I think this ECG is a good example for a multilevel learning environment. Something immediately apparent and something more subtle for the more advanced learner.
Follow-up for day 2 ECG.
This patient had been brought to hospital after having witnessed seizure in a McDonalds. Initially these were attributed to alcohol withdrawal (known use disorder). In ER was noted to have profound hypoK, hypoMg and hypoCa. Then this ECG was captured...
...showing PMVT initiated by a PVC couplet. The first at a longer coupling than the second.
But, prior to PMVT there is T wave alternans. These are sudden changes in temporal heterogeneity in ventricular repolarization and are associated with impending ventricular arrhythmias.
This is one of my favourite ECGs because it speaks so much to physiology.
This ECG is a good example of a rate dependent LBBB.
If you look carefully the sinus rate is unchanged. There is a rate dependent LBBB when sinus conducts one to one (latter part of the ECG) but after the PVC there is a compensatory pause and the bundle recovers....
...the RBBB beat is a PVC with slightly variable coupling intervals. In RBBB beats 3 and 4 the coupling is shorter and you can see the latter half of the upright P wave late in the QRS, but in beat 5 the coupling is longer and the P wave is seen early in the QRS.
This ECG was recorded in a patient with a potassium of 8.9.
Mild ⬆️K – extracellular K results in increased conductance via Ikr ➡️ ST depression, peak T & QT shortening
Moderate ⬆️K – persistently depolarises cell membrane inactivating Na channel ➡️ wide QRS and prolonged PR..
Severe K – sinoventricular conduction progresses to accelerated junctional with progressive QRST widening and ST-segment obliteration ➡️ smooth diphasic, sine wave.
Note – pseudo-ST segment elevation can be observed due to derangement in myocyte repolarization (same pt - K 8.1)
Of note - some have asked for context.
Most of these ECGs are from reading outpatient tests (ie they just show up in an inbox without context - no indication, no history, no medications, etc...).
So in a lot of circumstances we are reading blind.
This ECG demonstrates sinus rhythm with LBBB and PVC couplets. The PVCs are likely posterior fascicle in origin.
The point that catches some learners is the observation that the PVCs look narrower in V1 leading them to think this is PVC trigeminy.
This ECG shows SVT degenerating into self limited polymorphic VT following adenosine.
One proposed interpretation was SVT degenerating into AF with preexcitation but the SVT is likely AVNRT given the short VA interval (pseudo-S in inferior leads and pseudo-r’ in V1).
This ECG demonstrates complete heart block with a very slow escape rhythm. There is a clear escape in the middle of the twcibg, but right at the beginning of the ECG you see the T wave of the previous escape beat.
This ecg shows sinus rhythm with LBBB. There is a competing AIVR that is originating from the LV. This results in the 3rd and 4th beats having fusion, which narrows the QRS due to intrinsic resynchronisation (akin to what we do when we implant a CRT).
And why does this electrophysiologist find it interesting?
This ECG shows junctional rhythm with retrograde conduction alternating between a shirt and long VA time suggesting it’s alternating between the retrograde slow and fast pathways.
To be honest I’m not certain I can completely explain this ECG.
This is the initial post implant ECG for a @MicroPortCRMUSA Reply DR pacemaker implanted for AV block.
Breaking it down by its components. 1/n
The base rate is about 65-70 bpm (the rate between two sequential paced complexes).
Some PVCs are undersensed and do not reset the timing cycle (2nd paced beat).
Others are sensed and reset the timing cycle (4th paced beat). 2/n
The AVD is super short (~80 msec) which is less than the 95 msec crosstalk interval in a Sorin device, and consistent with the “as shipped” “exercise AVD”
Interrogation 5d post implant shows stable À (1.5mV & 0.75V) and V (8.5mV & 0.75V) lead parameters. 3/n
Got delayed digging up the operative reports on the previous ECG to try and explain it...
Whats going on here?
In addition to the above ECG, each of the following four ECGs were recorded in the same person. This should help point out the mechanism.
These ECGs demonstrate an atrial flutter (look to V1) with varying normal AV nodal conduction, fusion between AV node conduction and a AP, full AP conduction, and about conduction with LBBB.
The original ECG shows pre-excitation (fusion AVN/AP) then full AP then block in both
This ECG demonstrates a normally functioning @Medtronic pacemaker.
The patient is paced in atrium in MVP mode with a very long AVD. Note the 4th and 9th best don’t have a QRS complex between sequential P waves. This triggers the device to pace the ventricle 80ms after the AP.
What's going on and what would you do if this were your patient?
This ECG demonstrates AF with RVR. There is LBBB with discordant ST changes *BUT* looking to the high lateral leads (I, aVL) you see concordant ST elevation (ST segment and QRS in same direction) suggesting acute STEMI as per @ElenaSgarbossa criteria.
What is the finding(a) on this ECG, and what is the unifying diagnosis?
This ECG demonstrates sinus rhythm with atypical rsR’ pattern in V1 due to the presence of an epsilon wave (postexcitation in the RV) with associated right précordial TWI.
There is also a PVC which may be originating from the inferior RV.
This ECG is done post transplant. It shows sinus rhythm ~80 bpm in the recipients stump with sinus bradycardia in the donor heart with escape capture bigeminy.
- Abnormal precordial R wave progression with R/S ratio >1 in V1-2 and <1 in V6
- “Global negativity" in lead I (inverted P wave, negative QRS, inverted T wave) with inverted P wave in lead II
- Right Axis Deviation
- Upright QRS complex in aVR.
This ECG demonstrates automatic atrial tachycardia. The tachycardia is interesting as it fires at two different rate (slower in the first half, faster in the second)
Middle section has termination with A (simultaneous A termination and AV block)
There are only 2 sinus beats.
• • •
Missing some Tweet in this thread? You can try to
force a refresh
@drjohnm I think we gave drugs the best chance possible to succeed.
We undertook aggressive AAD titration over the first 90 days with standardised protocols and a target of AF suppression on continuous loop recorder monitor
- therapeutic achieved doses
- 30% used 2 AADs, 5% used 3 AAD
@drjohnm We had an independent committee review potential crossovers and offer therapeutic suggestions to try and keep people in their assigned group (we had 0 crossovers before a primary endpoint).
We used outcomes beyond « time to first »
@drjohnm And despite all that ablation was better in EARLY-AF.
- Less AF recurrences and burden
- Greater improvement in quality of life
- More likely to be a symptomatic at a year
- No apparent increased risk (and the counter point is the SAE in the control arm were substantial events)
1/ In October 2018 the @SCC_CCS released an update to the AF guidelines. This update included a significant revision of the recommendations for anticoagulation therapy around cardioversion. Space limited the discussion so... onlinecjc.ca/retrieve/pii/S…
3/ First, it is important to remember why AF is important. AF is increasingly common as the general population ages (and by extension our patients). The estimated lifetime-risk of developing AF is 22-26% for individuals 40-55 years of age.
1. Earlier in December I had the privilege to speak at the Cardiovascular Collaborative Medicine Conference in Manhattan on the role of catheter ablation post CABANA. I thought I'd present that talk via tweetorial. I'm not sure how well it will adapt to this form, but here goes..
2. As we work our way through this presentation I want you to keep in mind this patient profile. Specifically we are going to frame the conversation around a young patient with recurrent AF despite the use of AAD therapy as this is the profile where the evidence is most robust.
3. Why do we care about Atrial Fibrillation? Firstly, it is an important clinical problem. It is increasingly common as the general population ages (and by extension our patients). The estimated lifetime-risk of developing AF is 22-26% for individuals 40-55 years of age.