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Bigeminal rhythms, common and uncommon mechanisms
Journal of Electrocardiology 40 (2007) 135 – 138 www.elsevier.com/locate/jelectrocard
Bigeminal rhythms, common and uncommon mechanisms Kyuhyun Wang, MD,a,4 Richard W. Asinger, MD,a Henry J.L. Marriott, MDb a
Department of Internal Medicine, Hennepin County Medical Center and University of Minnesota, Minneapolis, MN, USA b Department of Internal Medicine, University of South Florida, Tampa, FL, USA Received 23 February 2006; accepted 21 April 2006
Abstract
Bigeminy is an often encountered arrhythmia in clinical practice. There are common and uncommon mechanisms for bigeminy. Typical examples are illustrated with their salient electrocardiographic and clinical features. When one encounters a bigeminal rhythm, an awareness of these numerous possibilities will facilitate arriving at the correct diagnosis, which is where quality patient care begins. D 2007 Elsevier Inc. All rights reserved.
The pairing of cardiac beats is an often encountered arrhythmia. The most common cause of such paired beats is bigeminy resulting from coupled ventricular or atrial premature beats. These can usually be recognized and distinguished with ease from the electrocardiogram. At times, however, they may be difficult to distinguish, as when the P wave of an atrial premature beat is lost on the T wave and its QRS is aberrantly conducted. There are many other less common causes of paired beats; some are clinically important, and some are inconsequential. It may be important to make a precise diagnosis. For this reason, we have assembled here the common and less common causes of bigeminy and reviewed their electrocardiographic differentiating features and, when pertinent, their appropriate management. Type 1 second-degree atrioventricular (AV) block (AV Wenckebach phenomenon) with a 3:2 AV conduction ratio is one of the causes of paired QRS complexes (Fig. 1A). In this situation, the longer cycle is less than twice the shorter cycle because the second of the paired QRS complexes is delayed by the amount of the PR interval increment. In type 2 second-degree AV block with a 3:2 conduction ratio (Fig. 1B), the longer cycle is equal to twice the shorter cycle because the second of the paired QRS complexes is not delayed. The distinction between types 1 and 2 second-degree AV block is important because the causes, the site of the block, 4 Corresponding author. Division of Cardiology, Department of Internal Medicine, Hennepin County Medical Center, 701 Park Avenue, South Minneapolis, MN 55415, USA. Tel.: +1 612 873 2875; fax: +1 612 904 4224. E-mail address: [email protected] 0022-0736/$ – see front matter D 2007 Elsevier Inc. All rights reserved. doi:10.1016/j.jelectrocard.2006.04.005
and the prognosis are all different.1 In type 1, the block is almost always within the AV node (rarely within or below the His bundle), due to reversible conditions (eg, drugs, ischemia, inflammation, or increased vagal tone), and is therefore transient. When it progresses to complete (38) AV block, an AV junctional pacemaker will escape at a reasonable rate (40-50/min) and is transient. On the other hand, in type 2, the block is below the His bundle due to irreversible conditions (eg, fibrosis or infarction), and the prognosis is poor. When it progresses to complete a 38 AV block, a ventricular escape rhythm will emerge at a slower rate (20-30/min), requiring an electronic pacemaker. If myocardial infarction is the cause of the 28 AV block, an inferior infarction results in type 1 and an anteroseptal infarction type 2. This is because the cause of the AV block in inferior infarction is either locally released adenosine2 or transient ischemia because the AV node has dual blood supply, the primary blood supply from either the right or the circumflex coronary artery (whichever is the dominant artery in that patient), and the secondary blood supply from the first septal perforator of the anterior descending coronary artery.3 On the other hand, the AV block in anteroseptal infarction results from the intraventricular conduction system being caught in the infarction process and is not transient. An example of atrial tachycardia with a 3:2 AV Wenckebach phenomenon is shown in Fig. 1C. The P waves occur regularly. The first atrial impulse is conducted to the ventricle with a normal PR interval, the second with a longer PR interval, and every third impulse is blocked. Atrial tachycardia with variable AV conduction is a common arrhythmia during digitalis intoxication. However, because digitalis is not frequently used today, it is more often a
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K. Wang et al. / Journal of Electrocardiology 40 (2007) 135 – 138
Fig. 1. Examples of 3:2 conduction at various conduction levels resulting in paired QRS complexes. A: 3:2 AV Wenckebach phenomenon. B: 3:2 AV block, type 2. C: Atrial tachycardia with 3:2 AV Wenckebach phenomenon. D: Junctional tachycardia with 3:2 exit block while the atria are fibrillating. E: Atrial flutter with 3:2 AV Wenckebach phenomenon. F: 3:2 SA block, type 1. G: 3:2 SA block, type 2. (See text for explanations).
primary rhythm problem in elderly patients. Some of these rhythms are atrial reentrant and can be converted with adenosine. Otherwise, it can be converted with intravenous ibutilide or electric shock to the precordium. If the rhythm is due to digitalis intoxication, electric shock to the precordium is contraindicated because there is the risk of precipitating fatal ventricular arrhythmias.4,5 In Fig. 1D, the atria are fibrillating, and AV junctional tachycardia has developed as a manifestation of digitalis intoxication. Instead of every junctional impulse conducting to the ventricles consistently, the second impulse is delayed, and every third impulse is blocked: junctional tachycardia with 3:2 exit block resulting in paired QRS complexes. Digitalis should be withheld. Atrial flutter with a 3:2 AV conduction ratio also results in paired QRSs (Fig. 1E). The atrial rate close to 300/min indicates that the rhythm is atrial flutter. The block between the sinus node and atria (SA block), with a 3:2 conduction ratio, also results in paired QRS complexes as seen in Fig. 1F. The SA block, like the AV block, can be either type 1 or type 2. If the longer cycle is less than twice the shorter cycle, it is type 1, and if the longer cycle is equal to 2 shorter cycles, it is type 2
(Fig. 1G). The SA block is a form of sinus node dysfunction and may be secondary to medications. In that case, withholding the medication will correct the rhythm. If it is intrinsic, it is a manifestation of sick sinus syndrome. Only if the patient is symptomatic from the bradycardia is an electronic pacemaker indicated. Symptoms include dizziness, syncope, or extreme weakness. Thus, AV or SA block with a 3:2 conduction ratio will always result in paired QRS complexes, but not all paired QRS complexes are due to 3:2 conduction. In fact, one of the common causes of paired QRS complexes is atrial bigeminy (ie, every other beat is an atrial premature beat; Fig. 2A). There is a premature, ectopic P wave in front of each of these premature QRS complexes, although at times the P wave may be obscured. If the premature beat occurs at a time when 1 bundle branch (more often the right) is still refractory when the other bundle branch has recovered, the impulse will be conducted to the ventricle aberrantly, resulting in different-looking, wide QRS complexes simulating ventricular bigeminy (Fig. 2B). Identifying a prematurely occurring P wave in front of these QRS complexes will clinch the correct diagnosis. In addition, if these premature impulses occur when the AV junction has
K. Wang et al. / Journal of Electrocardiology 40 (2007) 135 – 138
137
Fig. 2. Various causes of paired QRS complexes. A: Atrial bigeminy. B: Atrial bigeminy with aberrant conduction. C: Junctional bigeminy. D: Ventricular bigeminy. E: Sinus bradycardia with junctional escape beats. F: Atrial flutter with alternating conduction ratio. G. Non-conducted atrial trigeminy. H: Pacemaker bigeminy. (See text for explanations). A: P wave.
not fully recovered from the refractory period, they may conduct to the ventricles with a longer PR interval as in this tracing. If the premature narrow-QRS complex has no P wave in front of it, then one is dealing with AV junctional bigeminy (ie, every other beat is a junctional premature beat; Fig. 2C). When these junctional premature beats are aberrantly conducted, the rhythm certainly can be mistaken for ventricular bigeminy unless there is a retrograde P wave in front of each premature QRS complex. However, both junctional and ventricular premature beats can have a retrograde P wave after the QRS complex or an anterograde P wave in front of, within, or after the QRS complex. An example of ventricular bigeminy is shown in Fig. 2D. Langendorf et al6 observed that the precipitation of a ventricular premature beat (VPB) is favored by a long preceding R-R interval. The compensatory pause after the VPB constitutes a long R-R interval, which in turn causes another VPB. Thus, there is a tendency for a VPB to initiate and perpetuate ventricular bigeminy. They proposed the
term rule of bigeminy for this tendency. The clinical significance of ventricular bigeminy is that of frequent VPBs, and can be serious because they can precipitate ventricular tachycardia or benign, depending upon the underlying cardiac condition. Ventricular bigeminy may occur during hypokalemia and disappear when the potassium level is corrected. An example of sinus bradycardia where every other beat is a junctional escape beat (escape-capture bigeminy) is shown in Fig. 2E. In this situation, there has to be retrograde block to the atria, otherwise the junctional impulse will enjoy 1:1 retrograde conduction to the atria and to the sinus node, resulting in a regular junctional escape rhythm. The primary problem in this situation is sinus bradycardia that may be because of too much certain medications including digitalis, b-blockers, some calcium channel blockers, clonidine, lithium,7 and, rarely, H2 blockers.8 If it is an intrinsic problem, it is a form of sick sinus syndrome. During atrial flutter, if the AV conduction ratio alternates (eg, 2:1 alternating with 3:1 or with 4:1, etc), paired QRS complexes result as in Fig. 2F. Nonconducted atrial
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K. Wang et al. / Journal of Electrocardiology 40 (2007) 135 – 138
Table 1 Various causes of bigeminal rhythm Causes
Comments
A. Coupled premature beats a. Atrial bigeminy
Every other beat being a premature beat A prematurely occurring P wave in front of the premature QRS complex The P wave may be obscured by the T wave. If the P wave is lost in the T wave, this rhythm may be mistaken for ventricular bigeminy. There may be an anterograde P wave in front of, within, or after the premature QRS complex with AV dissociation or a retrograde P wave in front, within, or after the QRS complex. There may be an anterograde P wave in front of, within, or after the premature QRS complex with AV dissociation or a retrograde P wave only after the QRS complex. The longer cycle is less than twice the shorter cycle in type 1, and the longer cycle is equal to twice the shorter cycle in type 2.
Atrial bigeminy with ventricular aberration b. Junctional bigeminy c. Ventricular bigeminy B. 3:2 Conduction ratio a. 3:2 AV block during sinus rhythm Type 1 Type 2 b. 3:2 SA block Type 1 Type 2 c. 3:2 AV Wenckebach phenomenon during atrial tachycardia or flutter d. 3:2 Exit block during junctional tachycardia C. Miscellaneous a. Escape-capture bigeminy b. Alternating AV conduction ratio during atrial flutter c. Nonconducted atrial trigeminy d. Pacemaker bigeminy
For example, every other beat being a junctional escape during sinus bradycardia For example, 2:1 ratio alternating with 3:1 or with 4:1, etc Every third beat is an atrial premature impulse that is not conducted to the ventricles due to refractory period. Electronic pacemaker mistakes every other T wave for a QRS complex (oversensing).
trigeminy also results in paired QRS complexes (Fig. 2G). Every third beat is an atrial premature impulse that occurs during the refractory period of the conduction system, resulting in nonconducted atrial trigeminy. The clinical significance of this situation is that of frequent atrial premature beats, which is relatively benign. The paired QRS complexes in Fig. 2H result from a demand electronic ventricular pacemaker mistaking every other T wave for a QRS complex (oversensing). Note that the distance between the peak of the T wave and the next pacer spike during the longer cycle is equal to the pacer-pacer interval during the shorter cycle—a rare cause of paired QRS complexes. Thus, there is a long list of causes for paired QRS complexes (Table 1). Typical examples have been illustrated with their salient electrocardiographic and clinical features. When one encounters a bigeminal rhythm, an awareness of these numerous possibilities will facilitate arriving at the correct diagnosis, which is where quality patient care begins.
References 1. Zipes DP, Jalife J. Cardiac electrophysiology from cell to bedside. 2nd ed Philadelphia7 W.B. Saunders Company; 1995. p. 936. 2. Bertolet BD, McMurtrie EB, Hill JA, et al. Theophylline for the treatment of atrioventricular block after myocardial infarction. Ann Intern Med 1995;123:509. 3. Bassan R, Maia IG, Bozza A, et al. Atrioventricular block in acute inferior wall myocardial infarction: harbinger of associated obstruction of the left anterior descending coronary artery. J Am Coll Cardiol 1986; 8:773. 4. Rabbino MD, Likoff W, Dreifus LS. Complications and limitations of direct-current countershock. JAMA 1964;190:417. 5. Lown B, Kleiger R, Williams J. Cardioversion and digitalis drugs: changed threshold to electric shock in digitalized animals. Circ Res 1965;XVII:519. 6. Langendorf R, Pick A, Winternitz M. Mechanisms of intermittent ventricular bigeminy. I. Appearance of ectopic beats dependent upon length of cycle, the brule of bigeminyQ. Circulation 1955;11:422. 7. Wellens HJJ, Cats V, Duren DR. Symptomatic sinus node abnormalities following lithium carbonate therapy. Am J Med 1975;59:285. 8. Reding P, Devroede C, Barbier P. Bradycardia after cimetidine. Lancet 1977;2:1227.
Bigeminal rhythms, common and uncommon mechanisms Kyuhyun Wang, MD,a,4 Richard W. Asinger, MD,a Henry J.L. Marriott, MDb a
Department of Internal Medicine, Hennepin County Medical Center and University of Minnesota, Minneapolis, MN, USA b Department of Internal Medicine, University of South Florida, Tampa, FL, USA Received 23 February 2006; accepted 21 April 2006
Abstract
Bigeminy is an often encountered arrhythmia in clinical practice. There are common and uncommon mechanisms for bigeminy. Typical examples are illustrated with their salient electrocardiographic and clinical features. When one encounters a bigeminal rhythm, an awareness of these numerous possibilities will facilitate arriving at the correct diagnosis, which is where quality patient care begins. D 2007 Elsevier Inc. All rights reserved.
The pairing of cardiac beats is an often encountered arrhythmia. The most common cause of such paired beats is bigeminy resulting from coupled ventricular or atrial premature beats. These can usually be recognized and distinguished with ease from the electrocardiogram. At times, however, they may be difficult to distinguish, as when the P wave of an atrial premature beat is lost on the T wave and its QRS is aberrantly conducted. There are many other less common causes of paired beats; some are clinically important, and some are inconsequential. It may be important to make a precise diagnosis. For this reason, we have assembled here the common and less common causes of bigeminy and reviewed their electrocardiographic differentiating features and, when pertinent, their appropriate management. Type 1 second-degree atrioventricular (AV) block (AV Wenckebach phenomenon) with a 3:2 AV conduction ratio is one of the causes of paired QRS complexes (Fig. 1A). In this situation, the longer cycle is less than twice the shorter cycle because the second of the paired QRS complexes is delayed by the amount of the PR interval increment. In type 2 second-degree AV block with a 3:2 conduction ratio (Fig. 1B), the longer cycle is equal to twice the shorter cycle because the second of the paired QRS complexes is not delayed. The distinction between types 1 and 2 second-degree AV block is important because the causes, the site of the block, 4 Corresponding author. Division of Cardiology, Department of Internal Medicine, Hennepin County Medical Center, 701 Park Avenue, South Minneapolis, MN 55415, USA. Tel.: +1 612 873 2875; fax: +1 612 904 4224. E-mail address: [email protected] 0022-0736/$ – see front matter D 2007 Elsevier Inc. All rights reserved. doi:10.1016/j.jelectrocard.2006.04.005
and the prognosis are all different.1 In type 1, the block is almost always within the AV node (rarely within or below the His bundle), due to reversible conditions (eg, drugs, ischemia, inflammation, or increased vagal tone), and is therefore transient. When it progresses to complete (38) AV block, an AV junctional pacemaker will escape at a reasonable rate (40-50/min) and is transient. On the other hand, in type 2, the block is below the His bundle due to irreversible conditions (eg, fibrosis or infarction), and the prognosis is poor. When it progresses to complete a 38 AV block, a ventricular escape rhythm will emerge at a slower rate (20-30/min), requiring an electronic pacemaker. If myocardial infarction is the cause of the 28 AV block, an inferior infarction results in type 1 and an anteroseptal infarction type 2. This is because the cause of the AV block in inferior infarction is either locally released adenosine2 or transient ischemia because the AV node has dual blood supply, the primary blood supply from either the right or the circumflex coronary artery (whichever is the dominant artery in that patient), and the secondary blood supply from the first septal perforator of the anterior descending coronary artery.3 On the other hand, the AV block in anteroseptal infarction results from the intraventricular conduction system being caught in the infarction process and is not transient. An example of atrial tachycardia with a 3:2 AV Wenckebach phenomenon is shown in Fig. 1C. The P waves occur regularly. The first atrial impulse is conducted to the ventricle with a normal PR interval, the second with a longer PR interval, and every third impulse is blocked. Atrial tachycardia with variable AV conduction is a common arrhythmia during digitalis intoxication. However, because digitalis is not frequently used today, it is more often a
136
K. Wang et al. / Journal of Electrocardiology 40 (2007) 135 – 138
Fig. 1. Examples of 3:2 conduction at various conduction levels resulting in paired QRS complexes. A: 3:2 AV Wenckebach phenomenon. B: 3:2 AV block, type 2. C: Atrial tachycardia with 3:2 AV Wenckebach phenomenon. D: Junctional tachycardia with 3:2 exit block while the atria are fibrillating. E: Atrial flutter with 3:2 AV Wenckebach phenomenon. F: 3:2 SA block, type 1. G: 3:2 SA block, type 2. (See text for explanations).
primary rhythm problem in elderly patients. Some of these rhythms are atrial reentrant and can be converted with adenosine. Otherwise, it can be converted with intravenous ibutilide or electric shock to the precordium. If the rhythm is due to digitalis intoxication, electric shock to the precordium is contraindicated because there is the risk of precipitating fatal ventricular arrhythmias.4,5 In Fig. 1D, the atria are fibrillating, and AV junctional tachycardia has developed as a manifestation of digitalis intoxication. Instead of every junctional impulse conducting to the ventricles consistently, the second impulse is delayed, and every third impulse is blocked: junctional tachycardia with 3:2 exit block resulting in paired QRS complexes. Digitalis should be withheld. Atrial flutter with a 3:2 AV conduction ratio also results in paired QRSs (Fig. 1E). The atrial rate close to 300/min indicates that the rhythm is atrial flutter. The block between the sinus node and atria (SA block), with a 3:2 conduction ratio, also results in paired QRS complexes as seen in Fig. 1F. The SA block, like the AV block, can be either type 1 or type 2. If the longer cycle is less than twice the shorter cycle, it is type 1, and if the longer cycle is equal to 2 shorter cycles, it is type 2
(Fig. 1G). The SA block is a form of sinus node dysfunction and may be secondary to medications. In that case, withholding the medication will correct the rhythm. If it is intrinsic, it is a manifestation of sick sinus syndrome. Only if the patient is symptomatic from the bradycardia is an electronic pacemaker indicated. Symptoms include dizziness, syncope, or extreme weakness. Thus, AV or SA block with a 3:2 conduction ratio will always result in paired QRS complexes, but not all paired QRS complexes are due to 3:2 conduction. In fact, one of the common causes of paired QRS complexes is atrial bigeminy (ie, every other beat is an atrial premature beat; Fig. 2A). There is a premature, ectopic P wave in front of each of these premature QRS complexes, although at times the P wave may be obscured. If the premature beat occurs at a time when 1 bundle branch (more often the right) is still refractory when the other bundle branch has recovered, the impulse will be conducted to the ventricle aberrantly, resulting in different-looking, wide QRS complexes simulating ventricular bigeminy (Fig. 2B). Identifying a prematurely occurring P wave in front of these QRS complexes will clinch the correct diagnosis. In addition, if these premature impulses occur when the AV junction has
K. Wang et al. / Journal of Electrocardiology 40 (2007) 135 – 138
137
Fig. 2. Various causes of paired QRS complexes. A: Atrial bigeminy. B: Atrial bigeminy with aberrant conduction. C: Junctional bigeminy. D: Ventricular bigeminy. E: Sinus bradycardia with junctional escape beats. F: Atrial flutter with alternating conduction ratio. G. Non-conducted atrial trigeminy. H: Pacemaker bigeminy. (See text for explanations). A: P wave.
not fully recovered from the refractory period, they may conduct to the ventricles with a longer PR interval as in this tracing. If the premature narrow-QRS complex has no P wave in front of it, then one is dealing with AV junctional bigeminy (ie, every other beat is a junctional premature beat; Fig. 2C). When these junctional premature beats are aberrantly conducted, the rhythm certainly can be mistaken for ventricular bigeminy unless there is a retrograde P wave in front of each premature QRS complex. However, both junctional and ventricular premature beats can have a retrograde P wave after the QRS complex or an anterograde P wave in front of, within, or after the QRS complex. An example of ventricular bigeminy is shown in Fig. 2D. Langendorf et al6 observed that the precipitation of a ventricular premature beat (VPB) is favored by a long preceding R-R interval. The compensatory pause after the VPB constitutes a long R-R interval, which in turn causes another VPB. Thus, there is a tendency for a VPB to initiate and perpetuate ventricular bigeminy. They proposed the
term rule of bigeminy for this tendency. The clinical significance of ventricular bigeminy is that of frequent VPBs, and can be serious because they can precipitate ventricular tachycardia or benign, depending upon the underlying cardiac condition. Ventricular bigeminy may occur during hypokalemia and disappear when the potassium level is corrected. An example of sinus bradycardia where every other beat is a junctional escape beat (escape-capture bigeminy) is shown in Fig. 2E. In this situation, there has to be retrograde block to the atria, otherwise the junctional impulse will enjoy 1:1 retrograde conduction to the atria and to the sinus node, resulting in a regular junctional escape rhythm. The primary problem in this situation is sinus bradycardia that may be because of too much certain medications including digitalis, b-blockers, some calcium channel blockers, clonidine, lithium,7 and, rarely, H2 blockers.8 If it is an intrinsic problem, it is a form of sick sinus syndrome. During atrial flutter, if the AV conduction ratio alternates (eg, 2:1 alternating with 3:1 or with 4:1, etc), paired QRS complexes result as in Fig. 2F. Nonconducted atrial
138
K. Wang et al. / Journal of Electrocardiology 40 (2007) 135 – 138
Table 1 Various causes of bigeminal rhythm Causes
Comments
A. Coupled premature beats a. Atrial bigeminy
Every other beat being a premature beat A prematurely occurring P wave in front of the premature QRS complex The P wave may be obscured by the T wave. If the P wave is lost in the T wave, this rhythm may be mistaken for ventricular bigeminy. There may be an anterograde P wave in front of, within, or after the premature QRS complex with AV dissociation or a retrograde P wave in front, within, or after the QRS complex. There may be an anterograde P wave in front of, within, or after the premature QRS complex with AV dissociation or a retrograde P wave only after the QRS complex. The longer cycle is less than twice the shorter cycle in type 1, and the longer cycle is equal to twice the shorter cycle in type 2.
Atrial bigeminy with ventricular aberration b. Junctional bigeminy c. Ventricular bigeminy B. 3:2 Conduction ratio a. 3:2 AV block during sinus rhythm Type 1 Type 2 b. 3:2 SA block Type 1 Type 2 c. 3:2 AV Wenckebach phenomenon during atrial tachycardia or flutter d. 3:2 Exit block during junctional tachycardia C. Miscellaneous a. Escape-capture bigeminy b. Alternating AV conduction ratio during atrial flutter c. Nonconducted atrial trigeminy d. Pacemaker bigeminy
For example, every other beat being a junctional escape during sinus bradycardia For example, 2:1 ratio alternating with 3:1 or with 4:1, etc Every third beat is an atrial premature impulse that is not conducted to the ventricles due to refractory period. Electronic pacemaker mistakes every other T wave for a QRS complex (oversensing).
trigeminy also results in paired QRS complexes (Fig. 2G). Every third beat is an atrial premature impulse that occurs during the refractory period of the conduction system, resulting in nonconducted atrial trigeminy. The clinical significance of this situation is that of frequent atrial premature beats, which is relatively benign. The paired QRS complexes in Fig. 2H result from a demand electronic ventricular pacemaker mistaking every other T wave for a QRS complex (oversensing). Note that the distance between the peak of the T wave and the next pacer spike during the longer cycle is equal to the pacer-pacer interval during the shorter cycle—a rare cause of paired QRS complexes. Thus, there is a long list of causes for paired QRS complexes (Table 1). Typical examples have been illustrated with their salient electrocardiographic and clinical features. When one encounters a bigeminal rhythm, an awareness of these numerous possibilities will facilitate arriving at the correct diagnosis, which is where quality patient care begins.
References 1. Zipes DP, Jalife J. Cardiac electrophysiology from cell to bedside. 2nd ed Philadelphia7 W.B. Saunders Company; 1995. p. 936. 2. Bertolet BD, McMurtrie EB, Hill JA, et al. Theophylline for the treatment of atrioventricular block after myocardial infarction. Ann Intern Med 1995;123:509. 3. Bassan R, Maia IG, Bozza A, et al. Atrioventricular block in acute inferior wall myocardial infarction: harbinger of associated obstruction of the left anterior descending coronary artery. J Am Coll Cardiol 1986; 8:773. 4. Rabbino MD, Likoff W, Dreifus LS. Complications and limitations of direct-current countershock. JAMA 1964;190:417. 5. Lown B, Kleiger R, Williams J. Cardioversion and digitalis drugs: changed threshold to electric shock in digitalized animals. Circ Res 1965;XVII:519. 6. Langendorf R, Pick A, Winternitz M. Mechanisms of intermittent ventricular bigeminy. I. Appearance of ectopic beats dependent upon length of cycle, the brule of bigeminyQ. Circulation 1955;11:422. 7. Wellens HJJ, Cats V, Duren DR. Symptomatic sinus node abnormalities following lithium carbonate therapy. Am J Med 1975;59:285. 8. Reding P, Devroede C, Barbier P. Bradycardia after cimetidine. Lancet 1977;2:1227.