ECG Review
Why So Much ST Depression?
By Ken Grauer, MD, Professor Emeritus in Family Medicine, College of Medicine, University of Florida. Dr. Grauer is the sole proprietor of KG-EKG Press, and publisher of an ECG pocket brain book.
Figure 12-lead ECG from a patient with chest pain and heart failure. Why so much ST depression?
Scenario: Interpret the ECG shown above, obtained from an older woman on multiple drugs who presented to the emergency department with chest pain and an exacerbation of her chronic heart failure. What is the rhythm? Why so much ST depression? Clinically, what would you do?
Interpretation: The rhythm is rapid and regular at a rate of ~180/minute. The QRS complex is narrow in all 12 leads. This defines the rhythm as a SupraVentricular Tachycardia (SVT). No definite P waves are seen. It is impossible to know if the small upright deflection midway between QRS complexes in lead II represents a P wave, T wave, or both. This leaves us with the differential diagnosis of a regular SVT without definite sign of atrial activity (See below).
Otherwise, the rate is too fast for assessment of the QT interval to be meaningful; voltage criteria for LVH are easily satisfied (very deep S in V1 plus tall R in V5 easily exceeding 35 mm); and there is diffuse ST depression that exceeds 2-3 mm in many leads.
By far, the three most common entities to consider in the differential diagnosis of a regular SVT when atrial activity is uncertain are: 1) sinus tachycardia; 2) atrial flutter; and 3) paroxysmal supraventricular tachycardia (PSVT). That said, the rate of this rhythm (about 180/minute) makes it highly likely that PSVT is the diagnosis.
Sinus tachycardia rarely exceeds 160-170/minute in a nonexercising adult.
Untreated atrial flutter almost always presents with a ventricular rate that is close to 150/minute (usual range = 140-160/minute). This reflects the fact that the atrial rate of flutter in adults not on antiarrhythmic medication is almost invariably close to 300/minute and the most common conduction ratio (atria-to-ventricles) is 2:1. A ventricular response of ~180/minute as seen here would imply a flutter rate of 180 × 2 = 360/minute, which is well above that expected for atrial flutter.
Next to the rapid rate, the most remarkable finding in this case is the deep and diffuse ST segment depression. Although there are many possible causes of ST depression, we find it helpful to routinely consider the following six entities: 1) ischemia; 2) "strain" from LVH (left ventricular hypertrophy); 3) digitalis effect; 4) hypokalemia/ hypomagnesemia; 5) rate-related changes (tachycardia); and 6) any combination of these 5 entities. Given that the patient in this case is an older woman on multiple medications with chest pain and a history of heart failure, it is likely that at least several of these 6 entities (if not all of them) are contributing to the deep and diffuse ST depression on her initial 12 lead ECG. Clinically, the first priority in management is to address the tachycardia. Sudden onset of PSVT at 180/minute in an older patient with heart failure may certainly exacerbate her underlying condition. Chest pain (and ST depression) may result from the associated reduced coronary perfusion or the tachycardia itself. Both may resolve with conversion to sinus rhythm. Follow-up ECGs and serum troponin values after conversion to sinus rhythm will probably elucidate whether the deep and diffuse ST depression seen here was the result of a transient phenomenon (associated with her PSVT) or a primary cardiac event.
Scenario: Interpret the ECG shown above, obtained from an older woman on multiple drugs who presented to the emergency department with chest pain and an exacerbation of her chronic heart failure. What is the rhythm? Why so much ST depression? Clinically, what would you do?You have reached your article limit for the month. Subscribe now to access this article plus other member-only content.
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