This document provides an overview of approaches to evaluating and treating narrow complex tachycardia. It outlines steps to determine the mechanism, including examining P wave morphology and relationship to QRS. Common types discussed are AV nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), focal atrial tachycardia, and junctional tachycardias. Treatment options are also summarized, including vagal maneuvers, adenosine, calcium channel blockers, beta blockers, antiarrhythmic drugs, catheter ablation, and pacemaker therapy.

1. APPROACH TO NARROW QRS
COMPLEX TACHYCARDIA
Dr Dharam Prakash Saran

2. STEP wise
• Look for QRS duration.
• QRS complex regular/irregular.
• Then look for presence of p waves.
• P waves morphology
• P waves and QRS relationship 1:1
• AV block present.
• Termination initiation of tachycardia.
• Effect of BBB on tachycardia cycle length.

6. In brief from the diagram clues
• Response to carotid sinus massage or adenosine –with
termination of arrhythmia with Pwave –AVNRT
• Tachycardia persists with AV block –AT,AFL,SANRT
• Pseudo r ‘ wave in V1 –AVNRT
• SHORT RP interval – AVNRT,AVRT
• Long RP interval – AT,SANRT,AVNRT atypical

7. NARROW
COMPLEX QRS
TACHYCARDIA
SHORT RP
INTERVAL
TYPICAL
AVNRT
AVRT
LONG RP
INTERVAL
ATYPICAL AVNRT
AVRT slow
retrograde
conduction
Permanent Form
junctional
tachycardia
ATRIAL
TACHYCARDIA
SANRT
INAPPROPRIATE ST

8. ECG findings

9. Pwaves
no
Irregular
R-R interval
ATRIAL
FIBRILLATION
Regular
R-R interval
AVNRT
yes
NORMAL
MORPHOLOGY
SINUS TACHYCARDIA
SINUS NODE REENTRY
INAPPROPRIATE SINUS
TACHYCARDIA

14. Differentiation of AVNRT from AVRT

15. P wave present but
not of same
morphology as sinus
rhythm
Pseudo r’ wave
in
V1
AVNRT
Pseudo S wave
on lead II
AVNRT
Pwave
ST-T changes
Positive in lead
I
AVRT
Right posteroseptal
Accessory pathway
Negative in
lead I
AVRT
Left sided
accessory
pathway

16. AVNRT
• Presence of a narrow complex tachycardia with regular R-R
intervals and no visible p waves.
• P waves are retrograde and are inverted in leads II,III,AVF.
• P waves are buried in the QRS complexes –simultaneous
activation of atria and ventricles – most common presentation
of AVNRT –66%.
• If not synchronous –pseudo s wave in inferior leads ,pseudo r’
wave in lead V1---30% cases .
• P wave may be farther away from QRS complex distorting the
ST segment ---AVNRT ,mostly AVRT.

17. AV NODAL REENTRANT TACHYCARDIA

20. AVRT
• Typical – RP interval < PR interval
• RP interval > 80 milli sec
• Atypical –RP interval > PR interval
• Concealed bypass tract – only retrograde conduction
• Manifest bypass tract– both anterograde and retrograde.
• Electrical alternans –the amplitude of QRS complexes
varies by 5 mm alternatively.
• Rate related BBB occuring and the rate of tachycardia
is decreasing –then the bypass tract is on the same side
of the block.

21. AV REENTRANT TACHYCARDIA

25. WPW syndrome
• Two types
• Orthodromic
• Antidromic
• Antidromic is wide complex tachycardia
• In NSR detected by delta wave.
• Can ppt into AF and VF on use of AV nodal blockers
• MEMBRANE ACTIVE ANTIARRHTYHMIC DRUGS are safe.
• CONCEALED WPW syndrome – no delta wave .less risk of
AF

29. Focal Atrial Tachycardia
• P wave morphology changes.
• PR interval > 0.12 sec .
• Second,third degree AV block can occur.
• Tachycardia terminates with a qrs complex ..
• Right atrial origin– p wave inverted in V1.
• Upright in lead AVL
• Opposite if of left atrial origin
• Superior origin –upright p waves in inferior leads
• Inferior origin –p waves are inverted in inferior
leads.

31. Multifocal Atrial Tachycardia
• At least three consequtive p waves with different
morphologies with a rate > 100 bpm to be present.
• Isoelectric baseline between p waves.
• Also called as choatic atrial tachycardia
• Mostly seen in COPD ,electrolyte abn,theophylline
• Rate usually does not exceed 130-140 bpm.

32. Multifocal Atrial Tachycardia

33. SANRT
• Microreentrant tachycardia
• Usually precipitated and terminated by
premature atrial complexes.
• Atrial rate is usually 120-150 bpm.
• AV block can occur.

34. Junctional tachycardias
• Non paroxysmal – accelerated junctional rhythm
• Rate < 100 bpm Usually junctional node 40-60 bpm
• Paroxysmal or focal junctional tachycardia is rare –
automaticity.
• 110-250bpm.
• P waves may be before or after QRS complex
• Infrequent and nonsustained episodes –no treatment
• Acute termination of SVT establish the mechanism of SVT in
case of acute setting.
• Long term goal is abolishing the arryhthmia substrate.
• Precipitating factors – electrolyte
imbalance,hypoxia,ischemia,hyperthyroidism to be sought
out.

35. TREATMENT OF SVT

36. • A 12 lead ECG during tachycardia and NSR.
• No delay in therapy if the mechanism of SVT is not
known.
• Perform CAROTID SINUS MASSAGE,or give 6mg
bolus adenosine.
• In case of severe hemodynamic compromise a
synchronised cardioversion to be given.

37. Carotid sinus massage
• Check for carotid bruit before massage.
• At the level of cricoid cartilage,at the angle of mandible
the carotid sinus is situated.
• Gentle pressure is applied over the carotid sinus for 5 -
10 seconds.
• ECG recording to be present.
• In case of no response – try on the other side.
• Simultaneous pressure not to be applied both sides.
• Alternative manuevres are valsalva,gag reflex,ice water
pouring over the face.

38. • If SVT is suspected to be AVnode dependent –
drug of choice is adenosine and CCBs
verapamil and diltiazem.
• But digoxin,BBs,CCBs better control of
ventricular response in atrial tachycardias
• Class I agents to be combined with AV nodal
blocking drugs – to eliminate 1:1 conduction
of atrial to ventricles.

39. HEMODYNAMIC
STATUS
STABLE BP
>90/60 mmHg
Narrow QRS
and regular
R-R
Vagal maneuveres
IV adenosine
IV verapamil,diltiazem
IV sotalol
Refractory
Wide QRS
complex
Vagal manuevres
IV adenosine
procainamide
cardioversion
Digoxin
Verapamil
UNSTABLE
BP< 90/60
mmHg
Direct
Are contraindicated

40. DRUG DOSE SIDE EFFECTS
AV NODAL
BLOCKERS
ADENOSINE 6-12 mg bolus Flushing ,dyspnea
Chest pain
VERAPAMIL 0.15 mg/kg over 2 min Hypotension bradycardia
DILTIAZEM 0.25-0.35 mg/kg -2 min same
DIGOXIN 0.5-1.0 mg --- 2-10 min Digoxin toxicity
PROPANOLOL 1-3mg over I min Hypotension bradycardia
CLASS I AAD QUINIDINE 6-10MG/KG at 10 mg/min hypotension
PROCAINAMIDE 10-15mg/kg at 50 mg/min hypotension
DISOPYRAMIDE 1-2 mg/kg at 10 mg/min hypotension
PROPAFENONE 1-2mg/min at 10 mg/min Bradycardia,GI disturbance
FLECAINIDE 2 mg/kg at 10 mg/min Bradycardia,dizziness
CLASS III SOTALOL 1-1.5mg/kg at 10 mg/min Hypotension,proarrythmic
AMIODARONE 1.5 mg/kg during 15 min Hypotension,bradycardia

44. Pill in the pocket approach
 In whom recurrences are infrequent.
 But sustained.well tolerated hemodynamically.
 Patients who have had only a single episode of SVT..
 100-200mg of flecainide at the onset of SVT is a reasonable
approach…until he reaches the hospital.
 40-160 mg verapamil –without preexcitation,
 Betablockers
 Propafenone 150-450 mg.
 80% cases interrupted with a combination of CCBand BB in 2
hrs…

45. Long term control of SVT
• Frequency and severity of episodes.
• LVF
• Cost benefits of radiofrequency ablation
over the pharmacotherapy .
• Pharmacotherapy is considered in patients
who defer catheter ablation,whom in which
ablation failed,or carries a risk of AV block.
• Multifocal atrial tachycardia, Accessory
pathway – class Ia,Ic,III
• AV node blocking drugs
• Young patients – Ia drugs
• Class I agents LVD < 35% not used.
Long term
treatment
Membrane
active AAD
Catheter
ablation
Curative
surgery
Antitachycardia
pacing

46. Adenosine
 not to be used in bronchospastic pulmonary
disease.
 Adenosine precipitates asthma
 Given rapidly in 1-2 sec.
 If given by peripheral vein uplift the arm..
 Max dose is 30 mg
6- 12-12 mg
Terminates AVNRT .AFL with 2:1 block
 Potentiated by dipyradimole,carbamazepine –
decrease dose to 3 mg.

47. Other drugs
 Calcium channel blockers,beta blockers ,digoxin
are the next drugs to be used if not responded to
adenosine
 Usually 60 % cases respond to a dose of 6 mg and
95 % cases at 12 mg.
Type 1 a AAD, 1c,iii,AMIODARONE in
refractory cases.
 Beta blockers not to used IV in heart failure.
Long term treatment in case of recuurent
episodes,hemodynamic instability.

48. Catheter guided
Radiofrequency Ablation
• Several multipolar catheters are introduced
• High right atrium ,bundle of his
,RVapex,Coronary sinus.
• Radiofrequency is delivered at the site of earlier
activation
• Success is defined by elimination of the
tachycardia or loss of pre excitation.
• 90-98% success in AV node dependent
• 60-80% in case of AV node independent.
• Cryoablation more useful…

49. Catheter Ablation of Cardiac Arrhythmias.

50. Some important points
• When the QRS complex is wide and VT is mistaken as
SVT with ABERRANT conduction IV verapamil – not
recommended decreases BP.
• If DC cardioversion to be avoided because of possible
adverse response to digitalis adm …pacing Rt atrium and
ventricle via temp pacing.
• In WPW syndrome avoid VERAPAMIL,LIDOCAINE .
• Avoid digoxin.
• In SANRT –class IA,IC ,BB
• SANRT –digoxin.

51. Cont…
• Rx of ectopic atrial tachycardia – consider digitalis
toxicity,chronic lung disease,metabolic
abn,electrolyte abnormalities,acute MI ----temporary
pacing
• Removal or reversal of inciting factor
• Surgical excision of focus.
• Rx of MAT –chronic lung disease,metabolic,rare is
digitalis toxicity ---CCBS,BBs ..no role of
cardioversion,devices ,surgery.

52. In case of WPW syndrome
symptomatic concealed or
manifested ..and evidence of
preexcitation on NSR …send the
patient for catheter ablation…

53. Special problems
• 1.Coexisting Double Tachycardias
• May not be identified during noninvasive testing ..needs EP
study.
• Ex—typical AVNRT and AT.
• Concentric –eccentric –concentric.
• AVNRT –both APC,VPC
• AT only APC
• 2.Pseudo AF- infrequent presentation of PSVT.
• Occurs during onset and termination of tahcycardia.
• Multiple accessory AV pathways.
• In young who have AF without other risk factors.
• 5% of AVNRT.
• Group beating is seen

54. Thank
you