vt - diagnosis of broad complex tachycardia

7/28/2019 VT - Diagnosis of Broad Complex Tachycardia

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When confronted with a tachycardiahaving a broad QRS complex, it isimportant to be able to diVerentiate

between a supraventricular and a ventriculartachycardia. Medication given for the treat-ment of a supraventricular tachycardia (SVT)may be harmful to a patient with a ventriculartachycardia (VT).1 2 A reasonable haemody-namic condition during a tachycardia may

erroneously lead to the wrong diagnosis ofSVT.3 Familiarity with the ECG signs allowingthe diagnosis of a VT is therefore essential. Butas will be discussed here, the ECG should notonly tell you how to distinguish VT from othertachycardias with a broad QRS complex, butalso to suspect its aetiology and its site of originin the ventricle. Both aspects are important indecision making about the prognostic signifi-cance of VT and correct treatment.

Classification of tachycardias with abroad QRS complex

As shown in fig 1, broad QRS tachycardia canbe divided in three groups.x SVT with bundle branch blockBundle

branch block (BBB) may be pre-existing orcan occur when the refractory period of oneof the bundle branches is reached because of

the heart rate of the SVT (so calledtachycardia related or phase 3 block). BBBcan also occur because of retrograde invasionin one of the bundle branches.4 These causesof BBB can be found in patients with atrialtachycardia, atrial flutter, atrial fibrillation,atrioventricular (AV) nodal tachycardia, andalso during orthodromic circus movementtachycardia (with AV conduction over theAV node and ventriculo-atrial (VA)conduction over an accessory AV pathway).

x SVT with AV conduction over an accessoryAV pathwayThis may occur during atrialtachycardia, atrial flutter, atrial fibrillation,AV nodal tachycardia, and during

antidromic circus movement tachycardia(with AV conduction over an accessory AVpathway and VA conduction over the AVnode or a second accessory AV pathway). Itis also the case in the so called Mahaimtachycardia where AV conduction goes byway of a slowly conducting right sidedaccessory AV pathway or a nodo-ventricularfibre inserting into the right ventricle.

x Ventricular tachycardia.

ELECTROPHYSIOLOGY

Ventricular tachycardia:

diagnosis of broad QRS complex

tachycardia

Hein JJ WellensInteruniversity Cardiology Institute of the Netherlands (ICIN),

Utrecht, The Netherlands

Figure 1. Different types of SVT with BBB (diagram A), SVT with AV conduction over an accessory pathway (diagram B), and VT (diagramC) resulting in a broad QRS tachycardia. Acc, accessory; AV, atrioventricular; BBB, bundle branch block; CMT, circus movementtachycardia; SVT, supraventricular tachycardia; VA, ventriculo-atrial; VT, ventricular tachycardia.

A B C

SVT with BBB:

atrial tachy

atrial flutter

atrial fibrillation

AV nodal tachy

CMT with AV conduction over AV node

and VA conduction over Acc pathway

SVT with AV conduction over Acc pathway:

atrial tachy

atrial flutter

atrial fibrillation

AV nodal tachy

CMT with AV conduction over Acc

pathway and VA conduction over AV node

or second Acc pathway

VT

Heart2001;86:579585

579

Correspondence to:Prof. Dr. HJJ Wellens,Henric vanVeldekeplein 21, 6211TC Maastricht, [email protected]

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The ECG diagnosis

Importance of AV dissociationAlthough dissociation between atrial and ven-tricular activity during tachycardia is a hall-mark of VT (fig 2), some form of VA conduc-tion can be present during VT, especially atslow VT rates (fig 3).4 P waves can be diYcultto recognise during a broad QRS tachycardiaand it is always useful to look for non-electrocardiographic signs such as variations injugular pulsations, the loudness of the firstheart sound, and changes in systolic bloodpressure.5

In patients with slow VT rates occasionalconduction from atrium to ventricle over the

AV nodebundle branch system may happenresulting in capture or fusion beats (fig 4).Sudden narrowing of a QRS complex duringVT may also be the result of a premature ven-tricular depolarisation arising in the ventricle inwhich the tachycardia originates, or it mayoccur when retrograde conduction during VTproduces a ventricular echo beat leading tofusion with the VT QRS complex.5 Very rarely,

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400 msec84472Figure 2. Two types of VT (panel A and B) in the same patient(panel C during sinus rhythm). Atrioventricular dissociation ispresent during both VTs. Note the effect of the frontal plane axison the R:S ratio in lead V6 in RBBB shaped VT. R:S < 1 ispresent in case of a superior axis (panel B), but R:S > 1 with aninferior axis (panel A).

Figure 3. One to one ventriculo-atrial conduction during VT. The pwaves are negative in leads II, III, and avf and follow each QRScomplex. Left panelVT; right panelsame patient during sinus

rhythm.

Figure 4. Capture (QRS complexes: 5, 13, and 15)and fusion beats (QRS complex number 8) duringVT.

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Figure 5. VT origin and QRS width. Upper panel: anorigin close to the interventricular septum results inmore simultaneous right and left ventricular activationand therefore a more narrow QRS complex. Incontrast (lower panel) a VT origin in the lateralventricular wall results in sequential ventricularactivation and a wider QRS complex.

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VT origin far from interventricular septum

sequential ventricular activation

wide QRS

VT origin close to interventricular septum

more stimultaneous ventricular

more narrow QRSactivation

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AV dissociation is present in tachycardias otherthan VT. It may occur in AV junctional tachy-cardia with BBB after cardiac surgery or duringdigitalis intoxication.

Width of the QRS complexAs depicted in fig 5, the site of origin of the VTplays a role in the width of the QRS complex.When the arrhythmia arises in the lateral freewall of the ventricle sequential activation of theventricles occurs resulting in a very wide QRS.

The QRS complex will be smaller when the VThas its origin in or close to the interventricularseptum. Of course other factors also play a rolein the QRS width during VT, such as scar tissue(after myocardial infarction), ventricularhypertrophy, and muscular disarray (as inhypertrophic cardiomyopathy). It is of interestthat a QRS width of more than 0.14 seconds inright BBB (RBBB) tachycardias and 0.16 sec-onds during left BBB (LBBB) argues for a VT. 4

But a QRS width below such values may occurin VTs having their origin in or close to theinterventricular septum. Of course, QRS widthis not helpful in diVerentiating VT from atachycardia with AV conduction over an acces-

sory AV pathway because such a pathwayinserts into the ventricle leading to eccentricventricular activation and a wide QRS complex(fig 6).

An SVT can have a QRS width of more than0.14 (RBBB) or 0.16 (LBBB) seconds underthree circumstances: (1) in the presence of pre-existent BBB in the elderly with fibrosis in thebundle branch system and ventricular myocar-dium; (2) when during SVT AV conductionoccurs over an accessory AV pathway; (3) whenclass IC drugs (especially flecainide) arepresent during SVT.

QRS axis in the frontal plane

The QRS axis is not only important for the dif-ferentiation of the broad QRS tachycardia butalso to identify its site of origin and aetiology.As shown in fig 7, a VT origin in the apical partof the ventricle has a superior axis (to the left of30). An inferior axis is present when the VThas an origin in the basal area of the ventricle.Previous work4 showed that the presence of asuperior axis in patients with RBBB shapedQRS very strongly suggests VT. This does nothold for an LBBB shaped tachycardia. On thecontrary, presence of an inferior axis in LBBBshaped QRS tachycardia argues for a VT aris-ing in the outflow tract of the right ventricle.

Figure 6. An antidromic circus movement tachycardia with AV conduction over aright sided accessory pathway. The insertion of the accessory pathway in the freewall of the right ventricle results in sequential (right to left) ventricular activationand a wide QRS complex.

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Figure 7. VT origin and QRS axis. An apical originresults in a superiorly directed axis in the frontalplane. In contrast, a basal origin leads to an inferiorQRS axis (lower panel).

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VT origin infero-apical

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VT origin antero-apical

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Figure 8. Findings in lead V1 and V2 during LBBBshaped tachycardia pointing to a ventricular origin(see text).

V1 and V2

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A: > 30 ms FAVOURS VT

B: NOTCHING, SLURRING FAVOURS VT

C: > 70 ms FAVOURS VT

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Configurational characteristics of the QRScomplexLeads V1 and V6Marriott6 described that in RBBB shapedtachycardia, presence of a qR or R complex inlead V1 strongly argued for a ventricular originof the tachycardia, while a three phasic (RSR)pattern suggested a supraventricular origin.Apart from lead V1, lead V6 can also be veryhelpful in correctly diVerentiating RBBBshaped tachycardia. When in V6 the R:S ratiois < 1, a VT is very likely.4 As shown in fig 2B

an R:S ratio < 1 in V6 is typically found whenthere is left axis deviation in the frontal plane.If the axis is inferiorly directed, lead V6 oftenshows an R:S ratio > 1 (fig 2A). In LBBBshaped VT, lead V1 (and also V2) (fig 8)shows: an initially positive QRS with positivitymeasuring more than 0:03 seconds; slurring ornotching of the downstroke of the S wave; andan interval between the beginning of the QRSand the nadir of the S wave of 0.07 seconds ormore.7 When lead V6 shows a qR pattern dur-ing LBBB shaped tachycardia, VT is verylikely. In SVT with LBBB, lead V1 shows no orminimal initial positivity, a very rapid down-stroke of the S wave, and a short interval

between the beginning of the QRS and thenadir of the S wave (fig 9).

Interval onset QRS to nadir of S wave inprecordial leadsBrugada and colleagues8 suggested that an RSinterval > 100 ms in one or more precordialleads is highly suggestive for VT. One should becareful, however, because such a duration mayoccur in SVT with AV conduction over anaccessory pathway, SVT during administrationof drugs that slow intraventricular conduction(in particular, flecainide), and in SVT withpre-existent BBB, especially LBBB.

Concordant patternWhen all precordial leads show either negativeor positive QRS complexes this is called nega-tive or positive concordancy. Negative concor-dancy is diagnostic for a VT arising in the api-cal area of the heart (fig 10). Positiveconcordancy means that in the horizontalplane ventricular activation starts left posteri-orly. This can be found either in VT originatingin the left posterior wall or during tachycardiasusing a left posterior accessory AV pathway forAV conduction (fig 10).

Tachycardia QRS more narrow than sinus QRSWhen during tachycardia the QRS is morenarrow than during sinus rhythm a VT should

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Figure 9. SVT with LBBB. In panel A LBBB changes during tachycardia into a

narrow QRS following a ventricular premature beat. As described in the text, leadV1 during LBBB clearly shows signs pointing to a supraventricular origin of thetachycardia.

Figure 10. Concordant pattern. The left panel showsa VT arising in the apical area of the left ventricleresulting in negative concordancy of all precordialleads. In the right panel ventricular activation starts in

the left posterior area, resulting in positiveconcordancy of all precordial leads. The latter can befound in left posterior VT but also in SVT with AVconduction over a left posterior accessory pathway.

Figure 11. Tachycardia QRS smaller than QRS during sinus rhythm. On the leftsinus rhythm is present with a very wide QRS because of anterolateralmyocardial infarction and pronounced delay in left ventricular activation. On theright a VT arising on the right side of the interventricular septum results in moresimultaneous activation of the right and left ventricle than during sinus rhythmand therefore a smaller QRS complex.

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be diagnosed. As shown in fig 11, a very wideQRS is present during sinus rhythm because ofsequential activation of first the right and thenthe left ventricle. During tachycardia the QRSis more narrow. This can only be explained bya ventricular origin close to the intraventricularseptum, resulting in more simultaneous activa-tion of the right and left ventricle than duringsinus rhythm.

Presence of QR complexesCoumel and colleagues9 called attention to thesignificance of a QR (but not a QS) complex

during a broad QRS tachycardia, showing that

their presence indicates a scar in the myocar-dium usually caused by myocardial infarction.Figure 12 gives an example of QR complexesduring VT in patients with an anterior (panelA) and an old inferior myocardial infarction(panel B). QR complexes during VT arepresent in approximately 40% of VTs aftermyocardial infarction.10

Aetiology of VT

Most VTs have a previous myocardial infarc-

tion as their aetiology and,as pointed out,a QRcomplex during VT can be very helpful tomake that diagnosis. However, characteristicECG patterns can also be found in idiopathicVT11 and VT in patients with arrhythmogenicright ventricular dysplasia (ARVD).12 Figure 13shows three patterns of idiopathic VT arising inor close to the outflow tract of the right ventri-cle. All three have an LBBB-like QRS complexindicating a right ventricular origin. In panel Athe frontal QRS axis is +70 and lead 1 shows apositive QRS complex, indicating an origin ofthe tachycardia in the lateral part of the outflowtract of the right ventricle. In panel B the fron-tal QRS axis is inferior and the QRS is negative

in lead 1, pointing to an origin on the septalside in the right ventricular outflow tract. Inpanel C an inferior frontal QRS axis and QRSnegativity in lead 1 are also present, but leadsV1 and V2 clearly show initial positivity of theQRS complex. This is a tachycardia not arisingon the endocardial surface of the rightventricular outflow tract but epicardially inbetween the root of the aorta and the posteriorpart of the outflow tract of the right ventricle. Itis important to recognise this pattern becausethis site of origin of the VT cannot be treatedwith catheter ablation in contrast to the tachy-cardias depicted in panel A and B.

Figure 12. QRS complexes during VT indicating a myocardial scar. As shown bythe accompanying tracing, during sinus rhythm anterior wall myocardial infarctionis present in the left panel and inferior wall myocardial infarction in the right one.

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Figure 13. Three types of idiopathic VT arising in orclose to the outflow tract of the right ventricle (seetext).

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Figure 14. Three types of left ventricular idiopathicVT (see text).

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The QRS configuration in idiopathic left VT

is shown in fig 14. They all have an RBBB

shape because of an origin in the left ventricle.

The most common type is shown in panel A.

The frontal QRS axis shows left axis deviation.

The site of origin of the VT is in or close to the

posterior fascicle of the LBB. In panel B the

frontal QRS axis is further leftward (a so called

north-west axis). This tachycardia arises more

anteriorly close to the interventricular septum.

The least common idiopathic left VT is the

one shown in panel C. Now the frontal QRS

axis is inferiorly directed. This VT originates

in the anterior fascicle of the LBB. That area is

diYcult to reach by retrograde left ventricular

catheterisation and when catheter ablation is

considered an (atrial) transseptal catheterisa-

tion should be favoured. In ARVD there are

three predilection sites in the right ventricle:

the inflow and outflow tracts, and the apex.

While t he fir st two sites have a QRS

configuration during tachycardia which is dif-

ficult to diVerentiate from right ventricular

idiopathic VT, left axis deviation in a young

person with an LBBB shaped VT shouldimmediately lead to the suspicion of ARVD. In

fact, there is an important rule in LBBB

shaped VT with left axis deviation that cardiac

disease should be suspected and that idio-

pathic right ventricular VT is extremely

unlikely.

Figure 15 gives an example of an LBBB

shaped VT in a patient with ARVD. When the

broad QRS is identical during tachycardia and

sinus rhythm, one has to diVerentiate SVT

with pre-existent BBB from bundle branch

re-entrant tachycardia.13 In diseased hearts,

especially when the bundle branches and the

interventricular septum are involved, a tachy-

cardia may occur based upon a circuit withanterograde conduction down one bundle

branch or one of the left sided fascicles and

after septal activation retrograde conduction

over another branch of the bundle branch sys-

tem (fig 16).

This type of re-entry may occur in patients

with anteroseptal myocardial infarction, idio-

pathic dilated cardiomyopathy, myotonic dys-

trophy, after aortic valve surgery, and after

severe frontal chest trauma.

Value of the ECG during sinus rhythm

The ECG during sinus rhythm may show

changes such as pre-existent BBB, ventricular

pre-excitation, or an old myocardial infarction

which are very helpful in correctly interpreting

the ECG during broad QRS tachycardia. Also

the presence of AV conduction disturbances

during sinus rhythm make it very unlikely that a

broad QRS tachycardia in that patient has a

supraventricular origin and, as already shown in

fig 11, a QRS width during tachycardia more

narrow that during sinus rhythm points to a VT.

Figure 15. VT in arrhythmogenic right ventricular dysplasia (ARVD). VT showsLBBB shape and left axis deviation indicating an origin in the apex of the rightventricle. Note also the negative T waves in V1V3 during sinus rhythm, which isoften found in ARVD.

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Figure 16. Bundle branch re-entry VT. Following two electrically inducedpremature beats the tachycardia terminates in the middle of the recording.However, tachycardia resumes after two conducted sinus beats. The QRS isidentical during sinus rhythm and tachycardia. Note the presence of AVdissociation during tachycardia indicating a ventricular origin.

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Conclusion

Do not panic when confronted with a broadQRS tachycardia. Look for clinical signs of AVdissociation and evaluate the 12 lead ECG sys-tematically (see box above). Also, when avail-able, look at the 12 lead ECG during sinusrhythm. This approach usually gives the

correct diagnosis of VT versus SVT. Keep inmind that statistically VT is much more

common than SVT in the broad QRS tachycar-

dia. Never make the mistake of rejecting VTbecause the broad QRS tachycardia is haemo-dynamically well tolerated. When in doubt, do

not give verapamil or adenosine; procainamideshould be used instead.

1. Stewart RB, Bardy GH, Greene HL. Wide complextachycardia: misdiagnosis and outcome after emergenttherapy. Ann Intern Med 1986;104:76671.

2. Buxton AE, Marchlinski FE, Doherty JU. Hazards ofintravenous verapamil for sustained ventricular tachycardia.Am J Cardiol1987;59:110710.

3. Dancy M, Camm AJ, Ward D. Misdiagnosis of chronicrecurrent ventricular tachycardia. Lancet 1985;ii:3203. Three articles (refs 13) illustrating the dangers of giving

calcium antagonists to patients with a broad QRStachycardia erroneously interpreting a reasonablehaemodynamic condition as pointing to an SVT.

4. Wellens HJJ, Bar FWHM, Lie KI. The value of theelectrocardiogram in the differential diagnosis of atachycardia with a widened QRS complex. Am J Med1978;64:2733. First article systematically evaluating ECG findings in

broad QRS tachycardia indicating value and limitations ofAV dissociation, QRS width, QRS axis, and QRScharacteristics in leads V1 and V6 to differentiate betweenVT and SVT.

5. Harvey WP, Ronan JA. Bedside diagnosis ofarrhythmias. Prog Cardiovasc Dis 1966;8:41945. Physical examination is still of great value in the correct

diagnosis of the patient with a tachycardia.

6. Marriott HJL. Differential diagnosis of supraventricularand ventricular tachycardia. Geriatrics 1970;25:91101. The first systematic approach to use the ECG for

differentiating tachycardias.

7. Kindwall E,Brown J, Josephson ME.Electrocardiographic criteria for ventricular tachycardia inwide QRS complex left bundle-branch block morphologytachycardia. Am J Cardiol 1988;61:127983. Basic information for the correct interpretation of LBBB

shaped tachycardias.

8. Brugada P, Brugada J, Mont L, et al. A new approach tothe differential diagnosis of a regular tachycardia with a wideQRS complex. Circulation 1991;83:164959. A useful approach to the ECG diagnosis of the broad QRS

tachycardia.

9. Coumel P, Leclerq JF, Attuel P, et al. The QRSmorphology in postmyocardial infarction ventriculartachycardia: a study of 100 tracings compared with 70 casesof idiopathic ventricular tachycardia. Eur Heart J1984;5:792805. Important article indicating that the ECG contains

information about the aetiology of the broad QRStachycardia.

10. Wellens HJJ. The electrocardiographic diagnosis ofarrhythmias. In: Topol E, ed. Textbook of cardiovascularmedicine. Philadelphia: Lippincott, Raven, 1998:1591609. This chapter includes an analysis of the incidence of QR

complexes in a large series of patients with VT aftermyocardial infarction.

11. Wellens HJJ, Rodriguez LM, Smeets JL. Ventriculartachycardia in structurally normal hearts. In: Zipes DP, JalifeJ, eds. Cardiac electrophysiologyfrom cell to bedside, 2nded. Philadelphia: WB Saunders, 1995:7808. A review of the ECG characteristics of patients with right

and left sided idiopathic ventricular tachycardia.

12. Leclerq JF, Coumel PH. Characteristics, prognosis andtreatment of the ventricular arrhythmias of right ventriculardysplasia. Eur Heart J 1989:10 (suppl D):6170. ECG findings in patients with ARVD.

13. Touboul P, Kirkorian G, Atallah G, et al. Bundlebranch reentrant tachycardia treated by electrical ablation ofthe right bundle branch. J Am Coll Cardiol 1986;7:14049. A careful analysis of the bundle branch system as circuit

for a re-entry tachycardia.

Value and limitations of ECG findings indiagnosing broad QRS tachycardia

x AV dissociation suggests VT, but VAconduction may be present during VT

x A QRS width of > 160 ms suggests VT, butneed to rule out:

pre-existent BBB (especially LBBB)

SVT with AV conduction over an AP use of dr ugs slowing intraventricularconduction (flecainide).

Keep in mindVT arising close to or in theintraventricular conduction system may have awidth of < 140 ms

x Left axis deviation (to the left of 30)suggests VT, but is not helpful in:

LBBB shaped QRS SVT with conduction over a right sided

or posteroseptal AP SVT during use of class 1 C drugs

x Right axis deviation (to the right of +90)suggests VT in LBBB shaped QRS

x Concordant pattern in precordial leadssuggests VT, but positive concordancy mayoccur during SVT with AV conductionover a left posterior AP

x R nadir S > 100 ms in one or moreprecordial leads suggests VT, but may befound in:

SVT on drugs slowing intraventricularconduction

SVT with AV conduction over an AP pre-existent BBB (especially LBBB)

x QR complexes during VT suggest previousmyocardial infarction as aetiology

AP, accessory pathway; AV, atrioventricular; BBB, bundle

branch block; LBBB, left bundle branch block; SVT,

supraventricular tachycardia; VA, ventriculo-atrial;VT, ven-

tricular tachycardia

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vt - diagnosis of broad complex tachycardia

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