The next post is written by one of my great assistants, who is really an EKG-nerd! I hope you like it! Please respond if you have any comments and myself (Egon) and Iwan will take a look at it!
Have a look at this EKG. Go on, you know you want to!
What is the rhythm and what would be your treatment ?
At first glance it looked like an AVNRT (atrioventricular nodal reentrant tachycardia) to me and I had adenosine drawn up. But let’s be a good boy and follow the diagnostic tree from the ESC guidelines:
– Narrow ? Check.
– Tachycardia ? Yup.
– Visible P waves ? Hum, that’s a little tricky… Have a closer look:
Hey, what would you know, there do appear to be some funny looking p waves!
Atrial rate greater than ventricular rate ? It would seem so
Guess that makes it atrial flutter or atrial tachycardia.
Before we could do anything the rhythm spontaneously changed:
So what is the rhythm now? The computer seems to think it’s atrial flutter with a 2:1 atrioventricular block. (And we all know artificial intelligence beats natural stupidity.)
P waves are best seen in V2. Check it out:
2:1 block indeed but the PP segment is fairly straight, so no flutter.
And so my dear Watson, when all else is excluded the rhythm that remains must be the truth:
Paroxysmal atrial tachycardia (PAT) with block!!!
Although non sustained atrial tachycardia (AT) is frequently seen on Holter, sustained focal AT is actually relative rare.
In 1960 Lown. et al established following diagnostic criteria for PAT:
– abnormal P waves with a different morphology from the sinus P waves
– atrial rate between 150 and 250 bpm
– isoelectric intervals between P waves in all leads
The location of the ectopic atrial focus can be surmised from the P wave morphology:
a positive or biphasic P wave in aVL usually indicates a right atrial focus
a positive P wave in V1 usually indicates a left atrial focus
increased automaticity of an ectopic atrial focus (gradual onset and termination)
triggered by ‘delayed afterdepolarization’ (especially seen digitalis intoxication)
digitalis intoxication (especially AT with AV block)
Our patient received iv metoprolol which reduced the rate only marginally and because of persistent symptoms we ended up electrically cardioverting the patient back to sinus rhythm.
I wonder what would have happened if we had given the adenosine I had drawn up initially ? At the very least it would have slowed AV conduction and thereby revealing the atrial tachycardia, but apparently it could also have converted the patient. In fact, it is a IIa recommended treatment for AT according to the ESC as can be seen in the table below:
But hold on there for one freaking minute, young Padawan! I thought adenosine only caused a short AV block and surely the AV node is not part of an atrial tachycardia! How could it possibly convert AT ?
Adenosine has 2 mechanisms of action:
– it interacts with A1 receptors which increases potassium conductance, shortens the action potential and hyperpolarizes the membrane. This effect happens in both atrial and AV node tissue, but is absent in ventricular tissue.
– an indirect anti-adrenergic effect which decreases intracellular cAMP and inhibits calcium influx.
Triggered arrhythmias are thought to arise because of intracellular calcium overload and cAMP dependent. This is why adenosine can terminate triggered AT (and some forms of VT, since the anti-adrenergic effect is not tissue specific!). AT due to enhanced automaticity usually will only be transiently suppressed in response to adenosine.
Prognosis of AT is usually excellent but persistent forms may lead to tachycardia induced cardiomyopathy.
Hope you enjoyed this EKG case and remember: life will not break your heart, it will crush it!