M Chadi Alraies, MD

Cleveland Clinic Foundation

M C Alraies 1
The initial step in management of all patients with
tachycardia is to evaluate for hemodynamic instability:
 Is the patient experiencing signs and symptoms
related to the rapid heart rate?

 Hypotension, dyspnea, decreased level of

consciousness, chest pain, shock

 If hemodynamically unstable, often no time for

ECG and thorough evaluation

 If stable, 12-lead ECG can be used to differentiate

M C Alraies 2
Narrow or Wide Complex?
< 120 msec = narrow
> 120 msec = wide

 Narrow complex tachycardias reflect

synchronous activation of both ventricles via
supraventricular initiation, ie sinus node,
atria, AV node, His bundle
 Wide complex tachycardias (WCTs) may be
ventricular in origin, SVT with aberrant
conduction, or accessory pathway mediated

M C Alraies 3
SVT with aberrancy:
 Widening of the QRS complex due to
delayed or blocked conduction in the His-
Purkinje system, ie preexisting or rate-
dependent RBBB or LBBB with
superimposed sinus or atrial tachycardia,
Afib/flutter

M C Alraies 4
I. Wide Complex Tachycardia
 Is it VT or SVT with aberrancy?
 VT is most common cause of WCT, up to 80%1-4
 When evaluating the patient with WCT, cannot
exclude VT due to presence of hemodynamic
stability
 Misdiagnosis of VT as SVT and subsequent use of
AV nodal blocking agents (CCBs, beta blockers,
adenosine) may precipitate VF – ie, coronary steal
due to adenosine
 DC cardioversion is treatment of choice for unstable
WCTs

M C Alraies 5
M C Alraies 6
How do we differentiate between VT and SVT with
aberrancy?

 History is important:
 Presence of structural heart disease, especially
previous MI strongly suggestive of VT (greater
than 98% in one report5).
 Age: greater than 35, more likely VT – PPV 85%;
under 35 more likely SVT – PPV 70%6.
 Is there a history of arrhythmia, or is the patient on
antiarrhythmic or other cardiac meds?

M C Alraies 7
Physical Exam:

 Does the patient have a pacemaker, an ICD, or a

sternotomy scar?
 AV dissociation may cause cannon A waves of JVP:
intermittent and irregular pulsations of greater than
normal amplitude resulting from simultaneous atrial
and ventricular contraction. Contraction of RA
against closed TV produces transient increase in RA
and JVP
 Highly inconsistent fluctuations in BP due to
variability in the degree of LA contribution to LV
filling, stroke volume, and cardiac output

M C Alraies 8
ECG

Brugada criteria:
 An algorithm for the diagnosis of VT, most commonly
used method7.
 Overall 98.7% sensitivity and 96.5% specific for VT8.
 Algorithms for VT tend to misclassify SVT with
preexcitation (accessory pathway-mediated) as VT,
but preexcitation is an uncommon cause of WCT (6%
in one series8).

M C Alraies 9
Brugada Criteria7
1. Absence of an RS complex in all precordial leads?
- Yes: VT – sensitivity 21%, specificity 100% No: proceed to next question

2. R to S interval > 100 msec?

- Yes: VT – sensitivity 66%, specificity 98% No: proceed to next question

3. AV dissociation*?
- Yes: VT – sensitivity 82%, specificity 98% No: proceed to next question

4. Morphology criteria for VT present both in precordial

leads V1-V2 and V6?
- Yes VT – sensitivity 98.7%, specificity 96.5%
- No: SVT with aberrancy – sensitivity 96.5%, specificity 98.7%

* AV dissociation:

M C Alraies 10
R to S interval

M C Alraies 11
Brugada Criteria Algorithm7

M C Alraies 12
Morphology Criteria9
Features Favoring VT: Features Favoring SVT
w/Aberrancy:
RBBB pattern:
Monophasic R or Biphasic qR, QR, RBBB pattern:
or RS in V1 Triphasic rSR’ in V1
S > R or QS in V6 Triphasic rSR’ in V6
R > S in V6

LBBB pattern:
LBBB pattern:
Broad R wave or wide RS length (
> 30 msec in V1 or V2) No R in V1
Notched downstroke of S wave in Small narrow R in V2
V1 or V2 No slurring of S wave downstroke
> 60 msec to nadir of S in V1 or V2 Monophasic R in V6
qR or QS pattern in V6 Presence of septal Q in I and V6

M C Alraies 13
M C Alraies 14
Features Favoring VT:

M C Alraies 15
II. Narrow Complex Tachycardia:
The narrow complex tachycardias, aka “PSVT”:
 Sinus Tachycardia (ST)
 Inappropriate Sinus Tachycardia (IST)
 Sinoatrial Nodal Reentrant Tachycardia (SNRT)
 Atrial Tachyardia (AT)
 Multifocal Atrial Tachycardia (MAT)*
 Atrial Fibrillation (AF)*
 Atrial Flutter (AFl)*
 Junctional ectopic Tachycardia (JeT)
 Junctional Tachycardia (JT)
 Permanent Junctional Reciprocating Tachycardia (PJRT)
 Nonparoxysmal Junctional Tachycardia (NPJT)
 Atrioventricular Nodal Reentrant Tachycardia (AVNRT)
 Atrioventricular Reentrant Tachycardia (AVRT)

* AF, AFl, and MAT are PSVTs, but commonly classified as separate group
* Reentry is the most common cause of narrow complex tachycardia; increased
automaticity and triggered activity occur less frequently10.

M C Alraies 16
Initial Evaluation of Narrow Complex Tachycardias

Rate may be too fast to identify, can try the following to slow the rate:

I. Carotid sinus massage (CSM)

 Can slow or even terminate rhythm, as is often the
case with AVNRT or AVRT
 CSM induces temporary slowing of SA nodal activity
and AV nodal conduction by stimulating
baroreceptors, which causes increased vagus output
and sympathetic withdrawal
 Contraindicated if bruit present, prior CVA or TIA, MI
within 6 months, h/o VT/VF

M C Alraies 17
II. Adenosine
 Can be diagnostic and therapeutic in rhythms that depend on
AV node, ie AVNRT, AVRT
 6 mg IV followed by 12 mg through peripheral lines, or 1 mg
then 3 mg through CVC
 Transient asystole a “rare side effect”
 Common side effects include facial flushing (18%), palpitations,
CP, hypotension
 Effects blunted in patients on theophylline, and accentuated in
the denervated heart
 If using in pts suspected of having WPW, have defibrillator
ready (not recommended)

M C Alraies 18
When evaluating a narrow complex tachycardia, assess regularity
of rhythm

Irregular:
 AF = irregularly irregular, no identifiable P waves, atrial rate
350-600 impulses/min, irregularly irregular ventricular response
of 90-170 bpm, or higher if slick AV node. Coarse AF or
prominent U waves may give the appearance of P waves
 MAT = irregularly irregular, at least 3 distinct P wave
morphologies, varying P-P, R-R, and PR intervals. Typically
seen in elderly pts w/advanced pulmonary disease
 AFl with block = Mobitz Type I 2nd degree AV block
(Wenckebach) can look like AF because it’s irregular, but w/
pattern of grouped beats typical of Wenckebach

M C Alraies 19
Regular:

Do I see clearly discernible P waves? (best leads to look for P

waves are V1 and II)
If yes = ST, IST, AT, MAT, AFl, SNRT

P Waves Indiscernible:
- Most commonly AVNRT, but can also be AF, AVRT, JT11.
- JT arises from discrete focus within AV node or His bundle
- JT thought to be enhanced automaticity, not reentry
- JT seen with AMI, dig toxicity, myocarditis, or post-op due to
AV nodal injury
- Atrial activity usually retrograde, but AV dissociation can occur

M C Alraies 20
Atrial Flutter (AFl)
 Flutter has an easily identifiable classic appearance: P waves exhibit classic
sawtooth pattern
 Atrial rate > 250 bpm almost always flutter (cannot measure atrial rate in AF on
ECG)
- Ventricular rate of exactly 150 should be considered flutter until proven otherwise
 Macroreentrant atrial rhythm with reentry circuit involving large area of atrial
myocardium, with most common circuit around tricuspid annulus
 Atrial tissue between IVC and tricuspid annulus is called the isthmus, and RFA
of this region has >90% cure rate
 Typical A:V ratio is 2:1, with atrial rate of 300 in typical flutter
 Even ratios more common, ie 2:1 or 4:1 - beta blockers and CCBs can cause
this
 Classic/typical flutter is a counter-clockwise reentrant loop, with negative
sawtooth waves in leads II, III, and AVF; most common form of AFl
 - Atypical flutter is a clockwise reentrant loop, with positive sawtooth waves in
inferior leads, usually slower atrial (and ventricular) rate

M C Alraies 21
Typical Counter-Clockwise AFl

M C Alraies 22
Typical Atrial Flutter

M C Alraies 23
RFA

M C Alraies 24
Once the rhythm is sufficiently slowed, we must further
examine the P waves for characterization of atrial activity.

 Key features of atrial activity11:

 I. Atrial rate

 II. P wave morphology – sinus P’s, abnormal, or retrograde

 III. Correlation with ventricular rate – 1:1?

 IV. Position of P wave in relation to preceding or following QRS – Short RP

vs Long RP

M C Alraies 25
P Wave Morphology:

 Obtain old sinus ECG – if P wave is identical, then ST, IST, SNRT
 ST – rate usually 100-180 bpm, can be > 200 in young hearts (remember
220-age)
- Normal P wave morphology: axis of 0 to 90 degrees, ie upright in I, II, and
AVF
- A:V ratio always 1:1
 IST - chronic nonparoxysmal sinus tachycardia
- Unusual condition, cause unknown, thought to be abnormal autonomic
control
- Occurs in patients w/out apparent heart disease or physiologic cause for
ST
 SNRT -
- Uncommon, < 5% of EP referrals12.
- Rate 100-150
- Distinguised from ST by abrupt onset and termination

M C Alraies 26
Abnormal P Wave Morphology:

 If clearly different from sinus P, and RP > PR, likely some form of AT
 Can also occur in atypical AVNRT and AVRT w/slowly conducting
accessory pathway, aka PJRT
 AT:
-Regular w/rate 100-250 bpm
- Originating in atria outside of sinus node
- Often difficult to distinguish from sinus if close to sinus node
- Etiology: automatic, triggered, or reentrant
- Termination of the tachycardia with a QRS complex more common in
AT
- Not always 1:1 conduction, especially if atrial rate rapid and AV
conduction slow
- AT with block – seen with digitalis toxicity

M C Alraies 27
M C Alraies 28
Retrograde P Wave and Short RP:

 Most common cause of inverted P waves is improper lead placement

 True retrograde P waves caused by conduction from AV node toward
SA node
 Typically inverted in II, III, and AVF
 Retrograde P waves + short RP = Typical AVNRT (90%), AVRT, AT
w/1st degree block, and JT
 Short RP = P wave may appear nearer to the preceding QRS complex
(occasionally in or fused w/QRS complex) so that PR interval is
greater than RP interval
 Termination of the tachycardia with a P wave after the last QRS
complex most common in AVNRT or AVRT11.

M C Alraies 29
AVNRT

 60% of all PSVTs13.

 Two conduction pathways within the AV node

 Unidirectional block occurs with PAC

 Blocked pathway recovers as the impulse

conducts slowly down the other pathway and
conducts retrograde, creating reentrant loop

 Antegrade conduction occurs down the slow

pathway and retrograde conduction up the fast
pathway…remember “down the slow, up the
fast”

 Retrograde P waves may be obscured by QRS

complex

 V-A < 70 msec

 P waves may fall after or at the end of QRS

complex, creating a “pseudo R prime” in leads
where QRS negative, or “pseudo S wave” in
leads where QRS positive

M C Alraies 30
M C Alraies 31
M C Alraies 32
M C Alraies 33
AVRT
AVRT (orthodromic):
 Also known as AV reciprocating tachycardia
 Antegrade conduction occurs down AV node,
resulting in ventricular activation, then
retrograde atrial activation occurs later through
AV bypass tract
 Retrograde P wave follows QRS, usually in ST
segment
 Classic example is WPW, which is AVRT in
opposite direction – down node, up the
accessory pathway

AVRT (antidromic):
 Antegrade conduction occurs through AV
bypass tract and retrograde conduction occurs
through AV node
 This results in a wide complex tachycardia

M C Alraies 34
Orthodromic AVRT (WPW)

M C Alraies 35
Orthodromic AVRT (WPW)

M C Alraies 36
Retrograde P Wave and Long RP:

 Long RP = P wave may appear nearer to the following QRS complex, so that
RP interval is greater than the PR interval (AVRT, AT w/out 1st degree block,
PJRT, Atypical AVNRT)

 Combination of retrograde P waves and long RP usually caused by

atypical/uncommon AVNRT or AVRT w/slowly conducting accessory pathway

 Uncommon AVNRT = antegrade conduction down fast pathway and retrograde

conduction through a slow pathway; 10% of AVNRT14.

 P wave occurs very late in cardiac cycle, near next QRS, hence the long RP

 PJRT = AVRT w/slowly conducting accessory pathway; antegrade conduction

occurs through the AV node, and retrograde conduction occurs through slowly
conducting accessory pathway. Also produces long RP

M C Alraies 37
M C Alraies 38
M C Alraies 39
References:

1. Stewart, RB, Bardy, GH, Greene, HL. Wide complex tachycardia: misdiagnosis and outcome after emergency therapy. Ann Intern
Med 1986; 104:766.
2. Akhtar, M, Shenasa, M, Jazayeri, M, et al. Wide complex tachycardia. Reappraisal of a common clinical problem. Ann Intern Med
1988; 109:905.
3. Gupta, AK, Thakur, RK. Wide QRS complex tachycardias. Med Clin North Am 2001; 85:245.
4. Miller, JM, Hsia, HH, Rothman, SA, et al. Ventricular tachycardia versus supraventricular tachycardia with aberration:
electrocardiographic distinctions. In: Cardiac Electrophysiology From Cell to Bedside. Zipes, DP, Jalife, Jose (Eds), W.B.
Saunders, Philadelphia 2000. p.696.
5. Tchou, P, Young, P, Mahmud, R, et al. Useful clinical criteria for the diagnosis of ventricular tachycardia. Am J Med 1988; 84:53.
6. Baerman, JM, Morady, F, DiCarlo, LA Jr, de Buitleir, M. Differentiation of ventricular tachycardia from supraventricular tachycardia
with aberration: value of the clinical history. Ann Emerg Med 1987; 16:40.
7. Brugada, P, Brugada, J, Mont, L, et al. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS
complex. Circulation 1991; 83:1649.
8. Miller, JM, Hsia, HH, Rothman, SA, et al. Ventricular tachycardia versus supraventricular tachycardia with aberration:
electrocardiographic distinctions. In: Cardiac Electrophysiology From Cell to Bedside. Zipes, DP, Jalife, Jose (Eds), W.B.
Saunders, Philadelphia 2000. p.696.
9. Crawford PA, Lin TL. The Washington Manual Cardiology Subspecialty Consult. Lippincott, Williams, and Wilkins, New York, 2004:
pp 186-187.
10. Blomstrom-Lundqvist, C, Scheinman, MM, Aliot, EM, et al. ACC/AHA/ESC guidelines for the management of patients with
supraventricular arrhythmias--executive summary: a report of the American College of Cardiology/American Heart
Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines
(Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias). Circulation
2003; 108:1871.
11. Worldwide Web: Arnsdorf MF, Ganz LI. Approach to narrow QRS complex tachycardias. www.UpToDate.com. 5/24/06
12. Sanders, WE, Sorrentino, RA, Greenfield, RA, et al. Catheter ablation of sinoatrial node reentrant tachycardia. J Am Coll Cardiol
1994; 23:926.
13. Trohman, RG. Supraventricular tachycardia: implications for the intensivist. Crit Care Med 2000; 28:N129.
14. Akhtar, M, Jazayeri, MR, Sra, J, et al. Atrioventricular nodal reentry. Clinical, electrophysiological, and therapeutic considerations.
Circulation 1993; 88:282.
15. Worldwide Web: Suh, D. VT vs. SVT with aberrancy EKG criteria. http://intmedweb.wfubmc.edu/blurbs/cards/complex.html. 5/24/06

M C Alraies 40
Visit my blog

M C Alraies 41