The electrocardiogram in patients with pacemakers

The Electrocardiogram

in Patients

with Pacemakers

By AGUSTIN CASTELLANOS. JH., Jam M. ORTIZ, NICHOLAS PASTIS mD CEMR CASTILLO

E

LECTRONIC PACEMAKERS have been used primarily for the correction of life-threatening arrhythmias .I In addition, their use has provided secondary gains which have increased our knowledge of clectrophysiological events occurring in man213This information has been more direct than that obtained from extrapolation of animal experiments to the human heart. The majority of studies dealing with pacemaker electrocardiography have referred mainly to iatrogenic electrical arrhythmias. Less emphasis has been placed on the morphology of the pacemaker-induced QRS and ST-T changes. Analysis of the latter is of considerable academic and clinical importance as will be shown in this communication. Depolarization Changes Produced 1x1Ventricular Pacing Pacemaker-induced QRS changes are evaluated best during periods of complete A-V block when natural beats are absent; that is, when artificial stimuli are in total command of the ventricles. Pure beats produced by normally functioning electronic pacemakers consist of a stimulus artefact, or spike, and the corresponding ventricular response. The first step in the study of pacemaker electrocardiography consists in differentiating between the stimulus artefact and the QRS comples.“~4 Unless this is done correctly, serious conceptional errors can be made-which can lead to wrong clinical conclusions. Bipolar pacing yields small spikes in front of the usually well-delineated ventricular complexes. This occurs because both poles are within the heart itself, generally separated by a distance of 10 mm. On the other hand, during unipolar pacing, one electrode is inside the heart and the other on the body surface at a variable distance from the former, Unipolar spikes are generally of great amplitude and diphasic in nature.l Gersony et al. have stressed that the negative component is due to an electrical overshoot which is a function of the magnitude of the spike as received by the recording instrument.” It appears that the overshoot is directly proportional to the initial voltage and, when large enough, call make the identification of the onset of depolarization rather difficult. At times the QRS complexes are very small, or even completely masked by the spike. ..~--~

From Veterans

the University Administration

ACUSTIN

of Miami

School of Medicirz, Hospital, Miami, Fla. CASTELLANOS, JH. IvI.D.: Assistant Professor

~--~

~-

Department

Medicine,

of

of Medicine,

Unit;ersify

-_.

~. .-~~~~-

and

the

of Miami

School of Medicine; Chief, Division of Electrophysiology, Veterans Administration Hospital, Miami, Flu. JUAN nl. OHTIZ, k1.D.: Fellow in Cardiology, Veterans Administration Hospital, Miami, Fla. NICHOLAS PASTIS, R1.D: Fellow in Cardiology, Vetreans Administration Hospital, Miami, Flu. CESAR CASTILLO, M.D.: Assistant Professor of Medicine, University of Miami School of Medicine; Chief, Cardioptdmonary Laboratory, Veterans Administration Hospital, Miami, Fkz. 190

PRWRESS IN CAIIDIOVASWLAR DISEASES, \'oL. XIII,

No.

2 (

SEPTEMBEH), 1970

ELECTROCARDIOGRAM

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aVR

aVL

aVF

Fig. L-Right Ventricular Apical Pacing (RVAP). There is complete left bundle branch block (CLBBB) pattern associated with abnormal left-axis deviation (ALAD). Stimulus artefact should not be included in measurement of .&QRS of paced beats.

The size of the spike is not a function of the stimulating current but of the interelectrode distance. Its spatial orientation is influenced fundamentally by the position (on the body surface) of the positive pole. Different orientation

I

aVR

aVL

aVF

V6

Fig. 2.-Right CLBHB pattern

ventricular pacing between apex and outflow tract. is present, electrical axis not abnormally deviated to left.

Although

Fig. 3.-Right ventricular with right-axis deviation.

outflow

tract pacing. CLBBB

pattern now associated

will occur when the latter is in the right axilla, left axilla or abdomen. Unipolar pacing is best monitored from leads which arc perpendicular to the spatial axis of the spike. The orientation of the vectors of biporal spikes is that of rr line connecting the distal (negative ) and prosimal (positive) elcctrodrs.”

Right Ventricular

Stimulation

Classically, right ventricular pacing (either from the endocardium or epicardium) produces a complete left bundle branch block (CLBBB) pattern (Figs. l-3). The following sequence of events is observed when a catheter is advanced from the atria into the ventricles. First, when the tip is in the inflow tract, the electrical axis is normal. Abnormal left axis deviation occurs when stimulation is performed from the apex (Fig. 1). A normal axis again appears as the electrodes are moved toward the outflow tract (Fig. 2) .i Immediately below the pulmonary valves, a vertical axis or even right-axis deviation results (Fig. 3).

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Lead V6 and the frontal plane vectorcardiogram (obtained with the Frank system) have to be interpreted with caution in patients with right ventricular apical pacemakers.3.c If there is extreme left-axis deviation, both V6 and the X component of the vectorcardiogram can record a negative deflection,” which only indicates that the main forces are moving away (in this case superiorly) from the horizontal level in which these leads arc located. A CLBBB pattcm will not appear in V6, although it will be present in leads I and nVL. Hence, a ncsgative deflection in V6 cannot be identified with rightwards deviation of the electrical axis in the presence of abnormal left-axis deviation (ALAD). Moreover, the frontal planc maximal vector will be deviated superiorly and to the right, since both X and Y components record a negative deflection. Therefor{,, the frontal loop is artefnctual since the major forces arc moving to the left (and of course superiorly) and not to the right. At times, right ventricular apical pacing produces a true superior and rightward axis (Fig. 4) .I) In these cases, in contrast to those in which the classical pattcm is seen (Figs. 1 and 2), lead I is negative and aVL is still positive. Of c’oursc, Vl will show a predominant ncgativc deflection.

Left

Ventricular Stimulation

Left vcmtricular pacemakers usually produce right-axis deviation and a complete right bundle branch block ( CRBBB ) pattern.“~~~9-1:’ Leads I, aVL and V6 record a predominantly negative deflection. An R wave is seen in aVF and VI

I

II

III

aVR

aVL

aVF

Fig. 4.-Unusual (indeterminate) axis recorded during right ventricular apical pacing. Electrical forces are deviated superiorly, to left and posteriorly. Note aVL shows positive deflection.

V2

V3

AVR

AVL

AVF

V4

V5

V6

Fig. 5.-Left ventricular pacing produces right-axis deviation and complete right bundle branch block (CRBBB) Morphology. This is usual pattern obtained from patients with implanted epicardial pacemakers. (Fig. 5). Implantation is usually performed in the mid-to-high lateral portions of the left ventricle. However, when the electrodes are placed closer to the apex, an Sl-S2S3 pattern will result (Fig. 6). A positivity in Vl suggests left ventricular pacing; but when VI is negative, as shown in Fig. 3, Chapter I of the book by Castellanos and Lemberg,:’ it becomes impossible to determine whether the electrodes are (low) in the right or left ventricles. Transvenous pacing can induce QRS changes similar to the ones described as suggestive of left ventricular pacing. Stimulation from the more proximal parts of the coronary sinus (middle cardiac vein?) produces a predominant positivity in VI and V6, thus resembling WPW type A.:J,‘.1:‘.14R When the catheter is within the branches of the coronary sinus (great cardiac vein) or has perforated the anterior wall of the right ventricle and the extruded tip touches the epicardium of the left ventricle, pacing can produce the typical image of left ventricular stimulation, although the current is delivered through a transvenous catheter .3,4.14bA change from a CLBBB pattern to a CRBBB need not indicate perforation of the interventricular septum. This possibility was entertained in a recent article (without necropsy corroboration), but the position of thmecatheter in the X ray is more in keeping with pacing within a coronary sinus branch.lj Mower ct als have also observed right-axis deviation during right ventricular pacing.lO These authors postulated that the impulse could stimulate the specialized tissue in the right side of the heart, propagate in a retrograde direction to the A-V node,

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aVR

aVL

aVF

V6

Fig. K-Unusual pattern obtained from left ventricular apical pacing. Electrical axis points superiorly and to right. However, \‘I shows positive deflection (CRBBB pattern).

finally descending via the left branch to produce initial depolarization of the nonspecific myocardium on the left septal smface. It should be stressed that this assumption requires the following requisites: (a) that the impulse activate, exclusively, the right-sided Purkinjc system and not the ordinary myocardium; (b) the existence of functional longitudinal dissociation of the His bundle and or the A-V node (to allow retrograde conduction followed promptly by forward conduction through these structures): and (c) that initial left ventricular stimulation should invariably produce right-a,xis deviation. An alternative explanation was also offered by Mower et a1.l” They applied Sodi-Pallares’ earlier concepts of the structure of the interventricular septum.l” This author believed that parts of the anatomical right septal surface behave, electrically, as the left septal surface. Therefore, stimulation of these portions of the septum would produce patterns similar to those seen during initial activation of the left side of the heart. Clinical Applications Knowledge of the typical and atypical patterns produced by transvenous pacers is important to determine the site of the stimulating electrodes. A CRBBB pattern during transvenous stimulation should always raise the possibikty of coronary sinus pacing. Catheter malposition, although rare during permanent pacing, is not unusual when transient pacing is being performed. The intracardiac electrocardiogram can aid in locating the position of the catheter tip when the patient is in sinus rhythm, but is not of much

196

CASTELLANOS

El’

AL.

help if complete A-V block or idioventricular rhythms are present. Although the analysis of the various QRS patterns is helpful in determining the situ of stimulation, a definite conclusion should not be reached unless a hand-by-hand electroradiological correlation is performed. The influence that extensive acute or chronic infarction can have on the pacemaker-induced QRS complexes has not been evaluated and awaits further studies. AQRS

of

Ventricular

Extrasystoles

According

to M. B. Rosent)aum17~‘3

This author believes that the superior or inferior orientation of ventricular extrasystoles does not depend on their apical or basal origin (as presented in this communication), but as to whether they activate first the anterior or posterior wall of the left ventricle. This concept is based on the assumption that an ectopic beat originating close to the posteroinferior division of the left branch produces an image of CRBBB and block of the superior division of the left bundle branch (BSDLB). On the other hand, an extrasystole arising close to the anterosuperior division should resemble the pattern of CRBBB coexisting with block of the inferior division of the left bundle branch (BIDLB ). According to Rosenbaum, an apical (left ventricular) beat should produce forces directly posteriorly, its inferior or superior orientation depending on whether activation reaches the posterior or anterior wall first. We agree with Rosenbaum’s criteria for interpreting the origin of extrasystoles arising in the left ventricle at or close to the Purkinje network of the divisions of the left branch. Yet it becomes difficult to understand how a beat originating from a catheter electrode impinged in the apex of the right ventricle can produce an inferior axis, if there is practically no significant muscle mass below the electrode. Rosenbaum’s concept might apply to left ventricular pacemakers, considering that the anterior and posterior wall of this ventricle are really anterosuperior and posteroinferior. Anatomists usually use the terms “anterior” and “inferior” when referring to the divisions of the left branch. However, from the electrophysiological point of view, they behave as superior or inferior, since block in these structures tends to produce an inferior or superior axis shift and not changes in the anteroposterior direction. That is the reason why the characteristic patterns of left divisional blocks (hemiblocks) ‘;.I’ are seen in the frontal plane and not in the horizontal plane. Further research is needed to determine the types of QRS changes produced by endocardial stimulation of different left ventricular sites. Other QRS Patterns

Res8embling Pacemaker

Beats

The CLBBB pattern produced by right ventricular pacemakers is not identical to the one recorded in patients with sinus rhythm and CLBBB. Yet, except for an initial delay which almost invariably accompanies pacemaker beats, the resemblance is close enough to consider that the mechanism of CLBBB postulated by So&-Pallares et al. requires reevaluation.‘c These considerations, however, are beyond the scope of this paper. The diagram

on Fig. 7 shows

various

patterns

which

resemble

“classical”

ELlXXROCARDIOGRAM

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Fig. 7.-Frontal plane vectorcardiograms resembling right ventricular (apical) and left ventricular (epicardial) pacing. Left. (A) RVAP showing CLBBB morphology (with initial delay) and ALAD. During sinus rhythm this pattern has also been attributed to Wolff-Parkinson-White (WPW) coexisting with CLBBB (B) CLBBB with ALAD. (C) Hyperkalemia. (D) BSDLB with focal block. (E) Fusion WPW type B with ALAD. Right. (F) Left ventricular epicardial pacing showing CRBBB morphology (with initial delay) and RAD. Pattern has also been attributed to WPW coexisting with RBBB. (G) CRBBB + RVH. (H) CRBBB + BIDLB. (I) Fusion WPW type A with RAD. (J) E x t ensive posterolateral myocardial infarction with CRBBB. As suggested by Rosenbaum, 4B it is possible that loops similar to (A) and (F) could be seen in patients with WPW syndrome during what Durrer et al.‘” call “exclusive or predominant” Kent bundle conduction.

cndocardial apical right ventricular [ abnomlal left-axis deviation (ALAD) with prolonged intraventricular conduction time] and epicardial left ventricular (right axis deviation with prolonged intraventricular conduction time) pacing. As mentioned before, QRS complexes resulting from right ventricular apical pacing (RVAP) are similar to the ones seen in cases of CLBBB with abnormal left-axis deviation. The latter is defined as an axis between -30 and -90°. At present there are no uniform criteria as to how to classify the tracings showing sinus rhythm and “complete” left bundle branch block

ADVANCED

A-V

BLOCK

-

CLBBB

ALSO

PRESENT

Fig. B.-Implanted left ventricular pacemaker in patient with sinus rhythm and exclusive His bundle conduction. ALAD was attributed to BSDLB. Spikes falling in absolute refractory period (up to 0.32 sec. after onset of sinoatrial QRS complex) are ineffective. Those falling in relative refractory period (0.34 sec.) produce QRS complex different (negative in Vl) than other pacemaker beats (positive in Vl).

with ALAD. Some authors attribute this pattern to a simultaneous presence of block in the “trunk” of the left branch and in its anterosuperior division.” According to others, this double conduction disturbance cannot bc diagnosed electrocardiographically.‘o CLBBB with ALAD can be due to an abnormal (anatomical) position of the heart. The possibility that the impulse emerging from the unblocked right branch could “exit” at different septal levels should be evaluated. According to Rosenbaum et al., the association of left bundle branch block with ALAD suggeststhat, irrespective of QRS duration, an “incomplete” block of the trunk of the left bundle coexists with a block in the anterosuperior division (BSDLB ) .1s,21These authors have shown tracings with this combination in which the AQRS became normal after a further increase in the QRS complex; that is, when the block which appeared to be “complete” (but which was incomplete) became really complete. Although a BlSDLB produces ALAD, the QRS duration usually does not exceed 0.10 seconds.l”,‘” A BSDLB resembles the pattern of right ventricular apical pacing ( RVAP), if it is associated with a focal or myocardial fiber block which increases the QRS duration to over 0.12 seconds.22This pattern can also be simulated by that of WPW type B with ALAD.Z3-26 On the contrary, WPW type A with RAD is similar to the classical pattern produced by left ventricular pacemakers ( LVP),23-22 This type of QRS morphology can also be seen in patients with sinus rhythm and CRBBB, provided that the latter is distorted by the various factors which can deviate the axis to the right when CRBBB is present,1x,1gj’7-31 namely: (a) right ventricular hyper-

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Fig. 9.-Different types of fusion beats result when ventricles are depolarized from two different sites. Since both conducted and pacemaker beats have prolonged QRS complexes, fusion beats tend to shorten duration of depolarization. (Same patient as in Fig. 8.)

trophy; (b) block in the posteroinferior division of the left branch; and (c) cxtensive posterolateral infarction. Fusion Beats It is important to recognize that the morphology and AQRS of pacemakerinduced QRS complexes can change even when the stimulating electrodes remain in the same position. 3 In lead III this is a normal phenomenon due to respiratory movements and these physiological variations should not be taken as evidence of pacemaker malfunction. Artificial stimuli falling in the relative refractory period of an antecedent T wave can produce irregular ventricular propagation due to inhomogenous intraventricular conduction.” Hence, spikes appearing in the descending portion of the previous T wave can trigger QRS complexes of different morphology than that of beats initiated in late diastole. These changes are occasionally so marked that even the positive QRS complex in lead Vl (resulting from left ventricular pacing) have been transformed into a predominant negative deflection in this lead (Fig. 8) .3,4J3In addition, the morphology of a pure pacemaker beat varies when it “fuses” with a naturally occurring ventricular complex.3 Morphological QRS changes due to relative refractoriness and to “fusion” should be interpreted as such and not attributed to pacemaker failure. Moreover, the location of the pacing site cannot be made from these impure beats. Fusion beats are frequent during competition between a sinoatrial and continuous asynchronous paccmakers.“s3 In Fig. 9 the sinus beats show a CLBBB morphology (A) in Vl. Left ventricular pacing (LVP) produced a CRBRB pattern

(H

and

I)

in the same lead.

In this

case the fusion

beats

make

the

QRS duration more normal since the degree of asynchronous activation produced by the sinus beats (with CLBBB ) and by the ectopic left ventricular pacemaker is reduced (B through G) when the ventricles are activated more

i

I

Fig. lO.-His bundle electrograms recorded at onset of right ventricular apical pacing in patient with sinus (S) rhythm. Significance of abbreviations is as follows: F = fusion beat; ST = stimulus artefact; HBE = His bundle electrogram; H = His bundle deflection; UVE = unipolar ventricular electrogram. or less at the same time from two different sites. Note that fusion beats appear even when the spikes fall after the onset of the sinoatrial QRS complex. This occurs as long as the activation front propagated from the right septal surface (during CLBBB activation of the latter has precedence over that of the left septal surface) reaches the perielectrodes tissue before the pacemaker discharges. The interval between the onset of the QRS complex and last spike which produces a fusion beat is a measurement of the right to left (forward) intraventricular conduction time.3’-3R In addition, spikes falling in the terminal portions of the P-R interval also produce a fusion beat. (F and G). The interval between the P wave and the spike which produces the last pure CRBBB beat represents the time spent by the sinus impulses in traveling down through the ventricles and being unable to activate the site at the right septal surface which had just been rendered refractory by the impulse produced by the artificial pacemaker. The left-to-right retrograde conduction time can be obtained by substracting the corresponding P-to-spike interval from the basic P-R interva1.3z-3S The usefulness of the method of His bundle recordings (introduced by Scherlag et al.) can be extended to the understanding of fusion beats.39-42For instance, Fig. 10 shows three different types of QRS complexes. The first and last are pure sinus, and right ventricular apical pacemaker beats, respectively. The latter shows ALAD. The second ventricular complex is a fusion beat in which the ventricles are activated, in part, by the supraventricular. and in part, by the edopic ventricular, impulse. The stimulus artefact occurs IO

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msec. before excitation of the His bundle (H). A fusion beat is possible since the depolarizing wave propagating through the His bundle reaches th(> left side of the septum ahead of the artificial stimulus produced by thr right ventricular pacemaker. A fusion beat cannot occur if the impulse descending through the His bundle finds that the first area that it would normally have activated (in the left septal surface) had been rendered refractory by the excitation wa\‘e produced by the pacemaker. This occurs if the right-to-left (in this case, transeptal) conduction time is shorter than thus normal H-V interval measured from the onset of the H deflection to c3rliest site of ventricular activation. Jn Fig. 11 (same patient) the stimulus artefact was delivered 50 msec. ahead of the His bundle deflection. A fusion beat did not result because the artificially induced stimulus had activated the left side of the septum ahead of the impulse propagating through the His bundle and the latter. therefore. could not depolarize any portion of the ventricles. Classical examples of “fusion” beats are seen in patients with WPW syndrome when the ventricles are activated by impulses conducted via His and Kent bundles.43-*” His bundle recordings have been most valuable in these casc~s. The electrocardiograms shown in Figs. L-9 14 were obtained from a

ISt UVEJ--+-

St

.6 I H ;I

HBE&#’ Fig. Il.-Fusion beat did not occur with stimulus artefact delivered on top of P wave. (Same patient as in Fig. 10.)

502

CASTH,I,ASOS

El’

AI,.

III Fig. le.-Atria1 flutter (or fibrillation) exclusive His bundle conduction. ALAD

in patient with WPW syndrome was attributed to BSDLB.

during

I-

Fig. 13.-Fusion WPW beat (left) and exclusive or predominant kent bundle conduction after premature atria1 conkaction (PAC). High bipolar right atria1 lead (BAE) also recorded. (Same patient as in Fig. 12.)

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III

I i PBAE-p-+vk

p+

:

c I.

,

Fig. 14.-Pacing from outfiow tract of right ventricle shows similar morphology than one attributed to exclusive Kent bundle conduction (last QRS complex in Fig. 13). During sinus rhythm (P+), P wave is biphasic in bipolar lead obtained from upper portion of right atrium (BAE). Its onset preceeds that of low right atria1 (HBE) lead. Reverse true during retrograde conduction: P wave in BAE is inscribed after one in HBE. (Same patient as in Fig. 12.)

40-year-old male with WPW type A. Other tracings from this patient have been presented elsewhere.“” Exclusive (normal) conduction through the His bundle occurred mainly in the presence of atria1 fibrillation (Fig. 12). The AQRS of the corresponding ventricular complexes showed ALAD and fulfilled the criteria for BSDLB.l” During sinus rhythm the AQRS was around +60° (Fig. 13). The inscription of the H deflection almost coincided with that of the delta wave in lead II. This finding suggested that the ventricles were depolarized through both (Kent and His) bundles. 13A fusion beat resulted because the activation from the preexcited area reached the left ventricle after parts of the latter had been depolarized by the impulse descending through the His bundle. In the presence of iatrogenic or spontaneous premature atria1 contractions (Fig. 13, right) the H deflection appeared 30 msec. after the inscription of the delta wave, indicating that the ventricles had been preexcitated ahead of the His bundle.‘” In addition, the ventricular complex was wider and more bizarre. Both, AQRS and delta wave showed right-axis deviation. This beat was considered as representative of predominant or exclusive Kent bundle conduction.45 Thus, three types of QRS complexes were seen in this patient: (a) beats with right-axis deviation representing predominant or exclusive Kent bundle conduction; (1~) beats with left-axis deviation representing exclusive conduction through the

His bundle; and (c) fusion beats with a normal axis resulting from vcntriculai activation via Kent and His bundles. Three types of QRS con~p1exes arc also seen in Fig. 14. Thch last one is a fusion beat, as described previously. The second beat in this figure is a “His bundle” escape in which the sinus P wave appears “sandwiched” between the His bundle and ventricular deflections. The first QRS complex is the last of a series of pure pacemaker beats produced by stimulation of the outflow tract of the right ventricle. It shows right-axis deviation with a morphology similar to the one ascribed to predominant or exclusive Kent conduction (second ventricuIar complex in Fig. IS). This indicates that the ventricles were probably stimulated close to the area of preexcitation. However, since right-axis deviation can be seen during pacing of the right ventricular outflow tract (Fig. 3), as well as during left ventricular pacing ( Fig. 5 ) , no definite conclusions can be drawn in the absence of Vl. It is possible for the morphology and AQRS of an impulse propagating from the preexcitated area during exclusive Kent conduction to bc very similar to that produced by pacing from the same site (Rosenbaum) .46 This being the case, the exclusive initial delay characteristic of (fusion ) WPW complexes may be associated with diffuse delays resembling the pattern (which during sinus rhythm) has been ascribed to simultaneous coexisting WPW and bundle branch block.*‘-” Similar patterns are seen in pure pacemaker beats.g Fusion

Beats Produced

by Demand

and Synchronized

Pacemakers

Implanted ventricular-inhibited demand pacemakers are reset by the faster is due to the sensing natural complexcs.~” Resetting (the onset of inhibition) of an htracardiac signal; hence it need not occur at the beginning of ventricular depolarization in a peripheral lead. In consequence when the natural and artificial rates are similar, ventricular-inhibited pacemakers can produce fusion beats if the pacemaker discharges occur after the beginning of the QRS complex, before resetting has occurred.s1 Generally, the P-to-spike interval of patients with atrial-triggered pacemakers is shorter than the normal atrioventricular conduction time. Fusion beats appear if the P-to-spike interval and the P-R interva1 (of beats propagated via the A-V junction) are in the same range.“” This artificial arrhythmia resembles a WPW fusion beat in which A-V conduction occurs through the His and Kent bundle. The atrial-synchronized pacemaker behaves like an artificial Kent bundle.” Fusion beats can be seen when patients with ventricular-triggered pacemakers”3 are in sinus rhythm, if the interval between the onset of ventricular depolarization and the emission of the spike is short enough to allow the latter to occur before the onset of the refractory period of the perielectrode tissues.” Pseudofusion

Beats and Pseudo Currents

of

injury

A distortion of the ventricular complexes can occur when large unipolar spikes fall after the onset of the absolute refractory period,” even when the ventricles are not activated. In these cases the abnormal QRS complexes are

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not true fusion beats since they do not result from the more-or-less simultaneous activation of the ventricles by two centers. On the contrary, these beats are artefactual since they are produced by the effects (electrical overshoot) of the large unipolar spikes on the electrocardiographic recorder. According to Spitzer et al., 54 this is a “pseudofusion” beat which results from a pacemaker artefact superimposed on a supraventricular conducted beat superficially resembling a (true) fusion beat, The electrical overshoot can be long lasting, even extending to the ST segment.:’ This is the mechanism of false currents of injury in patients with ventricular-triggered pacemakers. 3 The resulting ST-T changes should not be attributed to injury due to coronary artery disease or pericarditis.“5*“6 On the contrary, true ST segment changes due to acute myocardial injury can indeed be seen during bipolar pacing in some patients with acute myocardial infarction. SUMMARY

A study of the pacemaker-induced ventricular complexes can be of help in determining the site of stimulation. The first step consists in separating the stimulus artefacts from the QRS complexes. Right ventricular pacing usually produces a complete left bundle branch block ( CLBBB ) morphology. The electrical axis can be left, normal or even right, as pacing is performed from the apex to the outflow tract. Rarely an Sl-X-S3 pattern (with negative deflection in Vl and V2) appears during right ventricular apical pacing. Left ventricular stimulation usually produces a right bundle branch block pattern with inferior and rightwards deviation of the AQRS, although a superior axis is rarely seen with inferior stimulation. In the absence of pacer failure the basic QRS morphology produced by late diastolic stimuli can change if: (a) there are significant respiratory moverncbnts; (b) stimulation occurs during the relative refractory period; and (c) fusion beats occur. The classical Wolff-Parkinson-White beat was interpreted as a fusion beat, as long as exclusive Kent bundle conduction was not present. In the latter instances pacin, 6 from the preescited area appeared to have produced similar QRS complexes. DEFINITIOXS

AND

ABBHEVIATIONS

ALAD: Abnormal left axis deviation (between -30 and -90’). ATRZAL-TRZGGERED PACEMAKER: Pacemaker triggered by the P wave. Spikes will appear even when P waves are absent. Artificial refractoriness has ranged between 400 and SO0 msec. in different models. RAE: Bipolar atria1 electrogram obtained when the catheter is close to the superior vena cava. This lead records the activity of the “high” right atrium. BZDLB: Block in the inferoposterior subdivision of the left branch; also known as left posterior hemiblock ( LPH) . BIPOLAR PACING: Pacing performed with the two poles (positive and negative) located within the heart itself. BSDLB: Block in the anterosuperior subdivision of the left branch, also known as left anterior hemiblock (LAH). is conduction disturbance has Th

also been called: hc~miblock, farction block, etc.

left superior

intravc~ntricular

block.

CLBBB PATTERN: Morphology of pacc~makcr-illdu~(!~l beats showing tive defection in VI and a predominant K wave in V6. The ,iQRS normal, or deviatrd to the left ( rarely to the right).

ptriina negacan be

CRBBB PATTERN: Morphology of pacemaker-induced beats showing rightwards deviation of the electrical forces with a prc~dominant positive deflection in lead Vl. CONTlNUOIrS ASYNCHRONOLr.5 PACEMAKER: Pacemaker which is constantly delivering impulses to the heart. The spikes are neither synchronized nor inhibited by natural beats. This term is preferred to the commonly used “fixed rate.” FOCAL BLOCK:

A block occurring distal to the Purkinje system.

FORWARD INTRAVENTRlCULAR CONDllCTZON TIME (FCT): Interval spent by the depolarizing wnvcx in propagating from the first ventricular site to be activated by the supraventricular impulse to the perielectrodes tissues. FUSION BEAT: QRS complex resulting from the more-or-less simultaneous activation of the ventricles from two or more sites. HBE: Bipolar lead recording the His bundle elcctrogram. This lead also records the activity of the “low” right atrium. PSEUDOFUSION BEAT: Stimulus artefact superimposed on a natural beat resembling a true fusion beat. However, the QRS distortion results from the electrical overshoot in the recorder and not from ventricular activation from two or more sites. PSEUDOCURREWT OF INJURY: ST segment changes resulting from the electrical overshoot produced by the spike. RAD: Right axis deviation; an axis between +llO and + 180’. RETROGRADE ZNTRAVENTRZCULAR CONDUCTION TlME (RCT): Interval spent by the depolarization wave to travel from the perielectrode tissues to the first part of the ventricular muscle activated by the supraventricular impulses. SECONDARY GAINS: Information regarding electrophysiological events in the human heart obtained from the use of electronic pacemakers. UNIPOLAR PACING: Pacing performed with one pole (negative) within the heart and the other pole (positive) at variable distances on the body surface. VENTRICULAR-INHIBITED DEMAND PACEMAKER: Pacemaker reset by natural beats and whose refractory period is not clinically significant. VENTRICULAR-TRIGGERED PACEMAKER: Pacemaker, triggered (not inhibited) by the ventricular complexes. The spikes will appear during the absence of natural beats. Artificial refractoriness has ranged between 400 and 500 msec. in different models.

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alIt left

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ELECTROCARDIOGRAM

IN

PATIENTS

WITH

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