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Monday, 6 August 2012

#ECGclass Case 4 - Working through and abnormal ECG

#ECG Class is an educational blog which runs alongside Twitter.
A new ECG "quizz" is launched most Monday evenings, in term time. 
Cases are generally aimed at Primary Care. 
All scenarios are completely fictitious and theoretical, but based on commonly occurring presentations in General Practice. 
This is an educational site, intended for healthcare professionals and shouldn't be construed as patient advice. 

Please use the Hashtag #ECGclass on Twitter, if you want to ask the patient any questions, or request any further investigations. Alternatively, please join in discussion and leave comments below.

Remember there are no right or wrong answers!  

ECG interpretation is often open to debate, and will usually evolve and change as new information becomes available.  Everyone's opinion is valid, and useful for others, as the evolution process takes place. 
Together we will try and form an interpretation based on the trace, and information, we have in front of us. 
Don't worry if you disagree - shout up and share your thoughts - the diagnosis is often arguable on the basis of a 12 lead trace, and may only become more obvious when a longer rhythm strip is available. 

Please feel free to join in, but most important of all, have fun! :-)

#ECGClass.  Case 4

So. This delightful 84yrs old man comes to see you in surgery. Amongst other things, he mentions some chest pains. His symptoms are a bit vague and non- specific. He’s been having them for 6yrs. They don’t sound cardiac, but you know him well, and know he has a history of IHD.
He’s not a fit man, but on the other hand, he’s not clinically unwell today. He seems much the same as usual. A long with his known IHD and CKD5, he’s also pretty immobile from his osteoarthritis and obesity. He seems a bit breathless today, as usual.
You think this could be anything....! He has a lot of potential problems. You note from his recent annual review blood checks that he has chronic stable anaemia (Hb10.5ish for many yrs) secondary to his CKD. His renal function is stably poor (eGFR is 10-12).

You decide it might be wise to get an ECG whilst you consider how best to take this forward. 
The practice nurse pops it back in front of you: 

Now what shall you do? Are you any the wiser?
Lets look at the ECG methodically and see if it helps. All ECG’s can be analysed with a few simple rules. If in doubt, just describe what you see. 

The rate has already been calculated for you at 52bpm. If not a quick ready reckoner is as follows:
For regular rhythms: Rate = 300 divided the number of large squares between 2 complexes.
For irregular rhythms: Rate = The number of complexes in 30 large squares (ie 6 seconds) multiplied by 10

Comment - Is this a regular or an irregular rhythm?
It’s regular. Best seen by studying the QRS complexes in long lead II in this case.
If there is no rhythm strip on a 12 lead ECG, you may only have 3 complexes to study. If so, regularity can be very difficult/impossible to determine.

Are there any P waves? Are they obvious – or perhaps hidden in other waves, or non-existent? How do they appear (Morphology? Orientation? Size?) Do they have a consistent appearance? Do they have a consistent relationship with the QRS?
I can just to say see P waves in the chest leads v1-6 but they are subtle! Because of poor quality baseline, I can’t see them in the limb leads or rhythm strip. (It may be impossible to see on your social media device – may need to zoom in or print a large copy)
(Cheats tip: If you’re not sure about seeing complexes – get a repeat ECG with the ‘gain’ increased to magnify the complexes. This is the second ECG I took on this man – you may have noticed the comment on the top right of the ECG: “non Standard lead gain”).
On his standard ECG I couldn’t be sure if he had P-waves or not. If there were no P-waves, then this would be a ventricular escape rhythm ie. No atrial activity seen, and the ventricles have helpfully responded by setting up their own pacemaker focus somewhere within them.
Of the few P-waves we can see, their shape is uniformly round. They appear to be upright in V1 but possibly inverted in v2-6. Not important for purposes of this lesson. 

The P-waves we can see appear to have a consistent relationship with the following QRS complexes, HOWEVER, this is prolonged...
The normal PR interval (start of P wave to the first deflection of the QRS complex) should be 3-5 small squares (0.11 to 0.20 seconds). In this case the PR interval is between 8-9 small squares. (>0.32 seconds)


Well done so far!

QRS Complexes.
Now we need to study the QRS complexes.
We’ve already decided they are regular.
We can’t really comment on the size, because we now know that the gain has been increased. So there’s no point thinking about LVH on this ECG.

We can consider their shape. Are they consistent in all leads? What about their orientation?
Is there any axis deviation?

(If you need help with calculating axis and normal conduction orientation, then refer back to link on previous #ECGclass – or search “ECG Teacher-Axis video” on You Tube!)
What is their duration?
(A normal QRS complex should be no wider than 1 and half to 2 and half small squares (0.06 – 0.11 seconds). 

In a heart with a healthy conduction system, once the impulse passes through the AV node, it travels through bundle of His, and down the Left and Right Bundle branches. As long as there is no delay in this conduction, this gives rise to a narrow QRS complex (less than 3 small squares).
If, however, after the impulse reaches the Bundle of His, there is any delay in the conduction, through either the Left or Right bundle branch, then the QRS complex will be widened.

LBBB usually gives rise to a wider QRS complex than RBBB. In LBBB, the width of the QRS is > 120ms (MORE than 3 small squares) whereas RBBB is often small squares.

LBBB = Left chest leads (I, V5 and V6) show RSR pattern (remember: WiLLiaM
RBBB = Right chest leads (V1 and 2) show RSR pattern. (remember MaRRoW)

If we go back to the ECG in Case 4, we notice that the QRS complexes are slightly broad, with RBBB formation.

But, that’ s not all....

If you have successfully worked out the cardiac axis, you will also see that there is

a Left Axis Deviation here. RBBB alone would not normally alter the cardiac axis.
Two common causes of LAD are:
1. Left ventricular Hypertrophy 

2. Inferior MI
3. May be normal variant in obese or stocky habitus

A none of these situations apply here, so we know something else must be going on.

The Left Bundle branch divides into two – the Anterior fascicle, and the Posterior fascicle. If both fascicles are blocked, then it becomes a full LBBB, but if only one fascicle is blocked, this is known as a “Hemiblock” or “Fasicular” block.
A Left Anterior Hemiblock (Left fasicular block), will always cause a LAD.
If you ever see RBBB + LAD, on an ECG, then you almost certainly have a LEFT ANTERIOR HEMIBLOCK.

In fact, he is relying entirely on his small posterior fascicle, of the left bundle branch for ventricular conduction. If that fails him, he’s in trouble.

Unsurprisingly, an ECHO revealed severely reduced LV systolic function. He needs a full cardiology assessment and consideration for pacing.

The End.
Well done those of you who read up to here!


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