I am frequently asked exactly how I approach 12-lead ECG interpretation. I use what I call the Six-Step Method.
It goes like this:
1.) Rate and rhythm
2.) Axis determination
3.) QRS duration (Intervals)
5.) STEMI mimics
6.) STEMI (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.
Let’s break them down one at a time.
1.) Rate and Rhythm
What is the rate? Are you dealing with a bradycardia or a tachycardia?
Is the rhythm regular or irregular?
Are P-waves present? Are they in a 1:1 relationship with the QRS complex? Look at P-wave morphology. Are they identical? Is the PR-interval within normal parameters and constant?
If we can’t establish that we’re dealing with sinus rhythm can we at least establish that we’re dealing with a supraventricular rhythm? Remember, wide QRS rhythms are ventricular until proven otherwise!
We shouldn’t look for a bundle branch block until we know we’re dealing with a supraventricular rhythm. This simple rule will keep you out of a lot of trouble.
2.) Axis Determination
See also: Cardiac Axis Determination
Is the front plane axis in the normal range (left inferior axis)?
Is the a left axis deviation which might suggest left anterior fascicular block, inferior MI, or paced rhythm?
Is it a right axis deviation 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 heart’s 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 don’t try to pinpoint the heart’s Z-axis (in 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 (Intervals)
If you’ve followed the first two steps there’s a good chance you’ve already picked up on a prolonged PR-interval or wide QRS complex, but “Step 3” is the designated time to check these intervals.
Does anything look bizarre? This is your chance to examine the P/QRS/ST/T to see if anything stands out.
We should also check the QT-interval, which starts at the beginning of the QRS complex and terminates at the end of the T-wave. In regular rhythms this interval should be less than 1/2 the R-R interval.
A. QT-interval is less than 1/2 the R-R interval. B. QT-interval is > 1/2 the R-R interval.
You’ll notice in computerized measurement two different measurements for the QT-interval. The “QT” and “QTc”. The QT is the raw measurement and the QTc is the “corrected” QT-interval which has been normalized for heart rate (using Bazett’s formula or something similar).
In men the QTc should be less than 450 ms and in women the QTc should be less than 460 ms. When the QTc is 500 ms or greater it should be considered clinically significant, particularly in a patient who has suffered syncope (increased risk of torsades de pointes).
If the QRS complex is “wide” (the QRS duration is = or > 120 ms), what is the QRS morphology in lead V1?
Is it right bundle branch block (RBBB) morphology or left bundle branch block (LBBB) morphology?
Typical or atypical? (Most clinicians do not understand this point which becomes important for differential diagnosis of wide complex tachycardias. It is beyond the scope of this blog post.)
Now check lead I to confirm! This an important step, because if lead V1 shows LBBB morphology and lead I shows RBBB morphology (or vice-versa) then it’s a nonspecific intraventricular conduction block which may suggest an electrolyte derangement or drug overdose.
If it’s RBBB morphology in lead V1, combine with axis determination to determine whether or not bifascicular block is present (or at least bifascicular morphology if we’re not confident we’re dealing with a supraventricular rhythm).
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 this is too important to be careless with terminology!
It can only be one or the other — a ventricular rhythm or a bundle branch block.
5.) STEMI Mimics
These are sometimes called “QRS confounders” or “STEMI imposters”.
Hyperkalemia – “the great imitator”
It’s important to realize that there are many conditions that cause ST-segment elevation on the 12-lead ECG.
- Acute myocardial infarction
- Left ventricular hypertrophy
- Left bundle branch block
- Ventricular paced rhythm
- Early repolarization
- Left ventricular aneurysm
- Brugada syndrome
- Wolff-Parkinson-White syndrome
- Osborn waves (hypothermia)
- Stress cardiomyopathy (Takotsubo)
- Aortic dissection
It’s good to remember that when you have an abnormal depolarization (as you do with bundle branch blocks, paced rhythms, ventricular rhythms, left ventricular hypertrophy, and Wolff-Parkinson-White syndrome) you will also have an abnormal repolarization (that’s what we mean by “secondary ST/T-wave abnormality”) which can cause ST-segment elevation on the 12-lead ECG.
6.) STEMI (Ischemia, Injury, Infarct)
Finally, I look for the obvious signs of acute ST-Elevation Myocardial Infarction (STEMI) or STEMI equivalents.
See also: Contiguous and Reciprocal Lead Charts
Acute inferior-posterior-lateral STEMI
I also look for signs of “old” acute myocardial infarction in the form of Q-waves, or ischemia in the form of ST-segment depression.
However, ischemia does not localize! So when you see ST-segment depression, especially when localized to a particular constellation of leads, think reciprocal changes first and ischemia second!
To be honest, it’s not this linear in my mind because I’ve been doing this for a long time and my eyes often shoot straight to the most obvious abnormality on a 12-lead ECG. As you get more experienced with ECG interpretation you require fewer decision rules. However, I do not violate any of these principles!
7.) Interpret the 12-lead ECG in light of the history and clinical presentation!
When pre-test probability is high we take even subtle ECG signs more seriously. Conversely, when the pre-test probability is low, the ECG evidence must be compelling to justify prehospital activation of the cardiac cath lab!
Do you need comprehensive training in 12-lead ECG interpretation?
Check out our video-based 12-lead ECG course at ECG Medical Training!