M Chadi Alraies, MD

Cleveland Clinic Foundation

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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

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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

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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

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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

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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?

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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 atrialand 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

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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).

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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:

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R to S interval

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Brugada Criteria Algorithm7

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Morphology Criteria9

Features Favoring VT:

RBBB pattern:

Monophasic R or Biphasic qR, QR,

or RS in V1

S > R or QS in V6

LBBB pattern:

Broad R wave or wide RS length (

> 30 msec in V1 or V2)

Notched downstroke of S wave in

V1 or V2

> 60 msec to nadir of S in V1 or V2

qR or QS pattern in V6

Features Favoring SVT

w/Aberrancy:

RBBB pattern:

Triphasic rSR’ in V1

Triphasic rSR’ in V6

R > S in V6

LBBB pattern:

No R in V1

Small narrow R in V2

No slurring of S wave downstroke

Monophasic R in V6

Presence of septal Q in I and V6

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Features Favoring VT:

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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.

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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

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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)

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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

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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

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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

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Typical Counter-Clockwise AFl

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Typical Atrial Flutter

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RFA

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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

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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

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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

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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.

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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

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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

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Orthodromic AVRT (WPW)

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Orthodromic AVRT (WPW)

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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

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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

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