Special Feature

Electrocardiographic ST Segment Depression

By William J. Brady, MD, FACEP, FAAEM

Introduction

ST segment depression (STD) is an important finding on the electrocardiogram (ECG) of the chest pain patient; in fact, this electrocardiographic finding is seen in approximately 30% of ED chest pain patients.1 While ST segment changes (both elevation and depression) are associated with an acute coronary syndrome (ACS), numerous other clinical entities manifest ST segment depression. For example, in an ED population, the following electrocardiographic diagnoses were associated with STD: ACS, 26%; left ventricular hypertrophy (LVH), 43%; bundle branch block (BBB), 21%; ventricular paced rhythm (VPR), 5%; and other patterns, 5%.1 Appropriate management partially is dependent upon differentiating these various causes of STD on the ECG.

Acute Coronary Syndrome

In the ACS patient, STD may be a presenting abnormality on the ECG resulting from one of several ischemic syndromes, including myocardial ischemia (without infarction), posterior wall AMI, non-ST segment elevation AMI, or reciprocal ST segment change in the setting of AMI. (See Figure 1.) Considering non-AMI ACS-related STD (i.e., myocardial ischemia), a combination of two electrocardiographic diagnostic criteria traditionally has been required to diagnose myocardial ischemia—at least 1 mm depression at the J point, with horizontal or down-sloping ST segment morphology.2 Such STD frequently is widespread, located simultaneously in both an inferior and anterior distribution; it does not necessarily localize to a particular anatomic segment. The morphology of the depressed ST segment may be of value in assessing the probability of a non-AMI ACS event. Extensive experience from cardiac stress testing shows that the actual configuration of the STD influences the specificity of this finding, with a down-sloping segment more specific for the diagnosis of ischemia than horizontal depression.3 In a review of ED chest pain patients, the presence of STD of any morphology was not predictive of ACS. If the clinician applies several simple rules to this electrocardiographic analysis, STD morphology is much more helpful. Certain electrocardiographic patterns with abnormal intraventricular conduction have STD as a "normal" finding, including LVH, BBB, and VPR; if these patterns are removed from this analysis, then the presence of STD is highly associated with ACS. Furthermore, the morphology of the depression is also helpful with horizontal morphology highly suggestive of ACS.1

Posterior wall AMI, from the perspective of the standard 12-lead ECG, will manifest STD in the right to mid-precordial leads. The majority of such acute infarcts will present with co-existing acute inferior wall infarction; isolated posterior wall AMIs, however, do occur.4 Electrocardiographic abnormalities suggestive of a posterior wall AMI include the following (in leads V1, V2, or V3): horizontal STD with tall, upright T waves; a tall, wide R wave; and an R/S wave ratio greater than 1.0 in lead V2.5,6 As such, STD in this distribution can represent either non-AMI ischemic change or posterior AMI. Boden et al noted that in patients presenting with STD in leads V1-V3, approximately half were found to have had a posterior wall infarction.7 The use of posterior leads will help distinguish between these two clinical presentations—the presence of ST segment elevation greater than 1 mm in the posterior leads V8 and V9 confirms the presence of posterior wall AMI.

Patients with non-ST segment elevation infarction may have transient and nonspecific findings, such as STD or T wave abnormalities in any of the leads of the 12-lead ECG. STD and inverted or biphasic T waves characteristically are seen. Differentiating non-ST segment elevation myocardial infarction from non-AMI ACS using only the ECG is difficult, if not impossible; serum marker analysis is required to rule in myocardial infarction in this particular presentation. (See Figure 2.)

Reciprocal ST segment depression, also referred to as reciprocal change, is defined as STD in leads that are separate from leads demonstrating ST segment elevation. It must be stressed that reciprocal STD can only exist when co-existing ST segment elevation is noted. Further, STD seen in patients with abnormal intraventricular conduction is not included in the definition of reciprocal change. Reciprocal change can be identified in approximately one-third of patients with anterior wall AMI and three-fourths of individuals with inferior AMI. The presence of reciprocal change increases the positive predictive value for a diagnosis of AMI to greater than 90%.8,9 In the setting of an inferior AMI with early, less pronounced ST segment elevation, the presence of STD in lead aVL alone may suggest early ACS.10

Left Bundle-Branch Block

Intraventricular conduction delays, such as with left BBB, will manifest significant ST segment/T wave abnormalities as a "normal" electrocardiographic finding; these changes mimic both acute and chronic ischemic changes. The left BBB pattern is the second most frequently encountered electrocardiographic pattern responsible for non-ischemic ST segment changes in the ED population, accounting for 15% of cases.11,12

Left BBB may present with significant STD. The rule of "appropriate discordance" states that in left BBB, ST segment/T wave configurations are directed opposite from the major, terminal portion of the QRS complex. As such, leads with predominantly positive QRS complexes (the monophasic R wave) will demonstrate ST segment depression with T wave inversion. In this electrocardiographic presentation, the ST segment usually is down-sloping in form. In fact, Sgarbossa and colleagues reported that in the setting of left BBB, STD—limited to leads V1, V2, and/or V3—is associated with AMI in the appropriate clinical presentation.13

Similar electrocardiographic issues are encountered in patients with right BBB and ventricular paced rhythms.

Left Ventricular Hypertrophy

Pressure and volume overload on the left ventricle leads to a sustained repolarization, which produces alterations in the morphology of the ST segment and T wave. In leads with either a leftward or posterior orientation, the sustained repolarization phase results in negativity of both the ST segment and the T wave (seen as STD with T wave inversion).2 These LVH-related repolarization abnormalities are referred to as a "strain pattern," encountered in approximately 70% of LVH cases, and are characterized by down-sloping STD with inverted T waves in leads with prominent R waves (leads I, aVL, V5 and V6).14 This T wave inversion is asymmetrical, with gradual down-sloping and a rapid return to baseline, often with the terminal portion of the T wave becoming positive (so-called "overshoot").

Digitalis Effect

At therapeutic levels, digitalis produces characteristic electrocardiographic changes, including STD. These changes are referred to as the digitalis effect, which must be distinguished from digitalis toxicity (which manifests primarily as cardiac dysrhythmia). The electrocardiographic manifestations of digoxin effect are as follows: "Scooped" ST segment depression, most prominent in the inferior and lateral precordial leads. Often, it may be impossible to differentiate the STD created by digitalis from ACS. In general, however, digitalis will create a "sagging" ST segment, while ischemia creates the typical horizontal or down-sloping depression. 

Dr. Brady, Associate Professor of Emergency Medicine and Internal Medicine, Vice Chair, Emergency Medicine University of Virginia, Charlottesville, is on the Editorial Board of Emergency Medicine Alert.

References

1. Brady WJ. Personal communication. January, 2004.

2. Wagner GS. Marriott’s Practical Electrocardiography 9th Ed. Baltimore: Williams & Wilkens;1994:1.

3. Goldschlager N, et al. Treadmill stress tests as indicators of the presence and severity of coronary artery disease. Ann Intern Med 1976;85:277.

4. Goldberger A. Electrocardiographic Differential Diagnosis 4th Ed. St. Louis: Mosby; 1991:1.

5. Aufderheide TD, et al. Electrocardiography in the patient with myocardial ischemia or infarction. In: Gibler WB, Aufderheide TP, eds. Emergency Cardiac Care 1st Ed. St. Louis: Mosby; 1994:169-216.

6. Brady WJ. Acute posterior wall myocardial infarction: Electrocardiographic manifestations. Am J Emerg Med 1998;16:409-413.

7. Boden WE, et al. Electrocardiographic evolution of posterior acute myocardial infarction: Importance of early precordial ST-segment depression. Am J Cardiol 1987; 59:782.

8. Otto LA, et al. Evaluation of ST segment elevation criteria for the prehospital electrocardiographic diagnosis of acute myocardial infarction. Ann Emerg Med 1994; 23:17-24.

9. Brady WJ, et al. Reciprocal ST segment depression: Impact on the electrocardiographic diagnosis of ST segment elevation acute myocardial infarction. Am J Emerg Med 2002;20:35-38.

10. Marriott HJL. Emergency Electrocardiography. Naples, FL: Trinity Press; 1997:28-40.

11. Brady WJ, et al. Electrocardiographic ST segment elevation: The diagnosis of AMI by morphologic analysis of the ST segment. Acad Emerg Med 2001;8:961-967.

12. Brady WJ, et al. Electrocardiographic ST segment elevation in emergency department chest pain center patients: Etiology responsible for the ST segment abnormality. Am J Emerg Med 2001;19:25-28.

13. 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.

14. Brady WJ, et al. Electrocardiographic manifestations: Patterns that confound the EKG diagnosis of acute myocardial infarction—left bundle branch block, ventricular paced rhythm, and left ventricular hypertrophy. J Emerg Med 2000;18:71-78.