28
CHAPTER 5 Intraventricular Conduction Abnormalities NORMAL CONDUCTION Many cardiac conditions cause electrical impulses to be conducted abnormally through the ventricular myocardium, producing changes in QRS complexes and T waves. Therefore, it is important to understand the conditions required to facilitate normal intraventricular impulse conduction. These are as follows The left and right ventricles are not in an enlarged state that would prolong the time required for their activation and recovery (Chapter 4, “Chamber Enlargement”). Myocardial ischemia or infarction is not present or is of insufficient magnitude to disrupt the spread of the activation and recovery waves (Chapter 7, “Myocardial Ischemia and Infarction”). There is rapid impulse conduction through the right- and left-ventricular Purkinje networks so that the endocardial surfaces are activated almost simultaneously (as discussed later in this chapter). There are no accessory pathways for conduction from the atria to the ventricles (Chapter 6, “Ventricular Preexcitation”). BUNDLE-BRANCH AND FASCICULAR BLOCK Since the activation of the ventricular Purkinje system is not represented on the surface electrocardiogram (ECG) (Fig. 1.9), abnormalities of its conduction must be detected indirectly by their effects on myocardial activation and recovery. The most specific changes indicative of such abnormalities occur within the QRS complex. A conduction disturbance within the right bundle branch (RBB), left bundle branch (LBB), left bundle fascicles , or between the Purkinje fibers and the adjacent myocardium may alter the QRS complex and T wave (Fig. 5.1). A conduction disturbance in the common bundle (Bundle of His) has similar effects on the entire distal Purkinje system, and therefore does not alter the appearance of the QRS complex or T wave.

CHAPTER 5cardioland.org/ECG/Marriott's Practical... · Figure 5.5. Twelve-lead ECGs from a 17-year-old girl with an ostium secundum atrial septal defect (A), an 81-year-old woman

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Page 1: CHAPTER 5cardioland.org/ECG/Marriott's Practical... · Figure 5.5. Twelve-lead ECGs from a 17-year-old girl with an ostium secundum atrial septal defect (A), an 81-year-old woman

CHAPTER 5

Intraventricular Conduction Abnormalities

NORMAL CONDUCTION Many cardiac condi t ions cause electr ica l impulses to be conducted abnormal ly through

the ventr icu lar myocardium, producing changes in QRS complexes and T waves.

Therefore, i t is important to understand the condi t ions required to fac i l i tate normal

in t raventr icu lar impulse conduct ion. These are as fo l lows

• The lef t and r ight ventr ic les are not in an enlarged state that would prolong the

t ime required for thei r act ivat ion and recovery (Chapter 4, “Chamber

Enlargement”) .

• Myocardia l ischemia or in farct ion is not present or is of insuf f ic ient magni tude

to d isrupt the spread of the act ivat ion and recovery waves (Chapter 7,

“Myocardia l Ischemia and Infarct ion”) .

• There is rapid impulse conduct ion through the r ight- and lef t -ventr icu lar

Purk in je networks so that the endocardia l sur faces are act ivated a lmost

s imul taneously (as d iscussed later in th is chapter) .

• There are no accessory pathways for conduct ion f rom the at r ia to the ventr ic les

(Chapter 6, “Ventr icu lar Preexci tat ion”) .

BUNDLE-BRANCH AND FASCICULAR BLOCK Since the act ivat ion of the ventr icu lar Purk in je system is not represented on the

sur face e lectrocardiogram (ECG) (F ig. 1.9) , abnormal i t ies of i ts conduct ion must be

detected indi rect ly by thei r ef fects on myocardia l act ivat ion and recovery. The most

speci f ic changes indicat ive of such abnormal i t ies occur wi th in the QRS complex. A

conduct ion d isturbance wi th in the r ight bundle branch (RBB), le f t bundle branch (LBB),

le f t bundle fascic les , or between the Purk in je f ibers and the adjacent myocardium may

al ter the QRS complex and T wave (F ig. 5.1) . A conduct ion d isturbance in the common

bundle (Bundle of His) has s imi lar ef fects on the ent i re d is ta l Purk in je system, and

therefore does not a l ter the appearance of the QRS complex or T wave.

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Figure 5.1. LAF and LPF indicate the lef t anter ior and

lef t poster ior fasc ic les, respect ive ly. (1 ) , (2 ) , and (3 )

indicate the locat ions at which int raventr icu lar

conduct ion abnormal i t ies can produce al terat ions of the

QRS complex and T wave. (Modi f ied f rom Wagner GS,

Waugh RA, Ramo BW. Cardiac arrhythmias. New York:

Churchi l l L iv ingstone, 1983;18.)

Block of an ent i re bundle branch requires that i ts ventr ic le be act ivated by myocard ia l

spread of e lectr ica l act iv i ty f rom the other ventr ic le, wi th pro longat ion of the overal l

QRS complex. Block of the ent i re RBB is termed complete r ight bundle-branch block

(RBBB), whi le b lock of the ent i re LBB is termed complete lef t bundle-branch block

(LBBB). In both of these condi t ions, the vent r ic les are act ivated successively instead

of s imul taneously. The other condi t ions in which the ventr ic les are act ivated

successively occur when one ventr ic le is preexci ted v ia an accessory atr ioventr icu lar

(AV) pathway (Chapter 6, “Ventr icu lar Preexci tat ion”) and when there are independent

ventr icu lar rhythms (Chapter 13 and Chapter 17) . Under these condi t ions, there is a

fundamental s imi lar i ty in the d is tor t ions of the ECG waveforms: the durat ion of the

QRS complex is pro longed and the ST segment s lopes into the T wave in the d i rect ion

away f rom the ventr ic le in which the abnormal i ty is located (F ig. 5.2) .

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Figure 5.2. Compar ison of pat terns of QRS

morphology in lead V1 when the two ventr ic les are

act ivated successively rather than s imul taneous ly:

A. A ventr icu lar beat . B. Bundle branch b lock. C. Ventr icu lar tachycardia. D. Ar t i f ic ia l ly paced

ventr icu lar rhythm.

A ventr icu lar conduct ion delay wi th only s l ight pro longat ion of the QRS complex could

be termed incomplete RBBB or incomplete LBBB. However, i t is important to remember

f rom Chapter 4 ( “Chamber Enlargement”) that enlargement of the r ight ventr ic le may

produce a d is tor t ion of the QRS complex that mimics incomplete RBBB (F ig. 4.9B),

whereas enlargement of the lef t ventr ic le may produce a prolongat ion of the QRS

complex that mimics incomplete LBBB (F ig. 4.8A). Since the LBB has mul t ip le

fasc ic les, another form of incomplete LBBB could be produced by a d is turbance in one

of i ts major fasc ic les.

The ventr icular Purk in je system is considered t r i fascicular . I t consists of the RBB and

the anter ior and poster ior por t ions of the LBB. The proximal RBB is smal l and

compact , and may therefore be considered ei ther a bundle branch or a fascic le. The

proximal LBB is a lso compact , but is too large to be considered a fascic le. I t remains

compact for 1 to 2 cm and then fans into i ts two fascic les.1 As Demoul in and Kulber tus

have shown in humans,2 there are mul t ip le anatomic var iat ions in these fascic les

among indiv iduals. Based on thei r anatomic locat ions, the two fascic les are termed the

lef t -anter ior fascic le (LAF) and lef t -poster ior fasc ic le (LPF), as seen in F igure 5.3. The

LAF of the LBB courses toward the anter ior-super ior papi l lary muscle, and the LPF of

the LBB courses toward the poster ior- in fer ior papi l lary musc le. There are a lso Purk in je

f ibers that emerge f rom the very proximal LBB that proceed along the sur face of the

interventr icu lar septum and in i t ia te le f t - to-r ight spread of act ivat ion through the

interventr icu lar septum.

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Figure 5.3. The lef t ventr ic le has been opened to reveal the LBB and i ts fascic les as or ig inal ly

presented in F igure 1.7C. Note that the anter ior and poster ior fascic les of the LBB are a lso

designated super ior and infer ior , respect ively, because these terms indicate thei r t rue

anatomic posi t ions. (From Netter FH. The Ciba col lect ion of medical i l lus t rat ions. vol 5. Heart .

Summit , NJ: Ciba–Geigy, 1978:13.)

Rosenbaum and coworkers descr ibed the concept of b locks in the fascic les of the LBB,

which they termed le f t anter ior and lef t poster ior hemiblock .3 However, these two

k inds of b lock are more appropr iate ly termed lef t anter ior fascicular b lock (LAFB) and

lef t poster ior fasc icular b lock (LPFB). Iso lated LAFB, LPFB, or RBBB is considered

uni fascicular b lock. Complete LBBB or combinat ions of RBBB wi th LAFB or wi th LPFB

are bi fascicular b locks , and the combinat ion of RBBB wi th both LAFB and LPFB is

considered t r i fasc icular b lock .

UNIFASCICULAR BLOCKS The term “uni fascicular b lock” is used when there is ECG evidence of b lockage of only

the RBB, LAF, or LPF. Isolated RBBB or LAFB occur commonly, whi le iso lated LPFB is

rare. Rosenbaum and coworkers ident i f ied only 30 pat ients wi th LPFB, as compared

wi th 900 pat ients wi th LAFB.3

Right Bundle-Branch Block Since the r ight ventr ic le contr ibutes minimal ly to the normal QRS complex, RBBB

produces l i t t le d is tor t ion of the QRS complex dur ing the t ime required for le f t -

ventr icu lar act ivat ion. F igure 5.4 i l lust rates the minimal d is tor t ion of the ear ly por t ion

and marked distor t ion of the late por t ion of the QRS complex that typ ica l ly occurs wi th

RBBB. The minimal contr ibut ion of the normal r ight-vent r icu lar myocardium is

complete ly subtracted f rom the ear ly por t ion of the QRS complex and then added later ,

when the r ight ventr ic le is act ivated v ia the spread of impulses f rom the lef t ventr ic le.

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This produces a late prominent posi t ive wave in lead V1 termed R¢, because i t fo l lows

the ear l ier posi t ive R wave produced by the normal le f t - to-r ight spread of act ivat ion

through the interventr icu lar septum (F ig. 5.4 and Table 5.1) .

Figure 5.4. The contr ibut ions f rom act ivat ion of the

interventr icu lar septum and the r ight and lef t

ventr icu lar f ree wal ls to the appearance of the QRS

complex in lead V1, wi th normal in t raventr icu lar

conduct ion ( top) and wi th RBBB (bottom) . The

numbers refer to the f i rs t , second, and th i rd sequent ia l

0.04-s per iods of t ime. Only two 0.04-s per iods are

required for normal conduct ion, but a th i rd is required

when RBBB is present .

Table 5.1. Cr i ter ia for Right Bundle Branch Block

RBBB has many var iat ions in i ts ECG appearance, as i l lust rated by the examples in

Figure 5.5A, Figure 5.5B and Figure 5.5C. In Figure 5.5A, the RBBB is considered

“ incomplete” because the durat ion of the QRS complex is only 0.10 s; but in F igure

5.5B and Figure 5.5C, the RBBB is considered “complete” because the durat ion of the

QRS complex is ≥ 0 .12 s.

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Figure 5.5. Twelve- lead ECGs f rom a

17-year-o ld g i r l wi th an ost ium

secundum atr ia l septa l defect (A) , an

81-year-o ld woman wi th f ibrosis of the

RBB (B) , and an 82-year-o ld man wi th

f ibrosis of both the RBB and the

anter ior fascic le of the LBB (C) .

Arrows in A , B , and C ind icate the

prominent terminal R¢ wave in V1, and

aster isks in A and C ind icate the

r ightward and lef tward axis shi f ts ,

respect ive ly.

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Left-Fascicular Blocks Normal act ivat ion of the lef t -ventr icular f ree wal l spreads s imul taneously f rom two

s i tes (near the inser t ions of the papi l lary muscles of the mi t ra l va lve) . Wavefronts of

act ivat ion spread f rom these endocardia l s i tes to the over ly ing epicardium. Since the

wavefronts t ravel in opposi te d i rect ions, they neutra l ize each other 's in f luence on the

ECG in a phenomenon cal led cancel lat ion . When block in e i ther the LAF or LPF is

present , act ivat ion of the f ree wal l proceeds f rom one s i te instead of two. Since the

cancel lat ion is removed, the waveforms of the QRS complex change, as descr ibed

below (F ig. 5.6 and Table 5.2 and Table 5.3) .

Figure 5.6. Schemat ic lef t ventr ic le v iewed f rom i ts apex upward toward i ts base. The

interventr icu lar septum (S ) , le f t -ventr icu lar f ree wal l (FW ) , and anter ior (A ) and infer ior ( I )

regions of the lef t ventr ic le are indicated. The typical appearances of the QRS complexes in

leads I ( top) and aVF (bottom) are presented for normal (A) , LAFB (B) , and LPFB lef t -

ventr icu lar act ivat ion (C) . Dashed l ines wi th in the inner c i rc les represent the fascic les; the two

wavy l ines crossing a fascic le indicate the s i tes of b lock. Smal l crosshatched c i rc les represent

the papi l lary muscles; outer r ings represent the endocardia l and epicardia l sur face of the lef t

ventr icu lar myocardium. Arrows wi th in the outer r ings indicate the d i rect ions of the wavefronts

of act ivat ion as they spread f rom the unblocked fascic les through the myocardium.

Table 5.2. Cr i ter ia for Lef t Anter ior Fascicular Block

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Table 5.3. Cr i ter ia for Lef t Poster ior Fascicular Block

Left Anterior Fascicular Block. I f the LAF of the LBB is b locked (F ig. 5.6B), the in i t ia l act ivat ion of the lef t -ventr icu lar

f ree wal l occurs v ia the LPF. Act ivat ion spreading f rom endocardium to the epicardium

in th is region is d i rected infer ior ly and r ightward. Since the b lock in the LAF has

removed the in i t ia l super ior and lef tward act ivat ion, a Q wave appears in leads that

have thei r posi t ive e lectrodes in a super ior / le f tward posi t ion ( i .e . , lead I ) and an R

wave appears in leads that have thei r posi t ive e lectrodes in an infer ior / r ightward

posi t ion ( i .e . , lead aVF). Fol lowing th is in i t ia l per iod, the act ivat ion wave spreads over

the remainder of the lef t -ventr icu lar f ree wal l in a super ior / le f tward d i rect ion,

producing a prominent R wave in lead I and a prominent S wave in lead aVF. This

change in the lef t -ventr icu lar act ivat ion sequence produces a lef tward shi f t o f the axis

of the QRS complex to at least –45 degrees. The overal l durat ion of the QRS complex

may be normal (F ig. 5.7A) or pro longed by 0.01 to 0.04 s (F ig. 5.7B).4

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Figure 5.7. Twelve- lead ECGs f rom a 53-year-o ld woman wi th no medical problems (A) and a

75-year-o ld man wi th a long h istory of poor ly t reated hypertension (B) . Arrows ind icate the

deep S waves in leads I I , I I I , and aVF that ref lect extreme lef t ax is deviat ion.

Left Posterior Fascicular Block. I f the LPF of the LBB is b locked (F ig. 5.6C), the s i tuat ion is reversed f rom that in LAF

block, and the in i t ia l act ivat ion of the lef t -ventr icu lar f ree wal l occurs v ia the LAF.

Act ivat ion spreading f rom the endocardium to the epicardium in th is region is d i rected

super ior ly and lef tward. Since the b lock in the LPF has removed the in i t ia l in fer ior and

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r ightward act ivat ion, a Q wave appears in leads wi th thei r posi t ive e lectrodes in an

infer ior / r ightward posi t ion ( i .e . , lead aVF) and an R wave appears in leads wi th thei r

posi t ive e lectrodes in a super ior / le f tward d i rect ion ( i .e . , lead I ) . Fol lowing th is in i t ia l

per iod, the act ivat ion spreads over the remainder of the lef t -ventr icu lar f ree wal l in an

infer ior / r ightward d i rect ion, producing a prominent R wave in lead aVF and a

prominent S wave in lead I . This change in the lef t -ventr icu lar act ivat ion sequence

produces a r ightward sh i f t of the axis of the QRS complex to at least +90 degrees.5

The durat ion of the QRS complex may be normal or s l ight ly pro longed (F ig. 5.8) .

Figure 5.8. Twelve- lead ECG from a heal thy 77-year-o ld woman. Arrows indicate the deep S

waves in leads I and aVL typical of both LPFB and RVH.

The considerat ion that LPFB may be present requires that there be no evidence of

r ight-ventr icu lar hypert rophy (RVH) f rom ei ther the precordia l leads (F ig. 5.8) or f rom

other c l in ical data. However, even the absence of RVH does not a l low diagnosis of

LPFB, because RVH can produce the same pat tern as LPFB in the l imb leads, and

RVH is much more common than is LPFB.

BIFASCICULAR BLOCKS The term “b i fascicular b lock” is used when there is ECG evidence of involvement of

any two of the RBBB, LAF, or LPF. Such evidence may appear at d i f ferent t imes or

may coexist on the same ECG. Bi fasc icular b lock is somet imes appl ied to complete

LBBB, and is commonly appl ied to the combinat ion of RBBB wi th e i ther LAFB or LPFB.

The term “b i la tera l bundle-branch block” is a lso appropr iate when RBBB and ei ther

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LAFB or LPFB are present .6 When there is b i fascicular b lock, the durat ion of the QRS

complex is pro longed to at least 0.12 s.

Left Bundle-Branch Block Figure 5.9 i l lust rates the marked distor t ion of the ent i re QRS complex produced by

LBBB. Complete LBBB may be caused by d isease in e i ther the main lef t bundle branch

(LBB) (prediv is ional ) or in both of i ts fascic les (postdiv is ional ) . When the impulse

cannot progress a long the LBB, e lectr ica l act ivat ion must f i rs t occur in the r ight

ventr ic le and then t ravel through the intervent r icu lar septum to the lef t ventr ic le.

Figure 5.9. The format of F igure 5.4 is repeated to i l lust rate the contr ibut ions f rom act ivat ion

of the var ious aspects of the ventr icu lar myocardium to the appearances of the QRS complex

in lead V1 wi th LBBB.

Normal ly, the interventr icu lar septum is act ivated f rom lef t to r ight , producing an in i t ia l

R wave in the r ight precordia l leads and a Q wave in leads I , aVL, and the lef t

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precordia l leads. When complete LBBB is present , however, the septum is act ivated

f rom r ight to le f t . This produces Q waves in the r ight precordia l leads and el iminates

the normal Q waves in the lef tward-or iented leads. The act ivat ion of the lef t ventr ic le

then proceeds sequent ia l ly f rom the interventr icu lar septum, to the adjacent anter ior

and infer ior wal ls , and then to the poster ior- la tera l f ree wal l . This sequence of

ventr icu lar act ivat ion in complete LBBB tends to produce monophasic QRS complexes,

wi th QS complexes in lead V1 and R waves in leads I , aVL, and V6 (Table 5.4) .

Table 5.4. Cr i ter ia for Lef t Bundle Branch Block

LBBB has many var iat ions in i ts ECG appearance, as i l lust rated by the examples in

F igure 5.10A, F igure 5.10B and Figure 5.10C. F igure 5.10A shows the typical

appearance of complete LBBB. In Figure 5.10B the extreme LAD indicates that

conduct ion is even s lower in the LAF than in the LPF, and only minimal R waves are

seen in leads V1 through V4. In F igure 5.10C the aberrat ion of a markedly pro longed

QRS complex is present , suggest ing the coexistence of le f t -ventr icu lar hypert rophy

(LVH).

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Figure 5.10. Twelve- lead ECGs f rom an

82-year-o ld woman wi th no medical

problems (A) , a 71-year-o ld man wi th

chronic heart fa i lure (B) , and a 74-year-o ld

man wi th a long history of hypertension

(C) . Arrows in A and C indicate the typical

character is t ics of LBBB in leads I and V1,

and arrows in B ind icate the deep S waves

in leads I I , I I I , and aVF and decreased R

waves in leads V2–V4.

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Right Bundle-Branch Block with Left Anterior Fascicular Block Just as LAFB appears as a uni fascicular b lock much more commonly than does LPFB,

i t more commonly accompanies RBBB as a b i fascicular b lock. The d iagnosis of LAFB

plus RBBB is made by observ ing the late prominent R or R¢ wave in precordia l lead

V1 of RBBB, and the in i t ia l R waves and prominent S waves in l imb leads I I , I I I , and

aVF of LAFB. The durat ion of the QRS complex should be at least 0.12 s and the

f ronta l -p lane axis of the complex should be between –45 degrees and –120 degrees

(F ig. 5.11) . In F igure 5.11A only LAFB is present , whi le in F igure 5.11B the presence

of RBBB indicates that a second fascic le has been blocked.

Figure 5.11. Twelve- lead ECGs f rom a 1-year previous (A) and a current (B) evaluat ion of a

73-year-o ld woman wi th no medical problems and no other ev idence of heart d isease. Arrows

indicate the deep S waves in I I , I I I , and aVF that are character is t ic of LAFB in A , and a

prominent R¢ wave character is t ic of RBBB in V1 in B .

Right Bundle-Branch Block with Left Posterior Fascicular Block The example of b i fascicular b lock consist ing of RBBB wi th LPFB rare ly occurs. Even

when changes in the ECG are ent i rely typ ical of th is combinat ion, the d iagnosis should

be considered only i f there is no c l in ical ev idence of RVH. The diagnos is of RBBB wi th

LPFB should be considered when precordia l lead V1 shows changes typ ical of RBBB

and l imb leads I and aVL show the in i t ia l R waves and prominent S waves typica l of

LPFB. The durat ion of the QRS complex should be at least 0.12 s and the f ronta l -

p lane axis of the complex should be at least +90 degrees (F ig. 5.12) .7

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Figure 5.12. Twelve- lead ECG from an 82-year-o ld woman wi th no complaints and no other

ev idence of heart d isease. Arrows ind icate the prominant S waves in I and aVL and RR'

complex in V1.

SYSTEMATIC APPROACH TO THE ANALYSIS OF BUNDLE-BRANCH AND FASCICULAR BLOCKS The fo l lowing steps should be taken in analyz ing bundle-branch and fascicular b locks:

• Examine the contour of the QRS complex.

RBBB and LBBB have opposi te ef fects on the contour of the QRS complex.

RBBB adds a new waveform di rected toward the r ight ventr ic le fo l lowing the

complet ion of s l ight ly a l tered waveforms di rected toward the lef t ventr ic le (F ig.

5.4) . Therefore, the QRS complex in RBBB tends to have a t r iphasic

appearance. In lead V1, which is opt imal for v isual iz ing r ight - versus lef t -s ided

conduct ion delay, the QRS in RBBB has the appearance of “ rabbi t ears” (F ig.

5.5) . Typical ly, the “ f i rs t ear” (R wave) is shorter than the “second ear” (R¢

wave). (Al though the term “rabbi t ears” in th is context refers to a t r iphasic

QRS, i t can a lso refer to two peaks found in monophasic QRS complexes.)

When RBBB is accompanied by b lock in one of the LBB fascic les, the posi t ive

def lect ion in lead V1 is of ten monophasic, as in F igure 5.12.

In LBBB, a sequent ia l spread of act ivat ion through the interventr icu lar septum

and lef t -ventr icu lar f ree wal l replaces the normal, compet ing and s imul taneous

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spread of act ivat ion through these areas. As a resul t , the QRS complex tends

to have a monophasic appearance that is notched rather than smooth.

Al though LBBB and LVH have many ECG simi lar i t ies, they a lso show marked

d i f ferences. Whereas the normal Q waves over the lef t ventr ic le may be

present or even exaggerated in LVH, they are absent in LBBB. When the LBB

is complete ly b locked, the septum is ent i re ly act ivated f rom i ts r ight s ide.

F igure 5.13 i l lust rates the appearance of incomplete (F ig 5.13B) and complete

(Fig. 5.13C) LBBB in a pat ient wi th LVH (Fig. 5.13A).

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Figure 5.13. The f ive representat ive ECG leads i l lust rate the evolv ing ECG changes in

a pat ient wi th severe hypertension as the LVH is compl icated by LBBB. A. Age 60

years. B. Age 63 years. C. Age 67 years.

• Measure the Durat ion of the QRS Complex.

Complete RBBB increases the durat ion of the QRS complex by 0.03 to 0.04 s,

and complete LBBB increases the durat ion of the complex by 0.04 to 0.05 s.

Block wi th in the LAF or LPF of the LBB usual ly pro longs the durat ion of the

QRS complex by on ly 0.01 to 0.02 s (F ig. 5.7B and Fig. 5.8) .4

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• Measure the Maximal Ampl i tude of the QRS Complex.

Bundle-branch block (BBB) produces QRS waveforms wi th lower vol tage and

more def in i te notching than those that occur wi th ventr icu lar hypert rophy.

However, the ampl i tude of the QRS complex does increase in LBBB because of

the re lat ive ly unopposed spread of act ivat ion over the lef t ventr ic le.

One general ru le for d i f ferent iat ing between LBBB and LVH is that the greater

the ampl i tude of the QRS complex, the more l ike ly is LVH to be the cause of

th is . Simi lar ly, the more prolonged is the durat ion of the QRS complex, the

more l ike ly is LBBB to be the cause of th is ef fect . Kle in and col leagues8 have

suggested that in the presence of LBBB, e i ther of the fo l lowing cr i ter ia are

associated wi th LVH:

o S wave in V2 + R wave in V6 > 45 mm.

o Evidence of le f t -at r ia l enlargement wi th a QRS-complex durat ion > 0.16

s.

• Est imate the Direct ion of the QRS Complex in the Two Planes of the ECG.

Since complete RBBB and complete LBBB al ter conduct ion to ent i re ventr ic les, they

might not be expected to produce much net a l terat ion of the f ronta l -p lane QRS axis.

However, Rosenbaum studied pat ients wi th intermi t tent LBBB in which b locked and

unblocked complexes could be examined s ide by s ide.4 LBBB was of ten observed to

produce a s igni f icant le f t -axis shi f t and somet imes even a r ight axis shi f t . The axis

was unchanged in only a minor i ty of pat ients.

However, b lock in e i ther the LAF or LPF of the LBB alone produces marked axis

deviat ion. The in i t ia l 0.20 s of the QRS complex is d i rected away f rom the b locked

fascic les, and the middle and late por t ions are d i rected toward the b locked fascic les,

causing the overal l d i rect ion of the QRS complex to be shi f ted toward the s i te of the

b lock (F ig. 5.7 and Fig. 5.8) .5 When block in e i ther of these LBB fascic les is

accompanied by RBBB, an even later waveform is added to the QRS complex, thereby

fur ther pro longing i ts durat ion. The di rect ion of th is f inal waveform in the f ronta l p lane

is in the v ic in i ty of 180 degrees, as a resul t of the RBBB (Fig. 5.5C).5

In BBB, the T wave is usual ly d i rected opposi te to the later por t ion of the QRS

complex (e.g. , in F igure 5.14A, the T wave in lead I is inver ted and the later par t of

the QRS complex is upr ight ; in F igure 5.14B the T wave is upr ight and the later par t of

the QRS complex is negat ive) . This opposi te polar i ty is the natura l resul t of the

depolar izat ion–repolar izat ion d isturbance produced by the BBB, and is therefore

termed secondary . Indeed, i f the d i rect ion of the T wave is s imi lar to that of the

terminal par t of the QRS complex (F ig. 5.14C), i t should be considered abnormal .

Such T-wave changes are pr imary and imply myocardia l d isease. The diagnosis of

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myocardia l in farct ion in the presence of BBB is considered in Chapter 10 ( “Myocardia l

In farct ion”) .

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Figure 5.14. Twelve- lead ECGs f rom

an 89-year-o ld woman dur ing a

rout ine heal th evaluat ion (A) , a 45-

year-o ld p i lo t dur ing an annual heal th

evaluat ion (B) , and a 64-year-o ld

woman on the f i rs t day af ter coronary

bypass surgery (C) . Arrows ind icate

the concordant d i rect ions of the

terminal QRS complex and of the T

wave in leads V2–V4 in C .

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One method of determining the c l in ical s igni f icance of T-wave changes in BBB is to

measure the angle between the axis of the T wave and that of the terminal par t of the

QRS complex. Obviously, i f the two are opposi te ly d i rected (as they are wi th

secondary T-wave changes), the angle between them wi l l be wide and may approach

180 degrees. I t has been proposed that i f th is angle is less than 110 degrees,

myocardia l d isease is present . In F igure 5.14B, the angle is about 150 degrees,

whereas in F igure 5.14C i t is only a few degrees.

CLINICAL PERSPECTIVE ON INTRAVENTRICULAR CONDUCTION DISTURBANCES Both RBBB and LBBB are of ten seen in apparent ly normal indiv iduals.9 The cause of

th is is f ibros is of the Purk in je f ibers, which has been descr ibed as Lenegre 's

d isease10 or Lev 's d isease.11 The process of Purk in je f ibrosis progresses s lowly: a

10-year fo l low-up study of heal thy av iators wi th BBB revealed no inc idence of

complete AV block, syncope, or sudden death.12 The pathologic process may be

accelerated by systemic hypertension: i t preceded the appearance of BBB in 60% of

the indiv iduals in the Framingham study. The mean age of onset of the BBB was 61

years.13

Ins ight in to the long-term prognosis for indiv iduals wi th chronic BBB but no other

ev idence of cardiac d isease comes f rom studies of the ECG changes preceding the

development of t ransient or permanent complete AV block. Fr iedberg and associates

have documented the common presence of some combinat ion of bundle-branch or

fascicular b lock immediate ly before onset of the AV block. The most common

combinat ion was RBBB wi th LAFB.14

The combined resul ts of these studies suggest that Lenegre 's or Lev 's d isease is a

s lowly developing process of f ibrosis of the Purk in je f ibers that has the u l t imate

potent ia l of causing complete AV block because of b i la tera l bundle-branch

involvement . Since the Purk in je cel ls lack the physio logic capaci ty of the AV-nodal

cel ls to conduct at varying speeds, a sudden progression f rom no AV block to

complete AV block may occur.15 When th is does occur, ventr icu lar act ivat ion can

resul t only f rom impulse format ion wi th in a Purk in je cel l beyond the s i te of the b lock.

Several c l in ical condi t ions may resul t , inc luding syncope and sudden death.

Bundle-branch or fascicular b lock may also be the resul t of other ser ious cardiac

d iseases. In Centra l and South Amer ica, Chagas disease, produced by infect ion wi th

Trypanosoma cruzi , is a lmost endemic and is a common cause of RBBB wi th LAFB.16

As indicated in Chapter 4, RBBB is commonly produced by the d istent ion of the r ight

ventr ic le that occurs wi th volume over loading. Transient RBBB may be produced

dur ing r ight-heart catheter izat ion, as i l lust rated in F igure 5.15.

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Figure 5.15. RBBB is induced by t rauma to the RBB. A catheter has been advanced f rom the

leg v ia the infer ior vena cava, and i ts t ip l ies against the r ight ventr icu lar endocardium in the

v ic in i ty of the RBB. The resul tant RBBB is i l lust rated in the th i rd and four th beats of the

schemat ic lead V1 ECG recording. (Modi f ied f rom Netter FH. The CIBA col lect ion of medical

i l lust rat ions. vol 5. Heart . Summit , NJ: CIBA–Geigy, 1978:13. )

Any combinat ion of the bundle branches or proximal fascic les may be b locked dur ing

an episode of myocardia l cel l death in a pat ient wi th coronary atherosclerosis. These

st ructures receive thei r b lood supply v ia the proximal septal per forat ing branch of the

lef t anter ior descending coronary ar tery (F ig. 5.16) . Therefore, the bundle branches

and thei r proximal fascic les become involved when there is an occlusion in e i ther the

lef t main coronary ar tery or the or ig in of i ts anter ior descending branch. Indiv iduals

who surv ive to reach the hospi ta l af ter occlus ion of such a major coronary ar tery may

have any combinat ion of bundle-branch or fascicular b locks compl icat ing extensive

myocardia l in farct ion. Since the acute and long-term morta l i ty rates in these pat ients

are very h igh, they do not represent a s igni f icant por t ion of the overal l populat ion of

indiv iduals wi th chronic bundle-branch and fascicular b lock.17

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Figure 5.16. The proximal por t ion of specia l ized conduct ion system is shown in re lat ion to i ts

b lood supply f rom a r ight anter ior obl ique v iew: A , AV node; B , Common bundle; C , LPF; D ,

LAF; E ; RBB. Note the lengths of the septa l per forat ing branches of the lef t anter ior

descending (LAD ) coronary ar tery in contrast to those of the poster ior descending ar tery

(PDA ) . (From Rotman M, Wagner GS, Wal lace AG. Bradyarrhythmias in acute myocardia l

in farct ion. Circulat ion 1972;45:703–722, wi th permiss ion. Copyr ight 1972 Amer ican Heart

Associat ion.)

In termi t tent BBB (pro longed QRS complexes present at some t imes but not at others)

usual ly represents a t ransi t ion stage before permanent b lock is establ ished. F igure

5.17A and Figure 5.17B show examples of the sudden onsets of LBBB and RBBB,

respect ive ly.

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Figure 5.17. Precordia l leads V1 and V5 are shown f rom a 62-year-o ld woman dur ing rout ine

ECG moni tor ing af ter uncompl icated abdominal surgery (A) and a 54-year-o ld man dur ing 24-

hour ECG moni tor ing for a complaint of d izz iness (B) . Arrows ind icate the onsets in the V1

leads of typical ly appear ing LBBB in A and RBBB in B .

At t imes, in termi t tent BBB is determined by the heart rate. As the rate accelerates, the

RR interval shortens and the descending impulse f inds one of the bundle branches st i l l

in i ts ref ractory per iod (F ig. 5.18) . With th is tachycardia-dependent BBB , s lowing of

the heart rate a l lows descending impulses to arr ive af ter the ref ractory per iod of the

ent i re conduct ion system, and normal conduct ion is resumed.

Figure 5.18. Precordia l leads V1 and V5 dur ing rout ine ECG moni tor ing of a 47-year-o ld

woman af ter breast cancer surgery. Arrows ind icate the appearance of incomplete RBBB

fo l lowing the shorter cyc le intervals.

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A rarer form of in termi t tent BBB, which develops only when the cardiac cycle

lengthens rather than shortens (F ig. 5.19) , is termed bradycardia-dependent BBB .

In termi t tent BBB is a form of intermit tent aberrant conduct ion of e lectr ica l impulses

through the ventr icu lar myocardium.

Figure 5.19. A l l beats are conducted s inus beats grouped in pai rs. Those ending the shorter

cycles are conducted normal ly, whi le those ending the longer cycles are conducted wi th LBBB.

GLOSSARY Atherosclerosis:

a th ickening of the inner ar ter ia l wal l caused by the deposi t ion of fat ty substances.

AV block:

a block in the cardiac conduct ion system that causes a d isrupt ion of at r ia l - to-

ventr icu lar e lectr ica l conduct ion.

Bifascicular block:

an int raventr icu lar conduct ion abnormal i ty involv ing any two of : the RBB, the anter ior

d iv is ion of the LBB, and the poster ior d iv is ion of the LBB.

Bilateral bundle-branch block:

an int raventr icu lar conduct ion abnormal i ty involv ing both the r ight and lef t bundle

branches, as indicated e i ther by the presence of some conducted beats wi th RBBB and

others wi th LBBB, or by AV block located dista l to the common bundle.

Bradycardia-dependent BBB:

RBBB or LBBB that is intermi t tent , appear ing only wi th a s lowing of the atr ia l rate.

Cancel lat ion: El iminat ion of an abnormal i ty produced by a par t icu lar cardiac problem by a s imi lar

abnormal i ty in another par t of the heart or by a d i f ferent abnormal i ty in the same part

of the heart , s ince the ECG waveforms represent the summat ion of the wavefronts of

act ivat ion and recovery wi th in the heart .

Chagas disease:

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a t ropical d isease caused by the f lagel late organism Trypanosoma cruzi , which is

marked by prolonged high fever, edema, and enlargement of the spleen, l iver , and

lymph nodes, and is compl icated by card iac involvement.

Fascicle:

a group of Purk in je f ibers too smal l to be cal led a “branch.”

Fibrosis: a condi t ion in which Purk in je f ibers are t ransformed into nonconduct ing interst i t ia l

f ibrous t issue.

Left anterior fascicular block:

a conduct ion abnormal i ty in the anter ior fascic le of the LBB.

Left posterior fascicular block:

to a conduct ion abnormal i ty in the poster ior fasc ic le of the LBB.

Lenegre's (Lev's) disease: both Lenegre and Lev descr ibed var iat ions of f ibrosis of the int raventr icu lar Purk in je

f ibers in the absence of other s igni f icant cardiac d isease.

Predivisional and postdivisional:

terms referr ing to b lock wi th in the LBB ei ther “pre-” or proximal to i ts d iv is ion into

fascic les, or “post- ” and involv ing both the anter ior and poster ior fasc ic les.

Primary and secondary T-wave changes:

in the presence of RBBB or LBBB, the term “pr imary T-wave changes” refers to

abnormal T waves that are d i rected s imi lar ly to the lat ter por t ion of the QRS complex,

and “secondary T-wave changes” refers to normal T waves that are d i rected opposi te

to the lat ter por t ion of the QRS complex.

Refractory period: the per iod fo l lowing e lectr ica l act ivat ion dur ing which a cardiac cel l cannot be

react ivated.

RR interval:

the per iod between successive QRS complexes.

Septal Q wave:

a normal , in i t ia l ly negat ive QRS waveform that appears in le f tward-or iented ECG leads

because of ear l iest act ivat ion of the interventr icu lar septum via the septal fascic les of

the LBB.

Syncope:

a br ief loss of consciousness associated wi th t ransient lack of cerebral b lood f low.

Tachycardia-dependent BBB: RBBB or LBBB that is intermi t tent , appear ing only wi th an accelerat ion of the atr ia l

rate.

Trifascicular block:

an int raventr icu lar conduct ion abnormal i ty involv ing the RBB and both the anter ior and

poster ior fasc ic les of the LBB.

Unifascicular block:

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an int raventr icu lar conduct ion abnormal i ty involv ing only one of the three pr inc ipal

fascic les of the int ravent r icu lar Purkin je system.

REFERENCES 1. Wel lens HJJ, L ie KI , Janse MJ, eds. The conduct ion system of the heart : s t ructure,

funct ion and c l in ical impl icat ions. The Hague: Mart inus Ni jhof f , 1978:287–295.

2. Demoul in JC, Kulbertus HE. Histopatholog ical examinat ion of the concept of le f t

hemiblock. Br Heart J 1972;34:807–814.

3. Rosenbaum MB, El izar i MV, Lazzar i JO. The hemiblocks. Oldsmar, FL: Tampa

Tracings, 1970.

4. Rosenbaum MB. Types of le f t bundle branch b lock and thei r c l in ical s igni f icance. J

Electrocardio l 1969;2:197–206.

5. Er iksson P, Hansson PO, Er iksson H, Del lborg M. Bundle-branch block in a general

male populat ion: the study of men born in 1913. Circulat ion 1998;98:2494–2500.

6. Hindman MC, Wagner GS, JaRo M, et a l . The c l in ical s igni f icance of bundle branch

block compl icat ing acute myocard ia l in farct ion. I I . Indicat ions for temporary and

permanent pacemaker inser t ion. Circulat ion 1978;58:689–699.

7. Wi l lems JL, Robles De Medina EO, Bernard R, et a l . Cr i ter ia for in t raventr icu lar-

conduct ion d isturbances and preexci tat ion. J Am Col l Cardio l 1985;5:1261–1275.

8. Kle in RC, Vera Z, DeMar ia AN, et a l . E lectrocardiographic d iagnosis of le f t

ventr icu lar hypert rophy in the presence of le f t bundle branch block. Am Heart J

1984;108:502–506.

9. Hiss RG, Lamb LE. Electrocardiographic f indings in 122,043 indiv iduals. Circulat ion

1962;25:947.

10. Lenegre J. Et io logy and pathology of b i la tera l bundle branch block in re lat ion to

complete heart b lock. Progr Cardiovasc Dis 1964;6:409.

11. Lev M. Anatomic basis for at r ioventr icu lar b lock. Am J Med 1964;37:742.

12. Rotman M, Tr iebwasser JH. A c l in ical and fo l low-up study of r ight and lef t bundle

branch block. Circulat ion 1975;51:477–484.

13. Schneider JF, Thomas HE, McNamara PM, et a l . Cl in ical -e lectrocardiographic

corre lates of newly acquired lef t bundle branch b lock: the Framingham study. Am J

Cardio l 1985;55:1332–1338.

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14. Lasser RP, Haf t J I , Fr iedberg CK. Relat ionship of r ight bundle-branch block and

marked lef t ax is deviat ion (wi th le f t par ieta l or per i - in farct ion b lock) to complete heart

b lock and syncope. Circulat ion 1968; 47:429–437.

15. Pick A, Langendorf R. Interpretat ion of complex arrhythmias. Phi ladelphia: Lea &

Febiger, 1979: 314–317.

16. Acquatel la H, Catal io t i F, Comez-Mancebo JR, et a l . Long term contro l of Chagas

disease in Venezuela: ef fects on serologic f indings, e lectrocardiographic abnormal i t ies

and c l in ical outcome. Circulat ion 1987;76:556–562.

17. Hindman MC, Wagner GS, JaRo M, et a l . The c l in ical s igni f icance of bundle branch

b lock compl icat ing acute myocard ia l in farct ion. I . Cl in ical character is t ics, hospi ta l

morta l i ty, and one-year fo l low-up. Ci rculat ion 1978;58:679–688.

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