types of repolarization abnormalities (e.g., left ventricular hypertrophy [LVH]), there are usually no significant differ-ences in the ST segments and T waves compared with normal individuals.1
Left Posterior Fascicular Block. LPFB, also termed left posterior hemiblock, is rare in contrast to LAFB. It is
characterized by a rightward axis shift and an rS pattern in leads I and aVL (Fig. 21-4). A qR pattern is present in lead III and often in leads II and aVF as well (see Box 21-2). LPFB should not be diagnosed in the presence of right ventricular hypertrophy (see Chapter 35, Ventricular Hypertrophy). The QRS complex duration is normal unless there is another cause of IVCA present. In a sense, LPFB manifests as the “opposite”
of LAFB; the axes are opposite (left in LAFB, right in LPFB), and the morphologic findings seen in the lateral leads (I, aVL) of each are seen in the inferior leads (II, III, aVF) in the other.
Bifascicular blocks
Right Bundle Branch Block Plus Left Anterior Fascicular Block. The combination of RBBB and LPFB is the most common form of bifascicular block.5This combination has the ECG manifestations of both RBBB and LAFB noted previously (Fig. 21-5). The leftward axis persists and the QRS complex duration is greater than 0.12 sec.
Right Bundle Branch Block Plus Left Posterior Fascicular Block. The combination of RBBB and LAFB is an uncom-mon form of bifascicular block. The ECG deuncom-monstrates the key features of both RBBB and LPFB (Fig. 21-6). The right-ward axis persists and the QRS complex duration is greater than 0.12 sec.
Left Bundle Branch Block. Because the left bundle branch is subdivided into anterior and posterior fascicles, complete LBBB can be considered a form of bifascicular block. The ECG in patients with LBBB (Fig. 21-7) demonstrates a QRS complex duration greater than 0.12 sec with a delayed intrin-sicoid deflection in lead V6of at least 0.08 sec.5If the QRS complex duration is less than 0.12 sec but other criteria for LBBB are met, the diagnosis of incomplete LBBB is made.
The right precordial leads in LBBB demonstrate QS or rS complexes. Leftward axis deviation may be present. Leads I and V6should manifest prominent monophasic R waves; the presence of even small q waves in these leads rules out the diagnosis. The ST segments and T waves should be oriented 90 SECTIONIII: ELECTROCARDIOGRAPHIC MANIFESTATIONS OF DISEASE
ELECTROCARDIOGRAPHIC HIGHLIGHTS
Right bundle branch block
• Lead V1: M-shaped QRS complex (rSR′); sometimes single wide or notched R wave or qR
• Lead V6: wide S wave
• Lead I: wide S wave
• QRS complex duration ≥0.12 sec (if preceding criteria are met but duration is <0.12 sec, “incomplete right bundle branch block” is evident)
• A unifascicular block Left anterior fascicular block
• Left axis deviation (between −30 (or −45) and −90 degrees;
usually ≥−60 degrees)
• Small q wave and prominent R wave or isolated prominent R wave in lead I
• Small q wave and prominent R wave in lead aVL
• Small r wave and prominent S wave in leads II, III, and aVF
• Usually normal QRS complex duration (unless associated with another cause of intraventricular conduction abnormality)
• A unifascicular block Left posterior fascicular block
• Right axis deviation (usually ≥+120 degrees)
• Small r wave and prominent S wave in leads I and aVL
• Small q wave and prominent R wave in lead III (often in leads II and aVF as well)
• No evidence for right ventricular hypertrophy or other causes of right axis deviation
• Usually normal QRS complex duration (unless associated with another cause of intraventricular conduction abnormality)
• A unifascicular block Left bundle branch block
• Right precordial leads: QS or rS complex
• Leads V5and V6: no q waves, monophasic prominent R wave
• Lead I: no q wave, monophasic prominent R wave
• QRS complex duration ≥0.12 sec (if preceding criteria are met but duration is <0.12 sec, “incomplete left bundle branch block” is evident)
• A bifascicular block Trifascicular blocks
• Evidence of permanent block in one fascicle and an intermittent/alternating block in the other two fascicles
• Definitive diagnosis requires His bundle recording; however, it is strongly suggested by the following:
- Incomplete trifascicular block: bifascicular block with first or second degree atrioventricular block
• Complete trifascicular block: bifascicular block with complete heart block
Nonspecific intraventricular conduction delay
• QRS complex duration of ≥0.11 sec
• Does not satisfy criteria for specific bundle branch or fascicular block
• Consider hyperkalemia as the cause of a new unifascicular or bifascicular block.
• ST segment elevation or upright T waves in leads V1to V3in the presence of right bundle branch block could suggest an acute coronary syndrome or Brugada syndrome.
• Left anterior fascicular block is often mistaken for past anteroseptal myocardial infarction.
• Other causes of right axis deviation should be ruled out before the diagnosis of left posterior fascicular block is made.
• Left bundle branch block (LBBB) is associated with signifi-cant secondary ST segment and T wave abnormalities that are discordant to the major vector of the QRS complexes across the precordium. Therefore, the presence of concordant ST segment elevation or concordant T wave orientation suggests myocardial ischemia.
• LBBB can be distinguished from left ventricular hypertrophy by the presence of prominent monophasic R waves and the absence of q waves in leads I and V6.
ELECTROCARDIOGRAPHIC PEARLS
CHAPTER21: Intraventricular Conduction Abnormalities 91
FIGURE 21-1 • Right bundle branch block. Note the rSR′ pattern of the wide QRS complex in lead V1(circle), and the wide S wave in leads I and V6(arrows).
FIGURE 21-2• Incomplete right bundle branch block. Note the QRS complex of intermediate width with an rSR′ pattern in lead V1(circle).
92 SECTIONIII: ELECTROCARDIOGRAPHIC MANIFESTATIONS OF DISEASE
FIGURE 21-3• Left anterior fascicular block (LAFB). Note the left axis deviation, prominent R wave in lead I, and prominent S wave in lead III. The QRS complex is of normal duration. Also typical of LAFB is the delayed transition zone in the precordial leads.
FIGURE 21-4• Left posterior fascicular block. The tracing demonstrates an evolving anteroseptal MI with Q waves and ST segment elevation in leads V1
through V4, along with left posterior fascicular block (LPFB). LPFB is diagnosed by right axis deviation, prominent S wave in lead I, and prominent R wave in lead III. The QRS complex is of normal duration.
CHAPTER21: Intraventricular Conduction Abnormalities 93
FIGURE 21-5• Bifascicular block (right bundle branch block [RBBB] + left anterior fascicular block [LAFB]). Although somewhat atypical, this ECG meets the criteria for RBBB and LAFB.
FIGURE 21-6• Bifascicular block (right bundle branch block + left posterior fascicular block).
94 SECTIONIII: ELECTROCARDIOGRAPHIC MANIFESTATIONS OF DISEASE
FIGURE 21-7• Left bundle branch block. Note the wide QRS complex associated with the prominent R wave in leads I, aVL, and V6and qS complex in lead V1. The ST segment/T wave changes are appropriately discordant to the QRS complex in the right and left precordial leads, as well as leads I and aVL.
FIGURE 21-8 • Trifascicular block (third degree heart block + right bundle branch block [RBBB] + left anterior fascicular block [LAFB]). A prior ECG demonstrated preexisting RBBB and LAFB, a bifascicular block. With the development of third degree heart block, a trifascicular block was diagnosed.
In this ECG, the atrial rate is 100 bpm, whereas the ventricular rate is 35 bpm.
CHAPTER21: Intraventricular Conduction Abnormalities 95
in a direction opposite (discordant) to the main deflection of the QRS complex in these leads. For this reason, the expected abnormalities of acute myocardial ischemia and infarction are not reliable (see Chapter 34, Acute Myocardial Infarction:
Confounding Patterns).
Trifascicular blocks
Trifascicular block is suspected when there is a permanent block in one fascicle and an intermittent block in the other two fascicles. For example, if the patient has a chronic RBBB and alternating LAFB and LPFB develop, trifascicular block is diagnosed. When a complete trifascicular block occurs, the ECG shows evidence of a bifascicular block with third degree AV block (Fig. 21-8). If the block in one of the fascicles is incomplete, the ECG demonstrates a bifascicular block with first or second degree AV block1 (Fig. 21-9). However, this pattern of AV block does not always guarantee that the conduction disturbance is due to fascicular disease; the conduction delay may be at the level of the AV node or the His bundle.1 Definitive diagnosis of trifascicular block requires His bundle recording.1,7 It is safer to assume that first or second degree AV block in the presence of bifascicular block heralds impending complete trifascicular block because there is no way to discern the cause of the AV block (fascicle versus AV nodal) at the bedside.
Nonspecific intraventricular conduction delay In NSIVCD, the QRS complex duration is greater than 0.12 sec, but the ventricular conduction delay does not meet strict
criteria for a specific bundle branch or fascicular block. In many cases, the delay is explained by the presence of drugs (e.g., cyclic antidepressants) or other conditions (e.g., hyper-kalemia, hypothermia) that slow ventricular conduction. LVH is often associated with conduction delay as well, and may produce significant prolongation of the QRS complex. This is not necessarily a pathologic condition. LVH with a widened QRS complex can sometimes be mistaken for LBBB, but the presence of small q waves and absence of a prominent monophasic R wave in leads I and V6rules out LBBB.
References
1. Surawicz BS, Knilans TK: Chou’s Electrocardiography in Clinical Practice, 5th ed. Philadelphia, WB Saunders, 2001.
2. Lenegre J: Etiology and pathology of bilateral bundle branch block in relation to complete heart block. Prog Cardiovasc Dis 1964;6:409.
3. Lev M: Anatomic basis for atrioventricular block. Am J Med 1964;37:742.
4. Mattu A, Brady WJ, Robinson DA: Electrocardiographic manifestations of hyperkalemia. Am J Emerg Med 2000;18:721.
5. Fowler NO: Clinical Electrocardiographic Diagnosis: A Problem Based Approach. Philadelphia, Lippincott Williams & Wilkins, 2000.
6. Wagner GS: Marriott’s Practical Electrocardiography, 10th ed. Philadelphia, Lippincott Williams & Wilkins, 2001.
7. Levitas R, Haft JL: Significance of first degree heart block (prolonged PR interval) in bifascicular block. Am J Cardiol 1975;34:259.
FIGURE 21-9 • Incomplete trifascicular block. This ECG shows suspected incomplete trifascicular block (first degree atrioventricular block + right bun-dle branch block + left posterior fascicular block [LPFB]), in a setting of previous anteroseptal myocardial infarction. Right ventricular hypertrophy (as a cause of the prominent R wave and qR pattern in lead V1, as well as for the right axis deviation) should be excluded by echocardiography before this pattern can be definitively concluded to represent LPFB.
Clinical Features
Atrial Fibrillation. The prevalence of atrial fibrillation is increasing and its incidence doubles with each decade of adult life, with 5% of persons aged 65 years and older affected.
Atrial fibrillation complicates 5% to 10% of acute myocardial infarctions and 40% of cardiac surgeries.1Presentations range from palpitations to pulmonary edema and stroke. Non-specific symptoms such as fatigue and altered mentation are common in the elderly.2 In patients with paroxysmal atrial fibrillation, asymptomatic episodes are more common than symptomatic episodes.
There are many causes for atrial fibrillation, including pericarditis, chronic hypertension, pulmonary embolism, coronary artery disease, alcohol abuse (holiday heart), rheu-matic valvular disease (particularly mitral and tricuspid), thy-rotoxicosis, and cardiac surgery. It is very rare for ischemic heart disease to present as atrial fibrillation in the absence of other signs and symptoms of ischemia.2Up to 30% of cases are not associated with hypertension or other demonstrable underlying cardiopulmonary disease (known as “lone” atrial fibrillation).3
The common pathophysiologic process is atrial enlarge-ment (especially the left atrium), atrial inflammation, and fibrosis. Triggering events include altered sympathetic or parasympathetic tone, acute or chronic changes in atrial wall tension, ischemia, bradycardia, atrial premature contractions, and conduction through accessory atrioventricular (AV) path-ways.1These triggers are prodysrhythmic because they accel-erate repolarization and shorten the refractory state of atrial tissue. Currently, the preeminent theory of the genesis of atrial fibrillation is the multiple wavelet hypothesis.1,2After a triggering event, multiple, random atrial micro-reentrant waves are generated, collide, and extinguish one another, and arise again. Another recently discovered mechanism for the initiation of atrial fibrillation involves a rapidly firing focus in or near the atrial sleeves of the pulmonary veins.1
There are four classifications of atrial fibrillation based on the duration of the dysrhythmia: (1) acute—lasting less than 48 hours; (2) paroxysmal—more than one acute self-terminating
episode; (3) persistent—lasting longer than 48 hours without spontaneous termination; and (4) permanent—resistant to pharmacologic or electrical cardioversion.4