Let’s talk about this heart rhythm a little bit, and when we do, let’s go back to the basics.
Is it regular or irregular?
Is it regularly irregular or irregularly irregular?
It’s irregularly irregular.
Does it have narrow QRS complexes or wide QRS complexes?
It has narrow QRS complexes.
Sight unseen, this heart rhythm has a high probability of being atrial fibrillation. However, wandering atrial pacemaker or multifocal atrial tachycardia is also part of the differential diagnosis.
Is the rate over 100?
So is this atrial fibrillation with rapid ventricular response or multifocal atrial tachycardia?
Let’s look at the isoelectric line. Does it appear fibrillatory?
We see atrial complexes before the QRS complexes. However, the P-wave morphology is not constant.
When you have 3 or more distinct P-wave morphologies, you are justified in calling a rhythm like this multifocal atrial tachycardia.
Now, I will tell you that on the cardiac unit a rhythm like this is often referred to as either atrial fibrillation or sinus tachycardia with frequent multi-focal PACs, but that is not correct.
Next, let’s look at the T-waves, because with a rhythm like this it can sometimes be difficult to differentiate P-waves and T-waves.
To find real T-waves, let’s only pay attention to cardiac cycles at the end of clusters of QRS complexes.
This should give you some idea as to the actual amplitude of the T-waves in lead II as well as the QT interval. Once you make a mental note of this, you can go back and decide if the other complexes are T-waves or P-waves superimposed on T-waves.
Now it should be obvious that the cardiac cycle circled in red is showing a P-wave masquerading (isn’t that a ridiculous word?) as a T-wave, whereas the cardiac cycle circled in blue shows an actual T-wave unspoiled by a mega P-wave.
Incidentally, these tall, pointy P-waves in lead II suggest significant right atrial enlargement. Remember, enlarged atria are not happy atria. They are predisposed to various arrhythmias like atrial fibrillation, atrial flutter, and multi-focal atrial tachycardia.
Granted, if you look at the 12-lead ECG, a right axis deviation is not present (right atrial enlargement and right ventricular hypertrophy go together) but the patient’s history includes “severe heart failure” which means that the patient’s entire heart is enlarged, not just the right side.
So what we see is “low voltage” in the limb leads (all QRS complexes < 10 mm), the result of electrical forces on the right and left side canceling each other out.
Especially with the history of COPD, I would call this a pulmonary disease pattern.
So how about the final rhythm strip showing a very fast narrow complex tachycardia?
This is where it’s nice to monitor a patient’s heart rhythm inside the hospital as opposed to inside the ambulance!
If you see a rapid heart rate inside the hospital you can “go back” in time and examine the onset of the arrhythmia to see whether or not it has a paroxysmal (sudden) onset. That would narrow it down to atrial flutter or some kind of reentrant tachycardia.
On the other hand, if the heart rate histogram shows a gradual increase in heart rate that maxed out at 216 you know it’s an automatic focus tachycardia for which adenosine would not be helpful (for example).
This particular arrhythmia turned out to be “self limiting” but even noting the termination of a tachycardia can be helpful in the diagnosis.
Did it stop abruptly (paroxysmal) or did it slow down gradually, revealing flutter waves (again, for example).
Since the patient’s chief complaint of dizziness seems to correlate with this rapid heart rate, definitive care for this condition will take place inside the hospital, and possibly the EP lab.
Sometimes the medications used to control rapid heart rates aren’t desirable for a patient with severe heart failure. Other times, they’re already taking these medications for the heart failure, but they’re experiencing rapid heart rates anyway!
I remember one patient with chronic AF who ultimately required RF ablation of the AV node and a pacemaker!
The atria continued to fibrillate but rapid ventricular response was no longer possible due to surgically induced third degree AV block. That was all the way back in 1997! Still pretty cool.
Thanks for the case, Mark!