPROPRIATE SINUS TACHYCARDIA:
-beta blockers and nondihydropyridine
calcium channel blockers such as
diltiazem and verapamil.
• POTS:
-pharmacologic
-non pharmacologic
-catheter ablation

17. Atrial fibrillation (AF) is a cardiac
arrhythmia characterized by seemingly
disorganized, rapid, and irregular atrial
electrical activation, resulting in loss of
organized atrial mechanical contraction.
These rapid and irregular electrical
signals input into the atrioventricular
(AV) node, which determines ventricular
activation and rate.
The conducted ventricular rate is variable,
resulting in an irregular, usually rapid
ventricular rate, ranging typically
between 110 and 160 beats/ min.

18. FOCAL
ACTIVATION –
ACTIVITY MAY
BETRIGGEREDDU
E TO INCREASED
AUTOMATICITY
OR FROM MICRO
RE-ENTRY.
MULTIPLE
WAVELET
MECHANISM–
THE
FIBRILLATION
ISMAINTAINEDBY
RE-ENTRY
CIRCUITS
FORMED BY SOME
OF THE
WAVELETS. THIS
PROCESS IS
POTENTIATED
BYA DILATED
LA(FACILITATES
CONTINUOUS
WAVEFORM
PROPAGATION)
,STRUCTURAL

19.  Irregularly irregular rhythm
 No P waves
 Absence of an isoelectric baseline
 Variable ventricular rate
 QRS complexes usually < 120ms,
unless pre-existing bundle branch
block, accessory pathway, or rate-
related aberrant conduction
 Fibrillatory waves may be present
and can be either fine (amplitude
< 0.5mm) or coarse (amplitude >
0.5mm)

20. CLASSIFIC
ATION OF
ATRIAL
FIBRILLAT
ION
 First episode – initial detection of AF regardless of
symptoms or duration
 Recurrent AF – More than 2 episodes of AF
 Paroxysmal AF – Self terminating episode < 7 days
 Persistent AF – Not self terminating, duration > 7 days
 Long-standing persistent AF – > 1 year
 Permanent (Accepted) AF – Duration > 1 yr in which
rhythm control interventions are not pursued or are
unsuccessful
 Lone: paroxysmal, persistent, or permanent AF with no
structural heart disease, typically in persons < 60 years
old, the lowest risk of complications → patients have
a CHA2DS2-VASc score of “0”
 Secondary: due to underlying condition, treatment
focuses on the underlying condition to resolve AF
 Subclinical: AF in asymptomatic individuals without a
prior diagnosis of AF

21. DIAGNOSIS OF AF
RATE CONTROL
RHYTHM CONTROL
ASSESSMENT FOR ANTICOAGULATION
TREATMENT OF UNDERLYING / ASSOCIATED

22. Electrocardiogram (ECG): confirms diagnosis
Irregularly irregular (pathognomonic)
Echocardiogram: used to identify etiology and complications
 Transthoracic echocardiogram (TTE)
• Used to assess cardiac function
• Rules out or confirms structural cardiac disease (e.g., valve stenosis)
 Transesophageal echocardiogram (TEE)
• Rules out or confirms the structural cardiac disease
• Indicated if AF lasted for > 48 hrs or if the duration is unknown
• Indicated if planning cardioversion on patients who haven’t received anticoagulation
therapy for at least 3 weeks
• Used to detect thrombi within the left atrium or left atrial appendage

23. • Ventricular rates should be adequately controlled
• ABCD ( Amiodarone , beta blockers , calcium channel blockers- non DHP
, digoxin )
• WITH NORMAL SYSTOLIC FUNCTION
• NON DIHYDROPYRIDINE CALCIUM CHANNEL BLOCKERS-
verapamil , diltiazem
• BETA BLOCKERS -metoprolol , atenolol , propranolol , esmolol
• DIGOXIN
• AMIODARONE
WITH LV SYSTOLIC DYSFUNCTION
• DIGOXIN
• AMIODARONE
NON PHARMACOLOGICAL
• AV NODAL ablation
• pulmonary vein isolation

24.  SPONTANEOUS CONVERSION -
Most frequently during first 24 to 48 hours
 PHARMACOLOGICAL
 AF OF <7 DAYS DURATION
WITH PRESERVED SYSTOLIC
FUNCTION : FLECAINIDE ,
PROPAFENONE, IBUTILIDE, DOFETILIDE,
AMIODARONE, QUINIDINE
WITH LV DYSFUNCTION : AMIODARONE
, DOFETILIDE
 AF OF >7 DAYS DURATION
AMIODARONE , IBUTILIDE , DOFEILIDE

25.  ELECTRICAL OR DIRECT CURRENT CARDIOVERSION
In IV sedation
 SURGICAL ABLATION
 CATHETER ABLATION

26.  ONE INTERMEDIATE
RISK FEATURE
 Option of T.ASPIRIN 81 to
325 mg daily or WARFARIN
(INR 2- 3)
 PREVIOUS STROKE OR, 2
OR MORE RISK FEATURE
 WARFARIN (INR 2-3)
CHA2DS2-VASc risk factor Points
C- Cardiac failure or left ventricular
dysfunction (EF <35%)
+1
H- Hypertension +1
A2- Age 75 years or older +2
D- Diabetes mellitus +1
S2- Stroke , TIA , or previous history of
thromboembolism
+2
V-Vascular disease +1
A- Age 65 –74 +1
Sc - Sex Category +1

28. • Cardiac enzymes → myocardial infarction
• BNP → heart failure
• TSH/fT4 → hyperthyroidism
• CBC → infection/sepsis
• BUN, creatinine → kidney function
• CT pulmonary angiography → pulmonary embolism
• Electrolytes(potassium, calcium, or magnesium) → electrolyte
imbalances
• Urine drug screen → cocaine, amphetamines, digoxin, or
alcohol
• Exercise tes􀆟ng → ischemic heart disease, also guides

29.  The accessory pathway allows for rapid conduction directly to the ventricles
bypassing the AV node
 Rapid ventricular rates may result in degeneration to VT or VF
 AV nodal blocking agents are contracindicated because they enhance conduction
across bypass tract andcause rapid ventricular rate and hemodynamic collapse
 Management of AF with WPW
 In unstable patients due to AF, urgent synchronised DC cardioversion is required.
 Medical management in stable patient is procainamide.

30. ECG features of Atrial Fibrillation
in WPW:
 Rate > 200 bpm
 Irregular rhythm
 Wide QRS complexes due to
abnormal ventricular
depolarisation via accessory
pathway
 QRS complexes change in shape
and morphology
 Axis remains stable, unlikely
polymorphic VT

32. ATRIAL FLUTTER
 Atrial flutter is a supraventricular arrhythmia caused by a re-entry circuit within the right atrium
with a regular atrial rate of 300 +/- 50 beats per minute
 It is usually precipitated by premature atrial complexes or repetitive impulses originating from
other areas contiguous to the atria such as the pulmonary veins
 Very regular and uniform flutter waves with a saw tooth or picket fence appearance.
 The flutter waves are typically inverted in leads II,III, and aVF and upright in V1.
 The baseline between two flutter waves is usually wavy and undulating

33. TYPES
TYPICAL ATRIAL FLUTTER (Anticlockwise
reentry)
 Inverted flutter waves in leads
II,III,aVF
 Positive flutter waves in V1- may
resemble upright P waves
REVERSE TYPICAL ATRIAL FLUTTER(Clock
wise reentry)
 Positive flutter waves in leads
II,IIIaVF
 Broad ,inverted flutter waves in
V1

35. ATRIAL FLUTTER V/S ATRIAL
TACHYCARDIA
Atrial Tachycardia with 2:1 AV block
 Atrial rate approximately 200 ± 50 bpm or 150 - 250 bpm
 Upright P waves in lead II
 Isoelectric baseline

36. ATRIAL FLUTTER WITH 2:1 AV BLOCK
 Atrial rate approximately 300 ± 50 bpm (minimum rate 240-250 bpm)
 Inverted atrial complexes in lead II
 Undulating or wavy baseline

37. ATRIAL FLUTTER V/S SVT
 Vagal maneuvers such as carotid sinus pressure, is useful in
differentiating atrial flutter from other types of regular narrow complex
SVT
 Atrial Flutter :In atrial flutter, carotid sinus pressure or AV nodal blockers
such as adenosine or verapamil will slow AV nodal conduction resulting
in a slower ventricular rate but will not convert atrial flutter to normal
sinus rhythm
 Regular narrow complex SVT: When the narrow complex tachycardia
is due to SVT, the tachycardia may convert to normal sinus rhythm with
carotid stimulation. SVT from reentry but not atrial flutter is frequently
terminated by AV nodal blockers to normal sinus rhythm

39. CLINICAL IMPLICATIONS
 It is more common in men than in women.
 Atrial flutter is usually associated with organic or structural cardiac
disease or it may be precipitated by an acute condition.
 An acute precipitating cause, usually surgery (cardiac or noncardiac),
pneumonia, acute myocardial infarction, or congestive heart failure can
be identified in 60% of cases.
 The remaining cases are associated with chronic cardiac or pulmonary
diseases or hypertension.
 Lone atrial flutter is rare occurring only in 1.7% of all cases.

40. TREATMENT
 Hemodynamically unstable and are hypotensive with low cardiac output,
immediate direct current cardioversion is indicated
 Similar to atrial fibrillation and include three considerations

41. 1 Anticoagulation to prevent thromboembolism: If duration of atrial flutter >/= 48hrs
2 .Control of ventricular rate
Poorly tolerated patient : Direct current cardioversion to convert atrial flutter to normal sinus
rhythm
Calcium channel blockers (Verapamil and Diltiazem) or Beta blockers
iv digoxin or amiodarone – acute decompensated
heartfailure/hypotension
Stable patients : Direct current cardioversion / atrial or transesophageal pacing
Calcium channel blockers or Beta blockers

42. 3. Conversion of atrial flutter to normal sinus rhythm can be accomplished
by the following:
 Antiarrhythmic agents
 Rapid atrial pacing
 Electrical cardioversion
 Catheter ablation
 Antitachycardia devices
 Surgery

43.  Antiarrhythmic agents: Class IA antiarrhythmic agents (procainamide)
Class IC (flecainide and propafenone)
Ibutilide, a Class III antiarrhythmic agent, -For patients weighing
> 60 kg, an initial 1 mg dose is injected intravenously for 10 minutes. The
same dose may be repeated after 10 minutes if the initial 1 mg bolus is not
effective
Procainamide, a Class IA antiarrhythmic agent, is given
intravenously with a loading dose of 10 to 14 mg/kg for 30 minutes. This is
followed by a maintenance infusion of 1 to 4 mg/minute.

44. Amiodarone: 5 mg/kg given intravenously in 10 minutes.
Recommened for both rate control and for
control of atrial flutter to normal sinus rhythm.
 Other agents: Propafenone and flecainide (Class IC agents) and sotalol
(Class III agent)
 Rapid atrial pacing: Among stable patients, atrial or transesophageal
pacing carries a Class I recommendation for converting atrial flutter to
normal sinus rhythm. Rapid atrial pacing is performed by introducing an
electrode catheter transvenously into the right atrium. It can also be
performed transesophageally by swallowing a pill electrode positioned
behind the left atrium.
Type1 : can be converted to normal sinus rhythm with rapid atrial
pacing
Type 2: cannot be interrupted by rapid atrial pacing

45. ATRIAL TACHYCARDIA
 The atria, including the atrial appendage, large veins draining into the
atria (pulmonary veins, vena cava, and coronary sinus) or even the mitral
or tricuspid annulus, may contain cells with properties of automaticity.
 The rate of discharge of these cells may be enhanced, resulting in atrial
tachycardia. The tachycardia may be unifocal or focal or it may be
multifocal

46. FOCAL ATRIAL TACHYCARDIA
 The tachycardia originates from a single focus in the atria or from a
venous connection contiguous to the atria such as the pulmonary veins
or vena cava.
 The atrial impulse spreads in a circumferential manner regardless of the
mechanism of the tachycardia.
 Due to enhanced automaticity (automatic atrial tachycardia), intra-atrial
micro-reentry (intraatrial reentrant tachycardia), or triggered automaticity
(atrial tachycardia with 2:1 AV block).
 May be paroxysmal or sustained

47. Electrical cardioversion.
Direct current cardioversion is the treatment of choice when rapid conversion to
normal sinus rhythm is desired and receives a Class I recommendation for both
stable and unstable patients
Catheter ablation of the reentrant pathway: Long-term therapy of atrial flutter
especially when recurrent includes ablation of the reentrant pathway with an
endocardial catheter.
Antitachycardia devices: Permanent pacemakers are capable of delivering rapid
atrial pacing and can be implanted in patients who are responsive to rapid atrial
pacing.
Surgery: This approach is feasible in patients who are also scheduled to
undergo coronary bypass surgery or open heart surgery for valvular disease.

48. ECG FINDINGS
 Presence of a regular narrow complex tachycardia > 100 bpm.
 Ectopic P waves, which are different from sinus P waves, precede the
QRS complexes usually with a PR interval > 0.12 seconds.
 The P waves are uniform and the atrial rate varies to as high as 250
bpm.
 The baseline between the P waves is usually flat or isoelectric
 Second-degree or higher grades of AV block may occur because the
tachycardia is not dependent on the AV node

49. LOCALIZING THE ORIGIN OF
TACHYCARDIA
RIGHT ATRIAL ORIGIN
 P waves are inverted in V1.
 If biphasic in V1, the P waves
are initially positive (upright) and
terminally negative (inverted).
 In lead aVL, the P waves are
upright or biphasic
LEFT ATRIAL ORIGIN
 P waves are upright in V1.
 If V1 is biphasic, the P waves are
initially negative (inverted) and
terminally positive (upright).
 In aVL, the P waves are negative
or isoelectric (flat)

51. SUPERIOR VS INFERIOR ORIGIN
 If the tachycardia originates
superiorly in either right or left
atria, the P waves are upright in
II, III, and aVF.
 Atrial appendages and superior
pulmonary veins .
 The tachycardia may be difficult
to differentiate from sinus
tachycardia.
 If the tachycardia originates
inferiorly in either right or left
atria, the P waves are inverted in
leads II, III, and aVF.
 Inferior vena cava and coronary
sinus orifice as well as the
inferior pulmonary veins

52. MULTIFOCAL ATRIAL
TACHYCARDIA
 MAT is characterized by the presence of atrial complexes originating
from different foci in the atria.
 It is most probably due to enhanced automaticity.
 Multiple independent automatic foci are present in the atria, resulting in
varying configurations of the P wave.

53. ECG FINDINGS
 At least three consecutive P waves with different morphologies with a
rate> 100 bpm should be present.
 The PR as well as the R-R interval is variable with isoelectric baseline
between P waves.

55. TREATMENT
 Treatment the underlying cause, which is usually COPD. If the patient is on
theophylline or beta agonist, the drug should be discontinued.
 Any electrolyte, blood gas, or metabolic abnormality should be corrected.
Any associated cardiac disease or pulmonary infection should be treated.
 MAT should be differentiated from atrial fibrillation. Patients with atrial
fibrillation need to be anticoagulated, whereas patients with MAT do not need
anticoagulation.
 Nondihydropyridine calcium channel blockers may be used to control the
ventricular rate and diminish the number of ectopic atrial impulses

56.  Diltiazem (20 mg IV) or verapamil (5 to 10 mg IV) may be given
intravenously. Diltiazem may be continued as an IV infusion drip at 5 to
15 mg per hour after the rate has been controlled with the initial bolus.
 Verapamil should not be given if there is left ventricular dysfunction
(ejection fraction 40%) or there is heart failure
 Beta blockers are contraindicated in bronchospastic pulmonary disease.
 Amiodarone may be tried for rate control and for suppression of ectopic
atrial impulses if the arrhythmia has not improved with the above agents.
 Intravenous magnesium

57. JUNCTIONAL TACHYCARDIA
 AV junctional tachycardia is due to repetitive impulses originating from
the AV node or bundle of His.
 The impulse follows the normal AV conduction system resulting in
narrow QRS complexes.
 2 types
Non paroxysmal junctional tachycardia
Paroxysmal or Focal junctional tachycardia

59. NON PAROXYSMAL JUNCTIONAL
TACHYCARDIA
 Ventricular rate is usually 70-120 bpm
 Despite the very slow rate of <100 bpm, the arrhythmia is considered a
tachycardia since the intrinsic rate of the AV junction is exceeded, which is
usually 40 to 60 bpm .
 AV junctional rhythm with a rate < 100 bpm is more appropriately called
accelerated junctional rhythm rather than junctional “tachycardia.”
 The tachycardia is nonparoxysmal with a slow onset and termination
 due to enhanced automaticity or triggered activity.
 When the retrograde P wave precedes the QRS complex, the PR interval is
usually < 0.12 seconds.
 When it follows the QRS complex, the R-P interval is usually < 0.20
seconds.

61. PAROXYSMAL JUNCTIONAL
TACHYCARDIA
 Paroxysmal or focal junctional tachycardia is rare.
 The SVT is more commonly seen in children than in adults.
 The tachycardia has no P waves making it difficult to differentiate from
AV nodal reentrant tachycardia

63. ECG FINDINGS OF JUNCTIONAL
TACHYCARDIA
 The QRS complexes are narrow unless there is preexistent bundle branch block or the
impulse is conducted with aberration.
 The QRS complexes are regular. In focal junctional tachycardia, the ventricular rate is
110 to 250 bpm. In nonparoxysmal junctional tachycardia, the ventricular rate is slower
and varies from 70 to 130 bpm.
 The P waves may occur synchronously with the QRS complex and may not be visible.
 When P waves are present, they are retrograde and are inverted in leads II, III, and
aVF. The retrograde P waves may occur before or after the QRS complexes. When the
retrograde P waves occur before the QRS complexes, the PR interval is short and is
usually 0.12 seconds. When the retrograde P waves follow the QRS complexes, the R-
P interval is usually 0.20 seconds.

64. ACUTE TREATMENT
NON PAROXYSMAL JUNCTIONAL TACHYCARDIA
 Often self-limiting and generally does not need any drug therapy
 Nonparoxysmal junctional tachycardia is frequently due to
digitalis toxicity. Digitalis should be discontinued if the drug is the cause
of the tachycardia
 Potassium should also be given if the serum level is < 4 mEq/L,
especially in postoperative patients.
 The rate of the tachycardia can be slowed with phenytoin 5 to
10 mg/ kg IV given as a 250-mg bolus diluted with saline and injected IV
slowly over 10 minutes, followed by 100 mg IV every 5 minutes as
needed to a maximum dose of 1 g. Phenytoin is effective only if the
tachycardia is digitalis induced.
 Beta blockers given IV have also been used to control the ventricular
rate

65. FOCAL JUNCTIONAL TACHYCARDIA
 Adenosine should be tried initially and if not effective, beta
blockers or nondihydropyridine calcium channel blockers should be tried.
 If AV nodal blockers are not effective, type IC (flecainide or
propafenone) and type III (amiodarone or sotalol) agents may be tried to
suppress the ectopic focus.
 In patients who do not respond to medications or in patients in
whom the tachycardia continues to become recurrent or incessant,
catheter ablation may be considered. Ablative procedures may be
associated with some risk of AV block because the foci involves the AV
node and bundle of His

67. Tachycardia
• Heart rate > 100bpm
• Supraventricular or ventricular
depending on the origin
• supra ventricular- origin above
BOH bifurcation (atria/av junction)
• Impulse follows normal AV
conduction system –activates
ventricles simultaneously---narrow
QRS (<120ms)
• Ventricular tachycardia- orgin
below BOH bifurcation-asynchronous

70. SUPRAVENTRICULAR
TACHYCARDIA
• Classified according to 3 general
mechanism
1. REENTRY
2. ENHANCED AUTOMATICITY
3. TRIGGERED ACTIVITY

71. SVT DUE TO REENTRY
• Abnormality in propagation of electrical
impulse
Presence of 2 separate pathways with
different electrophysiologic properties
SVT DUE TO ENHANCED AUTOMATICITY
• Abnormality in initiation rather than
conduction
• Cells in atria or AV junction exhibit
phase 4 depolarisation and may
spontaneously discharge faster than
sinus node if the discharge rate is
enhanced
SVT DUE TO TRIGGERED ACTIVITY
• Abnormality in initiation of impulse
• Resulting from after depolarisation

74. SVT DUE TO REENTRY
• 80-90% of all sustained SVT
• 4 TYPES
1. AVNRT
2. AVRT
3. SART
4. IART

75. AVNRT
• Reentrant SVT
with 2 pathways
with different
electrophysiogic
properties
• Slow pathway –
shorter
refractory
period
• Fast pathway –
longer
refractory
period

76. ECG FINDINGS
• Narrow complex tachycardia
• Regular R-R interval
• No visible P waves(atria &
ventricles are activated
simultaneously
-66% cases
• Retrograde P waves immediately
after QRS( pesudo S in II,III,aVF)
Pseudo r’ in V1)
• Retrograde P wave immediately
before QRS- (pseudo Q in inf

79. AVNRT WITH PSEUDO- S &
PSEUDO-R’WAVES

80. Atypical AVNRT
• Precipitate
d by
ectopic
ventricular
impulse
• Impulse is
conducted
anterograde
ly to
ventricle
through
slow
pathway
• Retrogradel
y to atria
through
fast
pathway
• Retrograde

82. Clinical significance
• SVT from reentry –most common
sustained narrow complex
tachycardia
• AVNRT –normal healthy individual
without structural cardiac da
• Females>males
• Episodic
• Recurrent
• Rarely persists for >12hrs
• Tolerable except pt with stenotic
valves/IHD/LV

83. • Presentations-palpitations
• Symptoms of low cardiac ouput
• Post palipitation diuresis
• Prominent neck vein pulsations

84. Acute treatment
• Vagal maneuvers
1. CAROTID SINUS PRESSURE
-neck hyperextended,at the angle of jaw,gentle but

85. • 4. Forceful.coughing
• 5.Diving reflex
PHARMACOLOGIC THERAPY
• ADENOSINE : 6MG BOLUS➡️ 12mg➡️12mg
• Helful in diagnosis of other
arrhythmias esp atrial flutter with 2:1
block
• Dose modification
• Initial dose -3mg if patient is on
dipyridamole or CBZ
• Higher dose may be needed if patient on
theophylline
• Contraindication –reactive airway
disease

86. Preseved LV function
• 1.calciun channel blockers
• Verapamil-5mg bolus (over 2min)
every 15minutes max 30mg
• Diltiazem-0.25mg/kg( 15-20mg)over
2minutes➡️0.35mg/kg after 15
minutes
• If patient become hypotensive- cal
• gluconate 10ml

87. 2. Beta blockers
• Metoprolol 5mg can be repeated every 5 min
max 15mg in 15min
• Atenolol- 5mg over 5min---can be repeated once
after 10min
• Propranolol -0.1mg/kg max 1mg/min , second
dose after 2min
• Esmolol-0.5mg/kg over a min➡️ 0.05mg/kg/min
infusion for next 4minutes
• 3.DIGOXIN- 0.5MG slow iv for 5min , subsequent
dose 0.25mg iv should be given after 4 hrs and
repeated if needed (max 1.5mg over 24 hrs)

88. • Other anti arrhythmics-if resistant to above drugs
• Type Ia –procainamide
• Ic –propafenone
• III- amiodarone ibutilide
• ELECTRICAL CARDIOVERSION- patient in shock
• IN LV SYSTOLIC DYSFUNCTION
• 1.DIGOXIN
• 2.AMIODARONE
• CONTAINDICATED- CCB/ BETA BLOCKERS

89. Long term therapy
• In patient with hemodynamic
instability during AVNRT/Recurrent
and prolonged arrhythmias
• Verapamil/diltiazem
• Digoxin
• Carvedilol/metoprolol
• Catheter ablation-96% success rate
• Complication-second or third degree
av block

90. ATRIOVENTRICULAR
RECIPROCATING
TACHYCARDIA
• Second most
common SVT
• 30.% all
reentrant
SVT
• Bypass
tract
connects
atria
directly to
ventricle
• Orthodromic
AVRT/
Antidromic
AVRT

91. ECG findings
• Definitive P waves+
• Inveted P inf leads
• Retrograde P waves Immediatelt
after QRS- deforming St segments
• R-P interval shorter than PR
interval

92. Types of orthodromic
AVRT
1. TYPICAL AVRT
*retrograde P after QRS
• conduction from ventricle to atria
across bypass tract
• Av node is the slow pathway
• Bypass tract-fast pathway
• RP interval shorter than PR
interval
• ATYPICAL AVRT
• Ventricle to atrium
across bypass tract
is slower than
conduction from
atrium to ventricle
across AV node
• Retrograde P infront
of QRS
• RP interval > PR
interval

95. Localising bypass
tract
• Free wall of LV
• Postero septal
• Free wall of RV
• Anteroseptal

97. Acute treatment- same
as that of Avnrt

98. Sinoatrial reentry
tachycardia
• Involving sinus node and contiguous
atrium
• P wave identical to sinus P waves
• Precipitated and terminated by a
premature atrial impulse
• Abrupt onset and abrupt termination
• Terminated by vagal maneuvers and
av nodal blocking agents
• Usually associated with structural
cardiac ds
• Well tolerated

99. Intra atrial re entry
tachycardia
• Electrical circuit confined to
small area in atrium
• P before QRS.
• Configuration of P depends on
origin of tachycardia –may be
upright/biphasic/inverted in inf
leads
• Ecg findings cannot differentiate
it from atrial tachycardia due to
enhanced or triggered automaticity

102. A 32 year old female presented to ER with c/o
palpitations for 2 days, on observation patient
was very anxious with profuse sweating, thin
built , with starry look , swelling in neck , BP –
160/100 mmHg , temp – 99.6*F. ECG taken
shows,

103.  12 lead ECG
 Normal standardisation
 Rate – 136/min
 Normal axis
 P wave – upright in L1 & inverted in avR
 Every p wave is followed by QRS complex
 Regular narrow complex tachycardia
 SINUS TACHYCARDIA
 HYPERTHYROIDISM

105. A 22 year old patient is hospitalized with
abdominal pain. She has no cardiac
symptoms. Her ECG shown below. What
does it demonstrate?

106.  12 lead ECG
 Normal standardisation
 Rate – 115/min
 Normal axis
 Regular narrow complex tachycardia
 PR interval < 120 ms
 No initial slurring in QRS ( delta wave )
 LOWN GANONG LEVINE SYNDROME

108. A 55 year old male visits hospital with c/o
feeling light headed and chest pain. He is
known chronic smoker and had repeated
admissions for breathlessness. ECG taken
shows ??

109.  12 lead ECG
 Normal standardisation
 Right axis deviation
 Right ventricular hypertrophy
 Rapid , irregular rhythm with multiple P wave
morphologies in single strip
 MULTIFOCAL ATRIAL TACHYCARDIA with cor
pulmonale

111. A 32 year old man brought to casualty after
he developed sudden onset dyspnea , chest
pain and palpitations at a party, his BP-
100/62 mmhg. ECG taken shows? Drug of
choice?

112.  12 lead ECG
 Normal standardisation
 Rate – 150/min
 Regular narrow QRS tachycardia with no obvious visible P
waves
 Pseudo R’ waves in V1-V2
 SUPRAVENTRICULAR TACHYCARDIA – AVNRT
 DOC- ADENOSINE

114. A 60 year old patient with chronic
kidney disease on maintenance hemo-
dialysis has recurrent episodes of
palpitations often requires
cardioversion. ECG of the patient at last
admission shows? What is the best
treatment option in this patient?

115.  12 lead ECG
 Normal standardisation
 Inverted flutter waves in II, III, & avF at atrial rate of
300 bpm
 Upright flutter waves in V1 simulating P waves.
 2:1 AV block resulting in ventricular rate of 150 bpm
 Occasional 3:1 conduction in v1-v3
 ANTICLOCKWISE ATRIAL FLUTTER
 Best Rx option – EP STUDY & ABLATION

117. A 66 year old female with H/O ischemic
cardiomyopathy and post-ICD status
with hypertension and diabetes has
come with a ECG taken for her few days
ago during routine check-up, she
denies any complaints at that time. ECG
shown below, what is the next step of
management??

118.  12 lead ECG
 Normal standardisation
 Irregularly irregular rhythm
 Ventricular rate - 70/min
 No definitive P waves present
 Fibrillatory waves present
 ATRIAL FIBRILLATION
 Eventhough patient had no complaints, applying
CHA-2DS2-VASc score, patient needs
ANTICOAGULANT THERAPY

120. A 30 year old male presented to ED
with c/o palpitations since half an hour,
he has similar episodes in the past
which settle on its own mostly, BP-
110/70 mmHg, ECG taken shows ?

121.  Regular , narrow QRS tachycardia
 Rate – 180/min
 Retrograde P waves are visible in V1 and in lead III (
notching at beginning of T wave ) with long RP interval
 ORTHODROMIC AVRT

123. A 52 year old male , known chronic
smoker presented with c/o
intermittent palpitations associated
with sweating and giddiness. He had
recent history of MI 2 months back on
treatment for the same. ECG taken
shows?

124.  12 lead ECG
 Normal standardisation
 Rapid , irregular , broad complex tachycardia with
LBBB morphology
 Ventricular rate ~ 200 bpm
 This could be easily mistaken for AF with LBBB
 Rate is too rapid ( 300bpm at places) i.e. too rapid to be
conducted via AV node
 Subtle beat to beat variation in QRS width present
 AF WITH PRE EXCITATION PROBABLY WPW

126. A 31 year old male had fever and
myalgia for 3 days , c/o chest
discomfort for 1 day, his BP was 90/60
mmHg. ECG taken shows? Probable
cause?

127.  12 lead ECG
 Normal standardisation
 Regular narrow QRS tachycardia at 115 bpm
 Retrograde P waves present and it is inverted in II, III,
avF and upright in V1 and avR
 Short PR interval (<120ms) indicates a junctional rather
than atrial focus
 ACCELERATED JUNCTIONAL RHYTHM
 Probably due to MYOCARDITIS

129. A 38 year old patient brought to
casualty with 2 hour history of rapid
heart beat associated with dizziness.
BP- 90/60 mmHg, ECG taken shows?
What is immediate line of
management?

130.  12 lead ECG
 Normal standardisation
 Northwest axis
 Very broad QRS complexes of similar morphology
(>200ms in V5 and V6 )
 Distance b/w onset of QRS to nadir of S-wave is >
100ms – BRUGADA SIGN
 Notching near nadir of S wave seen in leads II, III, avF
– JOSEPHSON’S SIGN
 MONOMORPHIC VT
 CARDIOVERSION

131. VT vs SVT WITH ABERRANCY
• Very high rate
• Very wide QRS > 160ms
• Absence of typical RBBB or LBBB morphology
• Extreme axis deviation
• Av dissociation
• Capture beats, fusion beats
• Positive / negative concordance throughout the leads
• Brugada sign
• Josephson sign

132. THANK YOU