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Second-degree atrioventricular block: mobitz type II
TheJournal of Emergency Medicine, Vol 11, pp47-54, 1993
Printed in the USA Copyright 0 1993 Pergamon Press Ltd.
Cardiology
Comm=ncary
SECOND-DEGREE ATRIOVENTRICULAR BLOCK: MOBITZ TYPE II John M. Wogan, *Department
of Emergency
MD, FACEP,’
Steven R. Lowenstein,
MD, bwti,t
and Gerald S. Gordon,
MD
Medicine, The Johns Hopkins Hospital, The Johns Hopkins University School of Medicine Baltimore,
Maryland, and Wniversity of Colorado Health Sciences Center Denver, Colorado Reprint Address: Steven R. Lowenstein, MD, MPH, Section of Emergency Medicine and Trauma, University of Colorado Health Scrences Center, Campus Box B215,4200 East Ninth Avenue, Denver, CO 80262
0 Abstract-Acute atrioventricular (AV) block occurs frequently in patients with myocardial infarction. Atrioventricular block is also a common manifestation of sclerodegenerative conduction system disease. Occasionally, heart block results from drug toxicity, hyperkalemia, cardiac valvular calcification, myocarditis, or infiltrative cardiomyopathy. Second-degree AV block is a form of “incomplete” heart block, in which some, but not all, atrial beats are blocked before reaching the ventricles. Mobitz type II second-degree block is an old term, which refers to periodic atrioventricular block with constant PR intervals in the conducted beats. The distinction between type II and type I block is descriptive; of greater importance to the clinician is the anatomic site of the block and the prognosis. In Mobitz type II block the site is almost always below the AV node; in Mobitz type I block the site is usually within the AV node. Type II AV block is more likely to progress to complete heart block and Stokes-Adams arrest. In most cases of second-degree heart block, including cases of 2 : 1 conduction, it is possible to determine the site of the AV block (intranodal or infranodal) using information about the age of the patient, the clinical setting, and the width of the QRS complex on the surface electrocardiogram. Second-degree atrioventricular block must be distinguished from other “causes of pauses.” Nonconducted premature atrial contractions and atrial tachycardia with block are common conditions, which may mimic second-degree AV
INTRODUCTION In 1906, Hay (1) and Wenckebach (2), working independently, described the atrioventricular block subsequently designated second-degree heart block, Mobitz type II. Their accomplishment was notable in that their conclusions predated the electrocardiogram and were based solely on observations of the arterial and jugular venous pulses. In 1921, following the development of the electrocardiogram (ECG), Mobitz (3) described in detail the electrocardiographic features of this type of heart block.
ELECTROCARDIOGRAPHIC
In second-degree block, Mobitz type II, sinus impulses are periodically blocked before reaching the ventricles. This disturbance is characterized by block of a single P wave; the preceding conducted sinus impulses have constant pulse rate (PR) intervals. The block is intermittent and is usually regularly repetitive (Figures l-3). This ECG pattern is in contrast to first-degree block, in which the PR interval is prolonged, but all sinus impulses are conducted. It is also different from third-degree block, where no si-
block. 0 Keywords-heart
= =
FEATURES
block; second degree; Mobitz II
Cardiology Commentary, a section devoted to topics in bedside cardiology and electrocardiography, nated by Steven R. Lowenstein, MD, MPH, University of Colorado Health Sciences Center, Denver.
RECEIVED: 7 November 1991; FINAL SUBMISSIONRECEIVED: 14 April 1992; ACCEPTED: 28 April 1992
47
0736-4679/93
is coordi$6.00 + 00
John M. Wogan, Steven R. Lowenstein, Gerald S. Gordon
Figure 1. Second-degree heart block. Note that 2 : 1 atrioventricuiar conduction is present along with intermittent bundle branch block. The atrioventricuiar block is probably type ii (that is, intranodai), based on the following clues: a) the presence of bundle branch and fascicuiar block, and b) the normal PR interval in the conducted beats.
nus impulses are conducted and the atria and ventricles beat independently. Second-degree Mobitz type II block must be differentiated from second-degree block, type I. In type I block, the PR interval varies. Typically, successive sinus impulses show progressive PR prolongation followed by a dropped beat (the Wenckebach phenomenon). The shortest PR interval occurs immediately after the dropped beat (4) (Figure 3). Second-degree block, Mobitz type II, must also be distinguished from “high-grade” or “advanced” block (Figure 4). In this condition, two or more consecutive P waves are blocked (i.e., the ECG shows a conduction ratio of 3 : 1 or higher). Type II AV block may be simulated by nonconducted premature atrial contractions (PAC’s). In Figure 5, nonconducted premature P waves are seen as small deformations of the preceding T wave. The differentiation between nonconducted PAC’s and second-degree heart block can be made readily by examining the P waves and P-P intervals, appreciating the prematurity and often abnormal shape of the P waves. Heart block is not really present; these P waves are not conducted because they occur ear-
ly, during the normal refractory period of the AV node. A second mimic of AV block is atrial tachycardia or flutter with “block” (Figure 6). Here, the atrial rate is unusually rapid. Heart block is not present; impulses are only being “filtered” by the normal refractoriness of the AV node (5).
ANATOMIC CONSIDERATIONS The site of Mobitz type II block is almost always below the AV node. In about 25% of cases (and more commonly in elderly patients), the delay is in the His bundle itself (6). In this circumstance, the QRS morphology may remain normal (6-8). More commonly, the block is in the bundle branchPurkinje system (that is, distal to the common His bundle). Therefore, in type II block, the QRS complexes usually show evidence of bundle branch or fascicular block (Figures 1, 2, 4) (9). The site of type I AV block is usually within the AV node. Therefore, the QRS complexes usually have a normal duration and contour.
Second-Degree
AV Block-II
49
Figure 2. His-bundle electrocardiogram from the same patient. The His-bundle electrode reveals block below the His-bundle. Note that during atrioventricular block (no QRS in leads I, II, aVF, Vl, and V6), depolarization occurs at both the AV node (see “A” on right atrial and His-bundle leads) and at the His-bundle (“H”) but is not transmitted below the His Bundle. Therefore, the block is Mobitz type II.
It should be emphasized that the terms type I and type II are semantic parameters, which describe the behavior of the PR intervals in consecutive, conducted sinus beats. Of greater significance to the clinician is the site of the block-either within or below the AV node. Although a certain diagnosis may be obtained only through an intracardiac His bundle recording, a reasonable inference regarding the site of the block is usually possible, just by knowing the clinical setting and reviewing the surface ECG. Furthermore (and contrary to popular belief), the site of the block can usually be ascertained even when 2 : 1 conduction is present. The salient features of intranodal (type I) and infranodal (type II) block are summarized later (and in Table 1).
DETERMINING THE SITE OF THE BLOCK IN THE PRESENCE OF 2 : 1 CONDUCTION It is often difficult to distinguish between Mobitz type I (intranodal) and II (infranodal) blocks when 2 : 1 conduction is present. In this setting, variability or prolongation of the PR interval supports a diagnosis of type I block. Therefore, a careful search of a long ECG tracing for two consecutive P waves should be made. A faster ECG paper speed may help to detect PR segment variability. If the PR intervals vary, then type I second-degree heart block is present. If the conduction ratios vary-for example, from 2 : 1 to 3 : 2-and the PR intervals remain fixed, then type II block is present (6).
50
John M. Wogan, Steven R. Lowenstein, Gerald S. Gordon
W
Figure 3. It may be difficult, at times, to differentiate between Yobitz types I and II second-degree heart block if 2 : 1 conduction is present. Rhythm strip A shows Mobitz type I block. In the early portion of the tracing, there is progressive prolongation of consecutive PR intervals, and the PR interval is shortest immediately after the dropped beat. Rhythm strip B is probably type II block; the conducted beats have constant PR intervals. Rhythm strip C is probably Mobitz type I block, based on the following clues: a) the QRS is narrow; b) the ST segment resembles digitalis effect (a common cause of vagotonia and intranodal block); and c) type I block is common, while type II block is rare.
Other criteria may help to differentiate type I and II blocks in the presence of 2 : 1 conduction (4,5) (Table 1). The presence of bundle branch, fascicular, or bifascicular block suggests type II block (Figures 1 and 4). In contrast, if 2 : 1 block is present with normal QRS complexes, the diagnosis of type I block is more likely (7). In an elderly patient with valvular calcification, type II block is likely. If a vagotonic drug has been administered to the patient (e.g., digitalis or morphine), type I AV block is more likely (Figure 3). Type I block is also more likely in the setting of an inferior wall myocardial infarction. Another helpful clue derives from the epidemiology of AV block: Mobitz type I block is ubiquitous, while type II block is rare (5,9). Simple bedside maneuvers may also permit localization of the site of AV block. For example, after administration of atropine, type I block (which is intranodal) improves. The reason is that the AV node is sensitive to atropine’s vagolytic effects. In contrast, atropine makes type II AV block worse. Type II block is located at the level of the His-Purkinje conducting tissue, where atropine has no direct effects.
However, by speeding the rate of sinus impulses and facilitating AV nodal conduction, atropine causes more impulses to penetrate these infranodal tissues, increases their refractoriness, and exacerbates the block (10). Exercise and catecholamines have effects similar to atropine: more impulses bombard the AV node, but fewer are conducted through. Carotid sinus massage (CSM) has the opposite effects. Type I AV block is made worse, because of the vagotonia. In contrast, CSM has no direct effect on infranodal block. However, CSM slows the sinus impulse rate, so that fewer impulses reach the AV node and His-Purkinje conducting tissue. Thus, the conduction ratio improves. In one recent series, the use of atropine and carotid sinus massage at the bedside predicted correctly the site of block in 13 of 15 patients with infra-His block and 9 of 10 patients with intranodal block (10). It is obvious that the responses to CSM, exercise, and catecholamines, while of physiologic interest, are seldom necessary in clinical practice. Certainly, CSM should not be employed in the emergency evaluation of a patient with heart block.
Second-Degree
AV Block-II
51
Figure 4. This 82-year-old man had a 2-week history of exercise intolerance, light-headedness, and fatigue. He presented after a sudden syncopal spell. The rhythm strips (lead II, not continuous) show high-grade AV block, with both 3 : 1 and 2 : 1 conduction. The wide GRS (left-bundle branch block pattern) auggests that the site of the block may be below the bundle of His. Note that there Is no variation In PR intervals regardless of the length of the preceding R-P Interval (no R-PIPR perlodlclty), suggeeting lnfranodal block. High-grade AV block can be type I (intranodal) or type II (infranodal); In cases where the QRS shows a bundle branch block pattern, It Is almost always infranodal (9). The 1Blead ECG from thls patient demonstrated the LBBB and high-grade AV block. lnfranodal conduction system disease seemed likely, and a permanent pacemaker was inserted. The final diagnosis was sclerodegeneratlve conduction system disease.
52
John M. Wogan, Steven R. Lowenstein, Gerald S. Gordon
Figure 5. Three rhythm strips, from different patients, are shown. Each demonstrates normal sinus rhythm. The pauses are the result of nonconducted premature atrial contractions (arrows). The P waves responsible for the pauses are premature and cause deformations of the T wave. Heart block is not present.
CLINICAL SIGNIFICANCE Type I AV block occurs commonly in patients with acute inferior wall myocardial infarction caused by ischemia of the AV node, adenosine release, heightened vagal tone (the Bezold-Jarish reflex), or other factors (11). Other vagotonic influences, such as digitalis excess, may also precipitate type I AV block. Type I AV block may even occur in healthy individuals during sleep, when sympathetic tone is low and parasympathetic tone predominates (12). Usually, the block is transient and the course is benign. In contrast, Mobitz II block is more often seen in acute anterior wall infarction, where actual myocardial necrosis extends through the septum to involve the bundle branches (13). In the absence of myocardial infarction, the most common etiology of Mobitz II AV block is sclerodegeneration of the conduction system. In this condition, which is primarily an affliction of the aged, fibrosis and fatty infiltration take place throughout the conduction system of the heart. The sinus node, atria1 conducting fibers, AV node, and His-Purkinje conducting tissues are often
affected. Figure 4 demonstrates high-grade AV block and left-bundle branch block in a patient who presented to an emergency department after a syncopal spell. The etiology of such diffuse conduction blocks is usually sclerodegenerative conduction system disease. The prognosis is one of continued progression and repeated episodes of symptomatic, advanced heart block. Type II block may occasionally result from betablocker or calcium blocker excess or other drug effects. Hyperkalemia, acidemia, and cardiac valvular calcification are sometimes implicated. Rarely, the etiology may be acute rheumatic fever, an infection (syphilis, toxoplasmosis, or diphtheria), myocarditis, or an infiltrative disease (such as amyloidosis or hemochromatosis) (5,14,15). The clinical significance of Mobitz type II heart block lies in its propensity to progress to complete heart block and cause left ventricular failure, StokesAdams syncope, or sudden death (4,16). Indeed, Mobitz warned that type II block is “the first step to Adams-Stokes attacks and complete permanent dissociation” (3,16).
Second-Degree
AV Block-II
Figure 6. The ECG demonstrates a right-bundle branch block, left ventricular hypertrophy, and a superior wall myocardial infarctlon (of indetermlnete age). The rhythm Is atrlal flutter with 4 : 1 conductlon (although the ECG was originally misread as high-grade AV block). Marriott contends that high-grade AV block should not be diagnosed unless two or more atrial impulses fail to be conducted at a “reasonably normal” atrlal rate (perhaps less than 135 beats/mm) (5).
TREATMENT The treatment of choice for type II block is pacemaker placement. Noninvasive, transcutaneous pacing is indicated as a temporizing maneuver, if imme-
diate transvenous pacing is not possible. In the setting of an acute myocardial infarction, type II AV block necessitates urgent pacemaker placement (16); type I block can often be treated expectantly. Indeed, type I block in patients with an acute inferior myo-
Table 1. Differentiation of lntranodal and lnfranodal Second-Degree Heart Block lntranodal ECG Most common ECG pattern PR interval QRS complex
Clinical Age of patient Common etiologies
Response to Maneuvers Exercise, atropine, and catecholamines Carotid sinus massage PROGNOSIS
lnfranodal
Type I-PR intervals vary in consecutive ducted beats Often prolonged in conducted beats Narrow
con-
Type II-PR intervals are fixed in consecutive conducted beats Usually normal Usually (75% of cases) wide, showing bundle branch or fascicular block. Narrow if intraHis block (25%)
Young or old 1. Inferior myocardial infarction 2. High vagal tone or drugs (digitalis, betablockers)
More often old 1. Anteroseptal myocardial infarction 2. Chronic sclerodegenerative conduction tem disease
Conduction
Conduction
ratio improves
Conduction ratio is made worse Often transient
sys-
ratios is made worse
Conduction ratio improves Often permanent or progressive ams attack
to Stokes-Ad-
54
John M. Wogan, Steven R. Lowenstein, Gerald S. Gordon
cardial infarction is often accompanied by an accelerated junctional tachycardia, assuring hemodynamic stability. Atropine (052.0 mg intravenously) has been advocated to treat type II AV block; indeed atropine is listed as “first line” in the current advanced cardiac life support (ACLS) protocol for heart block. However, as noted earlier, atropine seldom helps, and may actually worsen Mobitz type II AV block. This important caveat was noted by the American Heart Association/American College of Cardiology Task Force in its recent publication, “Guidelines for Early Management of Patients with Acute Myocardial Infarction” (17), which now warns against the use of
atropine where block at the His-Purkinje level is suspected. The Task Force stated that atropine is “not indicated and may be harmful [in] type II AV block and third degree block with new wide QRS complexes .” Isoproterenol may be a useful, temporary treatment for Mobitz II block, with the understanding that its use in the setting of acute ischemia may precipitate ventricular dysrhythmias and contribute to myocardial damage. Nonetheless, an infusion of isoproterenol (2 mg in 250 cc of D5W, beginning at 2 mcg/min) may be lifesaving until pacemaker placement is possible.
REFERENCES 1. Hay .I. Bradycardia and cardiac arrhythmia produced by depression of certain functions of the heart. Lancet 1906; i:139-43. 2. Wenckebach K. Beitrage Zurkenntis der Menschlichen Herztatigkeit. Arch Anat Physiol (Physiol Abth) 1906:297-354. 3. Mobitz W. Uber dei Unvollstandige Storung der Erregungsuberleitung Zwischen Vorhof und Kammer des Menschlichen Herzens. Z Geisamte Exp Med. 1924; 41:180-237. 4. Hart JI. Clinical implications of atrioventricular and intraventricular conduction abnormalities. I. Cardiovasc Clin. 1977;8: 41-64. 5. Marriott HJL. Practical electrocardiography. 8th ed. Baltimore: Williams & Wilkins; 1988. 6. Narula OS. His bundle electrocardiography and clinical electrophysiology. Philadelphia: F.A. Davis, 1975:139-75. 7. Chung EK. Electrocardiography. 3rd ed. Norwalk, CT: Appleton-century-crofts, 1985. 8. Narula 0, Samet P. Wenckebach and Mobitz type II AV block due to block within the His bundle and bundle branches. Circulation. 1970;41:947-65. 9. Zipes DP. Second-degree atrioventricular block. Circulation. 1979;60:465-72.
10. Mangiardi LM, Bonamini R, Conte M. Bedside evaluation of atrioventricular block with narrow QRS complexes: usefulness of carotid sinus massage and atropine administration. Am J Cardiol. 1982;49:1136-45. 11. Berger PB, Ryan TJ. Inferior myocardial infarction: High-risk subgroups. Circulation. 1990;81:401-4. 12. Hancock EW. The case of dropped beats after cardiac surgery. Hosp Practice. 1982;April:49-55. 13. Rosen KM, Loeb HS, Chuquimia R, et al. Site of Heart Block in Acute Myocardial Infarction. Circulation. 1970;42:92533. 14. Chou T. Electrocardiography in clinical practice, 3rd ed. Philadelphia: WB Saunders, 1991. 15. Friedman WH. Diagnostic electrocardiography and vectorcardiography. New York: McGraw-Hill, 1977. 16. Langendorf R, Pick A: Atrioventricular block, type II (Mobitz)-its nature and clinical significance. Circulation. 1968;38: 819-21. 17. ACC/AHA Task Force. ACC/AHA guidelines for the early management of patients with acute myocardial infarction. J Amer Co1 Cardiol. 1990;16:249-92.
Printed in the USA Copyright 0 1993 Pergamon Press Ltd.
Cardiology
Comm=ncary
SECOND-DEGREE ATRIOVENTRICULAR BLOCK: MOBITZ TYPE II John M. Wogan, *Department
of Emergency
MD, FACEP,’
Steven R. Lowenstein,
MD, bwti,t
and Gerald S. Gordon,
MD
Medicine, The Johns Hopkins Hospital, The Johns Hopkins University School of Medicine Baltimore,
Maryland, and Wniversity of Colorado Health Sciences Center Denver, Colorado Reprint Address: Steven R. Lowenstein, MD, MPH, Section of Emergency Medicine and Trauma, University of Colorado Health Scrences Center, Campus Box B215,4200 East Ninth Avenue, Denver, CO 80262
0 Abstract-Acute atrioventricular (AV) block occurs frequently in patients with myocardial infarction. Atrioventricular block is also a common manifestation of sclerodegenerative conduction system disease. Occasionally, heart block results from drug toxicity, hyperkalemia, cardiac valvular calcification, myocarditis, or infiltrative cardiomyopathy. Second-degree AV block is a form of “incomplete” heart block, in which some, but not all, atrial beats are blocked before reaching the ventricles. Mobitz type II second-degree block is an old term, which refers to periodic atrioventricular block with constant PR intervals in the conducted beats. The distinction between type II and type I block is descriptive; of greater importance to the clinician is the anatomic site of the block and the prognosis. In Mobitz type II block the site is almost always below the AV node; in Mobitz type I block the site is usually within the AV node. Type II AV block is more likely to progress to complete heart block and Stokes-Adams arrest. In most cases of second-degree heart block, including cases of 2 : 1 conduction, it is possible to determine the site of the AV block (intranodal or infranodal) using information about the age of the patient, the clinical setting, and the width of the QRS complex on the surface electrocardiogram. Second-degree atrioventricular block must be distinguished from other “causes of pauses.” Nonconducted premature atrial contractions and atrial tachycardia with block are common conditions, which may mimic second-degree AV
INTRODUCTION In 1906, Hay (1) and Wenckebach (2), working independently, described the atrioventricular block subsequently designated second-degree heart block, Mobitz type II. Their accomplishment was notable in that their conclusions predated the electrocardiogram and were based solely on observations of the arterial and jugular venous pulses. In 1921, following the development of the electrocardiogram (ECG), Mobitz (3) described in detail the electrocardiographic features of this type of heart block.
ELECTROCARDIOGRAPHIC
In second-degree block, Mobitz type II, sinus impulses are periodically blocked before reaching the ventricles. This disturbance is characterized by block of a single P wave; the preceding conducted sinus impulses have constant pulse rate (PR) intervals. The block is intermittent and is usually regularly repetitive (Figures l-3). This ECG pattern is in contrast to first-degree block, in which the PR interval is prolonged, but all sinus impulses are conducted. It is also different from third-degree block, where no si-
block. 0 Keywords-heart
= =
FEATURES
block; second degree; Mobitz II
Cardiology Commentary, a section devoted to topics in bedside cardiology and electrocardiography, nated by Steven R. Lowenstein, MD, MPH, University of Colorado Health Sciences Center, Denver.
RECEIVED: 7 November 1991; FINAL SUBMISSIONRECEIVED: 14 April 1992; ACCEPTED: 28 April 1992
47
0736-4679/93
is coordi$6.00 + 00
John M. Wogan, Steven R. Lowenstein, Gerald S. Gordon
Figure 1. Second-degree heart block. Note that 2 : 1 atrioventricuiar conduction is present along with intermittent bundle branch block. The atrioventricuiar block is probably type ii (that is, intranodai), based on the following clues: a) the presence of bundle branch and fascicuiar block, and b) the normal PR interval in the conducted beats.
nus impulses are conducted and the atria and ventricles beat independently. Second-degree Mobitz type II block must be differentiated from second-degree block, type I. In type I block, the PR interval varies. Typically, successive sinus impulses show progressive PR prolongation followed by a dropped beat (the Wenckebach phenomenon). The shortest PR interval occurs immediately after the dropped beat (4) (Figure 3). Second-degree block, Mobitz type II, must also be distinguished from “high-grade” or “advanced” block (Figure 4). In this condition, two or more consecutive P waves are blocked (i.e., the ECG shows a conduction ratio of 3 : 1 or higher). Type II AV block may be simulated by nonconducted premature atrial contractions (PAC’s). In Figure 5, nonconducted premature P waves are seen as small deformations of the preceding T wave. The differentiation between nonconducted PAC’s and second-degree heart block can be made readily by examining the P waves and P-P intervals, appreciating the prematurity and often abnormal shape of the P waves. Heart block is not really present; these P waves are not conducted because they occur ear-
ly, during the normal refractory period of the AV node. A second mimic of AV block is atrial tachycardia or flutter with “block” (Figure 6). Here, the atrial rate is unusually rapid. Heart block is not present; impulses are only being “filtered” by the normal refractoriness of the AV node (5).
ANATOMIC CONSIDERATIONS The site of Mobitz type II block is almost always below the AV node. In about 25% of cases (and more commonly in elderly patients), the delay is in the His bundle itself (6). In this circumstance, the QRS morphology may remain normal (6-8). More commonly, the block is in the bundle branchPurkinje system (that is, distal to the common His bundle). Therefore, in type II block, the QRS complexes usually show evidence of bundle branch or fascicular block (Figures 1, 2, 4) (9). The site of type I AV block is usually within the AV node. Therefore, the QRS complexes usually have a normal duration and contour.
Second-Degree
AV Block-II
49
Figure 2. His-bundle electrocardiogram from the same patient. The His-bundle electrode reveals block below the His-bundle. Note that during atrioventricular block (no QRS in leads I, II, aVF, Vl, and V6), depolarization occurs at both the AV node (see “A” on right atrial and His-bundle leads) and at the His-bundle (“H”) but is not transmitted below the His Bundle. Therefore, the block is Mobitz type II.
It should be emphasized that the terms type I and type II are semantic parameters, which describe the behavior of the PR intervals in consecutive, conducted sinus beats. Of greater significance to the clinician is the site of the block-either within or below the AV node. Although a certain diagnosis may be obtained only through an intracardiac His bundle recording, a reasonable inference regarding the site of the block is usually possible, just by knowing the clinical setting and reviewing the surface ECG. Furthermore (and contrary to popular belief), the site of the block can usually be ascertained even when 2 : 1 conduction is present. The salient features of intranodal (type I) and infranodal (type II) block are summarized later (and in Table 1).
DETERMINING THE SITE OF THE BLOCK IN THE PRESENCE OF 2 : 1 CONDUCTION It is often difficult to distinguish between Mobitz type I (intranodal) and II (infranodal) blocks when 2 : 1 conduction is present. In this setting, variability or prolongation of the PR interval supports a diagnosis of type I block. Therefore, a careful search of a long ECG tracing for two consecutive P waves should be made. A faster ECG paper speed may help to detect PR segment variability. If the PR intervals vary, then type I second-degree heart block is present. If the conduction ratios vary-for example, from 2 : 1 to 3 : 2-and the PR intervals remain fixed, then type II block is present (6).
50
John M. Wogan, Steven R. Lowenstein, Gerald S. Gordon
W
Figure 3. It may be difficult, at times, to differentiate between Yobitz types I and II second-degree heart block if 2 : 1 conduction is present. Rhythm strip A shows Mobitz type I block. In the early portion of the tracing, there is progressive prolongation of consecutive PR intervals, and the PR interval is shortest immediately after the dropped beat. Rhythm strip B is probably type II block; the conducted beats have constant PR intervals. Rhythm strip C is probably Mobitz type I block, based on the following clues: a) the QRS is narrow; b) the ST segment resembles digitalis effect (a common cause of vagotonia and intranodal block); and c) type I block is common, while type II block is rare.
Other criteria may help to differentiate type I and II blocks in the presence of 2 : 1 conduction (4,5) (Table 1). The presence of bundle branch, fascicular, or bifascicular block suggests type II block (Figures 1 and 4). In contrast, if 2 : 1 block is present with normal QRS complexes, the diagnosis of type I block is more likely (7). In an elderly patient with valvular calcification, type II block is likely. If a vagotonic drug has been administered to the patient (e.g., digitalis or morphine), type I AV block is more likely (Figure 3). Type I block is also more likely in the setting of an inferior wall myocardial infarction. Another helpful clue derives from the epidemiology of AV block: Mobitz type I block is ubiquitous, while type II block is rare (5,9). Simple bedside maneuvers may also permit localization of the site of AV block. For example, after administration of atropine, type I block (which is intranodal) improves. The reason is that the AV node is sensitive to atropine’s vagolytic effects. In contrast, atropine makes type II AV block worse. Type II block is located at the level of the His-Purkinje conducting tissue, where atropine has no direct effects.
However, by speeding the rate of sinus impulses and facilitating AV nodal conduction, atropine causes more impulses to penetrate these infranodal tissues, increases their refractoriness, and exacerbates the block (10). Exercise and catecholamines have effects similar to atropine: more impulses bombard the AV node, but fewer are conducted through. Carotid sinus massage (CSM) has the opposite effects. Type I AV block is made worse, because of the vagotonia. In contrast, CSM has no direct effect on infranodal block. However, CSM slows the sinus impulse rate, so that fewer impulses reach the AV node and His-Purkinje conducting tissue. Thus, the conduction ratio improves. In one recent series, the use of atropine and carotid sinus massage at the bedside predicted correctly the site of block in 13 of 15 patients with infra-His block and 9 of 10 patients with intranodal block (10). It is obvious that the responses to CSM, exercise, and catecholamines, while of physiologic interest, are seldom necessary in clinical practice. Certainly, CSM should not be employed in the emergency evaluation of a patient with heart block.
Second-Degree
AV Block-II
51
Figure 4. This 82-year-old man had a 2-week history of exercise intolerance, light-headedness, and fatigue. He presented after a sudden syncopal spell. The rhythm strips (lead II, not continuous) show high-grade AV block, with both 3 : 1 and 2 : 1 conduction. The wide GRS (left-bundle branch block pattern) auggests that the site of the block may be below the bundle of His. Note that there Is no variation In PR intervals regardless of the length of the preceding R-P Interval (no R-PIPR perlodlclty), suggeeting lnfranodal block. High-grade AV block can be type I (intranodal) or type II (infranodal); In cases where the QRS shows a bundle branch block pattern, It Is almost always infranodal (9). The 1Blead ECG from thls patient demonstrated the LBBB and high-grade AV block. lnfranodal conduction system disease seemed likely, and a permanent pacemaker was inserted. The final diagnosis was sclerodegeneratlve conduction system disease.
52
John M. Wogan, Steven R. Lowenstein, Gerald S. Gordon
Figure 5. Three rhythm strips, from different patients, are shown. Each demonstrates normal sinus rhythm. The pauses are the result of nonconducted premature atrial contractions (arrows). The P waves responsible for the pauses are premature and cause deformations of the T wave. Heart block is not present.
CLINICAL SIGNIFICANCE Type I AV block occurs commonly in patients with acute inferior wall myocardial infarction caused by ischemia of the AV node, adenosine release, heightened vagal tone (the Bezold-Jarish reflex), or other factors (11). Other vagotonic influences, such as digitalis excess, may also precipitate type I AV block. Type I AV block may even occur in healthy individuals during sleep, when sympathetic tone is low and parasympathetic tone predominates (12). Usually, the block is transient and the course is benign. In contrast, Mobitz II block is more often seen in acute anterior wall infarction, where actual myocardial necrosis extends through the septum to involve the bundle branches (13). In the absence of myocardial infarction, the most common etiology of Mobitz II AV block is sclerodegeneration of the conduction system. In this condition, which is primarily an affliction of the aged, fibrosis and fatty infiltration take place throughout the conduction system of the heart. The sinus node, atria1 conducting fibers, AV node, and His-Purkinje conducting tissues are often
affected. Figure 4 demonstrates high-grade AV block and left-bundle branch block in a patient who presented to an emergency department after a syncopal spell. The etiology of such diffuse conduction blocks is usually sclerodegenerative conduction system disease. The prognosis is one of continued progression and repeated episodes of symptomatic, advanced heart block. Type II block may occasionally result from betablocker or calcium blocker excess or other drug effects. Hyperkalemia, acidemia, and cardiac valvular calcification are sometimes implicated. Rarely, the etiology may be acute rheumatic fever, an infection (syphilis, toxoplasmosis, or diphtheria), myocarditis, or an infiltrative disease (such as amyloidosis or hemochromatosis) (5,14,15). The clinical significance of Mobitz type II heart block lies in its propensity to progress to complete heart block and cause left ventricular failure, StokesAdams syncope, or sudden death (4,16). Indeed, Mobitz warned that type II block is “the first step to Adams-Stokes attacks and complete permanent dissociation” (3,16).
Second-Degree
AV Block-II
Figure 6. The ECG demonstrates a right-bundle branch block, left ventricular hypertrophy, and a superior wall myocardial infarctlon (of indetermlnete age). The rhythm Is atrlal flutter with 4 : 1 conductlon (although the ECG was originally misread as high-grade AV block). Marriott contends that high-grade AV block should not be diagnosed unless two or more atrial impulses fail to be conducted at a “reasonably normal” atrlal rate (perhaps less than 135 beats/mm) (5).
TREATMENT The treatment of choice for type II block is pacemaker placement. Noninvasive, transcutaneous pacing is indicated as a temporizing maneuver, if imme-
diate transvenous pacing is not possible. In the setting of an acute myocardial infarction, type II AV block necessitates urgent pacemaker placement (16); type I block can often be treated expectantly. Indeed, type I block in patients with an acute inferior myo-
Table 1. Differentiation of lntranodal and lnfranodal Second-Degree Heart Block lntranodal ECG Most common ECG pattern PR interval QRS complex
Clinical Age of patient Common etiologies
Response to Maneuvers Exercise, atropine, and catecholamines Carotid sinus massage PROGNOSIS
lnfranodal
Type I-PR intervals vary in consecutive ducted beats Often prolonged in conducted beats Narrow
con-
Type II-PR intervals are fixed in consecutive conducted beats Usually normal Usually (75% of cases) wide, showing bundle branch or fascicular block. Narrow if intraHis block (25%)
Young or old 1. Inferior myocardial infarction 2. High vagal tone or drugs (digitalis, betablockers)
More often old 1. Anteroseptal myocardial infarction 2. Chronic sclerodegenerative conduction tem disease
Conduction
Conduction
ratio improves
Conduction ratio is made worse Often transient
sys-
ratios is made worse
Conduction ratio improves Often permanent or progressive ams attack
to Stokes-Ad-
54
John M. Wogan, Steven R. Lowenstein, Gerald S. Gordon
cardial infarction is often accompanied by an accelerated junctional tachycardia, assuring hemodynamic stability. Atropine (052.0 mg intravenously) has been advocated to treat type II AV block; indeed atropine is listed as “first line” in the current advanced cardiac life support (ACLS) protocol for heart block. However, as noted earlier, atropine seldom helps, and may actually worsen Mobitz type II AV block. This important caveat was noted by the American Heart Association/American College of Cardiology Task Force in its recent publication, “Guidelines for Early Management of Patients with Acute Myocardial Infarction” (17), which now warns against the use of
atropine where block at the His-Purkinje level is suspected. The Task Force stated that atropine is “not indicated and may be harmful [in] type II AV block and third degree block with new wide QRS complexes .” Isoproterenol may be a useful, temporary treatment for Mobitz II block, with the understanding that its use in the setting of acute ischemia may precipitate ventricular dysrhythmias and contribute to myocardial damage. Nonetheless, an infusion of isoproterenol (2 mg in 250 cc of D5W, beginning at 2 mcg/min) may be lifesaving until pacemaker placement is possible.
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10. Mangiardi LM, Bonamini R, Conte M. Bedside evaluation of atrioventricular block with narrow QRS complexes: usefulness of carotid sinus massage and atropine administration. Am J Cardiol. 1982;49:1136-45. 11. Berger PB, Ryan TJ. Inferior myocardial infarction: High-risk subgroups. Circulation. 1990;81:401-4. 12. Hancock EW. The case of dropped beats after cardiac surgery. Hosp Practice. 1982;April:49-55. 13. Rosen KM, Loeb HS, Chuquimia R, et al. Site of Heart Block in Acute Myocardial Infarction. Circulation. 1970;42:92533. 14. Chou T. Electrocardiography in clinical practice, 3rd ed. Philadelphia: WB Saunders, 1991. 15. Friedman WH. Diagnostic electrocardiography and vectorcardiography. New York: McGraw-Hill, 1977. 16. Langendorf R, Pick A: Atrioventricular block, type II (Mobitz)-its nature and clinical significance. Circulation. 1968;38: 819-21. 17. ACC/AHA Task Force. ACC/AHA guidelines for the early management of patients with acute myocardial infarction. J Amer Co1 Cardiol. 1990;16:249-92.