Review

right bundle-branch block in acute coronary syndrome: diagnostic and therapeutic implications for the emergency physician

Cheryl Lynn Horton, William J. Brady MD?

Department of Emergency Medicine, University of Virginia, Charlottesville, VA 22908, USA

Received 17 September 2008; accepted 23 September 2008

Abstract Right bundle-branch block (RBBB) in the patient with acute coronary syndrome is a marker of significant potential cardiovascular risk; the RBBB pattern in the patient with acute coronary syndrome identifies a subgroup of patients with quite high short- and long-term morbidity and mortality. Right bundle-branch block is not an uncommon finding on an electrocardiogram in the emergency department patient, noted incidentally and thus without clinical import or, conversely, encountered in the early phase of significant cardiovascular dysfunction. This review will address RBBB in the acute coronary syndrome setting.

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Right bundle-branch block

Impulse generation in the sinoatrial (SA) node or other default pacemaker sites occurs at least 60 times a minute in the healthy human heart; conduction of this impulse then follows with transmission of the electrical event in a rapid, orderly fashion. The rapid and efficient movement of this impulse is vital to appropriate cardiac function. The cardiac conduction system, the “electrical wiring” of the heart, is responsible for the transmission of this impulse throughout the myocardium.

The electrical impulse, once generated, is released from the SA node and travels throughout the atrial tissues via poorly defined, intra-atrial conduction pathways. As the electrical impulse is propagated throughout the atria, it also moves along more well-defined internodal tracts, traveling

* Corresponding author.

E-mail address: [email protected] (W.J. Brady).

from the SA node to the atrioventricular (AV) node. At the AV node, impulse transmission to the ventricular myocar- dium occurs; this transmission, however, is delayed at the AV node, allowing sufficient time for atrial depolarization and providing protection to the ventricular myocardium from excessive rates. Once the impulse moves through the AV node, it enters the bundle of His, which branches into 2 subdivisions at the interventricular septum; these branches are termed the left bundle and the right bundle branches. The 2 bundle branches continue with further subdivisions, ultimately ending in numerous Purkinje fibers; these fibers convey the impulse to the ventricular myocytes, depolarizing both ventricles in near-simultaneous fashion. Thus, the electrical event, initiated in the SA node, is rapidly and efficiently transmitted throughout the heart via the conduc- tion system, resulting in cardiac depolarization and ulti- mately, mechanical contraction.

Of the many portions of the conduction system, the right bundle branch plays a significant role in ventricular

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depolarization. The right bundle is a long, discrete, nonbranching structure that is located at the junction of the fibrous and muscular portions of the intraventricular septum. The proximal and terminal thirds of the right bundle traverse close to the endocardium and thus are the most vulnerable to stretch or traumatic injury; these specific areas of the right bundle branch are the sites where right bundle-branch block (RBBB) is most common. The right bundle has a dual Blood supply with most perfusion provided by the left anterior descending coronary artery; additional blood flow is provided by either the right coronary artery or the left circumflex coronary artery, depending on the dominance of the particular coronary system. In the anterior wall ST-elevation myocardial infarction patient with RBBB, Kurisu and colleagues [1] demonstrated higher rates of either left anterior descending artery or multivessel coronary disease, compared with other culprit vascular distributions.

The general mechanisms of injury to the right bundle branch are both structural and functional. Ischemia, infarc- tion, inflammation, cardiomyopathy, and congenital heart disease are structural causes of RBBB. Cor pulmonale and pulmonary embolism can cause RBBB by increasing right heart pressures, causing interventricular septal stretch. A rate-related bundle-branch block (BBB) is a type of functional BBB, occurring at excessive rates; in this setting, the rhythm’s rate is so rapid that the subsequent impulse arrives before the bundle branch has fully repolarized, thus producing dysfunctional conduction and the BBB. Iatrogenic events, such as placement of a right heart catheter, can also

produce RBBB; for instance, iatrogenic RBBB is reported in up to 5% of right heart catheterizations.

The prevalence of RBBB varies across populations; it is relatively rare, however, in an otherwise normal heart. A Swedish series of 7392 middle-aged men without a history of myocardial infarction or stroke had a 0.7% prevalence of RBBB [2]. Other investigations demonstrate that age [3- 5], diabetes mellitus, and anterior wall infarction are all significantly related to the development of RBBB [6]. With the increasing prevalence of RBBB as one ages, it is thought to be a marker of slowly progressive degenerative disease of the conduction system. One longitudinal prospective study illustrates this age association quite well, with RBBB found in 1% of the study population at 50 years and increasing to 17% at 80 years of age [7]. The prognosis of RBBB is often related to the presence, type, and severity of the underlying cardiac disease. Isolated RBBB has an excellent prognosis unlike isolated Left bundle-branch block (LBBB), which portends greater overt cardiac disease and a higher cardiac mortality rate [8]. Right bundle-branch block in the setting of known or suspected cardiac disease, however, is an independent predictor of all-cause mortality [9].

Electrocardiographic diagnosis of RBBB

Right bundle-branch block, regardless of its cause or location of the bundle injury, appears electrocardiographi-

Fig. 1 Normal sinus rhythm with RBBB. Note the wide QRS complex greater than 0.12 second in width, RsR? complex in lead V₁, and the RS complex in lead V₆. The R wave is of lower amplitude than the R? wave, a highly characteristic feature of the RBBB pattern.

cally similar. In the patient with RBBB, the depolarization wave initially arrives in the left ventricle via the left bundle branch. The electrical impulse is then transmitted to the right ventricle via the left bundle branch and myocyte-myocyte propagation, producing a “slurred” or widened appearance to the QRS complex. Because of the asynchronous activation of both ventricles as well as the inefficient propagation of the impulse, the QRS complex tends to be wide.

The traditional electrocardiographic criteria required for the diagnosis of RBBB includes the following criteria: a QRS complex width greater than 0.12 second; an RsR? QRS complex in lead V₁; and a widened or “slurred” S wave in leads I and V₆ (Figs. 1-3). The QRS complex is widened with a duration frequently greater than 0.12 second; note that an “incomplete” form of RBBB is encountered with a QRS complex width ranging from 0.08 to 0.12 second.

Fig. 2 A, Atrial fibrillation with rapid ventricular response and RBBB. Note the wide QRS complex greater than 0.12 second in width, RsR? complex in lead V₁, and the RS complex in lead V₆. B, After therapy, atrial fibrillation has slowed with persistence of the RBBB. Note the wide QRS complex greater than 0.12 second in width, RsR? complex in lead V₁, and the RS complex in lead V₆. As in A, the QRS complex in lead V₆, an RS complex, is much less dramatic in appearance than the RSR complex in lead V₁.

Fig. 3 Normal sinus rhythm with RBBB. In addition to the widened QRS complex, note the rsR? complex in lead V₁ as well as the RSR? wave in lead V₂. The RS complex in lead V₆ demonstrates equal R and S waves.

The most obvious electrocardiographic finding in RBBB is the configuration of the QRS complex in lead V₁, commonly referred to as the “rabbit ears” or M-shaped morphology (Figs. 1-5). The characteristic RBBB pattern is an RSR? complex found in lead V₁ (Figs. 4 and 5). The initial R wave (a positive deflection) reflects the normal septal activation and the S wave (a secondary negative deflection) reflects left ventricular activation; the R? wave (a secondary positive deflection) represents the delayed activation of the right ventricle from a left-to-right and anterior vector. The typical morphology of this QRS complex is the classic triphasic RSR? pattern, the uneven “M-shaped” structure [10]. Refer to Figs. 4 and 5 for complete graphical descriptions of the possible QRS complex morphologies found in lead V₁.

Fig. 4 The classic “rabbit ears” of RBBB in lead V₁ with an RSR? complex. Also note that the major, terminal portion of QRS complex is located on the opposite side of the isoelectric baseline from the initial portion of ST segment/T wave, illustrating the concept of appropriate discordance with discordant ST-segment depression.

In lead V₁, there are several distinct potential config- urations of the RSR? QRS complex that are clinically encountered (Fig. 5). Most commonly, the second peak of the QRS complex, the R? wave, is usually of a greater amplitude than the first peak, the r wave, producing the “M” configuration-and is termed the rsR? wave; recall that, by convention, capital letters represent deflections of the electrocardiogram (ECG) that are greater than 5 mm, whereas lower case letters symbolize smaller amplitude structures. The depth of the S wave in lead V₁ can vary depending on whether left ventricular activation is directed anteriorly or posteriorly; ranging from very small (1-3 mm) to quite prominent (3-6 mm). Other common lead V₁ QRS complex variations include the monophasic R wave (large, entirely positive structure), rsr?, rsR?, and rSR? patterns. A Q wave, at times prominent, can be seen in patients with septal myocardial infarction (MI), regardless of the MI age; the QRS complex configuration can be either the qR or qrsR? pattern.

Lead V₆ is generally less electrocardiographically impressive with an RS configuration. The delayed right- ward electrical activation typical of RBBB is manifested in the lateral leads (I, aVL, V5, and V₆) as a prolongation or “slurring” of the S wave. The RS wave is usually composed of a Prominent R wave with a wide S wave. The S wave is usually greater than 0.04 second in width; the S-wave duration can also be greater than the accompanying R wave; the depth of the S wave is variable, ranging from 1 to 5 mm [10,11]. Refer to Figs. 6 and 7 for complete graphical descriptions of the QRS complex in lead V₆.

Other Electrocardiographic features to consider include the axis and the presence of other Conduction abnormalities. The QRS complex axis in RBBB is usually normal but can be leftward or rightward. Left or Right axis deviation usually signifies concomitant block of either the anterior or posterior fascicle of the left bundle, which by definition is a bifascicular conduction block.

Fig. 5 Various configurations of RBBB in lead V₁. A, RSR? complex, the classic “rabbit ears.” B, RSR? complex, the classic “rabbit ears.” C, RSR? complex, the classic “rabbit ears.” D, QR complex. E, RSR? complex, the “m-shaped” variant. F, RSR? complex, the “m-shaped” variant. G, QR complex.

The appearance of the ST segment and, to a lesser extent, the T wave, is changed by the altered depolarization- repolarization patterns seen in RBBB. In fact, at times, ominous appearing ST-segment and T-wave changes are the new norm in patients with RBBB. The clinician must be familiar with these abnormalities such that both the expected

Fig. 6 Lead V₆ with prominent R wave and small S wave.

(ie, normal) and unexpected (ie, abnormal) ST-segment morphologies are recognized. The basic, normal relationship of the QRS complex and ST segment/T wave is described by the concept, or rule, of appropriate discordance. This concept suggests that the ST-segment and T-wave changes tend to be discordant to the primary QRS complex vector (Fig. 4).

The concept of appropriate discordance (Fig. 4) suggests that the major, terminal portion of the QRS complex is located on the opposite side of the isoelectric baseline from the ST segment and initial portion of the T wave. This concept, in the setting of RBBB, suggests that the predominantly positive RSR complex in the Right precordial leads will be accompanied by ST-segment depression and inverted T wave. By contrast, the left precordial leads, leads V5 or V₆, tend to be more variable in the RBBB Electrocardiographic presentation. The RS complex in these leads can demonstrate similar deflections of the QRS complex with equal amplitudes of the R and S waves, such that the ST segment is likely isoelectric or minimally elevated. In the setting of acute coronary syndrome (ACS) and RBBB, this concept of appropriate discordance is often violated and aids in the diagnosis of ACS, particularly in the right to mid precordial leads.

ACS diagnosis and RBBB

Investigations from the prefibrinolytic era reported the prevalence of RBBB in the setting of an acute MI (AMI) to

Fig. 7 Various lead V₆ configurations in RBBB. A, RS complex. B, RS complex. C, RS complex. D, RS complex. E, RS complex. F, RS complex with R wave equal to S wave.

range from 3 to 29% [12-17]; this rather broad range of occurrence results, of course, from differing selection criteria and the definition of RBBB. More recent studies have attempted to identify the time course of the RBBB develop- ment in the AMI patient: preexisting vs newly developed and transient vs permanent. Moreno and colleagues report that of the 10.8% of AMI cases who presented with RBBB, 65% of individuals demonstrated a new-onset RBBB; 56% of these patients demonstrated a transient RBBB in the periinfarct period [6]. In this patient group, a newly developed RBBB was more common in younger patients and women; furthermore, a large anterior wall infarction was almost always present. A preexisting RBBB, by contrast, was more likely in older individuals and in those with significant comorbidity (diabetes mellitus and cardiovascular disease) [18].

The ECG is a vital tool used in the emergency department (ED) evaluation of the chest pain patient suspected of ACS. conduction disturbances can impact the value of the ECG in this evaluation. Recall that, although the LBBB pattern obscures the electrocardiographic diagnosis of acute myo- cardial infarction, RBBB does not confound the ECG’s ability to diagnose AMI. The RBBB pattern can lead the unwary clinician to miss STEMI when, in fact, acute infarction is

present if he or she is not comfortable with the concept of appropriate discordance. Conversely, the often dramatic ST- segment and T-wave abnormalities of the RBBB pattern can suggest to the uninformed clinician that STEMI is present electrocardiographically when, in actual fact, the ECG demonstrates only appropriate waveforms for the RBBB.

Application of the concept of appropriate discordance, as discussed above, will assist in the electrocardiographic diagnosis of STEMI. Recall that the major, terminal portion of the QRS complex and the initial portion of the ST segment/T wave are discordant, meaning that they are located on opposite sides of the isoelectric baseline. Thus, in the right to mid precordial leads, the largely positive QRS complex will be associated with ST-segment depression and an inverted T wave. A “violation” of this concept will manifest as ST-segment elevation, which is concordant with the major, terminal portion of the QRS complex; the T-wave findings are more often variable with either continued inversion or disappearance (lost within the greater ST segment itself). Anterior wall STEMI is therefore usually quite obvious if the clinician is comfortable with the appropriate appearance of the ST segment in RBBB. Other STEMI patterns will demonstrate similar arrangements of

Fig. 8 Lead V₁ in patients with RBBB and anterior wall STEMI. A, Note R wave (large arrow) of the QRS complex is almost entirely obscured by the elevated ST segment (small arrow), which is concordant with the QRS complex. B, The R wave (large arrow) of the QRS complex is obvious in this example; concordant ST-segment elevation (small arrow) is also seen. C, The R wave of the QRS complex (large arrow) is prominent as is the concordant ST-segment elevation (small arrow).

Fig. 9 Examples of concordant ST-segment elevation in patients with anterior wall STEMI and RBBB (leads V₁ and V₂). A, Prominent, concordant ST-segment elevation. B, Less prominent, although still obvious, concordant ST-segment elevation. C, Prominent, concordant ST segment elevation. D, Concordant ST-segment elevation. E, Concordant ST-segment elevation. F, Concordant ST-segment elevation.

Fig. 10 A 65-year-old woman with chest pain, dyspnea, and weakness. The ECG demonstrates NSR with first-degree AV block and RBBB. Anterior wall STEMI is noted with concordant ST-segment elevation in leads V₁ to V₃. The patient developed cardiogenic shock and died despite aggressive therapy in the cardiac catheterization laboratory.

inappropriate ST segment waveform location-concordant ST-segment abnormalities. Refer to Figs. 8 to 13 for various examples of RBBB and STEMI.

A more complete discussion of Figs. 10 to 13 and related cases follows here. In each case, RBBB is seen in a patient with significant STEMI presentation. In Fig. 10, the ECG demonstrates normal sinus rhythm (NSR) with first-degree AV block and RBBB. The patient is a 65 year-old woman with chest pain, dyspnea, and weakness. Anterior wall STEMI is noted with concordant ST-segment elevation in leads V₁ to V₃. The patient developed cardiogenic shock and died despite aggressive therapy in the cardiac catheterization laboratory. Fig. 11 illustrates the ECG of a 72 year-old male patient who presented to the ED with chest pain. The examination was significant for pulmonary edema and borderline systemic perfusion. The initial ECG demonstrates NSR with RBBB. Anterior wall STEMI is noted with concordant ST-segment elevation in leads V₁ and V₂. Excessive discordant ST-segment elevation is seen in lead V₃. Concordant ST-segment elevation is seen also in lead I and aVL, indicative of a lateral wall STEMI as well. Repeat ECG before emergent coronary angiography demonstrated progressive ST segment changes not only in the anterolateral leads but also in the inferior distribution-concordant ST segment depression. Coronary angiography revealed prox- imal LAD occlusion with thrombus formation. This obstruc-

tion was successfully stented. The patient ultimately died of multiorgan failure in the intensive care unit 1 week later.

Fig. 12 is a prehospital ECG of a 56 year-old female patient with a history of myocardial infarction. The ECG demon- strated anterior STEMI, RBBB, and frequent premature ventricular contraction (PVC) with occasional R-on-T phe- nomenon. Before ED arrival, the patient developed pulseless ventricular tachycardia, which converted to sinus tachycardia with one defibrillation. The patient was transferred immedi- ately to the cardiac catheterization laboratory where a proximal LAD obstruction with thrombus was successfully opened.

Fig. 13 demonstrates an evolving anterolateral STEMI. The patient, a 61 year-old man, developed chest pain and new-onset RBBB. The first ECG demonstrated NSR with appropriate ST segment morphologies and RBBB pattern. Note the QR complex in lead V₁. Over the next 90 minutes, the patient continued to note chest pain with increasing dyspnea. Repeat ECGs revealed marked changes in the ST segment in leads I, aVL, V₁, V₂, and V₃. The ST-segment elevation in these leads is concordant and diagnostic of an anterolateral STEMI with RBBB. The patient was success- fully treated with tenecteplase (TNK) with complete resolution of chest pain, normalization of the ST-segment elevation, and disappearance of the RBBB pattern.

Most recently, there has been further clinical characteriza- tion of RBBB and AMI, differentiating STEMI from non-ST-

Fig. 11 A 72-year-old male patient presented to the ED with chest pain. The examination was significant for pulmonary edema and borderline systemic perfusion. A, The ECG demonstrates NSR with RBBB. Anterior wall STEMI is noted with concordant ST-segment elevation in leads V₁ and V₂. Excessive discordant ST-segment elevation is seen in lead V₃. Concordant ST-segment elevation is seen also in lead I and aVL, indicative of a lateral wall STEMI as well. B, Repeat ECG before emergent coronary angiography demonstrated progressive ST-segment changes not only in the anterolateral leads but also in the inferior distribution-concordant ST-segment depression. Coronary angiography revealed proximal LAD occlusion with thrombus formation. This obstruction was successfully stented. The patient ultimately died of multiorgan failure in the intensive care unit 1 week later.

elevation myocardial infarction (NSTEMI). Kleemann and colleagues [19] found that of the 11.5% of patients with AMI and RBBB, 4.4% had a STEMI, and 7.1% had a NSTEMI. The electrocardiographic features of NSTEMI-related RBBB were more varied and less easily diagnosed by standard electro- cardiography. As with the NSTEMI diagnosis in patients with normal conduction (ie, no RBBB pattern), the pivotal study is the serum marker that, of course, is elevated in the appropriate clinical setting-correct symptoms and ECG.

Implications of RBBB in ACS: treatment and prognosis

In the patient with ACS, the presence of RBBB is associated with more complex clinical presentations, with higher rates of high-risk coronary artery obstructive patterns, Cardiovascular complications, and death. For instance, in the anterior wall STEMI patient with RBBB, Kurisu and colleagues noted the presence of right bundle-branch block

Fig. 12 A prehospital ECG demonstrated anterior STEMI with RBBB and frequent PVC and occasional R-on-T phenomenon. A prehospital STEMI alert was activated. Before ED arrival, the patient developed pulseless ventricular tachycardia, which converted to sinus tachycardia with one defibrillation. The patient was transferred immediately to the cardiac catheterization laboratory where a proximal LAD obstruction with thrombus was successfully opened.

in 17% of this group. These patients were more often older and had higher rates of either left anterior descending artery or multivessel coronary disease. Thirty-day mortality was 14% compared to 2% in patients without the RBBB pattern; RBBB was a powerful independent predictor of 30-day mortality [1].

Patients with RBBB are more likely to experience Acute congestive heart failure, hypotension requiring treatment, cardiogenic shock, and cardiac arrest during their hospital stay [20]; these patients have also shown an increased requirement for transvenous pacemaker placement [6]. One study found that at the 1-year follow-up, patients with AMI and RBBB had a higher incidence of atrial fibrillation, ventricular tachycardia and fibrillation, left ventricular failure, and total mortality rates [6].

The ECG allows for risk stratification in patients with RBBB and AMI [21,22]. The characteristics of the RBBB and the AMI can carry important prognostic information. Of patients with AMI and RBBB, Moreno and colleagues [6] found that new-onset, permanent RBBB had the highest mortality rate at 1 year (73% vs 37%, P b.05) compared with the mortality rates of patients with a new, transient RBBB. Interestingly, Wong and colleagues [23] have also demon- strated that the increasing QRS complex width, in the setting of RBBB, is associated with progressively higher mortality rates in patients with anterior wall STEMI at 1 month postinfarction. There is a positive correlation between increasing QRS duration (by 20-millisecond increments) and increasing 30-day mortality in patients with both preexisting (P b .004) and new-onset (P b .003) RBBB. There is also a significant reduction in 30-day mortality (20.4% vs 35.3%) in patients whose ST-elevation resolved by >=50% compared with patients whose ST elevation did not resolve within 60 minutes of fibrinolysis (P = .006). Wong

and colleagues [23] call for an early and late risk stratification of AMI/RBBB patients using QRS duration in the acute setting and 50% resolution of the ST-elevation as a late marker of mortality.

In high-risk AMI groups, RBBB serves as a marker of even further cardiovascular risk and poor outcome. For instance, in a population of AMI patients with left main coronary artery obstruction and cardiogenic shock, predic- tors of in-hospital death included hypertension, increased heart rate, RBBB pattern, and low serum bicarbonate level. In fact, the RBBB pattern was noted to be the most powerful independent predictor of short-term mortality in patients presenting with left main-related AMI [24]. Investigators of the OPTIMAAL trial (a comparison of losartan and captopril in 5,477 patients with AMI-related left ventricular dysfunc- tion) addressed the presence of bundle branch block (both preexisting and newly developed) in AMI patients. In this study, they considered both short- and long-term outcomes relative to the presence of BBB. In this group, 8% of patients demonstrated BBB patterns at initial presentation with 54% RBBB and 46% LBBB. Both patterns were associated with an increased risk of poor outcome; sudden cardiac death was seen more frequently in the RBBB patients. During the follow-up period, an additional approximately 5% of patients developed BBB with 44% being RBBB; these patients, again, experienced higher rates of poor outcome, including increased mortality [25].

The treatment of patients with RBBB varies, but in general, patients are often undertreated. For instance, Go and colleagues report that compared with patients with normal conduction, fewer AMI/RBBB patients received aspirin, beta-adrenergic blocking agents, heparin, or Intravenous nitroglycerine within the first 24 hours of ED presentation. Of patients for whom fibrinolytic agents were clearly

Fig. 13 Twelve-lead NSR with RBBB is seen in this patient with evolving anterolateral STEMI. A, The patient, a 61 year-old man, developed chest pain and new-onset RBBB. The first ECG demonstrates NSR with appropriate ST-segment morphologies and RBBB pattern. Note the QR complex in lead V₁. B, Over the next 90 minutes, the patient continued to note chest pain with increasing dyspnea. Repeat ECGs revealed marked changes in the ST segment in leads I, aVL, V₁, V₂, and V₃. The ST-segment elevation in these leads is concordant, diagnostic of an anterolateral STEMI with RBBB. The patient was successfully treated with TNK with complete resolution of chest pain, normalization of the ST-segment elevation, and disappearance of the RBBB pattern.

indicated, those without BBB were more likely than those with RBBB or LBBB to receive emergent reperfusion treatment (P b .001). Those patients who are treated aggressively experience a delay to such therapy. For example, the median time to reperfusion treatment was longer for patients with both RBBB and LBBB than with no BBB [20].

Conclusion

The RBBB pattern in the patient with ACS is a particularly concerning finding; such patients are at increased risk of cardiovascular complications and death. Furthermore, the ECG itself can lead the unwary clinician down the wrong clinical pathway, thus missing the diagnosis and a reperfusion opportunity. In the patient

with RBBB and potential ACS, appropriate interpretation of the ECG and the recognition of associated cardiovas- cular risk are vital features in the early ED evaluation of such individuals.

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