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Mechanisms in reciprocal rhythm∗
Review Mechanisms in Reciprocal I
LEO SCHAMROTH, M.D. (Rand),
F.R.C.P. (Edin.)?
Lexington,
Rhythm* J
AND KARL F. YOSHONIS M.D.~
Kentucky
Reciprocal rhythm is defined and the mechanisms described in 2 cases. Reciprocal rhythm can occur with impulses of atrial, A-V nodal, or ventricular origin. Two separate A-V nodal pathways are an essential prerequisite. The two pathways may communicate with each other in the upper or lower parts, or both, of the A-V node to form upper or lower common pathways, or both. Reciprocal rhythm can occur in the presence of both upper and lower common pathways; it can also occur in the absence of a common pathway. The time of inscription of the “retrograde” P’ deflection does not necessarily reflect the return level of the reciprocal mechanism. An atria1 bridge is not an essential link in the reciprocal circuit. Unidirectional block in one of two pathways is necessary for the initiation of reciprocal rhythm. The nomenclature is reviewed.
R
with each other in both the upper and lower parts of the node to form upper and lower common pathways (Fig. 2B). 3. The pathways may be separated from each other in the lower A-V node and communicate in the upper part of the node to form an upper common pathway (Fig. 2C). 4. The pathways may be separated from each other throughout the entire A-V node. There is therefore no communication between the two pathways and consequently no common pathways are present (Fig. 2D).
ECIPROCAL RHYTHM may be defined as a rhythm wherein the atria1 or ventricular chamber § is activated two or more times by the same impulse. This occurs when an impulse arising in the sinus node, atria, atrioventricular (A-V) node or ventricles activates the atria1 or ventricular chamber but during its passage through the A-V node also enters another A-V nodal pathway, which permits the impulse to return to activate the same chamber once again (Fig. 1). There must therefore be at least two separate pathways within the A-V node. These pathways may communicate to form a common pathway, and there are four possible variations of their interrelation (Fig. 2). 1. The pathways may be separate from each other in the upper A-V node and communicate in the lower part of the node to form a lower common pathway (Fig. 2A). 2. The pathways may be situated in the middle of the A-V node and communicate
TYPES OF RECIPROCAL RHYTHM Reciprocal rhythm may, on the basis of impulse origin, be divided into three types (Fig. 1) : (1) reciprocal rhythm with impulses of sinus or atria1 origin; (2) reciprocal rhythm with impulses of A-V nodal or junctional origin; and (3) reciprocal rhythm with impulses of ventricular origin.
0 Electrophysiologically the two atria act as a functional unit and will be referred to as the atria1 chamber. Similarly, the two ventricles act as a functional unit and will be referred to as the ventricular chamber.
RECIPROCAL RHYTHM WITH ATRIAL
IMPULSES
OF
ORIGIN
In this type, a sinus or atria1 impulse activates
* From the Department of Medicine, Division of Cardiology, University of Kentucky, Lexington, Ky. Manuscript received August 9, 1968. t Visiting Professor of Cardiology. Present address: 155 Barry Hertzog Ave., Emmarentia, Johannesburg, South Africa. 1 Postdoctoral Fellow, U. S. Public Health Service Grant HE 05771. Address for reprints: Karl F. Yoshonis, M.D., Department of Medicine, Division of Cardiology, University of Kentucky, Lexington, Ky. 40506. 224
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Figure 1. Diagrammatic rejwesentationof reciprocal rhythm. Type 1, ventricular origin; Type 2, A-V nodal origin; Type 3, atria1 origin.
the atria1 chamber, resulting in the P wave, and is then conducted anterograde through the A-V node to activate the ventricular chamber, resulting in the QRS complex. During its passage through the A-V node, the impulse also enters another A-V nodal pathway and is conducted retrograde to activate the atria1 chamber once again, thereby resulting in a “retrograde” P wave-P’ (superiorly orientated frontal plane P wave axis). The sequence P-QRS-P’ is known as an atria1 echo1*2 (Fig. 1[3]). The sinus impulse during its passage through the A-V node thus divides into two activation frontsone continuing anterograde to activate the ventricular chamber, and the other returning retrograde to activate the atria1 chamber a second time. The return point, that is, the point or level at which the excitation front divides, will be termed the d point. Criteria for Diagnosis: It is difficult to prove the diagnosis of reciprocal rhythm with impulses of atria1 origin, for it may be argued that the P’ deflection represents an atria1 extrasystole and not retrograde atria1 activation.3 However, the diagnosis of this form of reciprocal rhythm has hitherto been suggested by the following criteria: 1. The presence of A-V nodal extrasystoles or A-V nodal escape beats with “retrograde” P’ deflections of the same shape and size as the P ’ of the postulated atria1 echo.4 This strongly suggests that the P’ deflection following the sinus P wave must also be the result of retrograde activation. 2. The P’ deflection of an atria1 echo only follows a long or relatively long P-R interval.4v5 The long P-R interval is necessary to allow the atria1 chamber sufficient recovery time before the arrival of the returning impulse. Such selective linkage would be very fortuituous in the case of true atria1 extrasystoles. Illustrative Case: The following case demonstrates further criteria for the diagnosis of reciprocal rhythm with impulses of atria1 origin, VOLUME
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Figure 2. Diagrammatic representationof the possible interrelation of two A-V nodal pathways within the A--V node (shaded area).
and, in addition, reveals other factors pertaining to the mechanisms of reciprocal rhythm. CASE 1. The electrocardiogram (Fig. 3) was recorded from a 50 year old woman who complained of occasional palpitations. There was no evidence of heart disease. The tracing (a continuous strip of standard lead II) shows paroxysms of tachycardia. Each paroxysm begins with a normal sinus P wave and continues with a tachycardia that is related to an abnormal P wave-the P’ deflection. The paroxysms are always terminated by a ventricular extrasystole. The P-R interval measures 16.* The first R-P’ interval of each paroxysm measures 34. All subsequent R-P’ intervals are slightly longer and measure 38. Ventricular extrasystoles occur during the paroxysms. Each ventricular extrasystole which occurs during a paroxysm is followed by a P’ deflection of the same shape and size as the P’ deflection associated with the normal QRS complexes (Fig. 3 to 6). Each ventricular extrasystole disturbs the P’-P’ rhythm. Thus, the sum of two consecutive P’-P’ intervals which do not include a ventricular extrasystole measures 100, whereas the sum of two consecutive P’-P’ intervals that include a ventricular extrasystole is slightly shorter and measures 92 (Fig. 5). The R to P’ time relation is nevertheless maintained (when allowances are made for the slightly increased width of the ventricular extrasystolic QRS complex; see later): the R-P’ interval of a normal QRS complex measures 34; the R-P’ interval of a ventricular extrasystole measures 40. It is evident that there is no compensatory pause following the ventricular extrasystole and that the P’ deflection following the extrasystole is also premature and must
* All time intervals are expressed in hundredths of a second.
Schamroth
226
FiKurc 3. Case 1. a&al origin.
Elechcardiogram
and Yoshonis
(strips of standard lead II) showing paroxysms of reciprocating
be related to the extrasystole. Furthermore, when two extrasystoles occur consecutively, the P’ deflection following each extrasystole is likewise premature. This R to P’ relation of the extrasystoles was always present in numerous observations. It is clear therefore that the P’ deflection must result from retrograde activation of the atria1 chamber by the extrasystolic impulse. And as all P’ deflections have the same configuration they must all result from retrograde activation, that is, the P’ deflection following the normal as well as the abnormal QRS complexes result from retrograde activation. This establishes the reciprocal origin of the P’ deflection following the normal QRS complex. The subsequent P’-R and
tachycardia
with
R-P’ intervals following the ventricular extrasystole remain constant unless disturbed once again by another ventricular extrasystole. The rhythm thus begins with a sinus impulse which is conducted to the ventricular chamber but also, during its passage through the A-V node, returns to activate the atria1 chamber once again, thereby constituting a reciprocal rhythm with impulse of sinus origin. The returning impulse is conducted anterograde once again, thereby initiating a reciprocating tachycardia (Fig. 5). When a ventricuiar extrasystole occurs, its premature impulse enters the retrograde pathway before the sinus impulse and continues the reciprocal rhythm which then becomes an example of
Figure 4. Case 1. Ekctrocardi~gram (continuous strips of simultaneous recordings from two esophageal leads) showing paroxysms of reciprocating tachycardia with atria1 origin. THE
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100
.
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l
A-V
V
Figure
5.
Case 1.
Electrocardiogram (esophageal
reciprocal rhythm with ventricular origin (Fig. 5). The reciprocal rhythm therefore begins with a sinus impulse and is interrupted and reset by a ventricular impulse which then continues the reciprocal mechanism. All the paroxysms are terminated by a ventricular extrasystole. This occurs when the ventricular impulse is relatively more premature and consequently encounters a refractory retrograde pathway that permits only partial penetration. Retrograde conduction is consequently blocked for the extrasystolic impulse, and this interferes with retrograde penetration of the succeeding sinus impulse, thereby terminating the reciprocal mechanism (Fig. 5). The shorter duration of the first R-P’ interval of each paroxysm is due to a pseudo-Wenckebach form of conduction, that is, the first retrograde impulse occurs after a long rest period and is therefore conducted with greater facility.
lead) with diagrammatic
analysis.
Comment: The reciprocal mechanism requires the presence of a dual conducting system within the A-V node. One pathway (pathway u) permits anterograde conduction, and another pathway (pathway b) permits retrograde conduction. Rosenblueth,6 Mendez et a1.7 and Moe and Mendez,s on the basis of animal experimenpostulated that the dual system is tation, situated in the upper regions of the A-V node and that a common pathway, termed the jinal common pathway,a is present in the lower regions of the A-V node (see Fig. 2A and 9A). Under these circumstances, the sinus impulse will begin its return journey at point d before its anterograde tricles
(Fig.
occurs
before
element 7A).
has
In other
the Ra
activated words,
complex
the
vcn-
the d point
is recorded
(Ra
Figure 6. Case 1. Electrocardiogram (simultaneous recordings of lead VI and an esophageal lead) showing two consecutive ventricular extrasystoles (labeled Rv) during a paroxysm of tachycardia. The P’ deflection following both extrasystoles is premature. VOLUME
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Figure 7. Diagrams illustrating the effect of a lower common pathway on the R-P’ interval resulting from (A) atria1 origin and (B) ventricular origin.
= QRS complex recorded by the complex sinus impulse). Furthermore, the longer the lower common pathway or the greater the delay in this pathway, the later the inscription of the Ra complex and the shorter the resulting Ra-P’ interval. This is in contrast to the situation resulting from retrograde activation of a ventricular impulse (Fig. 7B). The ventricular impulse must first activate the ventricular chamber (record-
Figure 8. Diagram illustrating the effect of no lower common pathway on the R-P’ intervals resulting from atria1 and ventricular origin.
Figure 9. Diagrams showing examples of various forms of reciprocal rhythm with different pathway interrelation. ing the Rv complex) and would only then be conducted through a potential lower common pathway (pathway c) before it can enter the retrograde pathway (pathway 6). The Rv-P’ interval is longer than the d-P’ interval and much longer than the Ra-P’ interval. Indeed, the ventricular extrasystolic impulse may be further delayed in the lower common pathway because this pathway has just been traversed by the preceding anterograde impulse and may, as a result, still be partially refractory. This will prolong the Rv-P’ interval even further. It is clear therefore that the R-P intervals resulting from sinus and ventricular impulses cannot be the same in the presence of a lower common pathway. In Case 1, however, both the Ra-P’ and Rv-P’ intervals are virtually the same. The slight discrepancy is due to the fact that in the case of the ventricular extrasystole the ventricles must be activated first i.e., the d point occurs after the beginning of ventricular activation, whereas in the case of the sinus impulse, the d point occurs before the beginning of ventricular activation (Fig. 8). It will be noted that the R-P’ interval measured from the beginning of the normal QRS complex is the same as the R-P ’ THE
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Mechanisms
Figure rkihach
10. C&e
2.
conduction
E/irctrocardio,.gam sc-quenres
ending
in Reciprocal
(continuous strip of lead in a reciprocal beat
interval measured from the end of the extrasystolic QKS complex (Fig. 3 to 5). The interval in both cases measures 36. The almost identical R-P’ intervals therefore indicate that there is essentially no lower common pathway in this particular case. The anatomic relation of the pathways and the reciprocal mechanism in this case is illustrated in Figure 9D. This case also demonstrates that reciprocal rhythm with atria1 origin can occur with a prolonged R-P’ time instead of a prolonged P-R time. The effect is essentially the same, for a prolonged R-P’ time will also allow the atria1 chamber sufficient time for recovery before arrival of the retrograde impulse. The basic prerequisite is, thus, a sufficiently long reciprocal time, which may be effected by an increase in the P-R interval or in the R-P’ interval, or both. RECIPROCAL
RHYTHM
WITH
A-V
NODAL
ORIGIN
In this form of reciprocal rhythm, the impulse arises in the A-V node and is conducted in two directions: anterograde to the ventricles, recording a QRS complex, and retrograde to the atria, recording a P’ deflection. The retrogradely conducted impulse may also enter another A-V nodal pathway and return anterogradely once again to reach the ventricles and record a second QRS complex, the reciprocal beat (Fig. 1[2]). This results in a P’ deflection that is “sandwiched” between two QRS complexes and is illustrated by the following case : CASE 2: ‘The electrocardiogram (Fig. 10 and 11) was recorded from a 47 year old woman who was
admitted to the hospital for carcinoma of the breast. There were no symptoms referrable to the cardiovascular system. She was a member of a family with congenital absence of the sinoatrial node.9 The electrocardiogram (Fig. 10, a continuous strip of lead V,) begins with three QRS complexes each of which is related to a succeeding P’ wave. (The frontal plane P’ axis was -9OO.) This represents A-V nodal VOLUME
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.\~-V nod;tl?hyth~u
with retrogrndr
\,Vm-
rhythm with retrograde conduction to the atria. There is a progressive increase in retrograde conduction time as reflected by an increasing R-P’ interval measuring 12, 16 and 18, respectively. This represents a retrograde Wenckebach sequence. The longest R-P’ interval is then followed by a premature QRS complex of the same shape and size as the preceding QRS complex. This represents a reciprocal beat. The reciprocal beat is always associated with a preceding long R-P’ interval, that is, an increased retrograde conduction time. This is necessary to allow a potential lower common pathway or the ventricles, or both, sufficient recovery time before arrival of the reciprocal impulse.rOJr The R-R interval of the reciprocal sequence is almost constant, measuring 34 to 35, and thus reflects an almost constant reciprocal time (see notes on nomenclature, to follow). The long R-P’ intervals associated with the reciprocal beats, however, vary considerably and measure either 18 or 28. Thus a considerable discrepancy exists between reciprocal time and R-P’ times.
The Upper Common Pathway: The association of constant reciprocal times with differing R-P’ or retrograde times indicates that the P’ deflection does not represent the return level of the reciprocal impulse. If the P’ deflection did represent the return level, then reciprocal sequence with different R-P’ intervals would most probably be associated with the different R-R times. Alternatively, if different R--P’ times were associated with constant reciprocal times, the highly unlikely postulate would have to be propounded that an increase in R-P’ time is exactly compensated by a proportional decrease in P’-R time. Furthermore, when a reciprocal sequence occurs with a long R-P’ interval of 28, the associated P’-R interval is 7, and this is clearly too short to represent anterograde conduction. Thus, return must have occurred before the inscription of the P’ deflection. The return level must therefore be situated
230
tia--N;
A-V
56 V
t-----t Rnl
Rn2
Rn3
11. Case 2. Electrocardiogram (enlarged and diagrammed lustrating concealed conduction mechanisms.
Figure
below
the
atria1 level (Fig. 12). This demonthe presence of an upper common pathway and also indicates that the atria do not participate in the reciprocal mechanism. The different R-P’ times must be due to different delays in the upper common pathway above the return level, since it is obvious that delay above the return level cannot affect reciprocal time (Fig. 12). RosenbluethG and Mendez et al.,’ on the basis of experimental work, state that an atria1 bridge strates
Pi
$2 4
A I
I
$ R’
12. Diagrammatic illustration showing the lack of effect of different conduction delays in an upper common pathway on reciprocal time.
Figure
Rn5
Rt-14
section of the end of the top strip of Fig. 10) il-
is always necessary in the reciprocal mechanism, that is, the impulse must traverse atria1 tissue to complete the reciprocal circuit. Their experimental observations, however, were not supported by Mignone and Wallace” who showed that an atria1 bridge was not an essential link. This confirmed a similar view, also based on experimental work, that was first propounded by Scherf and Shookhoff.13 This clinical case (Case 2) supports this latter concept. Thz Lower Common Pathway: The A-V nodal cycle begins from the moment the A-V nodal pacemaker discharges spontaneously or is itself discharged by another impulse. The first escape interval of an A-V nodal rhythm thus begins when a preceding impulse penetrates into the A-V nodal pacemaker and discharges it prematurely. As the A-V nodal cycle is usually constant, backward measurement of this cycle from the first A-V nodal escape beat will locate the moment of its preceding discharge. The impulse which effected the discharge then becomes evident and its conduction sequence is revealed. This principle can be applied to the present case (Case 2) as follows: The A-V nodal cycle or internodal interval is constant and measures 56 (illustrated as intervals Nl-N2 and N4-N5 in Fig. 11). The THE
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Figure 13. Diagrams illustrating (A) deduction of the presence of a lower common pathway from concealed conduction and (B) deduction of the presence of unidirectional block.
resultant R-R intervals of these nodal beats (illustrated as intervals Rnl-Rn2 and Rn4Rn5) will also be 56. Note that due to some conduction delay in the lower part of the node, the actual nodal discharge occurs just before the inscription of the QRS complex. The constancy of the A-V nodal rhythm is by the reciprocal disturbed or “dislocated” beat: the R-R interval following the reciprocal beat (Rn3-Rn4) is shorter than the A-V nodal cycle and measures 48 (Fig. 11). Backward measurement of the escape interval of 56 from Rn4--the first nodal escape beat following the reciprocal sequence-will locate the latest possible preceding discharge of the A-V nodal pacemaker. This moment is located before inscription of Rn3 (the QRS complex of the reciprocal beat), between Rn2 and Rn3. This discharge of the A-V nodal pacemaker could not be effected by the initial anterograde or retrograde A-V nodal impulses of the reciprocal sequence since these impulses cannot reach the pacemaker through the same pathway which they have just traversed and rendered refractory. The pacemaker could be reached only through another pathway. It is clear, therefore, that the discharge of the A-V nodal pacemaker was achieved by the reciprocal impulse and thus occurs later than the return or d point of the reciprocal sequence. This conclusion is supported by the observation that “dislocation” of the nodal rhythm only occurs with a reciprocal beat. VOLUME
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It is also clear that the A-V nodal pacemaker was discharged before the reciprocal impulse reached the ventricles to record the QRS complex. The reciprocal impulse must, therefore, have access to the A-V nodal pacemaker, and such access does not involve the ventricular musculature, that is, one reciprocal activation front (labeled x in Fig. 13A) reaches the A-V nodal pacemaker before the other component of the reciprocal activation front (labeledy) reaches the ventricles. Access to this A-V nodal pacemaker by a reciprocal impulse can only occur through a lower A-V nodal common pathway. The same hypothesis would apply if, alternatively, the pacemaker were situated in the lower common pathway. This explanation is much simpler, yet still supports the conclusion that a lower common pathway is obviously present. This case therefore demonstrates (1) the presence of both upper and lower A-V nodal common pathways (see Fig. 2 and 9B) and (2) that an atria1 bridge is not an essential link in the reciprocal pathway. THE RECIPROCAL PATHWAY AND UNIDIRECTIONAL BLOCK The essential prerequisite to the initiation of any reciprocal rhythm is unequal refractoriness or responsiveness of the two A-V nodal pathways. This condition is necessary so that an impulse arising in the ventricles, for example, will enter one pathway only and then return in the
232
Schamroth
opposite direction through the other pathway. If the two pathways were equally responsive, an impulse arising in the atria, for example, would enter both pathways simultaneously and then proceed in the same direction through both pathways. Retrograde return through either pathway would then become impossible and a reciprocal mechanism would thereby be obviated. This is indeed the case in the WolffParkinson-White syndrome when an atria1 impulse enters two A-V nodal pathways simultaneously; conduction proceeds anterograde through both pathways, and subsequent intraventricular conduction results in the typical Wolff-Parkinson-White complexes. When, however, the refractory periods of the two pathways become unequal, the atria1 impulse enters one pathway only, returns retrograde through the other pathway and thereby initiates a reciprocal rhythm.4J This observation emphasizes that the transient functional unidirectional block must exist in one of the conduction pathways for a reciprocal mechanism to occur. In the case of an impulse arising in the A-V node (Fig. 13B), the anterogradely conducted impulse (impulse a) reaches the lower regions of the reciprocal pathway (position 1) before the reciprocal impulse (impulse 6). Impulse a, however, cannot penetrate into the reciprocal pathway because of refractoriness (unidirectional block) and this permits impulse 6 to traverse the reciprocal pathway and effect a reciprocal return. If unidirectional block were absent, impulse a would penetrate into the reciprocal pathway (as shown by the dashed line) and prevent a reciprocal mechanism. Thus, in all forms of reciprocal rhythm, the second or reciprocal pathway must have the property of unidirectional block. NOTES ON NOMENCLATURE “Reversed Reciprocal Rhythm”14: This is the term applied to reciprocal rhythm with impulses of sinus or atria1 origin. It was so named because the rhythm results in a QRS complex that is sandwiched between two P waves-the reverse of reciprocal rhythm with nodal or ventricular origin, which results in a P wave that is sandwiched between two QRS complexes. However, the term is unsatisfactory, since names prefixed by non, pseudo or reversed are negative descriptions and state what the arrhythmia is not. Furthermore, it is clear that the reciprocal mechanism is basically the same irrespective of the originating
and Yoshonis impulse (see Case 1). Reciprocal rhythm is thus best classified on the basis of impulse origin, as described in the introduction. Common Pathway: The term common pathway is preferred to the term jnal commonpathway, as used by Moe and Mendez.8 Final common pathway implies the presence of a lower common pathway only, whereas both upper and lower common pathways may be present (Case 2). The term is further misleading since although a final common pathway may be the final pathway in cases of reciprocal rhythm with atria1 origin, it would be the initial pathway in the case of reciprocal rhythm with ventricular origin (Case 1). Return Level: This is the level within the A-V node where the impulse changes direction from an anterograde to a retrograde direction or vice versa. This is usually the level at which two pathways join to form a common pathway. Re-entry Time: This is the time taken for the reciprocal impulse to enter the same tissue a second time. The tissue that is stimulated twice may be (1) a common pathway, (2) the atria1 chamber, or (3) the ventricular chamber. Note that the re-entry time of a common pathway is not manifest electrocardiographically but may be calculated. Reciprocal Time: Reciprocal time is the reentry time applied to atria1 or ventricular chambers only, and is the time between consecutive activations of the atrial or ventricular chamber, that is, the R-R or P’-P’ intervals of reciprocal beats. The Reciprocal Pathway: This is the pathway used for re-entry, that is, the pathway that is not used initially. Abbreviations: The a pathway = the pathway grade conduction. The b pathway = the pathway grade conduction. The cpathway = the common
used for antero-
used for retropathway.
The d level = the return level. Ra = the QRS complex recorded pulse of atria1 or sinus origin.
by an im-
Rn = the QRS complex recorded pulse of A-V nodal origin.
by an im-
Rv = the QRS complex recorded pulse of ventricular origin.
by an im-
CONCLUSIONS 1. Reciprocal THE
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CARDIOLOGY
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pulses arising in the atria, A-V node, or ventricles. 2. The reciprocal mechanism can occur in the concomitant presence of both upper and lower A-V nodal common pathways. 3. The reciprocal mechanisms can also occur with two A-V nodal pathways that are separated from each other throughout the A-V junction. 4. An atria1 bridge is not an essential link in the reciprocal pathway. 5. The P’ deflection does not of necessity reflect the return point or level of a reciprocal circuit. 6. A prolonged reciprocal time is necessary for the occurrence of an atria1 echo. This may be effected by either a prolonged P-R interval or a prolonged R-P’ interval. 7. The diagnosis of reciprocal rhythm with impulse of atria1 origin is strongly suggested by the presence of A-V nodal or ventricular beats with “retrograde” P’ deflections of the same size and shape as the P’ deflection of the postulated atria1 echo. 8. Reciprocal rhythm may begin with sinus origin and be interrupted by an impulse of ventricular origin which then continues the reciprocal mechanism. 9. When reciprocal rhythm of sinus and ventricular origin coexist, the presence of a lower common pathway will create a discrepancy between the R-P’ intervals. Thus, the longer the lower common pathway or the longer the conduction delay within this pathway, the shorter the Ra-P’ interval, the longer the Rv-P’ interval and the greater the consequent discrepancy between the two. 10. Unidirectional block in one of the two A-V nodal pathways is an essential prerequisite to the initiation of reciprocal rhythm.
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REFERENCES 1. ROSENBLUETH, A. and RUBIO, R.
2.
3.
4.
5.
6. 7.
8.
9.
10.
11.
12.
13.
14.
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La influencia de la frecuencia de estimulacion sobre 10s tiempos de propagation auriculo-ventricular y ventriculoauricular. Arch. Inst. cardiol. Mexico, 25:535, 1955. MOE, G. K., PRESTON, J. B. and BURLINGTON,H. Physiologic evidence for a dual A-V transmission system. Circulation Res., 4~357, 1956. SCHERF, D. and COHEN, J. The Atrioventricular Node and Selected Cardiac Arrhythmias, p. 274. New York, 1964. Grune & Stratton. SCHAMROTH, L. Reversed reciprocating paroxysmal tachycardia and its relationship to the WolffParkinson-White syndrome. Am. Heart J., 59 :506. 1960. HARRIS, W. H., SEMLER, H. J. and GRISWOLD, H. E. Reversed reciprocating paroxysmal tachycardia controlled by guanethidine in a case of WolffParkinson-White syndrome. Am. Heart J., 67 :812, 1964. ROSENBLIJETH, A. Ventricular echoes. Am. J. Physiol., 195: 53, 1958. MENDEZ, C., HAN, J., GARCIA DE JALON, P. D. and MOE, G. K. Some characteristics of ventricular echoes. Circulation Res., 16 ~562, 1965. MOE, G. K. and MENDEZ, C. Physiologic basis of reciprocal rhythm. Progr. Cardiovar. Dis., 8: 461, 1966. BACOS, J. M., EAGEN, J. J. and ORGAIN, E. S. Congenital familial nodal rhythm. Circulation, 22 : 887, 1960. KISTIN, A. D. Mechanisms determining reciprocal rhythm initiated by ventricular premature systoles; multiple pathways of conduction. Am. J. Cardiol., 3 ~365, 1959. KISTIN, A. D. Multiple pathways of conduction and reciprocal rhythm with interpolated ventricular systoles. Am. Heart J., 65: 162, 1963. MIGNONE, R. J. and WALLACE, A. G. Ventricular echoes; evidence for dissociation of conduction and reentry within the A-V node. Circulation Res., 19 ~638, 1966. SCHERF, D. and SHOOKHOFF, C. Experimentelle Untersuchungen iiber die “Umkehr-Extrasystale.” Wien. Arch inn. Med.. 12: 501. 1926. KATZ, L. N. and PICK, A. Clinical Electrocardiography: The Arrhythmias, p. 623. Philadelphia, 1956. Lea & Febiger.
LEO SCHAMROTH, M.D. (Rand),
F.R.C.P. (Edin.)?
Lexington,
Rhythm* J
AND KARL F. YOSHONIS M.D.~
Kentucky
Reciprocal rhythm is defined and the mechanisms described in 2 cases. Reciprocal rhythm can occur with impulses of atrial, A-V nodal, or ventricular origin. Two separate A-V nodal pathways are an essential prerequisite. The two pathways may communicate with each other in the upper or lower parts, or both, of the A-V node to form upper or lower common pathways, or both. Reciprocal rhythm can occur in the presence of both upper and lower common pathways; it can also occur in the absence of a common pathway. The time of inscription of the “retrograde” P’ deflection does not necessarily reflect the return level of the reciprocal mechanism. An atria1 bridge is not an essential link in the reciprocal circuit. Unidirectional block in one of two pathways is necessary for the initiation of reciprocal rhythm. The nomenclature is reviewed.
R
with each other in both the upper and lower parts of the node to form upper and lower common pathways (Fig. 2B). 3. The pathways may be separated from each other in the lower A-V node and communicate in the upper part of the node to form an upper common pathway (Fig. 2C). 4. The pathways may be separated from each other throughout the entire A-V node. There is therefore no communication between the two pathways and consequently no common pathways are present (Fig. 2D).
ECIPROCAL RHYTHM may be defined as a rhythm wherein the atria1 or ventricular chamber § is activated two or more times by the same impulse. This occurs when an impulse arising in the sinus node, atria, atrioventricular (A-V) node or ventricles activates the atria1 or ventricular chamber but during its passage through the A-V node also enters another A-V nodal pathway, which permits the impulse to return to activate the same chamber once again (Fig. 1). There must therefore be at least two separate pathways within the A-V node. These pathways may communicate to form a common pathway, and there are four possible variations of their interrelation (Fig. 2). 1. The pathways may be separate from each other in the upper A-V node and communicate in the lower part of the node to form a lower common pathway (Fig. 2A). 2. The pathways may be situated in the middle of the A-V node and communicate
TYPES OF RECIPROCAL RHYTHM Reciprocal rhythm may, on the basis of impulse origin, be divided into three types (Fig. 1) : (1) reciprocal rhythm with impulses of sinus or atria1 origin; (2) reciprocal rhythm with impulses of A-V nodal or junctional origin; and (3) reciprocal rhythm with impulses of ventricular origin.
0 Electrophysiologically the two atria act as a functional unit and will be referred to as the atria1 chamber. Similarly, the two ventricles act as a functional unit and will be referred to as the ventricular chamber.
RECIPROCAL RHYTHM WITH ATRIAL
IMPULSES
OF
ORIGIN
In this type, a sinus or atria1 impulse activates
* From the Department of Medicine, Division of Cardiology, University of Kentucky, Lexington, Ky. Manuscript received August 9, 1968. t Visiting Professor of Cardiology. Present address: 155 Barry Hertzog Ave., Emmarentia, Johannesburg, South Africa. 1 Postdoctoral Fellow, U. S. Public Health Service Grant HE 05771. Address for reprints: Karl F. Yoshonis, M.D., Department of Medicine, Division of Cardiology, University of Kentucky, Lexington, Ky. 40506. 224
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Figure 1. Diagrammatic rejwesentationof reciprocal rhythm. Type 1, ventricular origin; Type 2, A-V nodal origin; Type 3, atria1 origin.
the atria1 chamber, resulting in the P wave, and is then conducted anterograde through the A-V node to activate the ventricular chamber, resulting in the QRS complex. During its passage through the A-V node, the impulse also enters another A-V nodal pathway and is conducted retrograde to activate the atria1 chamber once again, thereby resulting in a “retrograde” P wave-P’ (superiorly orientated frontal plane P wave axis). The sequence P-QRS-P’ is known as an atria1 echo1*2 (Fig. 1[3]). The sinus impulse during its passage through the A-V node thus divides into two activation frontsone continuing anterograde to activate the ventricular chamber, and the other returning retrograde to activate the atria1 chamber a second time. The return point, that is, the point or level at which the excitation front divides, will be termed the d point. Criteria for Diagnosis: It is difficult to prove the diagnosis of reciprocal rhythm with impulses of atria1 origin, for it may be argued that the P’ deflection represents an atria1 extrasystole and not retrograde atria1 activation.3 However, the diagnosis of this form of reciprocal rhythm has hitherto been suggested by the following criteria: 1. The presence of A-V nodal extrasystoles or A-V nodal escape beats with “retrograde” P’ deflections of the same shape and size as the P ’ of the postulated atria1 echo.4 This strongly suggests that the P’ deflection following the sinus P wave must also be the result of retrograde activation. 2. The P’ deflection of an atria1 echo only follows a long or relatively long P-R interval.4v5 The long P-R interval is necessary to allow the atria1 chamber sufficient recovery time before the arrival of the returning impulse. Such selective linkage would be very fortuituous in the case of true atria1 extrasystoles. Illustrative Case: The following case demonstrates further criteria for the diagnosis of reciprocal rhythm with impulses of atria1 origin, VOLUME
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AUGUST
1969
Figure 2. Diagrammatic representationof the possible interrelation of two A-V nodal pathways within the A--V node (shaded area).
and, in addition, reveals other factors pertaining to the mechanisms of reciprocal rhythm. CASE 1. The electrocardiogram (Fig. 3) was recorded from a 50 year old woman who complained of occasional palpitations. There was no evidence of heart disease. The tracing (a continuous strip of standard lead II) shows paroxysms of tachycardia. Each paroxysm begins with a normal sinus P wave and continues with a tachycardia that is related to an abnormal P wave-the P’ deflection. The paroxysms are always terminated by a ventricular extrasystole. The P-R interval measures 16.* The first R-P’ interval of each paroxysm measures 34. All subsequent R-P’ intervals are slightly longer and measure 38. Ventricular extrasystoles occur during the paroxysms. Each ventricular extrasystole which occurs during a paroxysm is followed by a P’ deflection of the same shape and size as the P’ deflection associated with the normal QRS complexes (Fig. 3 to 6). Each ventricular extrasystole disturbs the P’-P’ rhythm. Thus, the sum of two consecutive P’-P’ intervals which do not include a ventricular extrasystole measures 100, whereas the sum of two consecutive P’-P’ intervals that include a ventricular extrasystole is slightly shorter and measures 92 (Fig. 5). The R to P’ time relation is nevertheless maintained (when allowances are made for the slightly increased width of the ventricular extrasystolic QRS complex; see later): the R-P’ interval of a normal QRS complex measures 34; the R-P’ interval of a ventricular extrasystole measures 40. It is evident that there is no compensatory pause following the ventricular extrasystole and that the P’ deflection following the extrasystole is also premature and must
* All time intervals are expressed in hundredths of a second.
Schamroth
226
FiKurc 3. Case 1. a&al origin.
Elechcardiogram
and Yoshonis
(strips of standard lead II) showing paroxysms of reciprocating
be related to the extrasystole. Furthermore, when two extrasystoles occur consecutively, the P’ deflection following each extrasystole is likewise premature. This R to P’ relation of the extrasystoles was always present in numerous observations. It is clear therefore that the P’ deflection must result from retrograde activation of the atria1 chamber by the extrasystolic impulse. And as all P’ deflections have the same configuration they must all result from retrograde activation, that is, the P’ deflection following the normal as well as the abnormal QRS complexes result from retrograde activation. This establishes the reciprocal origin of the P’ deflection following the normal QRS complex. The subsequent P’-R and
tachycardia
with
R-P’ intervals following the ventricular extrasystole remain constant unless disturbed once again by another ventricular extrasystole. The rhythm thus begins with a sinus impulse which is conducted to the ventricular chamber but also, during its passage through the A-V node, returns to activate the atria1 chamber once again, thereby constituting a reciprocal rhythm with impulse of sinus origin. The returning impulse is conducted anterograde once again, thereby initiating a reciprocating tachycardia (Fig. 5). When a ventricuiar extrasystole occurs, its premature impulse enters the retrograde pathway before the sinus impulse and continues the reciprocal rhythm which then becomes an example of
Figure 4. Case 1. Ekctrocardi~gram (continuous strips of simultaneous recordings from two esophageal leads) showing paroxysms of reciprocating tachycardia with atria1 origin. THE
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100
.
92
l
A-V
V
Figure
5.
Case 1.
Electrocardiogram (esophageal
reciprocal rhythm with ventricular origin (Fig. 5). The reciprocal rhythm therefore begins with a sinus impulse and is interrupted and reset by a ventricular impulse which then continues the reciprocal mechanism. All the paroxysms are terminated by a ventricular extrasystole. This occurs when the ventricular impulse is relatively more premature and consequently encounters a refractory retrograde pathway that permits only partial penetration. Retrograde conduction is consequently blocked for the extrasystolic impulse, and this interferes with retrograde penetration of the succeeding sinus impulse, thereby terminating the reciprocal mechanism (Fig. 5). The shorter duration of the first R-P’ interval of each paroxysm is due to a pseudo-Wenckebach form of conduction, that is, the first retrograde impulse occurs after a long rest period and is therefore conducted with greater facility.
lead) with diagrammatic
analysis.
Comment: The reciprocal mechanism requires the presence of a dual conducting system within the A-V node. One pathway (pathway u) permits anterograde conduction, and another pathway (pathway b) permits retrograde conduction. Rosenblueth,6 Mendez et a1.7 and Moe and Mendez,s on the basis of animal experimenpostulated that the dual system is tation, situated in the upper regions of the A-V node and that a common pathway, termed the jinal common pathway,a is present in the lower regions of the A-V node (see Fig. 2A and 9A). Under these circumstances, the sinus impulse will begin its return journey at point d before its anterograde tricles
(Fig.
occurs
before
element 7A).
has
In other
the Ra
activated words,
complex
the
vcn-
the d point
is recorded
(Ra
Figure 6. Case 1. Electrocardiogram (simultaneous recordings of lead VI and an esophageal lead) showing two consecutive ventricular extrasystoles (labeled Rv) during a paroxysm of tachycardia. The P’ deflection following both extrasystoles is premature. VOLUME
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”
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1
Figure 7. Diagrams illustrating the effect of a lower common pathway on the R-P’ interval resulting from (A) atria1 origin and (B) ventricular origin.
= QRS complex recorded by the complex sinus impulse). Furthermore, the longer the lower common pathway or the greater the delay in this pathway, the later the inscription of the Ra complex and the shorter the resulting Ra-P’ interval. This is in contrast to the situation resulting from retrograde activation of a ventricular impulse (Fig. 7B). The ventricular impulse must first activate the ventricular chamber (record-
Figure 8. Diagram illustrating the effect of no lower common pathway on the R-P’ intervals resulting from atria1 and ventricular origin.
Figure 9. Diagrams showing examples of various forms of reciprocal rhythm with different pathway interrelation. ing the Rv complex) and would only then be conducted through a potential lower common pathway (pathway c) before it can enter the retrograde pathway (pathway 6). The Rv-P’ interval is longer than the d-P’ interval and much longer than the Ra-P’ interval. Indeed, the ventricular extrasystolic impulse may be further delayed in the lower common pathway because this pathway has just been traversed by the preceding anterograde impulse and may, as a result, still be partially refractory. This will prolong the Rv-P’ interval even further. It is clear therefore that the R-P intervals resulting from sinus and ventricular impulses cannot be the same in the presence of a lower common pathway. In Case 1, however, both the Ra-P’ and Rv-P’ intervals are virtually the same. The slight discrepancy is due to the fact that in the case of the ventricular extrasystole the ventricles must be activated first i.e., the d point occurs after the beginning of ventricular activation, whereas in the case of the sinus impulse, the d point occurs before the beginning of ventricular activation (Fig. 8). It will be noted that the R-P’ interval measured from the beginning of the normal QRS complex is the same as the R-P ’ THE
AMERICAN
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OF CARDIOLOGY
Mechanisms
Figure rkihach
10. C&e
2.
conduction
E/irctrocardio,.gam sc-quenres
ending
in Reciprocal
(continuous strip of lead in a reciprocal beat
interval measured from the end of the extrasystolic QKS complex (Fig. 3 to 5). The interval in both cases measures 36. The almost identical R-P’ intervals therefore indicate that there is essentially no lower common pathway in this particular case. The anatomic relation of the pathways and the reciprocal mechanism in this case is illustrated in Figure 9D. This case also demonstrates that reciprocal rhythm with atria1 origin can occur with a prolonged R-P’ time instead of a prolonged P-R time. The effect is essentially the same, for a prolonged R-P’ time will also allow the atria1 chamber sufficient time for recovery before arrival of the retrograde impulse. The basic prerequisite is, thus, a sufficiently long reciprocal time, which may be effected by an increase in the P-R interval or in the R-P’ interval, or both. RECIPROCAL
RHYTHM
WITH
A-V
NODAL
ORIGIN
In this form of reciprocal rhythm, the impulse arises in the A-V node and is conducted in two directions: anterograde to the ventricles, recording a QRS complex, and retrograde to the atria, recording a P’ deflection. The retrogradely conducted impulse may also enter another A-V nodal pathway and return anterogradely once again to reach the ventricles and record a second QRS complex, the reciprocal beat (Fig. 1[2]). This results in a P’ deflection that is “sandwiched” between two QRS complexes and is illustrated by the following case : CASE 2: ‘The electrocardiogram (Fig. 10 and 11) was recorded from a 47 year old woman who was
admitted to the hospital for carcinoma of the breast. There were no symptoms referrable to the cardiovascular system. She was a member of a family with congenital absence of the sinoatrial node.9 The electrocardiogram (Fig. 10, a continuous strip of lead V,) begins with three QRS complexes each of which is related to a succeeding P’ wave. (The frontal plane P’ axis was -9OO.) This represents A-V nodal VOLUME
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V,)
Rhythm
showing
.\~-V nod;tl?hyth~u
with retrogrndr
\,Vm-
rhythm with retrograde conduction to the atria. There is a progressive increase in retrograde conduction time as reflected by an increasing R-P’ interval measuring 12, 16 and 18, respectively. This represents a retrograde Wenckebach sequence. The longest R-P’ interval is then followed by a premature QRS complex of the same shape and size as the preceding QRS complex. This represents a reciprocal beat. The reciprocal beat is always associated with a preceding long R-P’ interval, that is, an increased retrograde conduction time. This is necessary to allow a potential lower common pathway or the ventricles, or both, sufficient recovery time before arrival of the reciprocal impulse.rOJr The R-R interval of the reciprocal sequence is almost constant, measuring 34 to 35, and thus reflects an almost constant reciprocal time (see notes on nomenclature, to follow). The long R-P’ intervals associated with the reciprocal beats, however, vary considerably and measure either 18 or 28. Thus a considerable discrepancy exists between reciprocal time and R-P’ times.
The Upper Common Pathway: The association of constant reciprocal times with differing R-P’ or retrograde times indicates that the P’ deflection does not represent the return level of the reciprocal impulse. If the P’ deflection did represent the return level, then reciprocal sequence with different R-P’ intervals would most probably be associated with the different R-R times. Alternatively, if different R--P’ times were associated with constant reciprocal times, the highly unlikely postulate would have to be propounded that an increase in R-P’ time is exactly compensated by a proportional decrease in P’-R time. Furthermore, when a reciprocal sequence occurs with a long R-P’ interval of 28, the associated P’-R interval is 7, and this is clearly too short to represent anterograde conduction. Thus, return must have occurred before the inscription of the P’ deflection. The return level must therefore be situated
230
tia--N;
A-V
56 V
t-----t Rnl
Rn2
Rn3
11. Case 2. Electrocardiogram (enlarged and diagrammed lustrating concealed conduction mechanisms.
Figure
below
the
atria1 level (Fig. 12). This demonthe presence of an upper common pathway and also indicates that the atria do not participate in the reciprocal mechanism. The different R-P’ times must be due to different delays in the upper common pathway above the return level, since it is obvious that delay above the return level cannot affect reciprocal time (Fig. 12). RosenbluethG and Mendez et al.,’ on the basis of experimental work, state that an atria1 bridge strates
Pi
$2 4
A I
I
$ R’
12. Diagrammatic illustration showing the lack of effect of different conduction delays in an upper common pathway on reciprocal time.
Figure
Rn5
Rt-14
section of the end of the top strip of Fig. 10) il-
is always necessary in the reciprocal mechanism, that is, the impulse must traverse atria1 tissue to complete the reciprocal circuit. Their experimental observations, however, were not supported by Mignone and Wallace” who showed that an atria1 bridge was not an essential link. This confirmed a similar view, also based on experimental work, that was first propounded by Scherf and Shookhoff.13 This clinical case (Case 2) supports this latter concept. Thz Lower Common Pathway: The A-V nodal cycle begins from the moment the A-V nodal pacemaker discharges spontaneously or is itself discharged by another impulse. The first escape interval of an A-V nodal rhythm thus begins when a preceding impulse penetrates into the A-V nodal pacemaker and discharges it prematurely. As the A-V nodal cycle is usually constant, backward measurement of this cycle from the first A-V nodal escape beat will locate the moment of its preceding discharge. The impulse which effected the discharge then becomes evident and its conduction sequence is revealed. This principle can be applied to the present case (Case 2) as follows: The A-V nodal cycle or internodal interval is constant and measures 56 (illustrated as intervals Nl-N2 and N4-N5 in Fig. 11). The THE
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Figure 13. Diagrams illustrating (A) deduction of the presence of a lower common pathway from concealed conduction and (B) deduction of the presence of unidirectional block.
resultant R-R intervals of these nodal beats (illustrated as intervals Rnl-Rn2 and Rn4Rn5) will also be 56. Note that due to some conduction delay in the lower part of the node, the actual nodal discharge occurs just before the inscription of the QRS complex. The constancy of the A-V nodal rhythm is by the reciprocal disturbed or “dislocated” beat: the R-R interval following the reciprocal beat (Rn3-Rn4) is shorter than the A-V nodal cycle and measures 48 (Fig. 11). Backward measurement of the escape interval of 56 from Rn4--the first nodal escape beat following the reciprocal sequence-will locate the latest possible preceding discharge of the A-V nodal pacemaker. This moment is located before inscription of Rn3 (the QRS complex of the reciprocal beat), between Rn2 and Rn3. This discharge of the A-V nodal pacemaker could not be effected by the initial anterograde or retrograde A-V nodal impulses of the reciprocal sequence since these impulses cannot reach the pacemaker through the same pathway which they have just traversed and rendered refractory. The pacemaker could be reached only through another pathway. It is clear, therefore, that the discharge of the A-V nodal pacemaker was achieved by the reciprocal impulse and thus occurs later than the return or d point of the reciprocal sequence. This conclusion is supported by the observation that “dislocation” of the nodal rhythm only occurs with a reciprocal beat. VOLUME
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It is also clear that the A-V nodal pacemaker was discharged before the reciprocal impulse reached the ventricles to record the QRS complex. The reciprocal impulse must, therefore, have access to the A-V nodal pacemaker, and such access does not involve the ventricular musculature, that is, one reciprocal activation front (labeled x in Fig. 13A) reaches the A-V nodal pacemaker before the other component of the reciprocal activation front (labeledy) reaches the ventricles. Access to this A-V nodal pacemaker by a reciprocal impulse can only occur through a lower A-V nodal common pathway. The same hypothesis would apply if, alternatively, the pacemaker were situated in the lower common pathway. This explanation is much simpler, yet still supports the conclusion that a lower common pathway is obviously present. This case therefore demonstrates (1) the presence of both upper and lower A-V nodal common pathways (see Fig. 2 and 9B) and (2) that an atria1 bridge is not an essential link in the reciprocal pathway. THE RECIPROCAL PATHWAY AND UNIDIRECTIONAL BLOCK The essential prerequisite to the initiation of any reciprocal rhythm is unequal refractoriness or responsiveness of the two A-V nodal pathways. This condition is necessary so that an impulse arising in the ventricles, for example, will enter one pathway only and then return in the
232
Schamroth
opposite direction through the other pathway. If the two pathways were equally responsive, an impulse arising in the atria, for example, would enter both pathways simultaneously and then proceed in the same direction through both pathways. Retrograde return through either pathway would then become impossible and a reciprocal mechanism would thereby be obviated. This is indeed the case in the WolffParkinson-White syndrome when an atria1 impulse enters two A-V nodal pathways simultaneously; conduction proceeds anterograde through both pathways, and subsequent intraventricular conduction results in the typical Wolff-Parkinson-White complexes. When, however, the refractory periods of the two pathways become unequal, the atria1 impulse enters one pathway only, returns retrograde through the other pathway and thereby initiates a reciprocal rhythm.4J This observation emphasizes that the transient functional unidirectional block must exist in one of the conduction pathways for a reciprocal mechanism to occur. In the case of an impulse arising in the A-V node (Fig. 13B), the anterogradely conducted impulse (impulse a) reaches the lower regions of the reciprocal pathway (position 1) before the reciprocal impulse (impulse 6). Impulse a, however, cannot penetrate into the reciprocal pathway because of refractoriness (unidirectional block) and this permits impulse 6 to traverse the reciprocal pathway and effect a reciprocal return. If unidirectional block were absent, impulse a would penetrate into the reciprocal pathway (as shown by the dashed line) and prevent a reciprocal mechanism. Thus, in all forms of reciprocal rhythm, the second or reciprocal pathway must have the property of unidirectional block. NOTES ON NOMENCLATURE “Reversed Reciprocal Rhythm”14: This is the term applied to reciprocal rhythm with impulses of sinus or atria1 origin. It was so named because the rhythm results in a QRS complex that is sandwiched between two P waves-the reverse of reciprocal rhythm with nodal or ventricular origin, which results in a P wave that is sandwiched between two QRS complexes. However, the term is unsatisfactory, since names prefixed by non, pseudo or reversed are negative descriptions and state what the arrhythmia is not. Furthermore, it is clear that the reciprocal mechanism is basically the same irrespective of the originating
and Yoshonis impulse (see Case 1). Reciprocal rhythm is thus best classified on the basis of impulse origin, as described in the introduction. Common Pathway: The term common pathway is preferred to the term jnal commonpathway, as used by Moe and Mendez.8 Final common pathway implies the presence of a lower common pathway only, whereas both upper and lower common pathways may be present (Case 2). The term is further misleading since although a final common pathway may be the final pathway in cases of reciprocal rhythm with atria1 origin, it would be the initial pathway in the case of reciprocal rhythm with ventricular origin (Case 1). Return Level: This is the level within the A-V node where the impulse changes direction from an anterograde to a retrograde direction or vice versa. This is usually the level at which two pathways join to form a common pathway. Re-entry Time: This is the time taken for the reciprocal impulse to enter the same tissue a second time. The tissue that is stimulated twice may be (1) a common pathway, (2) the atria1 chamber, or (3) the ventricular chamber. Note that the re-entry time of a common pathway is not manifest electrocardiographically but may be calculated. Reciprocal Time: Reciprocal time is the reentry time applied to atria1 or ventricular chambers only, and is the time between consecutive activations of the atrial or ventricular chamber, that is, the R-R or P’-P’ intervals of reciprocal beats. The Reciprocal Pathway: This is the pathway used for re-entry, that is, the pathway that is not used initially. Abbreviations: The a pathway = the pathway grade conduction. The b pathway = the pathway grade conduction. The cpathway = the common
used for antero-
used for retropathway.
The d level = the return level. Ra = the QRS complex recorded pulse of atria1 or sinus origin.
by an im-
Rn = the QRS complex recorded pulse of A-V nodal origin.
by an im-
Rv = the QRS complex recorded pulse of ventricular origin.
by an im-
CONCLUSIONS 1. Reciprocal THE
rhythm AMERICAN
can JOURNAL
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with
im-
CARDIOLOGY
Mechanisms
in Reciprocal
pulses arising in the atria, A-V node, or ventricles. 2. The reciprocal mechanism can occur in the concomitant presence of both upper and lower A-V nodal common pathways. 3. The reciprocal mechanisms can also occur with two A-V nodal pathways that are separated from each other throughout the A-V junction. 4. An atria1 bridge is not an essential link in the reciprocal pathway. 5. The P’ deflection does not of necessity reflect the return point or level of a reciprocal circuit. 6. A prolonged reciprocal time is necessary for the occurrence of an atria1 echo. This may be effected by either a prolonged P-R interval or a prolonged R-P’ interval. 7. The diagnosis of reciprocal rhythm with impulse of atria1 origin is strongly suggested by the presence of A-V nodal or ventricular beats with “retrograde” P’ deflections of the same size and shape as the P’ deflection of the postulated atria1 echo. 8. Reciprocal rhythm may begin with sinus origin and be interrupted by an impulse of ventricular origin which then continues the reciprocal mechanism. 9. When reciprocal rhythm of sinus and ventricular origin coexist, the presence of a lower common pathway will create a discrepancy between the R-P’ intervals. Thus, the longer the lower common pathway or the longer the conduction delay within this pathway, the shorter the Ra-P’ interval, the longer the Rv-P’ interval and the greater the consequent discrepancy between the two. 10. Unidirectional block in one of the two A-V nodal pathways is an essential prerequisite to the initiation of reciprocal rhythm.
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Rhythm
REFERENCES 1. ROSENBLUETH, A. and RUBIO, R.
2.
3.
4.
5.
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La influencia de la frecuencia de estimulacion sobre 10s tiempos de propagation auriculo-ventricular y ventriculoauricular. Arch. Inst. cardiol. Mexico, 25:535, 1955. MOE, G. K., PRESTON, J. B. and BURLINGTON,H. Physiologic evidence for a dual A-V transmission system. Circulation Res., 4~357, 1956. SCHERF, D. and COHEN, J. The Atrioventricular Node and Selected Cardiac Arrhythmias, p. 274. New York, 1964. Grune & Stratton. SCHAMROTH, L. Reversed reciprocating paroxysmal tachycardia and its relationship to the WolffParkinson-White syndrome. Am. Heart J., 59 :506. 1960. HARRIS, W. H., SEMLER, H. J. and GRISWOLD, H. E. Reversed reciprocating paroxysmal tachycardia controlled by guanethidine in a case of WolffParkinson-White syndrome. Am. Heart J., 67 :812, 1964. ROSENBLIJETH, A. Ventricular echoes. Am. J. Physiol., 195: 53, 1958. MENDEZ, C., HAN, J., GARCIA DE JALON, P. D. and MOE, G. K. Some characteristics of ventricular echoes. Circulation Res., 16 ~562, 1965. MOE, G. K. and MENDEZ, C. Physiologic basis of reciprocal rhythm. Progr. Cardiovar. Dis., 8: 461, 1966. BACOS, J. M., EAGEN, J. J. and ORGAIN, E. S. Congenital familial nodal rhythm. Circulation, 22 : 887, 1960. KISTIN, A. D. Mechanisms determining reciprocal rhythm initiated by ventricular premature systoles; multiple pathways of conduction. Am. J. Cardiol., 3 ~365, 1959. KISTIN, A. D. Multiple pathways of conduction and reciprocal rhythm with interpolated ventricular systoles. Am. Heart J., 65: 162, 1963. MIGNONE, R. J. and WALLACE, A. G. Ventricular echoes; evidence for dissociation of conduction and reentry within the A-V node. Circulation Res., 19 ~638, 1966. SCHERF, D. and SHOOKHOFF, C. Experimentelle Untersuchungen iiber die “Umkehr-Extrasystale.” Wien. Arch inn. Med.. 12: 501. 1926. KATZ, L. N. and PICK, A. Clinical Electrocardiography: The Arrhythmias, p. 623. Philadelphia, 1956. Lea & Febiger.