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Dysrhythmic dilemmas in coronary care
Diagnostic
Shelf
Dysrhythmic Dilemmas in Coronary Care
HENRY DIANE
J. L. MARRIOTT, C. THORNE,
MD, FACC
RN
St. Petersburg, F/a.
The many dysrhythmic vagaries of a single patient illustrate several practical points in the diagnosis of arrhythmias that bear emphasis because they are often not appreciated: The physical examination can provide useful information that is not available from the electrocardiogram; a right chest lead is superior for continuous monitoring, and a left chest lead is sometimes valuable for distinguishing between ventricular and supraventricular tachycardias; ventricular aberration of one bundle branch type may abruptly switch to aberration of the other bundle branch type; and advanced atrioventricular (A-V) block with accelerated ventricular rhythm can be simulated by A-V tachycardia with 2:l exit block and aberrant ventricular conduction. The practical significance of these facts is discussed.
After 8 years of coronary care, during which time the prompt recognition and treatment of arrhythmias and blocks have proved their worth, there are still many misconceptions about diagnosis that represent potential therapeutic hazards for the patient. These misconceptions include : (1) that the electrocardiogram is superior to physical examination at all stages of unraveling arrhythmias ; (2) that it makes little difference which lead is used for monitoring provided it registers distinct P waves and QRS complexes; (3) that ventricular aberration of both right and left bundle branch block type is unlikely to occur in quick succession in the same tracing ; and (4) that absence of conduction through the atrioventricular (A-V) junction, as manifested by independent P waves and QRS complexes at normal rates, always indicates a high degree of A-V block. One patient so well illustrated in a continuous clinical pageant the erroneousness of all these notions that we thought his case worth reporting, In the 24 hours after admission he demonstrated consecutively (1) that careful physical examination may reveal useful information about arrhythmias that is not contained in the electrocardiogram ; (2) the diagnostic value of using a right chest lead for continuous monitoring and a left chest lead for occasional confirmation ; (3) that aberration of right and left bundle branch block type may follow each other in quick succession in the same tracing ; and (4) that high-grade A-V block with accelerated idioventricular rhythm can be precisely mimicked by A-V tachycardia with 2 : 1 exit block and aberrant ventricular conduction. From the Coronary Care Center, St. Anthony’s Hospital, St. Petersburg, Fla. Manuscript received January 30, 1970, accepted March 12, 1970. Address for reprints: Henry J. L. Marriott, MD, St. Anthony’s Hospital, St. Petersburg, Fla. 33705.
VOLUME 27. MARCH 1971
Case Report A 66 year old white man was admitted to the Coronary Care Center at St. Anthony’s Hospital with a suspected acute myocardial infarction. Three hours after admission he began to have paroxysms of tachycardia that recurred repeatedly during the next 6 days at rates ranging be-
327
MARRIOTT
AND
THORNE
tween 152 and 220 beats/min. Edrophonium, digitalis, quinidine, propranolol, procainamide and lidocaine were all used in an effort to control the recurrent arrhythmia, but none was notably successful. A single d-c countershock of 60 or 100 watt seconds was invariably successful in terminating the longer paroxysms. When the patient’s tachycardia began, the right precordial monitoring lead (MCL,) revealed the pattern seen in Figure 1A. From this alone, one is compelled to plead uncertainty-it shows either ventricular tachycar&a or supraventricular tachycardia with ventricular aberration. Study of the jugular pulse told us that it was not atria1 tachycardia since the atria1 activity, of which there was no evidence in the electrocardiogram, had only half the frequency of the ventricular activity; this relationship was later documented in a jugular pulse tracing (Fig. 1B 1, We were therefore faced with either a ventricular or nodal tachycardia with 2: 1 retrograde block. A temporary switch to a left chest
AjMCL,’
lead (MCL,) informed us that the tachycardia was almost certainly supraventricular since there was a small Q, tall, thin R and small S wave (Fig. lC)-a pattern typical of ventricular aberration of right bundle branch block type and most unlikely in ventricular tachycardia.l We therefore made the provisional diagnosis of nodal tachycardia with aberrant ventricular conduction. Cardioversion was undertaken, and a successful dose of 100 jbules was administered. However, short bursts of tachycardia soon recurred, and the initial beats of these paroxysms were helpful and confirmatory in 2 ways (Fig. 1D) : the first beat always showed an rsR’ pattern with an initial r wave virtually identical with that of the flanking sinus beats ; and there was no evidence of preceding atria1 activity. We were therefore doubly assured of the diagnosis of A-V nodal tachycardia with ventricular aberration. Paroxysms showing a different ventricular pattern then developed (Fig. 2A). Since these showed a left bundle branch block contour, there was little hope of distinguishing between aberration and ectopy on the basis of morphologic features alone; however, finding that the rate of the tachycardia with the left bundle branch block pattern was identical with that of the paroxysms with right bundle branch block and fortified with the knowledge &hat aberration alternately A
Bi
: DKL, i8
,‘I
!;:I’.
‘I
:i.
Figure 1. A, tachycardia showing anomalous ventricular complexes indicating either left ventricular tachycardia or supraventricular tachycardia with ventricular aberration of right bundle branch block type. B, the jugular pulse tracing shows that cannon a waves occur only with every alternate ventricular beat, thus excluding atrial tachycardia. C, the left chest lead shows a ventricular complex of typical aberrant form, that is, small q wave, tall, slender R wave and small s wave. D, return of the tachycardia in which the initial beat confirms by its rsR’ contour the supraventricular origin of the paroxysms.
328
Figure 2. A, recurrence of the tachycardia but now with a left bundle branch block contour. B, the start of a paroxysm of left bundle branch block type: the first beat shows little aberration and is not preceded by a discernible P wave, thus confirming its atrioventricular (A-V) nodal origin; the second beat shows incomplete left bundle branch block and the subsequent beats complete left bundle branch block. C illustrates the astonishing abrupt switch from right bundle branch block type aberration to the incomplete left bundle branch block type without interruption and without measurable change in cycle length. D, the start of another paroxysm with typical right bundle branch block type aberration of the first beat, immediately switching to incomplete and then complete left bundle branch block type.
The American
Journal
of
CARDIOLOGY
DYSRHYTHMIC
DILEMMAS
IN CORONARY
CARE
the top strip. This immediately suggests 2: 1 exit block as an explanation for the half-rate in the top strip, and the impression is further borne out by the first premature and taller complex in the second strip. This beat ends a cycle that is slightly longer than the cycles of the subsequent tachycardia and therefore fits comfortably into the scheme of things as a 3:2 Wenckebach sequence-a common intermediary between 2:l and 1 :l conduction. Thus, in the upper strip, one’s revised diagnosis is the same A-V nodal tachycardia with a somewhat lesser degree of aberration (because of the longer ventricular cycles) and with 2:l exit block below the pacemaking site. Conduction of the sinus beats is prevented from reaching the ventricles, not because of A-V block but because of physiologic refractoriness constantly maintained by the rapid discharge of the junctional pacemaker. Figure 3. The electrocardiographic strips form a continuous tracing. The top strip shows an anomalous ventricular complex (rate 88/min) with independent P waves at a rate of 72, all the criteria necessary for diagnosing advanced atrioventricular (A-V) block with accelerated idioventricular rhythm. In the second half of the bottom strip the manifest tachycardia resumes, at exactly twice the rate of the beats in the top strip, suggesting that the rhythm in the top strip was actually the same A-V nodal tachycardia with 2:l exit block. In the first half of the second strip, there is 3:2 Wenckebach conduction below the nodal pacemaker. The sinus impulses fail to reach the ventricles because of constant physiologic refractoriness in the A-V junction due to the rapid rate of the pacemaker’s discharge. affecting both bundle branch systems is not uncommon, we were confident that both anomalous types of ventricular complex represented aberration. Subsequent sequences (Fig. 2, B to D) confirmed this. Figure 2B shows the beginning of a paroxysm in which the first beat is normally conducted, the second beat shows aberration of incomplete left bundle branch block type and the third and subsequent beats show fully developed left bundle branch block. Figure 2C shows a run of tachycardia with right bundle branch block changing to incomplete left bundle branch block without a pause and without any measurable change in cycle length. Figure 2D shows the beginning of another paroxysm in which the first beat shows unquestionable aberration of right bundle branch block type ; the next 5 beats show incomplete and the remainder complete left bundle branch block. Finally, our versatile A-V nodal tachycardia contrived to mimic second degree A-V block with accelerated idioventricular rhythm leading to A-V dissociation. This combination of disturbances is often seen in patients with acute myocardial infarction, and some, who have too little respect for the idioventricular rate in diagnosis, would label it complete A-V block and embark on inappropriate therapy. In Figure 3, the upper strip shows widened QRS complexes at a rate of 88 with independent sinus rhythm at a rate of 72. None of the sinus impulses are conducted to the ventricles, and a high grade of A-V block is therefore implied. But another explanation is much more likely and underscores the fact that one sometimes must look critically at cherished first impressions. In the second strip the manifest tachycardia resumes, and its rate is exactly double that of the rhythm in
VOLUME
27, MARCH 1971
Discussion Value of jugular pulse: The neck veins, when properly inspected, transmit many messages of value from the right atrium ; yet they are undoubtedly the most neglected of all cardiovascular signposts. In myocardial infarction they are of immense value in recognizing early congestive heart failure and are often helpful in the differentiation of arrhythmias. In this case, they gave the first clear indication that we were not dealing with an atria1 tachycardia. Atria1 activity is notoriously difficult to identify in the electrocardiogram in the presence of marked tachycardia with wide QRS complexes, and in some of these cases the jugular pulsations may clearly mirror atria1 activity and obviate the necessity for more sophisticated and time-consuming techniques. The safety and speed of inspecting neck veins can hardly be compared with that of invasive procedures such as passing an esophageal electrode or a pervenous atria1 wire. Lead selection : Students of arrhythmias have long appreciated the value of a right precordial lead (usually V,) for unravelling difficult rhythms. No one would deny that V1 is the best of our conventional 12 leads for differentiating the bundle branch block patterns, and attention has been drawn to its usefulness in distinguishing between left ventricular ectopy and ventricular aberration of the right bundle branch block type.2,3 Yet in the constant monitoring of patients with coronary disease, in whom the all-important function of monitoring is to identify arrhythmias and blocks, these widely accepted principles have been almost universally ignored. The present case illustrates the value of a right chest lead in separating a supraventricular mechanism with ventricular aberration from ventricular tachycardia. And aberration is no stranger-we have recognized it in no less than 8 percent of 250 consecutive patients with acute myocardial infarction, and it may well have gone unrecognized in many more. One illustration will suffice to underscore the
323
MARRIOTT
AND
THORNE
danger of mistaking aberration for ectopy. In the presence of atria1 fibrillation with rapid ventricular response, the appearance of a run of aberrant beats begets the notion of ventricular tachycardia. This may lead to a serious 2-fold error: Digitalis, though sorely needed, may be withheld, and lidoCaine, though contraindicated, may be administered. .Withholding digitalis may leave a too rapid ventricular response unchecked, and lidocaine may, like quinidine, facilitate A-V conduction and further dangerously accelerate the ventricular response. The resulting enhanced tachyarrhythmia may well precipitate shock, a disastrous consequence of well-meaning but misguided therapy. The value of a left chest lead in distinguishing between aberration and ectopy is also illustrated by our patient. Thus, it is expedient. to use a monitoring system that enables one to make a quick but temporary switch from a right to a left precordial lead. When a right chest lead still leaves doubt in the distinction between aberration and ectopy, a left chest lead may render an important clue: Aberration of right bundle branch type usually produces a qRs pattern in a left precordial lead and seldom an rS pattern; whereas .left ventricular ectopic beats usually produce an rS or QS pattern in left chest leads.‘,’ To achieve a practical precordial exploratory system, we have used for the past 3 years, in an experience with over 1,000 patients, a modified CL (“MCI,“) -hookup, details of which have been published elsewhere.Z--’ This hookup appears to retain the diagnostic advanta’ges of the more conventional lead V, while obviating the need to keep all 3 limbs wired in addition to the exploratory elec-
trode and ground. The modified CL attachment requires only 2 wires besides the ground. Guises of aberration : It is not widely realized that aberration may alternately don the cloaks of right and left bundle branch block in quick succession (“alternating aberration”), as this patient so well demonstrates. We have encountered a number of such cases, some of which have been reported.4,” An awareness of this not rare phenomenon is an important step toward avoiding the erroneous diagnosis of ventricular tachycardia. Problems in A-V block: A-V block poses some dilemmas in coronary care, both because criteria for diagnosis are shaky and inconsistent and also because methods of treatment are uncertain and unproved. Among those who report on its incidence in acute myocardial infarction, there is a tacit avoidance of any definition of complete A-V block, as though its criteria were so universally uniform and the diagnosis so transparently easy that no one has any difficulty in pinpointing it, But this is far from true. Many erroneously apply the term “complete A-V block” to disturbances for which others will rightly not accept the term; as a result, therapeutic claims made by different authors cannot be satisfactorily compared. It seems to be poorly understood that the success of A-V conduction is intimately related to the rate of the lower pacemaker. If its rate is so adjusted, conduction can be absent for significant periods not only in advanced A-V block but in mere first degree block and even in the absence of any block, as in our patient, if physiologic refractoriness in the A-V junction is maintained by a rapidly firing A-V nodal focus.
References 1.
Marriott HJL, LaCamera F: Diagnosis of arrhythmia (letter to editor). JAMA 203:527-528. 1968 2. Sandier IA, Marriott HJL: The differential morphology of anomalous ventricular complexes of RBBB-type in lead VI: ventricular ectopy versus aberration. Circulation 31: 551-556, 1965 3. Marriott HJL, Sandler IA: Criteria, old and new, for differentiating between ectopic ventricular beats and aberrant ventricular conduction in the presence of atrial fibrillation. Progr Cardiovasc Dis 9:18-28, 1966 Differential diagnosis of supraventricular 4. Marriott HJL:
and ventricular tachycardia. Geriatrics 25:91-101, 1970 5. Marriott HJL, Fogg E: Monitoring lead systems. JAMA 206:650, 1968 Prevention and treatment of cardiac ar6. Marriott HJL: rhythmias associated with myocardial infarction. Cardiovast Clinics 1:192-211, 1969 7. Marriott HJL, Fogg E: Constant monitoring for arrhythmias and blocks. Mod Cone Cardiovasc Dis 39:103-108, 1970 8. Marriott HJL: Sophisticated monitoring: slide reproductions, no. 40, Tampa Tracings, Oldsmar, Fla., 1969
The
American
Journal
of
CARDIOLOGY
Shelf
Dysrhythmic Dilemmas in Coronary Care
HENRY DIANE
J. L. MARRIOTT, C. THORNE,
MD, FACC
RN
St. Petersburg, F/a.
The many dysrhythmic vagaries of a single patient illustrate several practical points in the diagnosis of arrhythmias that bear emphasis because they are often not appreciated: The physical examination can provide useful information that is not available from the electrocardiogram; a right chest lead is superior for continuous monitoring, and a left chest lead is sometimes valuable for distinguishing between ventricular and supraventricular tachycardias; ventricular aberration of one bundle branch type may abruptly switch to aberration of the other bundle branch type; and advanced atrioventricular (A-V) block with accelerated ventricular rhythm can be simulated by A-V tachycardia with 2:l exit block and aberrant ventricular conduction. The practical significance of these facts is discussed.
After 8 years of coronary care, during which time the prompt recognition and treatment of arrhythmias and blocks have proved their worth, there are still many misconceptions about diagnosis that represent potential therapeutic hazards for the patient. These misconceptions include : (1) that the electrocardiogram is superior to physical examination at all stages of unraveling arrhythmias ; (2) that it makes little difference which lead is used for monitoring provided it registers distinct P waves and QRS complexes; (3) that ventricular aberration of both right and left bundle branch block type is unlikely to occur in quick succession in the same tracing ; and (4) that absence of conduction through the atrioventricular (A-V) junction, as manifested by independent P waves and QRS complexes at normal rates, always indicates a high degree of A-V block. One patient so well illustrated in a continuous clinical pageant the erroneousness of all these notions that we thought his case worth reporting, In the 24 hours after admission he demonstrated consecutively (1) that careful physical examination may reveal useful information about arrhythmias that is not contained in the electrocardiogram ; (2) the diagnostic value of using a right chest lead for continuous monitoring and a left chest lead for occasional confirmation ; (3) that aberration of right and left bundle branch block type may follow each other in quick succession in the same tracing ; and (4) that high-grade A-V block with accelerated idioventricular rhythm can be precisely mimicked by A-V tachycardia with 2 : 1 exit block and aberrant ventricular conduction. From the Coronary Care Center, St. Anthony’s Hospital, St. Petersburg, Fla. Manuscript received January 30, 1970, accepted March 12, 1970. Address for reprints: Henry J. L. Marriott, MD, St. Anthony’s Hospital, St. Petersburg, Fla. 33705.
VOLUME 27. MARCH 1971
Case Report A 66 year old white man was admitted to the Coronary Care Center at St. Anthony’s Hospital with a suspected acute myocardial infarction. Three hours after admission he began to have paroxysms of tachycardia that recurred repeatedly during the next 6 days at rates ranging be-
327
MARRIOTT
AND
THORNE
tween 152 and 220 beats/min. Edrophonium, digitalis, quinidine, propranolol, procainamide and lidocaine were all used in an effort to control the recurrent arrhythmia, but none was notably successful. A single d-c countershock of 60 or 100 watt seconds was invariably successful in terminating the longer paroxysms. When the patient’s tachycardia began, the right precordial monitoring lead (MCL,) revealed the pattern seen in Figure 1A. From this alone, one is compelled to plead uncertainty-it shows either ventricular tachycar&a or supraventricular tachycardia with ventricular aberration. Study of the jugular pulse told us that it was not atria1 tachycardia since the atria1 activity, of which there was no evidence in the electrocardiogram, had only half the frequency of the ventricular activity; this relationship was later documented in a jugular pulse tracing (Fig. 1B 1, We were therefore faced with either a ventricular or nodal tachycardia with 2: 1 retrograde block. A temporary switch to a left chest
AjMCL,’
lead (MCL,) informed us that the tachycardia was almost certainly supraventricular since there was a small Q, tall, thin R and small S wave (Fig. lC)-a pattern typical of ventricular aberration of right bundle branch block type and most unlikely in ventricular tachycardia.l We therefore made the provisional diagnosis of nodal tachycardia with aberrant ventricular conduction. Cardioversion was undertaken, and a successful dose of 100 jbules was administered. However, short bursts of tachycardia soon recurred, and the initial beats of these paroxysms were helpful and confirmatory in 2 ways (Fig. 1D) : the first beat always showed an rsR’ pattern with an initial r wave virtually identical with that of the flanking sinus beats ; and there was no evidence of preceding atria1 activity. We were therefore doubly assured of the diagnosis of A-V nodal tachycardia with ventricular aberration. Paroxysms showing a different ventricular pattern then developed (Fig. 2A). Since these showed a left bundle branch block contour, there was little hope of distinguishing between aberration and ectopy on the basis of morphologic features alone; however, finding that the rate of the tachycardia with the left bundle branch block pattern was identical with that of the paroxysms with right bundle branch block and fortified with the knowledge &hat aberration alternately A
Bi
: DKL, i8
,‘I
!;:I’.
‘I
:i.
Figure 1. A, tachycardia showing anomalous ventricular complexes indicating either left ventricular tachycardia or supraventricular tachycardia with ventricular aberration of right bundle branch block type. B, the jugular pulse tracing shows that cannon a waves occur only with every alternate ventricular beat, thus excluding atrial tachycardia. C, the left chest lead shows a ventricular complex of typical aberrant form, that is, small q wave, tall, slender R wave and small s wave. D, return of the tachycardia in which the initial beat confirms by its rsR’ contour the supraventricular origin of the paroxysms.
328
Figure 2. A, recurrence of the tachycardia but now with a left bundle branch block contour. B, the start of a paroxysm of left bundle branch block type: the first beat shows little aberration and is not preceded by a discernible P wave, thus confirming its atrioventricular (A-V) nodal origin; the second beat shows incomplete left bundle branch block and the subsequent beats complete left bundle branch block. C illustrates the astonishing abrupt switch from right bundle branch block type aberration to the incomplete left bundle branch block type without interruption and without measurable change in cycle length. D, the start of another paroxysm with typical right bundle branch block type aberration of the first beat, immediately switching to incomplete and then complete left bundle branch block type.
The American
Journal
of
CARDIOLOGY
DYSRHYTHMIC
DILEMMAS
IN CORONARY
CARE
the top strip. This immediately suggests 2: 1 exit block as an explanation for the half-rate in the top strip, and the impression is further borne out by the first premature and taller complex in the second strip. This beat ends a cycle that is slightly longer than the cycles of the subsequent tachycardia and therefore fits comfortably into the scheme of things as a 3:2 Wenckebach sequence-a common intermediary between 2:l and 1 :l conduction. Thus, in the upper strip, one’s revised diagnosis is the same A-V nodal tachycardia with a somewhat lesser degree of aberration (because of the longer ventricular cycles) and with 2:l exit block below the pacemaking site. Conduction of the sinus beats is prevented from reaching the ventricles, not because of A-V block but because of physiologic refractoriness constantly maintained by the rapid discharge of the junctional pacemaker. Figure 3. The electrocardiographic strips form a continuous tracing. The top strip shows an anomalous ventricular complex (rate 88/min) with independent P waves at a rate of 72, all the criteria necessary for diagnosing advanced atrioventricular (A-V) block with accelerated idioventricular rhythm. In the second half of the bottom strip the manifest tachycardia resumes, at exactly twice the rate of the beats in the top strip, suggesting that the rhythm in the top strip was actually the same A-V nodal tachycardia with 2:l exit block. In the first half of the second strip, there is 3:2 Wenckebach conduction below the nodal pacemaker. The sinus impulses fail to reach the ventricles because of constant physiologic refractoriness in the A-V junction due to the rapid rate of the pacemaker’s discharge. affecting both bundle branch systems is not uncommon, we were confident that both anomalous types of ventricular complex represented aberration. Subsequent sequences (Fig. 2, B to D) confirmed this. Figure 2B shows the beginning of a paroxysm in which the first beat is normally conducted, the second beat shows aberration of incomplete left bundle branch block type and the third and subsequent beats show fully developed left bundle branch block. Figure 2C shows a run of tachycardia with right bundle branch block changing to incomplete left bundle branch block without a pause and without any measurable change in cycle length. Figure 2D shows the beginning of another paroxysm in which the first beat shows unquestionable aberration of right bundle branch block type ; the next 5 beats show incomplete and the remainder complete left bundle branch block. Finally, our versatile A-V nodal tachycardia contrived to mimic second degree A-V block with accelerated idioventricular rhythm leading to A-V dissociation. This combination of disturbances is often seen in patients with acute myocardial infarction, and some, who have too little respect for the idioventricular rate in diagnosis, would label it complete A-V block and embark on inappropriate therapy. In Figure 3, the upper strip shows widened QRS complexes at a rate of 88 with independent sinus rhythm at a rate of 72. None of the sinus impulses are conducted to the ventricles, and a high grade of A-V block is therefore implied. But another explanation is much more likely and underscores the fact that one sometimes must look critically at cherished first impressions. In the second strip the manifest tachycardia resumes, and its rate is exactly double that of the rhythm in
VOLUME
27, MARCH 1971
Discussion Value of jugular pulse: The neck veins, when properly inspected, transmit many messages of value from the right atrium ; yet they are undoubtedly the most neglected of all cardiovascular signposts. In myocardial infarction they are of immense value in recognizing early congestive heart failure and are often helpful in the differentiation of arrhythmias. In this case, they gave the first clear indication that we were not dealing with an atria1 tachycardia. Atria1 activity is notoriously difficult to identify in the electrocardiogram in the presence of marked tachycardia with wide QRS complexes, and in some of these cases the jugular pulsations may clearly mirror atria1 activity and obviate the necessity for more sophisticated and time-consuming techniques. The safety and speed of inspecting neck veins can hardly be compared with that of invasive procedures such as passing an esophageal electrode or a pervenous atria1 wire. Lead selection : Students of arrhythmias have long appreciated the value of a right precordial lead (usually V,) for unravelling difficult rhythms. No one would deny that V1 is the best of our conventional 12 leads for differentiating the bundle branch block patterns, and attention has been drawn to its usefulness in distinguishing between left ventricular ectopy and ventricular aberration of the right bundle branch block type.2,3 Yet in the constant monitoring of patients with coronary disease, in whom the all-important function of monitoring is to identify arrhythmias and blocks, these widely accepted principles have been almost universally ignored. The present case illustrates the value of a right chest lead in separating a supraventricular mechanism with ventricular aberration from ventricular tachycardia. And aberration is no stranger-we have recognized it in no less than 8 percent of 250 consecutive patients with acute myocardial infarction, and it may well have gone unrecognized in many more. One illustration will suffice to underscore the
323
MARRIOTT
AND
THORNE
danger of mistaking aberration for ectopy. In the presence of atria1 fibrillation with rapid ventricular response, the appearance of a run of aberrant beats begets the notion of ventricular tachycardia. This may lead to a serious 2-fold error: Digitalis, though sorely needed, may be withheld, and lidoCaine, though contraindicated, may be administered. .Withholding digitalis may leave a too rapid ventricular response unchecked, and lidocaine may, like quinidine, facilitate A-V conduction and further dangerously accelerate the ventricular response. The resulting enhanced tachyarrhythmia may well precipitate shock, a disastrous consequence of well-meaning but misguided therapy. The value of a left chest lead in distinguishing between aberration and ectopy is also illustrated by our patient. Thus, it is expedient. to use a monitoring system that enables one to make a quick but temporary switch from a right to a left precordial lead. When a right chest lead still leaves doubt in the distinction between aberration and ectopy, a left chest lead may render an important clue: Aberration of right bundle branch type usually produces a qRs pattern in a left precordial lead and seldom an rS pattern; whereas .left ventricular ectopic beats usually produce an rS or QS pattern in left chest leads.‘,’ To achieve a practical precordial exploratory system, we have used for the past 3 years, in an experience with over 1,000 patients, a modified CL (“MCI,“) -hookup, details of which have been published elsewhere.Z--’ This hookup appears to retain the diagnostic advanta’ges of the more conventional lead V, while obviating the need to keep all 3 limbs wired in addition to the exploratory elec-
trode and ground. The modified CL attachment requires only 2 wires besides the ground. Guises of aberration : It is not widely realized that aberration may alternately don the cloaks of right and left bundle branch block in quick succession (“alternating aberration”), as this patient so well demonstrates. We have encountered a number of such cases, some of which have been reported.4,” An awareness of this not rare phenomenon is an important step toward avoiding the erroneous diagnosis of ventricular tachycardia. Problems in A-V block: A-V block poses some dilemmas in coronary care, both because criteria for diagnosis are shaky and inconsistent and also because methods of treatment are uncertain and unproved. Among those who report on its incidence in acute myocardial infarction, there is a tacit avoidance of any definition of complete A-V block, as though its criteria were so universally uniform and the diagnosis so transparently easy that no one has any difficulty in pinpointing it, But this is far from true. Many erroneously apply the term “complete A-V block” to disturbances for which others will rightly not accept the term; as a result, therapeutic claims made by different authors cannot be satisfactorily compared. It seems to be poorly understood that the success of A-V conduction is intimately related to the rate of the lower pacemaker. If its rate is so adjusted, conduction can be absent for significant periods not only in advanced A-V block but in mere first degree block and even in the absence of any block, as in our patient, if physiologic refractoriness in the A-V junction is maintained by a rapidly firing A-V nodal focus.
References 1.
Marriott HJL, LaCamera F: Diagnosis of arrhythmia (letter to editor). JAMA 203:527-528. 1968 2. Sandier IA, Marriott HJL: The differential morphology of anomalous ventricular complexes of RBBB-type in lead VI: ventricular ectopy versus aberration. Circulation 31: 551-556, 1965 3. Marriott HJL, Sandler IA: Criteria, old and new, for differentiating between ectopic ventricular beats and aberrant ventricular conduction in the presence of atrial fibrillation. Progr Cardiovasc Dis 9:18-28, 1966 Differential diagnosis of supraventricular 4. Marriott HJL:
and ventricular tachycardia. Geriatrics 25:91-101, 1970 5. Marriott HJL, Fogg E: Monitoring lead systems. JAMA 206:650, 1968 Prevention and treatment of cardiac ar6. Marriott HJL: rhythmias associated with myocardial infarction. Cardiovast Clinics 1:192-211, 1969 7. Marriott HJL, Fogg E: Constant monitoring for arrhythmias and blocks. Mod Cone Cardiovasc Dis 39:103-108, 1970 8. Marriott HJL: Sophisticated monitoring: slide reproductions, no. 40, Tampa Tracings, Oldsmar, Fla., 1969
The
American
Journal
of
CARDIOLOGY