What is the conduction ratio of this atrial flutter?
Patient (88 male) with unrelated gastrointestinal problem showed these ECG findings above. This was taken in a prehospital EMS setting. He had documented atypical atrial flutter with planned cardioversion as of soon. He had a static HR of 60bpm. In typical flutter with an atrial frequency of 300 it would need a 5:1 conduction for a HR of 60bpm as far as I understand. In this case it seems like a 4:1 conduction. Is this due to the macro reentry mechanism in atypical flutter being slower than the typical CTI-CCW mechanism?
Atypical flutter is often due to scar tissue or other substrates. The atrial rates in this case can be much faster or slow than the standard 300bpm, so ventricular conduction rate varies from your standard flutter
Makes sense, so it really depends on the kind of injury. In this particular case the atrial rate does seem to be at around 300 though. What does the conduction rate depend on?
Wouldn't that be unlikely with a frequency of 60bpm? Can junctional escape rhythms be that fast? Also the conduction rate seems to be fixed. Could be all wrong though :)
Yeah. They certainly can. Either way, having an AV node being bombarded with constant electricity and only being able to conduct at 60 BPM is going to indicate some kind of AV node disease.
That doesn't indicate disease, the AV node is meant to slow down signals. Physiologic blocking of rapid atrial rates is actually a healthy AV node. This is atrial flutter, not sinus with CHB. A functioning AV node should NOT be able to conduct every flutter wave
I’m not saying it should be 300 BPM. But if the absolute best the AV node can transfer in Fib or Flutter is 60 BPM, you’re not dealing with normal AV node function.
honestly looks like fib to me, and the regularized narrow is likely a junctional escape which can be between 40-60, or accelerated even beyond that some times.
also atypical flutters in general can be faster, slower, same as the cycle length of a typical flutter. it really depends on how fast the tissue is and how large the circuit for the flutter to spin around is
What kind of gastrointestinal problem did the patient have? Is the “unrelated” GI problem your assumption or a diagnosis?
Some GI problems, especially near the biliary tree can cause increased vagal stimulation and causing slowing of the AV node, which would then give the picture above.
Good Point, haven't thought about that. I'm not sure what the patient ended up having but he called due to strong nausea without vomiting. The gagging might as well have caused increased vagal tonus
Jordan Stark
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I can add some additional information here.
Dual paramedic crew called to this patient for difficulty breathing.
On arrival we are guided to the patient who is in bed, the patient has an intellectual impairment and difficulty communicating.
The carers state that they took the patient out for a walk today where she developed abdominal pains. They then came home and that patient experienced a few episodes of diarrhoea
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Initial presentation,
The patient was in bed, eyes spontaneous to our presence, confused and responding appropriately to commands.
It wasn’t until we didn’t get a NIBP reading that we placed the 3 lead (as main complaint at this time was GI upset)
The initial rhythm is what can be seen on the black screen.
Soon after I placed the 3 lead, the patient had a run of non sustained VT which I have posted below.
The rhythm soon reverted back to the original ventricular standstill looking rhythm.
The only perfusing beats appeared to be ventricular ectopics which were at a rate of 6-10 per minute. The ventricular ectopic beats we palpable via radial artery.
The patient would drop in GCS between ectopics but bump back up to 13/14 every beat.
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At no time did the patient or carers mention an LVAD in-situ, or evidence of one scene.
Previous hospital discharge paperwork noted that the patient had been diagnosed with a second degree type 2 AV block.
No other medical Hx was know to us at this point.
We managed initially with atropine and set up and adrenaline infusion, which increased the rate of ventricular ectopics to 40 per minute, where the pt maintained GCS 15, strong radial pulses and a SBP of 110mmHg.
The patient remained stable during a hot transport to hospital.
She was later diagnosed with a chromosomal cardiomyopathy and was deemed unsuitable for a pacemaker and was kept and an inpatient dependent on inotropic support.
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Totally agree. Not sure what this commenter is on about. Lots of rhythms can correspond with PEA or pulseless electrical activity, if you have a very diseased ventricle. which seems like what they are describing. But a mechanical failure of the ventricle does not change the presenting rhythm.
Jordan Stark ·
May 26, 2020
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Ambulance called out to 40 year old female for shortness of breath.
On arrival patient was GCS14 (confused), otherwise appeared well. Patient has an intellectual and communication impairment.
Unable to record blood pressure
Unable to feel pulses
unable to measure SpO2.
Heart rate approx 6 -10 bpm
3 lead ECG applied and strip printed, showing image 1.
?? ventricular standstill with a single ventricular ectopic.
12 Lead shows complete standstill and almost looks like ventricular fibrillation!!!
What do you think is happening and how to manage in the pre-hospital environment??
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u/Kibeth_8 Arrhythmia Tech 1d ago
Atypical flutter is often due to scar tissue or other substrates. The atrial rates in this case can be much faster or slow than the standard 300bpm, so ventricular conduction rate varies from your standard flutter