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Myocardial infarction unmasked by an unusual arrhythmia
Diagnostic
Shelf
Myocardial
Infarction
Unmasked by an
Unusual Arrhythmia* MICHAEL LECH WAGNER,
M.D. and SIDNEY R.
ARBEIT, M.D., F.A.c.~.
.Jersey City, New Jersey
T
HIS CASE is reported
currence cardiographic
to illustrate the conof several interesting electrophenomena in a single tracing.
penicillin. responsive
CASE REPORT
un-
The electrocardiogram displays second degree sinoatrial block with Wenckebach periods, a rate-conditioned left bundle branch block, the masking of an acute anteroseptal myocardial infarction by this conduction disturbance, and its unmasking by normally conducted beats occurring in the pauses occasioned by the sinoatrial block. Sinoatrial Block with M’enckrbacfr Periods: The phenomenon of second degree sinoatrial block with Wenckebach periods is strictly analogous in structure to the more usual form of Wenckebath periods occurring on an A-V nodal level.1.2 In the latter, there is a progressive prolongation of atrioventricular conduction, as manifested by a progressive increase in the P-R interval, culminating finally in failure of conduction of one of the atria1 impulses to the ventricles and a dropped ventricular beat. The greatest increments in A-V conduction time characteristically occur in the earliest beats, with each successive beat showing a smaller increment in its P-R Thus, while the P-R intervals lengthen, interval. the R-R intervals paradoxically shorten, and there is an acceleration of the ventricular rate prior to the dropped beat. In the analogous situation of second degree sinoatrial block with Wenckebach periods, the sinus node may initiate its impulses with regularity, but there is a progressive delay in their conduction to the atria, culminating in complete failure of this conduction and a
woman was admitted to the Jersey City Medical Center because of severe “squeezing” anterior chest pain of eight hours’ duration, dyspnea and diaphoresis. She was known to be diabetic for 12 years and was controlled with diet and tolbutamide. For 12 years, and especially over the past year, she noted gradually progressive dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea and occasional pedal edema. She was not taking digitalis at the time of her admission. There was no prior history of chest pain or myocardial infarction. On admisricn, she was found to be moderately obese and in no distress; she had a regular pulse rate of 84/min., blood pressure 120/70, respirations 26/min. and a rectal temperature of 101’~. There was no venous distention, hepatomegaly nor edema. Her thorax had a kyphotic configuration. Bilateral moist inspiratory basilar rales were heard, with flatness and diminished breath sounds at the right base. The apex impulse was not palpable, and the heart sounds were distant. No cardiac murmurs were heard; the cardiac rhythm was regular. A chest roentgenogram showed an enlarged heart with congestive pulmonary changes and a bilateral pleural effusion. The hematocrit was 417&,, white blood cell count 16,OOOjcu. mm. with a normal differential count, BUN 26 mg.%, and blood sugar 368mg.gb. A diagnosis of acute myocardial infarction, suspected clinically, was corroborated by a rise in serum glutamic oxalacetic transaminase. The electrocardiogram taken on admission is shown in Figure 1, The patient was treated with salt restriction, digitalization and diuretics. She continued to be febrile. Pneumonia was diagnosed and treated with
JANUARY 1964
week, she became
DISCUSSION
.4n 85 year old Puerto Rican
* From the Electrocardiography Station, Department ment of Medicine, Seton Hall College of Medicine.
During the second and died.
of Medicine,
81
the Jersey City Medical
Center, and The Depart-
Wagner
82
FIG. 1.
Elrctrocardiogram
and Arbeit
taken on April 4, 1063, at 7:15 A.M.
dropped atria1 beat1 Here, too, the greatest increments in sinoatrial conduction must occur in the earliest beats, for the P-P intervals progressively shorten and the atria accelerate prior to the dropped beat. Intermittent Bundle Branch Block and Myocardial Infarction: The second phenomenon which these tracings illustrate is the interplay between cardiac rate and the refractory state of conducting tissues in the production of intermittent conduction disturbances. Shortening of the R-R interval below a critical level, with exrate of conduction,” ceeding of the “critical may result in impingement of succeeding impulses upon conducting tissues still refractory from those preceding. This may be manifested
as aberrancy of intraventricular conduction, or, if one of the bundle branches is more specifically involved, as a rate-conditioned bundle branch block.3 --7 In this tracing, the dominant beats have a left bundle branch block configuration. However, those beats terminating the long R-R occasioned by the second degree intervals, sinoatrial block, have a normal QRS duration, indicating that they are normally conducted. Hence, the left bundle branch block of this electrocardiogram is rate-conditioned, with the longer R-R intervals allowing time for the refractory tissues of the “fatigued” left bundle branch to recover and conduct normally. Inspection of these normally conducted THE
AMERICAN
JOURNAL
OF
CARDIOLOGY
Myocardial
Infarction
cu~nplescs re\-eals a (2 wave in VI-V?, with ele\.ated RS-7’ segments and inverted T waves, the classic pattern of an acute anteroseptal m).ocardial infarction. The dominant left bundle branch block complexes give no indication of this. The masking of an infarction pattern by a block in the left bundle branch is a well known occurrence, explained by the fact that both conditions affect initial depolarization forces. This is particularly well illustrated in this tracing. SUMMARY A case is presented of second degree sinoatrial block with Wenckebach periods, and a rateconditioned left bundle branch block masking an acute anteroseptal myocardial infarction which is revealed in the normally conducted beats occurring in the pauses caused by the second degree sinoatrial block. The mechanisms underlying this unusual tracing are discussed.
JANUARY
1964
IJnmasked
t)y :b-rhythmia
1.
DXIIERI~,
2.
GREENWOOD,
G.
M., .IK., RUSNN, .\. and
83
BRIXLJLI:\
, P.
lnteratrial and sinoatrial block, with an illtlstratix-c case. :lm. Hm,_t J., 31: 352, 1946.
R. J., FINKELSTEIN, D. and MONHEIT, R. Sinoatrial blcck with \venrkebach phenomenon. Alnz.J. Cnrdiol., 8: 140, 1961.
3. VESELL, H.
Critical rates in ventricular conduction. Unstable bundle branch block. .+u. J. .\f. SC., 202 : 138, 1941.
4. VESELI.,H. Critical rates in ventricular conduction. II. Simulation of localized bundle branch block. :inl. Hmt J., 41: 46, 1951. 5. VESELL, H. and KRAEMER, L. B. Critical rates in ventricular conduction. m. Simulation of ventricular tachycardia. Am. Heart J., 41 : 280, 1951. 6. VESELL, H. and FRIEDFELD, L. Critical rates in ventricular conduction. IV. Duration of unstable bundle branch block. ;Im. Hrart J., 44: 830, 1952. 7. SHEARN, M. A. and KYTAND, D. A. Intermittent bundle branch block. Observations with special reference to the critical heart rate. .Irch. Int. .\fcd., 91: 448. 1953.
Shelf
Myocardial
Infarction
Unmasked by an
Unusual Arrhythmia* MICHAEL LECH WAGNER,
M.D. and SIDNEY R.
ARBEIT, M.D., F.A.c.~.
.Jersey City, New Jersey
T
HIS CASE is reported
currence cardiographic
to illustrate the conof several interesting electrophenomena in a single tracing.
penicillin. responsive
CASE REPORT
un-
The electrocardiogram displays second degree sinoatrial block with Wenckebach periods, a rate-conditioned left bundle branch block, the masking of an acute anteroseptal myocardial infarction by this conduction disturbance, and its unmasking by normally conducted beats occurring in the pauses occasioned by the sinoatrial block. Sinoatrial Block with M’enckrbacfr Periods: The phenomenon of second degree sinoatrial block with Wenckebach periods is strictly analogous in structure to the more usual form of Wenckebath periods occurring on an A-V nodal level.1.2 In the latter, there is a progressive prolongation of atrioventricular conduction, as manifested by a progressive increase in the P-R interval, culminating finally in failure of conduction of one of the atria1 impulses to the ventricles and a dropped ventricular beat. The greatest increments in A-V conduction time characteristically occur in the earliest beats, with each successive beat showing a smaller increment in its P-R Thus, while the P-R intervals lengthen, interval. the R-R intervals paradoxically shorten, and there is an acceleration of the ventricular rate prior to the dropped beat. In the analogous situation of second degree sinoatrial block with Wenckebach periods, the sinus node may initiate its impulses with regularity, but there is a progressive delay in their conduction to the atria, culminating in complete failure of this conduction and a
woman was admitted to the Jersey City Medical Center because of severe “squeezing” anterior chest pain of eight hours’ duration, dyspnea and diaphoresis. She was known to be diabetic for 12 years and was controlled with diet and tolbutamide. For 12 years, and especially over the past year, she noted gradually progressive dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea and occasional pedal edema. She was not taking digitalis at the time of her admission. There was no prior history of chest pain or myocardial infarction. On admisricn, she was found to be moderately obese and in no distress; she had a regular pulse rate of 84/min., blood pressure 120/70, respirations 26/min. and a rectal temperature of 101’~. There was no venous distention, hepatomegaly nor edema. Her thorax had a kyphotic configuration. Bilateral moist inspiratory basilar rales were heard, with flatness and diminished breath sounds at the right base. The apex impulse was not palpable, and the heart sounds were distant. No cardiac murmurs were heard; the cardiac rhythm was regular. A chest roentgenogram showed an enlarged heart with congestive pulmonary changes and a bilateral pleural effusion. The hematocrit was 417&,, white blood cell count 16,OOOjcu. mm. with a normal differential count, BUN 26 mg.%, and blood sugar 368mg.gb. A diagnosis of acute myocardial infarction, suspected clinically, was corroborated by a rise in serum glutamic oxalacetic transaminase. The electrocardiogram taken on admission is shown in Figure 1, The patient was treated with salt restriction, digitalization and diuretics. She continued to be febrile. Pneumonia was diagnosed and treated with
JANUARY 1964
week, she became
DISCUSSION
.4n 85 year old Puerto Rican
* From the Electrocardiography Station, Department ment of Medicine, Seton Hall College of Medicine.
During the second and died.
of Medicine,
81
the Jersey City Medical
Center, and The Depart-
Wagner
82
FIG. 1.
Elrctrocardiogram
and Arbeit
taken on April 4, 1063, at 7:15 A.M.
dropped atria1 beat1 Here, too, the greatest increments in sinoatrial conduction must occur in the earliest beats, for the P-P intervals progressively shorten and the atria accelerate prior to the dropped beat. Intermittent Bundle Branch Block and Myocardial Infarction: The second phenomenon which these tracings illustrate is the interplay between cardiac rate and the refractory state of conducting tissues in the production of intermittent conduction disturbances. Shortening of the R-R interval below a critical level, with exrate of conduction,” ceeding of the “critical may result in impingement of succeeding impulses upon conducting tissues still refractory from those preceding. This may be manifested
as aberrancy of intraventricular conduction, or, if one of the bundle branches is more specifically involved, as a rate-conditioned bundle branch block.3 --7 In this tracing, the dominant beats have a left bundle branch block configuration. However, those beats terminating the long R-R occasioned by the second degree intervals, sinoatrial block, have a normal QRS duration, indicating that they are normally conducted. Hence, the left bundle branch block of this electrocardiogram is rate-conditioned, with the longer R-R intervals allowing time for the refractory tissues of the “fatigued” left bundle branch to recover and conduct normally. Inspection of these normally conducted THE
AMERICAN
JOURNAL
OF
CARDIOLOGY
Myocardial
Infarction
cu~nplescs re\-eals a (2 wave in VI-V?, with ele\.ated RS-7’ segments and inverted T waves, the classic pattern of an acute anteroseptal m).ocardial infarction. The dominant left bundle branch block complexes give no indication of this. The masking of an infarction pattern by a block in the left bundle branch is a well known occurrence, explained by the fact that both conditions affect initial depolarization forces. This is particularly well illustrated in this tracing. SUMMARY A case is presented of second degree sinoatrial block with Wenckebach periods, and a rateconditioned left bundle branch block masking an acute anteroseptal myocardial infarction which is revealed in the normally conducted beats occurring in the pauses caused by the second degree sinoatrial block. The mechanisms underlying this unusual tracing are discussed.
JANUARY
1964
IJnmasked
t)y :b-rhythmia
1.
DXIIERI~,
2.
GREENWOOD,
G.
M., .IK., RUSNN, .\. and
83
BRIXLJLI:\
, P.
lnteratrial and sinoatrial block, with an illtlstratix-c case. :lm. Hm,_t J., 31: 352, 1946.
R. J., FINKELSTEIN, D. and MONHEIT, R. Sinoatrial blcck with \venrkebach phenomenon. Alnz.J. Cnrdiol., 8: 140, 1961.
3. VESELL, H.
Critical rates in ventricular conduction. Unstable bundle branch block. .+u. J. .\f. SC., 202 : 138, 1941.
4. VESELI.,H. Critical rates in ventricular conduction. II. Simulation of localized bundle branch block. :inl. Hmt J., 41: 46, 1951. 5. VESELL, H. and KRAEMER, L. B. Critical rates in ventricular conduction. m. Simulation of ventricular tachycardia. Am. Heart J., 41 : 280, 1951. 6. VESELL, H. and FRIEDFELD, L. Critical rates in ventricular conduction. IV. Duration of unstable bundle branch block. ;Im. Hrart J., 44: 830, 1952. 7. SHEARN, M. A. and KYTAND, D. A. Intermittent bundle branch block. Observations with special reference to the critical heart rate. .Irch. Int. .\fcd., 91: 448. 1953.