- Email: [email protected]
Electrocardiographic manifestations: diagnosis of atrioventricular block in the Emergency Department
The Journal of Emergency Medicine, Vol. 26, No. 1, pp. 95–106, 2004 Copyright © 2004 Elsevier Inc. Printed in the USA. All rights reserved 0736-4679/04 $–see front matter
doi:10.1016/j.jemermed.2003.10.001
Selected Topics: Cardiology Commentary
ELECTROCARDIOGRAPHIC MANIFESTATIONS: DIAGNOSIS OF ATRIOVENTRICULAR BLOCK IN THE EMERGENCY DEPARTMENT Geoffrey E. Hayden,
MD,*
William J. Brady, MD,† Marc Pollack, Richard A. Harrigan, MD§
MD, PhD,‡
and
*Department of Emergency Medicine, Vanderbilt University, Nashville, Tennessee, †Department of Emergency Medicine, University of Virginia, Charlottesville, Virginia, ‡Department of Emergency Medicine, York Hospital, York, Pennsylvania, and §Department of Emergency Medicine, Department of Internal Medicine, Temple University, Philadelphia, Pennsylvania Reprint Address: William Brady, MD, Department of Emergency Medicine, Box 800699, University of Virginia Medical Center, Charlottesville, VA 22908
e Abstract—Patients with bradycardia are commonly encountered by the Emergency Physician. Of the possible bradydysrhythmias, atrioventricular blocks (AVB) represent a significant portion of these presentations. In this article, we provide four illustrative cases of patients presenting to the Emergency Department (ED) with AVB. We review the various types of AV block dysrhythmias (1st, 2nd, and 3rd degrees) and their underlying etiologies. This discussion also focuses on the presentation, clinical considerations, management and acute treatment of AVB dysrhythmias in the emergent setting. © 2004 Elsevier Inc.
in hemodynamically unstable patients. These patients, if properly diagnosed and appropriately treated, may have significantly improved outcomes. The following scenarios provide illustrative cases of patients presenting to the ED with atrioventricular block.
CASE PRESENTATIONS Case 1
e Keywords— electrocardiogram; atrioventricular block
A 51-year-old man without past medical history experienced a ground-level fall, resulting in a complex ankle fracture. The Emergency Medical Service (EMS) personnel were summoned and found the man, alert and in no obvious distress with the exception of significant left lower extremity deformity at the ankle. The patient was transported to the ED via ambulance. Examination revealed the ankle injury without other complicating issue; the vital signs were normal. Electrocardiographic (EKG) monitoring (Figure 1) and 12-lead electrocardiogram demonstrated normal sinus rhythm (NSR) with firstdegree AVB. The patient was admitted to the hospital for operative repair. His hospital course was uneventful; no further care of his AVB was felt necessary.
INTRODUCTION The presentation of a patient with compromising bradydysrhythmia to the Emergency Department (ED) requires a timely, effective diagnostic and therapeutic approach by the Emergency Physician (EP). Of the possible bradycardic rhythms, atrioventricular blocks (AVB) represent a significant portion of these presentations (1,2). Immediate consideration of several potential causes, including both ischemic and non-ischemic etiologies, is essential. Presentations range from the incidental finding in asymptomatic patients to life-threatening heart block
Selected Topics: Cardiology Commentary is coordinated by Theodore Chan, MD, of the University of California San Diego Medical Center, San Diego, California and William Brady, MD, of the University of Virginia, Charlottesville, Virginia 95
96
G. E. Hayden et al.
Figure 1. Rhythm strip revealing sinus rhythm with prolongation of the PR interval and constant 1:1 atrioventricular relationship – findings consistent with first-degree AVB.
Case 2 A 55-year-old man with a history of myocardial infarction presented to EMS personnel with chest pain. EMS found the patient to be alert with vital signs of a blood pressure 125/88 mm Hg, a pulse 65 beats/min (regular with occasional irregularity), and respirations of 24 breaths/min. The remainder of the examination was significant for diaphoresis and anxiety. The single-lead EKG monitor revealed NSR with second-degree, type I AVB (Figure 2). The patient was transported to the ED with nitroglycerin therapy and aspirin. On arrival, he remained alert with unchanged vital signs. Cardiopulmonary findings were significant for clear lung fields. Multi-lead rhythm strips and 12-lead
EKG monitoring was initiated, revealing NSR with second-degree, type I AVB as seen by EMS; evidence of inferior ST segment depression was also seen. The patient received additional anti-anginal therapy with resolution of chest pain; atropine was given without effect. Transcutaneous pacing pads were applied while Cardiology was consulted for a transvenous pacing wire. He was admitted to the hospital with a course remarkable for positive troponins and recurrent chest pain. Cardiac catheterization demonstrated proximal right coronary disease with thrombus that was successfully opened and stented. The patient was ultimately discharged with a diagnosis of non-ST segment elevation acute myocardial infarction and AVB that resolved with restoration of coronary perfusion.
Figure 2. Rhythm strip revealing sinus rhythm with progressive prolongation of the PR interval, ultimately resulting in a dropped beat – findings consistent with second-degree, type I AVB.
Electrocardiographic Diagnosis of Atrioventricular Block
97
Figure 3. Rhythm strip revealing a wide QRS complex rhythm; evidence of atrioventricular conduction was noted with consistent P wave—QRS complex relationship. The PR interval is constant with abrupt dropped beats—findings consistent with seconddegree, type II AVB. In two instances on this rhythm strip, high-degree AVB is noted with several non-conducted P waves occurring before restoration of atrioventricular conduction.
Case 3 A 65-year-old woman with a history of angina and coronary artery disease experienced progressive weakness followed by syncope; she also noted chest discomfort. The EMS personnel were summoned and found an alert female. The EKG monitor revealed a wide QRS complex with irregularity (Figure 3). The patient had vital signs within normal limits with the exception of the pulse (50 beats/min). On arrival in the ED, the clinical situation was unchanged with the notable exception of hypotension. The EKG revealed a regular wide QRS complex rhythm with frequent dropped beats; further analysis revealed AVB (second degree, type II). The patient underwent transcutaneous pacing with normalization of perfusion and resolution of chest pain; arrangements were made with Cardiology for a transvenous pacemaker. She was admitted to the coronary care unit with a course remarkable for negative rule-out myocardial infarction protocol. A permanent ventricular pacemaker was inserted and the patient was discharged with a diagnosis of symptomatic second-degree AVB.
Case 4 A 48-year-old man was doing yard work when he gradually developed chest pain, dyspnea, and profound dizziness. Upon EMS arrival, the patient appeared diaphoretic but alert. Monitoring revealed a wide QRS complex rhythm at a rate of approximately 50 beats per minute; evidence of complete AV dissociation was noted, consistent with third-degree AVB (Figure 4). Appropriate therapy was initiated and the patient was trans-
ported to the ED. Upon arrival, he was awake and alert, complaining only of chest discomfort. Soon after ED arrival, he became unresponsive associated with a marked reduction in his blood pressure; the monitor revealed continued third-degree AVB with a significantly slower ventricular escape rhythm. Immediate transcutaneous pacing was applied with restoration of mental status and normal perfusion. The patient was admitted to the hospital with placement of a transvenous pacing wire and complete reliance on the pacemaker for approximately 20 h. He slowly developed sinus rhythm with bradycardia that normalized to NSR. It was ultimately determined that the patient had inadvertently used excessive metoprolol in conjunction with his long-term verapamil therapy for hypertension.
DISCUSSION Heart block is a descriptive term used to characterize a disturbance in the conduction of the electrical impulse in the heart—in this case, in and around the atrioventricular (AV) node. This disturbance can be partial or complete, resulting in either a delayed or an entirely blocked impulse. The conduction disturbance most commonly results from dysfunction in the following areas of the heart’s conduction system: between the sinus node and atrium (sinoatrial block), between the atria and ventricles (AV block [AVB]), within the atria (intra-atrial block), or within the ventricles (intra-ventricular block) (3). This review focuses on AVB (Figure 5), which generally results from dysfunction in one of three areas of the cardiac conduction system: the AV node (above the His bundle); the His bundle (intra-Hisian); or the distal His bundle or the bundle branches (infra-Hisian); these forms
98
G. E. Hayden et al.
Figure 4. Rhythm strip revealing a wide QRS complex rhythm; evidence of complete atrioventricular dissociation was noted without evidence of atrioventricular communication. The rhythm disturbance was diagnosed as third-degree AVB.
of AVB include first-degree, second-degree (types I and II), and third-degree disturbances (3,4). Although the surface electrocardiogram (EKG) may not definitively identify the site of the AV block, certain electrocardiographic patterns serve not only to differentiate the various blocks but also to identify the site of origin. Multiple etiologies of AVB are encountered with the most common being acute myocardial infarction. Also of note among etiologies are myocardial ischemia,
Figure 5. Atrioventricular block. (A) First-degree AVB. (B) Second-degree, type I AVB. (C) Second-degree, type II AVB with narrow QRS complex. (D) Second-degree, type II AVB with wide QRS complex.
primary conduction disease, and medication effect (intentional and unintentional) (Figures 6 and 7) (1).
First-Degree Atrioventricular Block In first degree AVB, the PR interval is prolonged with a duration greater than 0.20 s and is constant without progressive change (Figure 8A and 8B). The P wave has normal morphology and precedes every QRS complex. The QRS complex also has a normal morphology and axis for the given patient and clinical situation. Every atrial impulse is conducted to the ventricles (Figures 1 and 8A, 8B). The increased PR interval is secondary to delayed impulse conduction in the atrium, the AV node, or the His-Purkinje system (4). The vast majority of first-degree AVBs present with narrow QRS complexes; the block is localized to the proximal conducting system in 87% of cases, whereas 13% of cases are located within the common bundle of His (5). First-degree block with wide QRS complexes (duration longer than 0.12 s) result from the following sites of dysfunction: proximal to the bundle (22%), distal to the bundle (33%), intra-Hisian (12%), and supra- or infra-Hisian (33%). In summary, in first-degree AVB with a normal QRS, the delay almost always occurs in the AV node; wide QRS may indicate delay in the AV node or His-Purkinje system. Epidemiologically, prolongation of the PR interval is a normal variant in 1 to 2% of the population (6). Reports have indicated that between 0.5% and 2% of normal young persons have prolonged PR intervals (7,8). Further, in a study of healthy middle-aged men with prolonged PR intervals and normal QRS complexes, the authors conclude that the EKG findings have no prog-
Electrocardiographic Diagnosis of Atrioventricular Block
99
Figure 6. Etiology of AVB in unstable prehospital patients.
nostic significance and are not associated with any ischemic heart disease (9). The clinical presentation of patients with first-degree AVB is generally benign. Rarely, various symptoms and signs may be observed, including palpitations, dizziness, syncope, and angina; these would correspond to insufficient cardiac output precipitated by the AVB. Overall, the prognosis for patients with first-degree AVB is excellent; no therapy is indicated in the asymptomatic patient. This statement includes asymptomatic individuals with chronic bifascicular block, in whom the rate of progression to third-degree AVB remains low; prophylactic pacing is still not indicated (10). Some dispute surrounds patients with first-degree AVB and symptoms of low cardiac output that is relieved by temporary pacing; similar controversy regards management of patients with coexistent chronic heart failure (CHF). These presentations are deemed Class II indications for pacing; in other words, there is a divergence of opinion or conflicting evidence regarding its usefulness and effectiveness, though, in this case, existing evidence favors its usefulness (11). Otherwise, the patient can be monitored over time for development of other conduction disturbances or hemodynamic compromise. Though
rare, first-degree AV block can be seen with acute rheumatic fever. The significance here is for valvular dysfunction and not rhythm disturbance.
Type I, Second-Degree Atrioventricular Block In Mobitz type I block, also known as Wenkebach AVB, P waves and QRS complexes are usually normal in terms of morphology and total duration (Figures 2 and 9A–C). The site of the block is usually at or above the AV node; as such, the QRS complex is narrow and the rate is sufficient to maintain adequate perfusion. In type I block, a specific pattern to the P wave-QRS complex relationship is encountered. The PR interval is often normal in the first beat of the series. Progressive PR interval lengthening with subsequent beats is observed until an impulse is unable to reach the ventricles, resulting in a nonconducted P wave. After the dropped beat, the PR interval returns to normal and the cycle repeats itself. A pattern to the RR interval is also seen. As the PR lengthens with subsequent beats, the RR interval becomes shorter. After the dropped beat, the RR interval in the subsequent beats tends to shorten. In fact, the RR interval
Figure 7. Incidence of various forms of AVB in ischemic and non-ischemic presentations.
100
G. E. Hayden et al.
Figure 8. First-degree AVB. (A) Sinus rhythm with prolongation of the PR interval and constant 1:1 atrioventricular relationship; note that PR interval is constant in length. (B) Insert below the rhythm strip (thick bar) demonstrates the characteristics of the PR interval – prolonged in each cycle and constant in length.
containing the dropped beat is less than two of the shorter cycles. One will also notice on the rhythm strip a grouping of beats that is especially noticeable with a tachycardia. Such a finding is referred to as grouped beating of Wenckebach (Figure 9C). Evidence on the EKG for Mobitz type I AVB includes the following: 1) progressive lengthening of the PR interval, then dropped beat; 2) progressive shortening of the RR interval; 3) the RR length of the dropped beat is less than twice the shortest cycle; and 4) grouped beating (Figures 2 and 9A–C) (3,4). Unfortunately, these “typical” features of Wenckebach group beating are observed in fewer than 50% of all cases of type I block (3,12). Denes et al. report that 86% of Wenckebach periods vary from the defining criteria in one or more ways (12). Rather, one may observe a number of divergences from the classic pattern. The PR intervals may not lengthen progressively; several PR intervals may share the same duration or a PR interval may decrease in duration. The second PR interval may not represent the greatest incremental increase in duration. The last PR increment may be of the greatest magnitude. Lastly, a non-conducted impulse may not be observed (4,12). These variations from the typical presentation have been explained by the role of the autonomic nervous system in regulating sinus rate and AV conduction (4). Most importantly, however, is that differentiation of these atypical forms has no clinical importance. His bundle recordings in patients with type I, seconddegree AVB have identified conduction disturbances in
the AV node in 72% cases as compared to only 9% intra-Hisian and 19% infra-Hisian (5). These numbers are consistent with other literature, which in the setting of a normal QRS localizes the block to the AV node (proximal to the His bundle) in almost all cases (13,14). A widened QRS complex, however, may indicate a block in the AV node, in the His bundle, or distal to the His bundle. Epidemiologically, type I, second-degree AVB may be infrequently observed in both trained athletes and normal persons during sleep, perhaps due to increased vagal tone (3,15,16). Outside of AMI, it may also occur with the ingestion of various medications used to prevent cardiac ischemia, control atrial fibrillation, or treat systemic hypertension (17). The clinical presentation of patients is generally benign. Accordingly, the prognosis and indicated management are based on the clinical setting and the presence of related heart disease. Asymptomatic individuals with no heart disease generally do well without therapy; in patients with structural heart disease, the prognosis is dependent on the natural history of the heart disease itself as opposed to the AVB (4). Patients may require only cardiac monitoring to follow the rare symptomatic presentation or progression to higher-grade AV block, which is unlikely except in cases involving acute myocardial infarction (AMI). In the occasional patient, this block is associated with systemic hypoperfusion and should be treated with atropine. Atropine should be given in 0.6 to 1 mg boluses, repeated every 5 min, not to exceed a total dose of 0.04
Electrocardiographic Diagnosis of Atrioventricular Block
101
Figure 9. Second-degree, type I AVB. (A) NSR with progressively prolonged PR interval, culminating in a dropped beat. (B) Insert below the rhythm strip (thick bar) demonstrates the characteristics of the PR interval—prolonged in each cycle with progression, ultimately resulting in a dropped beat (arrow)—i.e., no conduction to the ventricle and no QRS complex. (C) Grouped beating is demonstrated in these two examples of second-degree, type I AVB.
mg/kg. In patients with AMI, atropine and other medications are more likely to be effective if AVB develops within the first 6 h of signs of infarction. When effective, atropine will either abolish the block or accelerate the ventricular rhythm. In a significant minority of patients, atropine seems ineffective. Recently, it has been shown that adenosine may mediate some of the AVBs during AMI, possibly explaining atropine’s lack of efficacy in certain clinical situations (18). Methylxanthines, such as aminophylline and theophylline, are competitive antag-
onists of adenosine and may be successful in abolishing AVB when atropine is ineffective. If pharmacotherapy is ineffective, then a temporary transvenous pacemaker can be inserted in the symptomatic patient. During placement of the transvenous pacer, a transcutaneous pacemaker can be placed if the patient is hemodynamically unstable. Additionally, transvenous pacing is not recommended unless these patients are symptomatic with hypoperfusion, syncope, acute congestive heart failure, or ischemic chest pain (4). Asymp-
102
G. E. Hayden et al.
Figure 10. Second-degree, type II AVB. (A) Upper panel—Fixed PR interval without progressive change with sudden dropped beat and narrow QRS complex. Lower panel—Similar to upper panel example with wide QRS complex. (B) Nature of PR interval is seen in these examples of second-degree, type II AVB. Note the constant PR interval (constant length as indicated by the thick bars) and dropped beats (arrow).
tomatic patients with type I, second-degree AVB should not undergo transcutaneous or transvenous pacing (19).
Type II, Second-Degree Atrioventricular Block The PR interval in type II second-degree AVB is constant. The PR interval may be either normal or prolonged, but it is always constant without progressive PR interval lengthening. The QRS complex, conversely, is widened in most instances of type II second-degree AVB though narrow QRS complex rhythms are encountered (Figures 3 and 10A–B). This may help to distinguish it from 2:1 type I block that by EKG is not able to be differentiated from type II. The magnitude of the AVB is expressed as a ratio of P waves to QRS complexes (4). The QRS complex, in most cases, is wide (i.e., greater than 0.12 s). This finding is explained by its association
with bundle branch block (20,21). His bundle recordings indicate that the block is never localized to the His bundle; instead, 20% of cases occur in the common bundle and 80% in the bundle branches (5). Consistent with the general rule that blocks distal to the His bundle presume a more serious prognosis, type II blocks often progress to complete heart block (CHB) and produce Stokes-Adams syncope (3,4). This progression to CHB is a common finding in particular with patients suffering from extensive anterior infarctions. Patients with type II, second-degree AVB may be unstable at the time of assessment or may develop thirddegree block suddenly. If so, transvenous pacing should be instituted immediately. Patients can sometimes be supported with isoproterenol or transcutaneous pacing while the transvenous pacing wire is positioned. Patients concurrently suffering from AMI may be managed more aggressively. Atropine is rarely if ever the drug of choice
Electrocardiographic Diagnosis of Atrioventricular Block
103
Figure 11. Second-degree AVB with 2:1 conduction pattern (nontypable AVB).
for Mobitz II block. Atropine may increase the sinus rate while not affecting AV conduction, thus enhancing the degree of AVB. The American College of Cardiology/ American Heart Association (ACC/AHA) guidelines favor permanent pacing even in asymptomatic patients with type II, second-degree AVB (19). Atrioventricular Block with 2:1 Conduction Pattern At times, it may be difficult to distinguish between types I and II, second-degree block, based on the EKG. This non-typable second-degree AVB results from a 2:1 AVB ratio, or two P waves for one QRS complex (Figure 11). In this setting, the determination of progressively lengthening PR intervals versus stable intervals with intermittent non-conducted impulses may be impossible; precise identification would necessitate two or more consecutive impulse conductions. Therefore, it is reasonable to state that this EKG presentation preempts classification as a type I or type II, second-degree AVB (22). The precise location of 2:1 blocks is similarly confounding, with reports that the site of the block can be determined only in His recordings (23,24). A reasonable diagnostic approach is to patiently follow the EKG strips; appearance of an AVB pattern with two consecutive P waves conducted (e.g., a 3:2 block) would allow for more definitive determination of type I versus type II, second-degree AVB. Other diagnostic measures are described in the literature. Kaushik et al. note the value of certain maneuvers: 1) vagal maneuvers and beta-adrenergic blocking agents decrease conduction if the block results from a lesion in the AV node; 2) vagal maneuvers and beta-adrenergic blocking agents do not affect the conduction if the block results from a lesion located infranodally; 3) atropine increases conduction when the block results from an AV nodal lesion; and 4) atropine does not alter conduction if the block results from an infranodal lesion (25). Further, a number of EKG findings may favor a particular designation, in particular the
nature of the QRS complex interval. Specifically, a normal QRS duration is consistent with an AV nodal block, whereas a prolonged QRS is supportive of an infranodal block (4). PR intervals are less helpful, as fixed intervals in a 2:1 block have no diagnostic usefulness, and variable PR intervals in the absence of a narrow QRS do not specify an AV nodal block (25). The medical management of 2:1 AVB is also the subject of controversy. Although it is reasonable to treat the hemodynamically unstable patient with a narrow QRS complex with atropine, infranodal blocks (i.e., those presentations with widened QRS complex) may respond poorly to this approach. As the degree of AVB may be worsened by atropine, Kaushik et al. describe two important contraindications to atropine use in the setting of likely intra- or infra-Hisian AVB: 1) stable, wide QRS 2:1 AVB; and 2) 2:1 AVB that evolves into type II block (regardless of QRS duration) (25–28). Kusomoto and Goldschlager state that in an asymptomatic patient, a 2:1 block with a coexisting bundle branch block is an appropriate indication for pacing; the assumption is that, in this setting, the block is infranodal (29). This recommendation may be disputed by the finding of an AV nodal block in 15–20% of cases with 2:1 block and bundle branch block (25).
High-Degree (Advanced) Second-Degree Atrioventricular Block By definition, high-degree or advanced AV block indicates a block of two or more consecutive P waves (3). This form of second-degree block is diagnosed when a block of consecutive sinus impulses occurs (Figures 3 and 12) (4). When the patient is suffering an anterior MI, the high-degree AVB is likely a variation on type II, second-degree AVB with bilateral bundle branch block (4).
104
G. E. Hayden et al.
Figure 12. High-degree AVB. Note the presence of two non-conducted P waves.
Third-Degree Atrioventricular Block In complete or third-degree AVB, no impulses are conducted from the atria to the ventricles. With the absence of conduction of P waves to the ventricle, the atria and ventricle remain under the control of their respective pacemakers. Generally, if there is a junctional pacemaker, the ventricular rate is 40 – 60 beats/min and the QRS complex is narrow; a rate of 20 – 40 beats/min and a wide QRS usually indicate a ventricular pacemaker (Figures 4 and 13) (3,4). The escape rhythm, whether junctional or ventricular, is almost always regular, due in part to decreased autonomic control as compared to the sinus node (30). In contrast, the atrial pacemaker can be either sinus or ectopic (of normal rate), bradycardic, tachycardic, flutter, or fibrillation. Further, the atrial rate is almost always greater than the ventricular rate in patients with third-degree AVB, although in rare cases the block may be “isorhythmic,” with similar atrial and ventricular rates. In general, complete heart block can be confidently diagnosed only when the dissociation is prolonged and the ventricular rate is 45 beats/min or less (4). Specific EKG findings are dependent on the location of the block, with consequent prognostic significance. In general, third-degree blocks may occur within the AV node (narrow QRS and rate ⬎ 40 bpm) or infra-Hisian (wide QRS and rate ⬍ 40 bpm); these locations in general correspond to either congenital or acquired etiologies, respectively (4). A wide array of conditions may produce acquired third-degree AVB. Among these are surgery, electrolyte
disturbances (hyperkalemia), myoendocarditis (valve ring abscess, rheumatic fever, viral myocarditis, Lyme disease), tumors, Chagas disease, rheumatoid nodules, calcific aortic stenosis, myxedema, polymyositis, infiltrative processes (such as amyloid, sarcoid, or scleroderma), cardiomyopathy, hypothyroidism, hypothermia, sepsis, etc. In adults, drug toxicity (beta-blockers, calcium channel blockers, digoxin, quinidine, procainamide), coronary disease, and degenerative processes seem to be the most common causes of complete heart block (3,4,6,25). Other literature identifies idiopathic fibrosis as the most common finding in chronic complete AVB (30). The most common cause of third-degree AVB in children is congenital pathology, in particular, abnormal embryonic development of the AV node (3,4). Complete heart block (third-degree AVB) is a relatively common complication in myocardial infarctions, particularly in the setting of unstable bradydysrhythmias. These patients generally are either hemodynamically unstable at presentation or become unstable suddenly. The clinical manifestations reflect insufficient cardiac output, with palpitations, dizziness, presyncope or syncope, and angina. Sudden cardiac death is not rare. Elderly patients with third-degree AVB may manifest only symptoms of weakness or fatigue. In this population, special consideration is given to the medication regimen of cardioactive drugs. Patients with third-degree AVB and anterior MI are likely to be hemodynamically unstable at the initial assessment or develop hemodynamic embarrassment suddenly. These patients should have a transvenous pacemaker placed urgently. Many of these patients require
Figure 13. Third-degree AVB with wide QRS complex. No relationship of the P waves and QRS complexes is noted. The two structures are occurring independently of one another.
Electrocardiographic Diagnosis of Atrioventricular Block
permanent pacemakers. If the patient is unstable, atropine, isoproterenol, or transcutaneous pacing therapy should be instituted while placing the transvenous wire. In patients with inferior MI, the ventricular rate tends to be adequate to maintain cardiac output. If the ventricular rate is greater than 40 beats/min and the patient is stable, one can elect to place a transvenous pacer only if the clinical situation deteriorates. If the patient develops hypotension, heart failure, oliguria, or ventricular dysrhythmia, then atropine, isoproterenol, or transvenous pacing should be initiated. Patients with anterior infarctions and third-degree block should be treated aggressively for cardiogenic shock. A considerable body of literature has grown around the issue of the risk of progression to complete heart block in patients with AMI. A useful method to predict the potential for such progression considers the electrocardiographic presence of the following risk factors, including first-degree AVB, second-degree (types I and II) AVB, right bundle branch block (BBB), left BBB, left anterior fascicular block, and left posterior fascicular block (31). Each risk factor when noted on the 12-lead electrocardiogram receives a score of 1. The total score is added, which is then translated to the rate of occurrence of such AVB, giving the clinician the risk of progression to complete heart block in patients with AMI. A score of 0 carries a 1.2% risk of complete heart block development, whereas a score of 3 or more is associated with a significant possibility of complete heart block—36.4%. Intermediate scores of 1 and 2 have rates of occurrence of 7.8% and 25%, respectively (32). The ACC/AHA guidelines support permanent pacing for third-degree AVB at any anatomical level associated with any of the following: 1. Bradycardia with symptoms presumed to be due to AV block. 2. Dysrhythmias and other medial conditions that require drugs that result in symptomatic bradycardia. 3. Documented periods of asystole of ⱖ 3.0 s or any escape rate of ⬍ 40 beats/min in awake, symptomfree patients. 4. After catheter ablation of the AV junction. 5. Postoperative AVB that is not expected to resolve. 6. Neuromuscular diseases with AVB such as myotonic muscular dystrophy, Erb’s dystrophy (limb-girdle), and peroneal muscular atrophy. 7. Second-degree AVB, regardless of the type or site of block, with associated symptomatic bradycardia (19). Guidelines favor permanent pacing, albeit with a divergence of opinion, in cases of asymptomatic third-degree AVB at any anatomical site with average awake ventricular rates of 40 beats/min or faster (19).
105
Atrioventricular Dissociation Atrioventricular (AV) dissociation is a non-specific term to describe all cases of independently functioning atrial and ventricular pacemakers. Both P waves and QRS complexes occur at regular rates, though without an electrical association. The dissociation may be intermittent, with occasional capture beats, or permanent. Four mechanisms of AV dissociation are discussed: 1. AV dissociation by default: sino-atrial impulses discharge at a rate lower than that of a junctional or ventricular pacemaker (sinus dysrhythmia, sinus bradycardia, sinus arrest, or sinoatrial block). 2. AV dissociation by usurpation: a subsidiary pacemaker may accelerate (e.g., during ventricular tachycardia or non-paroxysmal junctional tachycardia) and control ventricular contraction by exceeding the atrial rate. 3. Complete heart block: in the setting of third-degree heart block, as aforementioned, the atria and ventricles are controlled by their respective pacemakers. 4. Mixed etiology: a combination of conduction pathology; for example, acceleration of a lower pacemaker in the setting of an AVB (3,4,27,31,33). Whereas the first mechanism may manifest in a normal heart, accelerated AV dissociation is caused by the abnormally enhanced excitability of a subsidiary pacemaker (34). Third-degree heart block is similarly pathological, and is always considered a form of AV dissociation. Finally, isorhythmic AV dissociation may be observed, with remarkably similar atrial and ventricular rates but independent electrical activity. As with 2:1 AVB, examining extensive EKG strips may uncover PR interval variations consistent with AV dissociation (34). AV dissociation is only a descriptive term for an EKG finding; importantly, it always represents the result of some underlying rhythm disturbance. This underlying cause must be identified and addressed. Finally, it occurs most commonly in elderly patients with degenerative cardiovascular disease (31). Clinical features again may include symptoms of decreased cardiac output, including dizziness, presyncope or syncope, and angina; palpitations, as a reflection of irregular conduction, are also common. Prognosis and management depends on the defined etiology of the AV dissociation. Generally, it is transient, although active medical and interventional management may be indicated if conduction block or an accelerated subsidiary pacemaker is the underlying cause (35).
106
G. E. Hayden et al.
REFERENCES 1. Brady WJ, Swart G, DeBehnke DJ, Ma OJ, Aufderheide TP. The efficacy of atropine in the treatment of hemodynamically unstable bradycardia and atrioventricular block: prehospital and emergency department considerations. Resuscitation 1999;41:47–55. 2. Swart G, Brady WJ, DeBehnke DJ, Ma OJ, Aufderheide TP. Acute myocardial infarction complicated by hemodynamically unstable bradyarrhythmia: Prehospital and ED treatment with atropine. Am J Emerg Med 1999;17:647–52. 3. Braunwald E, Zipes DP, Libby P, eds. Heart disease: a textbook of cardiovascular medicine, 6th edn. Philadelphia: WB Saunders; 2001. 4. Rardon DP, Miles WM, Zipes DP. Atrioventricular block and dissociation. In: Zipes DP, Jalife J, eds. Cardiac electrophysiology: from cell to bedside, 3rd edn. Philadelphia: WB Saunders; 2000: 451–9. 5. Puech P. Incidence of different types of AV block and their localization by His bundle recordings. In: Wellen HJJ, Lie KI, Janse MJ, eds. The conduction system of the heart. Philadelphia: Lea & Febiger; 1976:467– 84. 6. Abedin Z, Conner R. Interpretation of cardiac arrhythmias: selfassessment approach. Boston: Kluwer Academic Publishers; 2000. 7. Johnson RL, Averill KH, Lamb LE. Electrocardiographic findings in 67,375 asymptomatic individuals. VII. Atrioventricular block. Am J Cardiol 1960;6:153–77. 8. Van Hemelen NM, Robles de Medina EO. Electrocardiographic findings in 791 young men between the ages of 15 and 23 years. I. Arrhythmias and conduction disorders (Dutch). Ned Tijdschr Geneeskd 1975;119:45–52. 9. Erikssen J, Otterstad JE. Natural course of a prolonged PR interval and the relation between PR and incidence of coronary heart disease. A 7-year follow-up study of 1832 apparently healthy men aged 40 –59 years. Clin Cardiol 1984;7:6 –13. 10. McAnulty JH, Rahimtoola SH, Murphy E, et al. Natural history of “high-risk” bundle-branch block: final report of a prospective study. N Engl J Med 1982;307:137– 43. 11. Ellenbogen KA. Pacing for acute and chronic atrioventricular conduction system disease. In: Ellenbogen KA, Kay GN, Wilkoff BL, eds. Clinical cardiac pacing and defibrillation, 2nd edn. Philadelphia: WB Saunders; 2000:426 –53. 12. Denes P, Levy L, Pick A, Rosen KM. The incidence of typical and atypical A-V Wenckebach periodicity. Am Heart J 1975;89:26 – 31. 13. Pick A, Langendorf R. Interpretation of complex arrhythmias. Philadelphia: Lea & Febiger; 1979. 14. Narula OS. Wenckebach type I and II atrioventricular block (revisited). Cardiovasc Clin 1974;6:137– 67. 15. Strasberg B, Amat-Y-Leon F, Dhingra RC, et al. Natural history of chronic second-degree atrioventricular nodal block. Circulation 1981;63:1043–9. 16. Meytes I, Kaplinsky E, Yahini JH, Hanne-Paparo N, Neufeld HN.
17. 18.
19.
20. 21. 22. 23.
24. 25.
26.
27. 28.
29. 30. 31. 32.
33.
34. 35.
Wenckebach A-V block: a frequent feature following heavy physical training. Am Heart J 1975;90:426 –30. Sloan SB, Weitz HH. Postoperative arrhythmias and conduction disorders. Med Clin North Am 2001;85:1171– 89. Vidaillet HJ Jr, Broste SK, Marx JJ Jr, et al. The 12-lead electrocardiogram of “healthy” ambulatory subjects with positive Lyme immunoserology. Am J Cardiol 1993;71:1249 –51. Lee TH. Use of cardiac pacemakers and antiarrhythmia devices: ACC/AHA guidelines summary. In: Braunwald E, Zipes DP, Libby P, eds. Heart disease: a textbook of cardiovascular medicine, 6th edn. Philadelphia: WB Saunders; 2001:810 – 4. Rosen KM, Gunnar RM, Rahimtoola SH. Site and type of second degree AV block. Chest 1972;61:99 –100. Damato AN, Lau SH, Helfant RH, et al. A study of heart block in man using His bundle recordings. Circulation 1969;39:297–305. Barold S. 2:1 Atrioventricular block: order from chaos. Am J Emerg Med 2001;19:214 –7. Dunn MI, Lipman BS. AV blocks, AV dissociation and reciprocal or reentrant rhythms. In: Dunn MI, Lipman BS, Lipman-Massie, eds. Clinical electrocardiography, 8th edn. Chicago: Year Book Publisher; 1989:445–70. Scheidt S. Basic electrocardiography. West Caldwell, NJ: CibaGeigy; 1986. Kaushik V, Leon AR, Forrester JS Jr, Trohman RG. Bradyarrhythmias, temporary and permanent pacing. Crit Care Med 2000;28(10 suppl):N121– 8. Narula OS. Clinical concepts of spontaneous and induced atrioventricular block. In: Manel WJ, ed. Cardiac arrhythmias, 3rd edn. Philadelphia: J.B. Lippincott; 1995:441–59. Kastor JA. Atrioventricular block. In: Kastor JA, ed. Arrhythmias, 2nd edn. Philadelphia: WB Saunders; 2000:509 – 65. Ellenbogen KA, de Guzman M, Kawanishi DT, et al. Pacing for acute and chronic atrioventricular conduction system disease. In: Ellenbogen KA, Kay GN, Wilkoff BL, eds. Clinical cardiac pacing and defibrillation, 2nd edn. Philadelphia: WB Saunders; 2000:426 – 53. Kusomoto FM, Goldschlager N. Cardiac pacing. N Engl J Med 1996;334:89 –98. Wagner GS. Marriott’s practical electrocardiography, 10th edn. Philadelphia: Lippincott Williams & Wilkins; 2001. Harrigan RA, Perron AD, Brady WJ. Atrioventricular dissociation. Am J Emerg Med 2001;19:218 –22. Lamas FA, Muller JE, Turi ZG, et al. A simplified method to predict occurrence of complete heart block during acute myocardial infarction. Am J Cardiol 1986;57:1213–9. Zipes DP. Specific arrhythmias: diagnosis and treatment. In: Braunwald E, ed. Heart disease: a textbook of cardiovascular medicine, 5th edn. Philadelphia: WB Saunders; 1997:640 –704. Marriott HJL, Menendez MM. A-V dissociation revisited. Prog Cardiovasc Dis 1966;8:522–38. Schott A. Atrioventricular dissociation with and without interference. Prog Cardiovasc Dis 1960;2:444 – 64.
doi:10.1016/j.jemermed.2003.10.001
Selected Topics: Cardiology Commentary
ELECTROCARDIOGRAPHIC MANIFESTATIONS: DIAGNOSIS OF ATRIOVENTRICULAR BLOCK IN THE EMERGENCY DEPARTMENT Geoffrey E. Hayden,
MD,*
William J. Brady, MD,† Marc Pollack, Richard A. Harrigan, MD§
MD, PhD,‡
and
*Department of Emergency Medicine, Vanderbilt University, Nashville, Tennessee, †Department of Emergency Medicine, University of Virginia, Charlottesville, Virginia, ‡Department of Emergency Medicine, York Hospital, York, Pennsylvania, and §Department of Emergency Medicine, Department of Internal Medicine, Temple University, Philadelphia, Pennsylvania Reprint Address: William Brady, MD, Department of Emergency Medicine, Box 800699, University of Virginia Medical Center, Charlottesville, VA 22908
e Abstract—Patients with bradycardia are commonly encountered by the Emergency Physician. Of the possible bradydysrhythmias, atrioventricular blocks (AVB) represent a significant portion of these presentations. In this article, we provide four illustrative cases of patients presenting to the Emergency Department (ED) with AVB. We review the various types of AV block dysrhythmias (1st, 2nd, and 3rd degrees) and their underlying etiologies. This discussion also focuses on the presentation, clinical considerations, management and acute treatment of AVB dysrhythmias in the emergent setting. © 2004 Elsevier Inc.
in hemodynamically unstable patients. These patients, if properly diagnosed and appropriately treated, may have significantly improved outcomes. The following scenarios provide illustrative cases of patients presenting to the ED with atrioventricular block.
CASE PRESENTATIONS Case 1
e Keywords— electrocardiogram; atrioventricular block
A 51-year-old man without past medical history experienced a ground-level fall, resulting in a complex ankle fracture. The Emergency Medical Service (EMS) personnel were summoned and found the man, alert and in no obvious distress with the exception of significant left lower extremity deformity at the ankle. The patient was transported to the ED via ambulance. Examination revealed the ankle injury without other complicating issue; the vital signs were normal. Electrocardiographic (EKG) monitoring (Figure 1) and 12-lead electrocardiogram demonstrated normal sinus rhythm (NSR) with firstdegree AVB. The patient was admitted to the hospital for operative repair. His hospital course was uneventful; no further care of his AVB was felt necessary.
INTRODUCTION The presentation of a patient with compromising bradydysrhythmia to the Emergency Department (ED) requires a timely, effective diagnostic and therapeutic approach by the Emergency Physician (EP). Of the possible bradycardic rhythms, atrioventricular blocks (AVB) represent a significant portion of these presentations (1,2). Immediate consideration of several potential causes, including both ischemic and non-ischemic etiologies, is essential. Presentations range from the incidental finding in asymptomatic patients to life-threatening heart block
Selected Topics: Cardiology Commentary is coordinated by Theodore Chan, MD, of the University of California San Diego Medical Center, San Diego, California and William Brady, MD, of the University of Virginia, Charlottesville, Virginia 95
96
G. E. Hayden et al.
Figure 1. Rhythm strip revealing sinus rhythm with prolongation of the PR interval and constant 1:1 atrioventricular relationship – findings consistent with first-degree AVB.
Case 2 A 55-year-old man with a history of myocardial infarction presented to EMS personnel with chest pain. EMS found the patient to be alert with vital signs of a blood pressure 125/88 mm Hg, a pulse 65 beats/min (regular with occasional irregularity), and respirations of 24 breaths/min. The remainder of the examination was significant for diaphoresis and anxiety. The single-lead EKG monitor revealed NSR with second-degree, type I AVB (Figure 2). The patient was transported to the ED with nitroglycerin therapy and aspirin. On arrival, he remained alert with unchanged vital signs. Cardiopulmonary findings were significant for clear lung fields. Multi-lead rhythm strips and 12-lead
EKG monitoring was initiated, revealing NSR with second-degree, type I AVB as seen by EMS; evidence of inferior ST segment depression was also seen. The patient received additional anti-anginal therapy with resolution of chest pain; atropine was given without effect. Transcutaneous pacing pads were applied while Cardiology was consulted for a transvenous pacing wire. He was admitted to the hospital with a course remarkable for positive troponins and recurrent chest pain. Cardiac catheterization demonstrated proximal right coronary disease with thrombus that was successfully opened and stented. The patient was ultimately discharged with a diagnosis of non-ST segment elevation acute myocardial infarction and AVB that resolved with restoration of coronary perfusion.
Figure 2. Rhythm strip revealing sinus rhythm with progressive prolongation of the PR interval, ultimately resulting in a dropped beat – findings consistent with second-degree, type I AVB.
Electrocardiographic Diagnosis of Atrioventricular Block
97
Figure 3. Rhythm strip revealing a wide QRS complex rhythm; evidence of atrioventricular conduction was noted with consistent P wave—QRS complex relationship. The PR interval is constant with abrupt dropped beats—findings consistent with seconddegree, type II AVB. In two instances on this rhythm strip, high-degree AVB is noted with several non-conducted P waves occurring before restoration of atrioventricular conduction.
Case 3 A 65-year-old woman with a history of angina and coronary artery disease experienced progressive weakness followed by syncope; she also noted chest discomfort. The EMS personnel were summoned and found an alert female. The EKG monitor revealed a wide QRS complex with irregularity (Figure 3). The patient had vital signs within normal limits with the exception of the pulse (50 beats/min). On arrival in the ED, the clinical situation was unchanged with the notable exception of hypotension. The EKG revealed a regular wide QRS complex rhythm with frequent dropped beats; further analysis revealed AVB (second degree, type II). The patient underwent transcutaneous pacing with normalization of perfusion and resolution of chest pain; arrangements were made with Cardiology for a transvenous pacemaker. She was admitted to the coronary care unit with a course remarkable for negative rule-out myocardial infarction protocol. A permanent ventricular pacemaker was inserted and the patient was discharged with a diagnosis of symptomatic second-degree AVB.
Case 4 A 48-year-old man was doing yard work when he gradually developed chest pain, dyspnea, and profound dizziness. Upon EMS arrival, the patient appeared diaphoretic but alert. Monitoring revealed a wide QRS complex rhythm at a rate of approximately 50 beats per minute; evidence of complete AV dissociation was noted, consistent with third-degree AVB (Figure 4). Appropriate therapy was initiated and the patient was trans-
ported to the ED. Upon arrival, he was awake and alert, complaining only of chest discomfort. Soon after ED arrival, he became unresponsive associated with a marked reduction in his blood pressure; the monitor revealed continued third-degree AVB with a significantly slower ventricular escape rhythm. Immediate transcutaneous pacing was applied with restoration of mental status and normal perfusion. The patient was admitted to the hospital with placement of a transvenous pacing wire and complete reliance on the pacemaker for approximately 20 h. He slowly developed sinus rhythm with bradycardia that normalized to NSR. It was ultimately determined that the patient had inadvertently used excessive metoprolol in conjunction with his long-term verapamil therapy for hypertension.
DISCUSSION Heart block is a descriptive term used to characterize a disturbance in the conduction of the electrical impulse in the heart—in this case, in and around the atrioventricular (AV) node. This disturbance can be partial or complete, resulting in either a delayed or an entirely blocked impulse. The conduction disturbance most commonly results from dysfunction in the following areas of the heart’s conduction system: between the sinus node and atrium (sinoatrial block), between the atria and ventricles (AV block [AVB]), within the atria (intra-atrial block), or within the ventricles (intra-ventricular block) (3). This review focuses on AVB (Figure 5), which generally results from dysfunction in one of three areas of the cardiac conduction system: the AV node (above the His bundle); the His bundle (intra-Hisian); or the distal His bundle or the bundle branches (infra-Hisian); these forms
98
G. E. Hayden et al.
Figure 4. Rhythm strip revealing a wide QRS complex rhythm; evidence of complete atrioventricular dissociation was noted without evidence of atrioventricular communication. The rhythm disturbance was diagnosed as third-degree AVB.
of AVB include first-degree, second-degree (types I and II), and third-degree disturbances (3,4). Although the surface electrocardiogram (EKG) may not definitively identify the site of the AV block, certain electrocardiographic patterns serve not only to differentiate the various blocks but also to identify the site of origin. Multiple etiologies of AVB are encountered with the most common being acute myocardial infarction. Also of note among etiologies are myocardial ischemia,
Figure 5. Atrioventricular block. (A) First-degree AVB. (B) Second-degree, type I AVB. (C) Second-degree, type II AVB with narrow QRS complex. (D) Second-degree, type II AVB with wide QRS complex.
primary conduction disease, and medication effect (intentional and unintentional) (Figures 6 and 7) (1).
First-Degree Atrioventricular Block In first degree AVB, the PR interval is prolonged with a duration greater than 0.20 s and is constant without progressive change (Figure 8A and 8B). The P wave has normal morphology and precedes every QRS complex. The QRS complex also has a normal morphology and axis for the given patient and clinical situation. Every atrial impulse is conducted to the ventricles (Figures 1 and 8A, 8B). The increased PR interval is secondary to delayed impulse conduction in the atrium, the AV node, or the His-Purkinje system (4). The vast majority of first-degree AVBs present with narrow QRS complexes; the block is localized to the proximal conducting system in 87% of cases, whereas 13% of cases are located within the common bundle of His (5). First-degree block with wide QRS complexes (duration longer than 0.12 s) result from the following sites of dysfunction: proximal to the bundle (22%), distal to the bundle (33%), intra-Hisian (12%), and supra- or infra-Hisian (33%). In summary, in first-degree AVB with a normal QRS, the delay almost always occurs in the AV node; wide QRS may indicate delay in the AV node or His-Purkinje system. Epidemiologically, prolongation of the PR interval is a normal variant in 1 to 2% of the population (6). Reports have indicated that between 0.5% and 2% of normal young persons have prolonged PR intervals (7,8). Further, in a study of healthy middle-aged men with prolonged PR intervals and normal QRS complexes, the authors conclude that the EKG findings have no prog-
Electrocardiographic Diagnosis of Atrioventricular Block
99
Figure 6. Etiology of AVB in unstable prehospital patients.
nostic significance and are not associated with any ischemic heart disease (9). The clinical presentation of patients with first-degree AVB is generally benign. Rarely, various symptoms and signs may be observed, including palpitations, dizziness, syncope, and angina; these would correspond to insufficient cardiac output precipitated by the AVB. Overall, the prognosis for patients with first-degree AVB is excellent; no therapy is indicated in the asymptomatic patient. This statement includes asymptomatic individuals with chronic bifascicular block, in whom the rate of progression to third-degree AVB remains low; prophylactic pacing is still not indicated (10). Some dispute surrounds patients with first-degree AVB and symptoms of low cardiac output that is relieved by temporary pacing; similar controversy regards management of patients with coexistent chronic heart failure (CHF). These presentations are deemed Class II indications for pacing; in other words, there is a divergence of opinion or conflicting evidence regarding its usefulness and effectiveness, though, in this case, existing evidence favors its usefulness (11). Otherwise, the patient can be monitored over time for development of other conduction disturbances or hemodynamic compromise. Though
rare, first-degree AV block can be seen with acute rheumatic fever. The significance here is for valvular dysfunction and not rhythm disturbance.
Type I, Second-Degree Atrioventricular Block In Mobitz type I block, also known as Wenkebach AVB, P waves and QRS complexes are usually normal in terms of morphology and total duration (Figures 2 and 9A–C). The site of the block is usually at or above the AV node; as such, the QRS complex is narrow and the rate is sufficient to maintain adequate perfusion. In type I block, a specific pattern to the P wave-QRS complex relationship is encountered. The PR interval is often normal in the first beat of the series. Progressive PR interval lengthening with subsequent beats is observed until an impulse is unable to reach the ventricles, resulting in a nonconducted P wave. After the dropped beat, the PR interval returns to normal and the cycle repeats itself. A pattern to the RR interval is also seen. As the PR lengthens with subsequent beats, the RR interval becomes shorter. After the dropped beat, the RR interval in the subsequent beats tends to shorten. In fact, the RR interval
Figure 7. Incidence of various forms of AVB in ischemic and non-ischemic presentations.
100
G. E. Hayden et al.
Figure 8. First-degree AVB. (A) Sinus rhythm with prolongation of the PR interval and constant 1:1 atrioventricular relationship; note that PR interval is constant in length. (B) Insert below the rhythm strip (thick bar) demonstrates the characteristics of the PR interval – prolonged in each cycle and constant in length.
containing the dropped beat is less than two of the shorter cycles. One will also notice on the rhythm strip a grouping of beats that is especially noticeable with a tachycardia. Such a finding is referred to as grouped beating of Wenckebach (Figure 9C). Evidence on the EKG for Mobitz type I AVB includes the following: 1) progressive lengthening of the PR interval, then dropped beat; 2) progressive shortening of the RR interval; 3) the RR length of the dropped beat is less than twice the shortest cycle; and 4) grouped beating (Figures 2 and 9A–C) (3,4). Unfortunately, these “typical” features of Wenckebach group beating are observed in fewer than 50% of all cases of type I block (3,12). Denes et al. report that 86% of Wenckebach periods vary from the defining criteria in one or more ways (12). Rather, one may observe a number of divergences from the classic pattern. The PR intervals may not lengthen progressively; several PR intervals may share the same duration or a PR interval may decrease in duration. The second PR interval may not represent the greatest incremental increase in duration. The last PR increment may be of the greatest magnitude. Lastly, a non-conducted impulse may not be observed (4,12). These variations from the typical presentation have been explained by the role of the autonomic nervous system in regulating sinus rate and AV conduction (4). Most importantly, however, is that differentiation of these atypical forms has no clinical importance. His bundle recordings in patients with type I, seconddegree AVB have identified conduction disturbances in
the AV node in 72% cases as compared to only 9% intra-Hisian and 19% infra-Hisian (5). These numbers are consistent with other literature, which in the setting of a normal QRS localizes the block to the AV node (proximal to the His bundle) in almost all cases (13,14). A widened QRS complex, however, may indicate a block in the AV node, in the His bundle, or distal to the His bundle. Epidemiologically, type I, second-degree AVB may be infrequently observed in both trained athletes and normal persons during sleep, perhaps due to increased vagal tone (3,15,16). Outside of AMI, it may also occur with the ingestion of various medications used to prevent cardiac ischemia, control atrial fibrillation, or treat systemic hypertension (17). The clinical presentation of patients is generally benign. Accordingly, the prognosis and indicated management are based on the clinical setting and the presence of related heart disease. Asymptomatic individuals with no heart disease generally do well without therapy; in patients with structural heart disease, the prognosis is dependent on the natural history of the heart disease itself as opposed to the AVB (4). Patients may require only cardiac monitoring to follow the rare symptomatic presentation or progression to higher-grade AV block, which is unlikely except in cases involving acute myocardial infarction (AMI). In the occasional patient, this block is associated with systemic hypoperfusion and should be treated with atropine. Atropine should be given in 0.6 to 1 mg boluses, repeated every 5 min, not to exceed a total dose of 0.04
Electrocardiographic Diagnosis of Atrioventricular Block
101
Figure 9. Second-degree, type I AVB. (A) NSR with progressively prolonged PR interval, culminating in a dropped beat. (B) Insert below the rhythm strip (thick bar) demonstrates the characteristics of the PR interval—prolonged in each cycle with progression, ultimately resulting in a dropped beat (arrow)—i.e., no conduction to the ventricle and no QRS complex. (C) Grouped beating is demonstrated in these two examples of second-degree, type I AVB.
mg/kg. In patients with AMI, atropine and other medications are more likely to be effective if AVB develops within the first 6 h of signs of infarction. When effective, atropine will either abolish the block or accelerate the ventricular rhythm. In a significant minority of patients, atropine seems ineffective. Recently, it has been shown that adenosine may mediate some of the AVBs during AMI, possibly explaining atropine’s lack of efficacy in certain clinical situations (18). Methylxanthines, such as aminophylline and theophylline, are competitive antag-
onists of adenosine and may be successful in abolishing AVB when atropine is ineffective. If pharmacotherapy is ineffective, then a temporary transvenous pacemaker can be inserted in the symptomatic patient. During placement of the transvenous pacer, a transcutaneous pacemaker can be placed if the patient is hemodynamically unstable. Additionally, transvenous pacing is not recommended unless these patients are symptomatic with hypoperfusion, syncope, acute congestive heart failure, or ischemic chest pain (4). Asymp-
102
G. E. Hayden et al.
Figure 10. Second-degree, type II AVB. (A) Upper panel—Fixed PR interval without progressive change with sudden dropped beat and narrow QRS complex. Lower panel—Similar to upper panel example with wide QRS complex. (B) Nature of PR interval is seen in these examples of second-degree, type II AVB. Note the constant PR interval (constant length as indicated by the thick bars) and dropped beats (arrow).
tomatic patients with type I, second-degree AVB should not undergo transcutaneous or transvenous pacing (19).
Type II, Second-Degree Atrioventricular Block The PR interval in type II second-degree AVB is constant. The PR interval may be either normal or prolonged, but it is always constant without progressive PR interval lengthening. The QRS complex, conversely, is widened in most instances of type II second-degree AVB though narrow QRS complex rhythms are encountered (Figures 3 and 10A–B). This may help to distinguish it from 2:1 type I block that by EKG is not able to be differentiated from type II. The magnitude of the AVB is expressed as a ratio of P waves to QRS complexes (4). The QRS complex, in most cases, is wide (i.e., greater than 0.12 s). This finding is explained by its association
with bundle branch block (20,21). His bundle recordings indicate that the block is never localized to the His bundle; instead, 20% of cases occur in the common bundle and 80% in the bundle branches (5). Consistent with the general rule that blocks distal to the His bundle presume a more serious prognosis, type II blocks often progress to complete heart block (CHB) and produce Stokes-Adams syncope (3,4). This progression to CHB is a common finding in particular with patients suffering from extensive anterior infarctions. Patients with type II, second-degree AVB may be unstable at the time of assessment or may develop thirddegree block suddenly. If so, transvenous pacing should be instituted immediately. Patients can sometimes be supported with isoproterenol or transcutaneous pacing while the transvenous pacing wire is positioned. Patients concurrently suffering from AMI may be managed more aggressively. Atropine is rarely if ever the drug of choice
Electrocardiographic Diagnosis of Atrioventricular Block
103
Figure 11. Second-degree AVB with 2:1 conduction pattern (nontypable AVB).
for Mobitz II block. Atropine may increase the sinus rate while not affecting AV conduction, thus enhancing the degree of AVB. The American College of Cardiology/ American Heart Association (ACC/AHA) guidelines favor permanent pacing even in asymptomatic patients with type II, second-degree AVB (19). Atrioventricular Block with 2:1 Conduction Pattern At times, it may be difficult to distinguish between types I and II, second-degree block, based on the EKG. This non-typable second-degree AVB results from a 2:1 AVB ratio, or two P waves for one QRS complex (Figure 11). In this setting, the determination of progressively lengthening PR intervals versus stable intervals with intermittent non-conducted impulses may be impossible; precise identification would necessitate two or more consecutive impulse conductions. Therefore, it is reasonable to state that this EKG presentation preempts classification as a type I or type II, second-degree AVB (22). The precise location of 2:1 blocks is similarly confounding, with reports that the site of the block can be determined only in His recordings (23,24). A reasonable diagnostic approach is to patiently follow the EKG strips; appearance of an AVB pattern with two consecutive P waves conducted (e.g., a 3:2 block) would allow for more definitive determination of type I versus type II, second-degree AVB. Other diagnostic measures are described in the literature. Kaushik et al. note the value of certain maneuvers: 1) vagal maneuvers and beta-adrenergic blocking agents decrease conduction if the block results from a lesion in the AV node; 2) vagal maneuvers and beta-adrenergic blocking agents do not affect the conduction if the block results from a lesion located infranodally; 3) atropine increases conduction when the block results from an AV nodal lesion; and 4) atropine does not alter conduction if the block results from an infranodal lesion (25). Further, a number of EKG findings may favor a particular designation, in particular the
nature of the QRS complex interval. Specifically, a normal QRS duration is consistent with an AV nodal block, whereas a prolonged QRS is supportive of an infranodal block (4). PR intervals are less helpful, as fixed intervals in a 2:1 block have no diagnostic usefulness, and variable PR intervals in the absence of a narrow QRS do not specify an AV nodal block (25). The medical management of 2:1 AVB is also the subject of controversy. Although it is reasonable to treat the hemodynamically unstable patient with a narrow QRS complex with atropine, infranodal blocks (i.e., those presentations with widened QRS complex) may respond poorly to this approach. As the degree of AVB may be worsened by atropine, Kaushik et al. describe two important contraindications to atropine use in the setting of likely intra- or infra-Hisian AVB: 1) stable, wide QRS 2:1 AVB; and 2) 2:1 AVB that evolves into type II block (regardless of QRS duration) (25–28). Kusomoto and Goldschlager state that in an asymptomatic patient, a 2:1 block with a coexisting bundle branch block is an appropriate indication for pacing; the assumption is that, in this setting, the block is infranodal (29). This recommendation may be disputed by the finding of an AV nodal block in 15–20% of cases with 2:1 block and bundle branch block (25).
High-Degree (Advanced) Second-Degree Atrioventricular Block By definition, high-degree or advanced AV block indicates a block of two or more consecutive P waves (3). This form of second-degree block is diagnosed when a block of consecutive sinus impulses occurs (Figures 3 and 12) (4). When the patient is suffering an anterior MI, the high-degree AVB is likely a variation on type II, second-degree AVB with bilateral bundle branch block (4).
104
G. E. Hayden et al.
Figure 12. High-degree AVB. Note the presence of two non-conducted P waves.
Third-Degree Atrioventricular Block In complete or third-degree AVB, no impulses are conducted from the atria to the ventricles. With the absence of conduction of P waves to the ventricle, the atria and ventricle remain under the control of their respective pacemakers. Generally, if there is a junctional pacemaker, the ventricular rate is 40 – 60 beats/min and the QRS complex is narrow; a rate of 20 – 40 beats/min and a wide QRS usually indicate a ventricular pacemaker (Figures 4 and 13) (3,4). The escape rhythm, whether junctional or ventricular, is almost always regular, due in part to decreased autonomic control as compared to the sinus node (30). In contrast, the atrial pacemaker can be either sinus or ectopic (of normal rate), bradycardic, tachycardic, flutter, or fibrillation. Further, the atrial rate is almost always greater than the ventricular rate in patients with third-degree AVB, although in rare cases the block may be “isorhythmic,” with similar atrial and ventricular rates. In general, complete heart block can be confidently diagnosed only when the dissociation is prolonged and the ventricular rate is 45 beats/min or less (4). Specific EKG findings are dependent on the location of the block, with consequent prognostic significance. In general, third-degree blocks may occur within the AV node (narrow QRS and rate ⬎ 40 bpm) or infra-Hisian (wide QRS and rate ⬍ 40 bpm); these locations in general correspond to either congenital or acquired etiologies, respectively (4). A wide array of conditions may produce acquired third-degree AVB. Among these are surgery, electrolyte
disturbances (hyperkalemia), myoendocarditis (valve ring abscess, rheumatic fever, viral myocarditis, Lyme disease), tumors, Chagas disease, rheumatoid nodules, calcific aortic stenosis, myxedema, polymyositis, infiltrative processes (such as amyloid, sarcoid, or scleroderma), cardiomyopathy, hypothyroidism, hypothermia, sepsis, etc. In adults, drug toxicity (beta-blockers, calcium channel blockers, digoxin, quinidine, procainamide), coronary disease, and degenerative processes seem to be the most common causes of complete heart block (3,4,6,25). Other literature identifies idiopathic fibrosis as the most common finding in chronic complete AVB (30). The most common cause of third-degree AVB in children is congenital pathology, in particular, abnormal embryonic development of the AV node (3,4). Complete heart block (third-degree AVB) is a relatively common complication in myocardial infarctions, particularly in the setting of unstable bradydysrhythmias. These patients generally are either hemodynamically unstable at presentation or become unstable suddenly. The clinical manifestations reflect insufficient cardiac output, with palpitations, dizziness, presyncope or syncope, and angina. Sudden cardiac death is not rare. Elderly patients with third-degree AVB may manifest only symptoms of weakness or fatigue. In this population, special consideration is given to the medication regimen of cardioactive drugs. Patients with third-degree AVB and anterior MI are likely to be hemodynamically unstable at the initial assessment or develop hemodynamic embarrassment suddenly. These patients should have a transvenous pacemaker placed urgently. Many of these patients require
Figure 13. Third-degree AVB with wide QRS complex. No relationship of the P waves and QRS complexes is noted. The two structures are occurring independently of one another.
Electrocardiographic Diagnosis of Atrioventricular Block
permanent pacemakers. If the patient is unstable, atropine, isoproterenol, or transcutaneous pacing therapy should be instituted while placing the transvenous wire. In patients with inferior MI, the ventricular rate tends to be adequate to maintain cardiac output. If the ventricular rate is greater than 40 beats/min and the patient is stable, one can elect to place a transvenous pacer only if the clinical situation deteriorates. If the patient develops hypotension, heart failure, oliguria, or ventricular dysrhythmia, then atropine, isoproterenol, or transvenous pacing should be initiated. Patients with anterior infarctions and third-degree block should be treated aggressively for cardiogenic shock. A considerable body of literature has grown around the issue of the risk of progression to complete heart block in patients with AMI. A useful method to predict the potential for such progression considers the electrocardiographic presence of the following risk factors, including first-degree AVB, second-degree (types I and II) AVB, right bundle branch block (BBB), left BBB, left anterior fascicular block, and left posterior fascicular block (31). Each risk factor when noted on the 12-lead electrocardiogram receives a score of 1. The total score is added, which is then translated to the rate of occurrence of such AVB, giving the clinician the risk of progression to complete heart block in patients with AMI. A score of 0 carries a 1.2% risk of complete heart block development, whereas a score of 3 or more is associated with a significant possibility of complete heart block—36.4%. Intermediate scores of 1 and 2 have rates of occurrence of 7.8% and 25%, respectively (32). The ACC/AHA guidelines support permanent pacing for third-degree AVB at any anatomical level associated with any of the following: 1. Bradycardia with symptoms presumed to be due to AV block. 2. Dysrhythmias and other medial conditions that require drugs that result in symptomatic bradycardia. 3. Documented periods of asystole of ⱖ 3.0 s or any escape rate of ⬍ 40 beats/min in awake, symptomfree patients. 4. After catheter ablation of the AV junction. 5. Postoperative AVB that is not expected to resolve. 6. Neuromuscular diseases with AVB such as myotonic muscular dystrophy, Erb’s dystrophy (limb-girdle), and peroneal muscular atrophy. 7. Second-degree AVB, regardless of the type or site of block, with associated symptomatic bradycardia (19). Guidelines favor permanent pacing, albeit with a divergence of opinion, in cases of asymptomatic third-degree AVB at any anatomical site with average awake ventricular rates of 40 beats/min or faster (19).
105
Atrioventricular Dissociation Atrioventricular (AV) dissociation is a non-specific term to describe all cases of independently functioning atrial and ventricular pacemakers. Both P waves and QRS complexes occur at regular rates, though without an electrical association. The dissociation may be intermittent, with occasional capture beats, or permanent. Four mechanisms of AV dissociation are discussed: 1. AV dissociation by default: sino-atrial impulses discharge at a rate lower than that of a junctional or ventricular pacemaker (sinus dysrhythmia, sinus bradycardia, sinus arrest, or sinoatrial block). 2. AV dissociation by usurpation: a subsidiary pacemaker may accelerate (e.g., during ventricular tachycardia or non-paroxysmal junctional tachycardia) and control ventricular contraction by exceeding the atrial rate. 3. Complete heart block: in the setting of third-degree heart block, as aforementioned, the atria and ventricles are controlled by their respective pacemakers. 4. Mixed etiology: a combination of conduction pathology; for example, acceleration of a lower pacemaker in the setting of an AVB (3,4,27,31,33). Whereas the first mechanism may manifest in a normal heart, accelerated AV dissociation is caused by the abnormally enhanced excitability of a subsidiary pacemaker (34). Third-degree heart block is similarly pathological, and is always considered a form of AV dissociation. Finally, isorhythmic AV dissociation may be observed, with remarkably similar atrial and ventricular rates but independent electrical activity. As with 2:1 AVB, examining extensive EKG strips may uncover PR interval variations consistent with AV dissociation (34). AV dissociation is only a descriptive term for an EKG finding; importantly, it always represents the result of some underlying rhythm disturbance. This underlying cause must be identified and addressed. Finally, it occurs most commonly in elderly patients with degenerative cardiovascular disease (31). Clinical features again may include symptoms of decreased cardiac output, including dizziness, presyncope or syncope, and angina; palpitations, as a reflection of irregular conduction, are also common. Prognosis and management depends on the defined etiology of the AV dissociation. Generally, it is transient, although active medical and interventional management may be indicated if conduction block or an accelerated subsidiary pacemaker is the underlying cause (35).
106
G. E. Hayden et al.
REFERENCES 1. Brady WJ, Swart G, DeBehnke DJ, Ma OJ, Aufderheide TP. The efficacy of atropine in the treatment of hemodynamically unstable bradycardia and atrioventricular block: prehospital and emergency department considerations. Resuscitation 1999;41:47–55. 2. Swart G, Brady WJ, DeBehnke DJ, Ma OJ, Aufderheide TP. Acute myocardial infarction complicated by hemodynamically unstable bradyarrhythmia: Prehospital and ED treatment with atropine. Am J Emerg Med 1999;17:647–52. 3. Braunwald E, Zipes DP, Libby P, eds. Heart disease: a textbook of cardiovascular medicine, 6th edn. Philadelphia: WB Saunders; 2001. 4. Rardon DP, Miles WM, Zipes DP. Atrioventricular block and dissociation. In: Zipes DP, Jalife J, eds. Cardiac electrophysiology: from cell to bedside, 3rd edn. Philadelphia: WB Saunders; 2000: 451–9. 5. Puech P. Incidence of different types of AV block and their localization by His bundle recordings. In: Wellen HJJ, Lie KI, Janse MJ, eds. The conduction system of the heart. Philadelphia: Lea & Febiger; 1976:467– 84. 6. Abedin Z, Conner R. Interpretation of cardiac arrhythmias: selfassessment approach. Boston: Kluwer Academic Publishers; 2000. 7. Johnson RL, Averill KH, Lamb LE. Electrocardiographic findings in 67,375 asymptomatic individuals. VII. Atrioventricular block. Am J Cardiol 1960;6:153–77. 8. Van Hemelen NM, Robles de Medina EO. Electrocardiographic findings in 791 young men between the ages of 15 and 23 years. I. Arrhythmias and conduction disorders (Dutch). Ned Tijdschr Geneeskd 1975;119:45–52. 9. Erikssen J, Otterstad JE. Natural course of a prolonged PR interval and the relation between PR and incidence of coronary heart disease. A 7-year follow-up study of 1832 apparently healthy men aged 40 –59 years. Clin Cardiol 1984;7:6 –13. 10. McAnulty JH, Rahimtoola SH, Murphy E, et al. Natural history of “high-risk” bundle-branch block: final report of a prospective study. N Engl J Med 1982;307:137– 43. 11. Ellenbogen KA. Pacing for acute and chronic atrioventricular conduction system disease. In: Ellenbogen KA, Kay GN, Wilkoff BL, eds. Clinical cardiac pacing and defibrillation, 2nd edn. Philadelphia: WB Saunders; 2000:426 –53. 12. Denes P, Levy L, Pick A, Rosen KM. The incidence of typical and atypical A-V Wenckebach periodicity. Am Heart J 1975;89:26 – 31. 13. Pick A, Langendorf R. Interpretation of complex arrhythmias. Philadelphia: Lea & Febiger; 1979. 14. Narula OS. Wenckebach type I and II atrioventricular block (revisited). Cardiovasc Clin 1974;6:137– 67. 15. Strasberg B, Amat-Y-Leon F, Dhingra RC, et al. Natural history of chronic second-degree atrioventricular nodal block. Circulation 1981;63:1043–9. 16. Meytes I, Kaplinsky E, Yahini JH, Hanne-Paparo N, Neufeld HN.
17. 18.
19.
20. 21. 22. 23.
24. 25.
26.
27. 28.
29. 30. 31. 32.
33.
34. 35.
Wenckebach A-V block: a frequent feature following heavy physical training. Am Heart J 1975;90:426 –30. Sloan SB, Weitz HH. Postoperative arrhythmias and conduction disorders. Med Clin North Am 2001;85:1171– 89. Vidaillet HJ Jr, Broste SK, Marx JJ Jr, et al. The 12-lead electrocardiogram of “healthy” ambulatory subjects with positive Lyme immunoserology. Am J Cardiol 1993;71:1249 –51. Lee TH. Use of cardiac pacemakers and antiarrhythmia devices: ACC/AHA guidelines summary. In: Braunwald E, Zipes DP, Libby P, eds. Heart disease: a textbook of cardiovascular medicine, 6th edn. Philadelphia: WB Saunders; 2001:810 – 4. Rosen KM, Gunnar RM, Rahimtoola SH. Site and type of second degree AV block. Chest 1972;61:99 –100. Damato AN, Lau SH, Helfant RH, et al. A study of heart block in man using His bundle recordings. Circulation 1969;39:297–305. Barold S. 2:1 Atrioventricular block: order from chaos. Am J Emerg Med 2001;19:214 –7. Dunn MI, Lipman BS. AV blocks, AV dissociation and reciprocal or reentrant rhythms. In: Dunn MI, Lipman BS, Lipman-Massie, eds. Clinical electrocardiography, 8th edn. Chicago: Year Book Publisher; 1989:445–70. Scheidt S. Basic electrocardiography. West Caldwell, NJ: CibaGeigy; 1986. Kaushik V, Leon AR, Forrester JS Jr, Trohman RG. Bradyarrhythmias, temporary and permanent pacing. Crit Care Med 2000;28(10 suppl):N121– 8. Narula OS. Clinical concepts of spontaneous and induced atrioventricular block. In: Manel WJ, ed. Cardiac arrhythmias, 3rd edn. Philadelphia: J.B. Lippincott; 1995:441–59. Kastor JA. Atrioventricular block. In: Kastor JA, ed. Arrhythmias, 2nd edn. Philadelphia: WB Saunders; 2000:509 – 65. Ellenbogen KA, de Guzman M, Kawanishi DT, et al. Pacing for acute and chronic atrioventricular conduction system disease. In: Ellenbogen KA, Kay GN, Wilkoff BL, eds. Clinical cardiac pacing and defibrillation, 2nd edn. Philadelphia: WB Saunders; 2000:426 – 53. Kusomoto FM, Goldschlager N. Cardiac pacing. N Engl J Med 1996;334:89 –98. Wagner GS. Marriott’s practical electrocardiography, 10th edn. Philadelphia: Lippincott Williams & Wilkins; 2001. Harrigan RA, Perron AD, Brady WJ. Atrioventricular dissociation. Am J Emerg Med 2001;19:218 –22. Lamas FA, Muller JE, Turi ZG, et al. A simplified method to predict occurrence of complete heart block during acute myocardial infarction. Am J Cardiol 1986;57:1213–9. Zipes DP. Specific arrhythmias: diagnosis and treatment. In: Braunwald E, ed. Heart disease: a textbook of cardiovascular medicine, 5th edn. Philadelphia: WB Saunders; 1997:640 –704. Marriott HJL, Menendez MM. A-V dissociation revisited. Prog Cardiovasc Dis 1966;8:522–38. Schott A. Atrioventricular dissociation with and without interference. Prog Cardiovasc Dis 1960;2:444 – 64.