Special Feature
ECG Diagnosis of Acute Myocardial Infarction: Difficult Cases
By William J. Brady, MD
The ecg is a powerful clinical tool used in the evaluation of chest pain patients. Concomitant left bundle branch block (LBBB), ventricular paced rhythm (VPR), or left ventricular hypertrophy (LVH), however, may mask acute ischemic changes due to myocardial infarction, confounding this evaluation. Several strategies are available to assist in the correct interpretation of these electrocardiographic patterns, including a knowledge of the associated, or anticipated, ST segment-T-wave changes resulting from the abnormal ventricular conduction; the performance of serial ECGs that may demonstrate the dynamic changes encountered in acutely ischemic patients; and a comparison to previous ECGs.
In LBBB, the ventricular depolarization pattern is abnormal with activation of the ventricles occurring from the right to the left, a direction opposite from the norm. Since the left ventricle cannot be depolarized from the left bundle branch, the impulse must proceed down the right bundle and across the interventricular septum, eventually reaching the left ventricle. After leaving the right bundle branch, the impulse travels through the myocardium rather than the specialized conduction fibers, resulting in a prolonged duration of ventricular depolarization and the widened QRS complex. In the patient with LBBB, the 12-lead ECG records the abnormal ventricular activation producing a broad, mainly negative QS or rS complex in lead V1. In lead V6, a positive, monophasic R wave is seen; similar complexes are frequently found in leads 1 and aVL. Poor R-wave progression or QS complexes are noted in the right-to-mid precordial leads, rarely extending beyond leads V4 or V5. QS complexes may also be encountered in leads III and aVF. The T wave, especially in the right-to-mid precordial leads, has a convex upward shape or a tall, vaulting appearance, similar to the hyperacute T wave of early acute myocardial infarction (AMI). The T waves in leads with the monophasic R wave are frequently inverted. The anticipated or expected ST segment/T- wave configurations are discordant, directed opposite from the terminal portion of the QRS complex; this relationship is called QRS complex-T wave axes discordance-or the rule of appropriate discordance. As such, leads with either QS or rS complexes may have markedly elevated ST segments, mimicking AMI. Leads with a large monophasic R wave demonstrate ST segment depression (STD). An inspection of the ECG in patients with LBBB must be performed, looking for a loss of this "normal" discordant relationship.
Sgarbossa and associates developed a clinical prediction rule to assist in the ECG diagnosis of AMI in the setting of LBBB.1 They identified three criteria suggestive of AMI and assigned each a risk score, including: concordant ST segment elevation (STE) more than 1mm (score of 5); STD more than 1 mm in leads V1, V2, or V3 (score of 3); and discordant STE more than 5 mm (score of 2). A total score of 3 or more suggests that the patient may be experiencing an AMI based on the ECG; with a score less than 3, the electrocardiographic diagnosis is less certain, requiring additional evaluation. Such an understanding of ECG changes in AMI in patients with LBBB consequently allows the clinician to recognize unanticipated morphologies that may be suspicious for AMI.
In VPR, the ventricular depolarization pattern is abnormal with activation of the ventricles occurring from the right to the left, resembling the LBBB pattern in most cases. A pacer spike, a narrow negative or positive deflection, is seen in most leads immediately preceding the QRS complex. In the patient with VPR, the 12-lead ECG records the altered ventricular activation producing a broad, mainly negative QS or rS complex in leads V1 to V6 with either poor R-wave progression or QS complexes; QS complexes may also be encountered in leads II, III, and aVF. These leads may demonstrate significant STE. A large monophasic R wave is encountered in leads I and aVL and, on occasion, in leads V5 and V6. T waves in the right-to-mid precordial and inferior leads may have a "hyperacute" morphology, suggestive of AMI, while the T waves in leads with the monophasic R wave are frequently inverted. Loss of this normal QRS complex-T wave axes discordance in patients with VPR may imply an acute process, such as AMI. The anticipated ST segment/T-wave/QRS complex relationship is discordant-that is, these aspects of the complex are located on opposite sides of the isoelectric baseline with the terminal portion of the QRS complex directed opposite from the ST segment/T-wave. This relationship is described by the rule of appropriate discordance and is similar to the electrocardiographic principles applied in the setting of LBBB. As such, leads with QS complexes may have marked STE, mimicking AMI. Leads with a large, monophasic R wave demonstrate STD.
Sgarbossa et al published a report detailing the ECG changes encountered in patients with VPR.2 Three ECG criteria were found to be useful in the early diagnosis of AMI, including: discordant STE more than 5 mm; concordant STE more than 1 mm; and STD more than 1 mm in leads V1, V2, or V3. Interestingly, no criteria involving QRS complex or T-wave morphologies were found to be useful. This article, in contrast to much of the existing cardiology literature, distinguishes between past myocardial infarction and AMI and provides the physician with the electrocardiographic tools to make the early ECG diagnosis of AMI.
The ECG in the patient with LVH will demonstrate ST segment/T-wave changes in approximately 70% of cases; these changes result from altered repolorization of the ventricular myocardium due to hypertrophy. These ST segment/T-wave abnormalities are the new " in many patients with LVH and may mask and/or mimic the early findings consistent with AMI; this effect, however, occurs to a lesser extent than encountered in the LBBB and VPR situations. LVH is associated with poor R-wave progression and loss of the septal R-wave in the right-to-mid precordial leads, most commonly producing a QS pattern. In general, these QS complexes are located in leads V1 and V2, rarely extending beyond lead V3. As predicted by the rule of appropriate discordance, STE is encountered in this distribution along with prominent, "hyperacute" T waves. The STE seen in this distribution may be greater than 5 mm in height and is difficult to distinguish from that associated with AMI. The initial, up-sloping portion of the ST segment/T- wave complex is frequently concave in LVH compared to the either flattened or convex pattern observed in the AMI patient. This morphologic feature is imperfect, however; early AMI may reveal such a concave feature.
The ECG diagnosis of AMI in the setting of certain confounding electrocardiographic patterns including LBBB, VPR, and LVH is difficult but possible. The emergency physician must be an expert in ECG interpretation, possessing a working knowledge of the ST segment/T-wave changes seen with these confounding patterns-and also be able to recognize the pathologic changes. Additional tools for these situations include the performance of serial ECGs, ST segment trend monitoring, and a comparison to previous ECGs. Using a knowledge of the anticipated electrocardiographic changes of LBBB, VPR, and LVH supported by the criteria proposed by Sgarbossa et al, the physician's approach in the early phase of care can then move from a "non-diagnostic" ECG with a "rule-out" myocardial infarction admission diagnosis to a "rule-in" approach, thereby offering more appropriate, and potentially more aggressive, treatment in timely fashion-including early cardiology consultation with urgent cardiac catheterization and/or thrombolysis.1,2 The physician must realize, however, that these ST segment changes are only suggestive of AMI in patients with complicated ECGs; morphologic changes alone are not diagnostic of AMI. Therapeutic decisions must be made keeping this caveat in mind.
References
1. Sgarbossa EB, et al. Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle branch block. N Engl J Med 1996; 334:481-487.
2. Sgarbossa EB, et al. Early electrocardiographic diagnosis of acute myocardial infarction in the presence of ventricular paced rhythm. Am J Cardiol 1996;77: 423-424.
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