Chest Pain in Woman With Recent Coronary Stent
A 66-year-old woman with a history of coronary artery disease, hypertension, diabetes mellitus, and end-stage renal disease presents to the emergency department 1 week after a coronary artery stent was placed to treat ischemic heart disease. She has had severe substernal chest pain with dyspnea and diaphoresis for roughly an hour, and she is in obvious distress.
Her vital signs are normal. No jugular venous distention is noted; lungs are clear; and heart rate is regular, without murmurs, gallops, or rubs. The initial ECG is shown here.
Which of the following best explains the ECG findings?
•Left bundle-branch block (BBB).
•Right ventricular hypertrophy.
•Right BBB.
•Wolff-Parkinson-White syndrome.
•Right BBB and acute anterolateral myocardial infarction (MI).
•Left BBB and acute anterolateral MI.
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Answer
WHAT THE ECG SHOWS
The ECG shows a regular, wide QRS–complex rhythm and a normal rate (Figure 1). The differential diagnosis for a widened QRS complex is listed in the Table. Some of the entities in the differential can be excluded clinically (eg, ventricular paced rhythm, sodium channel blocker toxicity, ventricular tachycardia, myocarditis). Others can be excluded by closer scrutiny of the morphologic characteristics of the QRS complex and T waves. For example, right ventricular hypertrophy can be excluded because the patient’s ECG does not meet voltage criteria for this condition (eg, Rwave amplitude greater than 7 mm in lead V1 and S-wave amplitude greater than 7 mm in lead V5 or V6); Wolff-Parkinson-White syndrome is excluded by the lack of delta waves and short PR intervals; and hyperkalemia is unlikely because the ECG shows no peaked T waves. Thus, some type of intraventricular conduction delay is the most likely explanation for her ECG findings.
ECG FEATURES OF BUNDLE-BRANCH BLOCKS
The QRS-complex width criterion is the same in both left BBB and right BBB: a duration of more than 0.12 s. To distinguish between left and right BBB, it is essential to focus on the morphologic characteristics of the precordial leads (V1 through V6). The presence of an rSR—or less commonly (as in this tracing), a qR complex—in the rightsided precordial leads (V1 and V2) together with a relatively shallow, wide S wave in the left-sided leads (V6, I, aVL) suggests right BBB (Figures 1 and 2). The rSR pattern results because a delay in conduction through the right bundle branch delays depolarization of the right ventricle. Normally, the weaker electrical forces of the right ventricle are obscured by the more powerful forces of the left ventricle, whose activity dominates on the ECG tracing. However, when right ventricular forces occur after those of the left, they become visible on the ECG. Thus, the “R” of the rSR represents depolarization spreading to the right side of the heart.
In left BBB, a QS or rS pattern in the right-sided precordial leads and a notched/slurred monophasic R wave (without a preceding septal Q wave) in the left-sided leads are typical (Figure 3). Nonspecific intraventricular conduction delays also show QRS complexes wider than 0.12 s, but do not meet the morphologic criteria of either right or left BBB.
In the presence of right (and also left) BBB, the ST-segment/ T-wave complex in the leads that define the BBB (in this case, V1 and V2 ) follows the “rule of appropriate discordance.” In right BBB, this means that the major vector of the QRS complex (positive) follows a direction that is discordant with, or opposite to, that of the ST-segment/T-wave vector (negative) in the right precordial leads.
Under normal circumstances, ventricular depolarization (reflected in the QRS complex) and repolarization (reflected in the ST-segment/T-wave complex) are often in the same direction. In persons with a BBB, altered ventricular activation begets altered ventricular repolarization. In the case of right BBB, repolarization, like depolarization, proceeds in a “left first, then right” manner; because the left ventricle was activated first, it recovers first. Thus, the ST and T vectors of repolarization are directed leftward (downward in leads V1 and V2 ) and are discordant with the QRS complex in the right precordial lead(s) and concordant with the QRS complex in the left precordial leads (V5 , V6 ). Although an upright T wave may occasionally be seen in lead V1 in persons with right BBB,1 following the rule of appropriate discordance, the ST segment is usually relatively isoelectric before it dives down toward the inverted T wave.
The ECG tracing in this case thus exhibits a number of features that are consistent with a right BBB: widened QRS complex (with the qR variant of right BBB); the expected prominent, wide S wave in lead V6 ; and ST-segment/T-wave changes discordant with (opposite to) the principal vector of the QRS complex, which is upward. However, the morphology of the ST segment needs closer scrutiny.
ECG FEATURES THAT SUGGEST MI
Once right BBB has been identified, the morphology of the complexes must be analyzed closely to determine whether it is fully consistent with that of right BBB or whether other elements—perhaps suggestive of another disease process—are also present. In fact, this is the key to deciphering this patient’s ECG.
The most important aspect of this tracing is revealed by close analysis of the subtleties of the ST-segment/T-wave complex. Note the hint of ST-segment elevation in lead V1 , which becomes more pronounced in leads V2 through V5 (see Figure 1). This is not characteristic of right BBB and is reflective of an acute anterolateral injury pattern (or MI). In addition, the T waves in leads V5 and, especially, V6 are hyperacute in appearance—another telltale marker of acute MI.
Finally, the QRS axis is leftward as a result of the QS complexes in leads II and aVF, which together with the commonly occurring, predominantly positive QRS complex in lead I, localize the axis deviation to somewhere between 30 and 90 degrees. This may constitute evidence of an age-indeterminate inferior MI; the Q waves are responsible for the left axis deviation.
Keep in mind, however, that the existence of an inferior wall MI can be incorrectly inferred from a tracing that shows right BBB.1 The qR pattern seen in the right precordial leads in a patient with right BBB may actually result from an isoelectric initial r wave that appears before the qR but is masked (an [r]sR that has become a qR pattern). Likewise, an apparent QS or Qr pattern, as seen in leads III and aVF in this tracing, may in reality be an (r)Sr in which the isoelectric initial r wave has been lost in the baseline. In these ways, right BBB can masquerade as an ageindeterminate inferior MI. Ultimately, cardiac catheterization will be required to determine the cause of this patient’s ECG findings.
The ECG of a different patient—one who was found to have sustained an acute MI in the presence of right BBB—is shown in Figure 4. The key to detecting acute MI in this tracing lies, as with the tracing in Figure 1, in careful scrutiny of the ST segments in the precordial leads. In the presence of right BBB, the ST segments should not be elevated across the precordium as they are in Figure 4. Moreover, because the T waves are upright, the appropriate discordance of the T waves is lost; this is another clue to the presence of acute coronary ischemia.
OUTCOME OF THIS CASE
The patient was taken promptly to the cardiac catheterization laboratory. A critical stenosis in the left anterior descending artery was opened and re-stented, and the patient recovered uneventfully. A neartotal occlusion of the right coronary artery was also noted, with bridging collaterals. Thus, the ST-segment/T-wave changes seen in the precordial leads on her initial ECG can be attributed to the left anterior descending artery stenosis. The findings in the inferior leads (II, III, and aVF) most likely represent Q waves from a previous inferior wall MI.
REFERENCES:
1. Surawicz B, Knilans TK. Chou’s Electrocardiography in Clinical Practice. 5th ed. Philadelphia: WB Saunders Co; 2001.
2. Raitt MH, Maynard C, Wagner GS, et al. Appearance of abnormal Q waves early in the course of acute myocardial infarction: implications for efficacy of thrombolytic therapy. J Am Coll Cardiol. 1995; 25:1084-1088.