Context is Crucial

The patient is a 56 year old healthy woman who presented with a 30 minute history of palpitations, chest discomfort and dyspnoea. There is no past history of cardiac problems or arrhythmias.  She is not on any medications.  Her systolic BP on arrival was 95 mm Hg.



Figure_1 is the ECG taken at 2029. The main findings are:

  • A regular and narrow QRS complex tachycardia is present at a rate of about 188 per minute. Upright P waves are seen immediately after each QRS complex in many leads e.g. Lead 1. Lead II, Lead III and Lead aVR
  • There is horizontal depression of the ST segment in Leads I, aVF and V6.
  • There is an upward sloping depression of the ST segment in Lead II and Leads V2 to V6.
  • There is 2 mm ST elevation in Lead aVR and in Lead V1.
  • The QT interval is prolonged (the QT interval in the rhythm strip is longer than the R-R interval of consecutive QRS complexes)

The widespread ST changes suggest widespread subendocardial ischaemia, while the elevated ST segment in aVR raises the possibility of coronary artery disease involving the main stem of the left coronary artery. As the ST changes are associated with a very fast ventricular rate they are (more likely) to be caused by the tachycardia rather than acute coronary artery disease.

Supraventricular tachycardia (SVT) is an encompassing and acceptable diagnosis for this rhythm. Most episodes of SVT are due to a re-entry circuit that incorporates the AV node and adjacent "slow" and "fast" pathways. If the re-entry circuit takes a slow-fast route the atria are activated at the same time as the ventricles and P waves are obscured by the QRS complex. If the re-entry circuit takes a fast-slow route the atria are activated just after the ventricles, and P waves are seen immediately after the QRS complex (retrograde P waves).

Key findings in the initial ECG:

  • A narrow complex tachycardia with a ventricular rate of about 188 per minute. This is due to AVN re-entry with a "fast-slow" sequence of conduction producing retrograde P waves.
  • Widespread ST depression
  • ST elevation in Lead aVR

The immediate priority is to stop the SVT. The initial method is to interrupt the conduction of the re-entry circuit through the AV node by:

  • Increasing vagal discharge using the Valsalva manoeuvre or (less commonly these days) by carotid sinus massage.
  • Drug treatment with adenosine or verapamil

The following ECG (Figure_2) was taken at 2107 after treatment with intravenous adenosine. Her symptoms have revolved, and her systolic BP is now 120 mm Hg.



The most important findings in the ECG taken at 2107 are:

  • Sinus tachycardia is present with a ventricular rate of 100 per minute. The P waves and the PR interval are normal.
  • There is sagging ST depression in Leads I - III, Lead aVF and Leads V4 to V6. The ST depression in Leads V2 and V3 is upward sloping and horizontal respectively.
  • ST elevation persists in Lead aVR.
  • The QT interval is now at the upper limit of normal.

At this point there are two issues to consider:
Do we need to measure the serum troponin concentration ?
An increased troponin concentration is often found if the serum troponin is measured after an episode of SVT. This can occur after SVT in young persons with normal coronary arteries, meaning that the elevation is caused by ischaemia secondary to the tachycardia. An elevated troponin level in this middle age woman would not distinguish between myocyte ischaemia due to the SVT and infarction due to acute coronary artery disease. The serum troponin was not measured this patient.

What is the significance of the ST segment changes ?

The observed ST segment changes are a combination of:

  • Horizontal ST depression
  • Upward sloping ST depression
  • ST elevation in Leads aVR and V1

We can approach these finding in different ways:
1. Paroxysmal tachycardia may be associated with inversion of the T wave or the ST segment that can persist for hours or days after the tachycardia has resolved. This has been called the "post tachycardia syndrome". These changes are a poor predictor of underlying coronary artery disease; most patients with such changes have normal coronary arteries if they undergo coronary angiography.
2. Are these ECG changes simply those seen during exercise, or do they represent a positive exercise stress test ?

The normal electrocardiographic changes during exercise are:

  • P wave increases in height
  • R wave decreases in height
  • J point becomes depressed
  • ST segment becomes sharply up-sloping
  • Q-T interval shortens
  • T wave decreases in height

The standard criterion for an abnormal ST segment response in a exercise stress test are:

  • Horizontal (planar) or downsloping depression of 1 mm or more
  • ST elevation of more than 1 mm, particularly in the absence of Q waves.
  • A highly specific sign for ischaemia is inversion of the U wave.

T wave changes such as inversion and pseudo-normalisation (an inverted T wave that becomes upright) are non-specific changes. The presence of extrasystoles that have been induced by exercise is neither sensitive nor specific for coronary artery disease.

Some of the ECG changes during SVT in this case are the same as those seen in a positive exercise stress test.
The ST-segment depression in exercise stress testing reflects ischaemia, which may indicate the presence of obstructive coronary artery disease. However ST-segment depression in exercise stress testing is thought to be less accurate in identifying coronary artery disease in women than in men. In particular women are more likely to have a “false-positive” exercise ECG; a negative exercise stress test is useful in effectively ruling out a diagnosis of coronary artery disease.

3. Is the ST elevation in Lead aVR in this case part of the "post tachycardia syndrome" (where the ECG changes are 'benign'), or does it mean that the patient has (obstructive) coronary artery disease of the left main stem coronary artery? Published reports of the post tachycardia syndrome include examples of reversible elevation of the ST segment in Lead aVR, so in this case the changes are unlikely to bedue to coronary artery disease.

Suppose that this patient's palpitations had resolved before she reached hospital, so the first ECG you see is the one in Figure_2. TheseECG changes and the history of chest discomfort suggest left main stem coronary artery disease, so the patient would be admitted and have a coronary angiogram.

We return to the actual presentation, where we have access to both ECGs. The patient is keen to go home after resolution of her palpitations, but agrees to stay in the ED for a period of cardiac monitoring.




Figure 3 show that the ST-T changes have completely resolved during two and a half hours of cardiac monitoring and observation. The patient was discharged to have an outpatient stress thallium test and review by the Cardiology Unit.

Key Points

  • Narrow complex SVT due to AVN re-entry with a "fast-slow" sequence of conduction producing retrograde P waves.
  • Widespread ST depressionduring and immediately after the SVT, consistent with the post tachycardia syndrome
  • SVT can cause marked elevation of the ST segment in Lead aVR that is reversible and is not a sign of left main stem coronary artery disease


  1. Kernohan RJ. Post-paroxysmal tachycardia syndrome. Brit Heart J. 1969; 31:803-806
  2. Imrie JR, Yee R, Klein GJ, Sharma AD. Incidence and clinical significance of ST segment depression in supraventricular tachycardia. Can J Cardiol. 1990; 6:323-326.
  3. Hill J, Timmis A. ABC of clinical electrocardiography. Exercise tolerance testing. BMJ. 2002; 324: 1084-1087
  4. Miranda RC, Machado MN, Takakura IT et al. Elevated troponin levels after prolonged SVT in patients with normal coronary angiography. Cardiology 2006; 106: 10-13
  5. George M, Arumugham PS, Figueredo VM. aVr – the forgotten lead. Exp Clin Cardiol 2010; 15: 36-44.
  6. Kohli P, Gulati M. Exercise stress testing in women. Circulation. 2010; 122:2570-2580
  7. McLellan A, Prior D. Cardiac stress testing. Stress electrocardiography and stress echocardiography. Australian Family Physician. 2012; 41:119-122