The Six-Step Method for 12-Lead ECG

Interpretation
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Im sometimes asked how I approach 12-lead ECG interpretation. I use what I call the Six-
Step Method (which actually has seven steps).
It goes like this:
1.) Rate and rhythm
2.) Axis determination
3.) QRS duration (Intervals)
4.) Morphology
5.) STE-mimics
6.) Ischemia, Injury, Infarct
Step 7 is a rule I started throwing in to remind students that one should always interpret an
ECG (or any other diagnostic test) in light of the history and clinical presentation.
Lets break them down one at a time.
1.) Rate and rhythm
Are you dealing with a bradycardia or a tachycardia? If the exact rhythm is unknown, are we
certain were dealing with a supraventricular rhythm?
This is critical because if the rhythm has wide QRS complexes (fast or slow) its ventricular
until proven otherwise!
Failure to observe this simple rule can cause a lot of problems.
2.) Axis determination
Is the axis in the normal range?
Is it a left axis deviation (left superior axis), which might suggest left anterior fascicular
block, inferior MI, or paced rhythm?
Is it a right axis deviation (right inferior axis), which might suggest left posterior fascicular
block, lateral MI, right ventricular hypertrophy or acute right-sided strain?
Is it an extreme axis deviation (right superior axis), which might suggest VT, electrolyte
derangement, or misplaced limb lead electrodes?
Examining the hearts electrical axis in the frontal plane is one of the techniques I use to get a
feel for a 12-lead ECG.
Similarly, while I dont try to pinpoint the hearts Z-axis (the horizontal plane), I do notice R-
wave progression, the transition, and whether or not there is positive or negative concordance
of QRS complexes in the precordial leads.
3.) QRS duration (and other intervals like the PR interval and QT interval)
If youve followed the first two steps theres a good chance youve already picked up on a
prolonged PR interval or wide QRS complex, but Step 3 is the designated time to make
sure youre dealing with a narrow QRS rhythm (or a supraventricular rhythm with wide QRS
complexes).
Time and time again I see paramedics who are new to 12-lead ECG interpretation saying
things like paced rhythm with left bundle branch block or VT with right bundle branch
block.
Maybe they mean paced rhythm with left bundle branch block morphology or VT with
right bundle branch morphology but something like this is too important to be lazy with
terminology!
This is also the designated time that you look at the QT/QTc and verify that the QTc is < 500
ms (and hopefully < 460 ms).
4.) Morphology
If the QRS complex is wide (the QRS duration is = or > 120 ms), what is the QRS
morphology in lead V1?
Is it RBBB morphology or LBBB morphology? Typical or atypical? Now check lead I to
confirm! Thats an important step, because if lead V1 shows LBBB morphology and lead I
shows RBBB morphology (or vice-versa) then its a nonspecific intraventricular conduction
block which may suggest an electrolyte derangement or drug overdose.
If its RBBB morphology in lead V1, combine with axis determination to determine whether
or not bifascicular block is present (or at least bifascicular morphology).
Does anything look bizarre? This is your chance to examine the P/QRS/ST/T to see if
anything stands out. This is where you might pick up on things like Brugadas syndrome.
5.) STE-mimics (QRS confounders, Imposters of AMI)
By now weve already determined whether or not a bundle branch block or paced rhythm is
present, and theres an excellent chance youve already picked up on several other
abnormalities that could mimic or mask acute myocardial infarction.
However, this is where I explicitly rule out the STE-mimics (paced rhythm, left bundle
branch block, left ventricular hypertrophy, benign early repolarization, pericarditis, Wolff-
Parkinson-White pattern, ventricular aneurysm, hyperkalemia).
6.) Ischemia, Injury, Infarct.
Finally, I look for the obvious signs of acute STEMI (ST-elevation or hyperacute T-waves). I
also look for ST-depression, T-wave inversion, abnormal Q-waves, and so on.
If an STE-mimic is present, I look for acute STEMI in the presence of an STE-mimic using
things like Sgarbossas criteria, the rule of appropriate T-wave discordance, and reciprocal
changes.
To be honest, its not this linear in my mind because Ive been doing this for a long time and
my eyes often shoot straight to the most obvious abnormality on a 12-lead ECG.
However, I do not violate any of these principles!