You can get fooled if you don't read the ECG systematically

A middle-aged woman presented with chest pain continuous since the previous day.  Here was the inital ECG:

What is it?
The treating physicians interpreted ST and T-wave abnormalities worrisome for ischemia

The patient was treated for ACS medically.  Cardiology was consulted for persistent pain in a patient with presumed ACS.

What is really going on?  See below.





















Remember to read the ECG systematically.  Don't look at the ST segments and T-waves first! Your eye is drawn to them, but resist!

Instead, read:

1. Rate
2. Rhythm
3. Intervals
4. QRS voltage, axis, duration, conduction delays and bundle branch blocks.
5. Repolarization (ST, T, U)


Here is an annotated version:

Notice there a no P-waves in front of the QRS complexes!
The black arrow points to a retrograde P-wave (atrial activity would be more accurate)
The red arrow also points to retrograde atrial activity in V3.
The blue lines point out the retrograde atrial activity in every lead.

Possible rhythms:
1.  A slow re-entrant rhythm with retrograde atrial activity
            a. AVNRT
            b. AVRT (accessory pathway)
2. Junctional tachycardia with retrograde P-waves

Why do we think it is not simply atrial tachycardia?

Because the atrial activity comes after the QRS and is inverted.

If it is atrial tachycardia, then:
1.  There would have to be a VERY long PR interval (400 ms) and
2.  The atrial activity would have to be low in the atrium for the P-wave to be inverted.

This is all possible, but much less likely than a re-entrant rhythm.

Why do the ST segments and T-waves look so abnormal?

This is just a result of a large and inverted, superimposed P-wave.  The atrial activity is simultaneous with the ST segment and T-wave.


The patient was given adenosine and converted:

There is now sinus rhythm and normal ST segments and T-waves.

This proves that it is an adenosine sensitive (re-entrant) paroxysmal supraventricular tachycardia.

In this case, failure to read rhythm first led to error.  

While there may be some underlying ST-T abnormalities, any ischemia must first be managed by managing the dysrhythmia and re-assessing with a repeat ECG.  When this was done, there was no residual ischemia.

Some points:
1.  This conversion by adenosine would work in both AVNRT and AVRT.
2.  It was a very slow rhythm for both AVNRT and AVRT, but especially for AVNRT.  A slow accessory pathway is likely.
3.  If it is an accessory pathway, should there not be delta waves?  No!  See explanation below.
4.  Does conversion with adenosine help in diagnosis of atrial tachycardia?  No!  Some atrial tachycardia is automatic and does not respond to adenosine.  Some is re-entrant and does not responds.  But some is re-entrant and does respond to adenosine.

There was a slight rise in troponins which is consistent with type II MI.  However, the rate was not so fast, and some significant coronary disease may be involved.  She will therefore get a stress test.


I received this question:

How do you tell that the retrograde P is not a T wave, and the T wave is not a P wave with a 1st degree heart block? Is it just their relative shapes?

And answered it thus:

Not at all a dumb question.  With experience, you can tell that the T-wave is deformed by another wave.  You can suspect this, and then test your hypothesis by looking in other leads to see if the T-wave is deformed at the same time in those other leads.   

One cannot say for certain that it is not an inverted P-wave with a long PR interval, but: 1) a PR interval of 400 ms is very uncommon and 2) if not retrograde, then an inverted P-wave must come from low in the atrium.  

Therefore, you have to hypothesize two unusual occurrences: 1) very long PR interval and 2) low atrial pacemaker.  And you also have to explain a fast rhythm.

All this can be explained by a low atrial tachycardia with a prolonged PR interval.  But it also has to be an atrial tach that is adenosine sensitive, and not all of them are.

Steve Smith





Absence of delta wave in WPW:

The below refers to this case: http://hqmeded-ecg.blogspot.com/2015/09/a-large-r-wave-in-lead-v1.html

Preexcitation and delta waves may not be apparent in sinus rhythm in patients with WPW who have a left-lateral bypass tract.   In this setting, the time for the atrial impulse to reach the atrial insertion of the accessory pathway is longer than the time to reach, and transmit through, the AV node.  This patient does in fact have a left lateral bypass tract and that is why it has right axis deviation and some of the characteristics of RBBB, with the majority of forces going from left to right, causing large R-wave in V1.

If there were a normal conduction through the AV node (here it is slowed - 1st degree AV block), then the impulse would have gotten through the AV node before pre-excitation and there would be no delta wave.   Some call this "concealed conduction," because on the baseline ECG you cannot see a delta wave, yet the patient can have WPW related tachycardias.

You can read more about concealed conduction here.

See this fascinating case of WPW with a normal PR interval.