(See previous post for explanatory information about #ECGclass)
The wife of this 48yr old man, called the paramedics when she witnessed his collapse at home.
The paramedics arrived within minutes, noted his complete loss of cardiac output, initiated CPR and gave 2 shocks, with return of spontaneous circulation.
The shock strip is seen below:
Q1. What is the pre-shock rhythm?
He was taken directly to the catheter labs at the local hospital, but his coronary arteries were entirely normal.
As his GP, you hear about his admission. His three small children attend the local school with your own. He's not someone you see very often, so you check his notes. According to your records, he was previously fit and well, other than one mention of palpitations a few years ago. He had only mentioned these in passing. They did not worry him and rarely caused him anything more than a trivial and transient discomfort. You had advised him about caffeine intake, and work stress, but neither you nor he felt they warranted further investigation. You had advised him to contact you again, if they became more frequent, or troublesome.
Q3. What might you be thinking about now?
Once stable in hospital, a post-collapse, resting ECG is taken:
Q4. What is the PR interval? is it normal?
Q5. Is the morphology of the QRS complex normal?
Q6. What is the QT interval? is it normal?
Q1. The pre-shock strip shows completely disorganised, chaotic ventricular activity. This is Ventricular Fibrillation (VF). This is a life threatening arrhythmia, which is inexcusable to miss. Hope you got it!
Q2. The first rhythm on the post-shock strip shows an irregular Broad Complex Tachycardia (BCT), at a very rapid rate (300 bpm). All the complexes look similar, a bit like monomorphic Ventricular Tachycardia (VT) - but unlike VT, they are irregular (zoom in and map out, to confirm this, if you're in any doubt).
So far so good. I think this is a reasonable level of interpretation for most of us.
But, there's more detail to follow, for the advanced enthusiasts!
The second rhythm looks like a possible return to sinus rhythm (alternatively, this could be a CPR artefact - we'd need a longer strip to be sure).
Q3. What might you be thinking about?
Well, apart from your defence union... ;o You might be wondering about that history of palpitations. Was it significant? We start thinking about things like Wolf Parkinson White syndrome, The hereditary channelopathies, long QT/Brugada etc. etc.
To exclude these disorders, we need to consider the PR interval, the QRS morphology and the QT interval.
You can chose any lead you like when it comes to measuring waves and intervals - so always just plump for the one with the clearest, most well-defined complexes.
For this reason, in this ECG, let's study Lead I.
Q4. The PR interval on this ECG is short at around 2 small squares (0.08 seconds), slurring directly on to a stepped upsloping R wave.
Q5. As already eluded to, The R wave is 'stepped' - or slurred - with a slightly broad base. Given that the QRS complex represents ventricular depolarisation, and this is a very rapid process (thanks to the ventricular conduction systems, the Bundle of His and Purkinje fibres) the R wave should be likewise, a rapid, pretty much vertical, upstroke (or downstroke depending on the lead).
This ECG shows beautiful pre-excited Delta waves indicative of Wolff Parkinson White.
Q6. Again using Lead 1 for calculation purposes, the QT interval is normal at 10 small squares, or 0.40 seconds. (Normal range 9-11 small squares, or 0.36 - 0.44 seconds). This can be most easily measured using the very first complex in lead I as it sits perfectly on the grid lines! Tip: Always look out for complexes sitting on the grid lines - to make measuring easy on yourself.
For more information of WPW, it's presentation and management, refer back to the previous post by clicking on the link.
But remember - Delta waves alone, do not constitute WPW syndrome - that diagnosis relies on associated symptoms of syncope or palpitations.
Now here's the tricky bit, for advanced followers.
Back to the post shock rhythm:
This irregular BCT is a result of atrial fibrillation being conducted direct to the ventricles by way of an accessory pathway. So the VF has been shocked into pre-excited AF.
Because the conduction is going the 'right' way down the accessory pathway (atria to ventricles), it's termed anterograde. (If the conduction travels from ventricles to atria it's termed retrograde).
Because the accessory pathway is abnormal, it doesn't have the delaying and rate-limiting properties of the AV node that usually protect the ventricles from abnormally fast rates. In EP studies, they can stimulate VT by bombarding the ventricles with rapid impulses. This is why the combination of WPW and AF is dangerous: the anterograde conduction down the accessory pathway can act like a natural VT stimulator.
If you want to understand this better, there's a good BMJ article which does a great job:
Physiology of WPW - Emergency Medicine Journal
This man went on to have ablation therapy.
Just out of interest, here's the post-ablation ECG on the same patient which shows complete absence of the previous delta waves:
It's really unusual to capture a shock strip like the one above, and it's certainly not something we're likely to see as GP's, but it does serve to alert and remind us, of the possible fatal complication of WPW.
In this case, hindsight is a wonderful thing. But it was almost too late for the advantage-of-the-retrospectoscope in this husband and father.
Almost...but not quite, thanks to our wonderful paramedic colleagues. :)
I'm really grateful to Mark Hammond for kindly providing, and helping talk me through, these strips. Thanks Mark! H.