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The QRS complex
Because the component parts Q, R, S are intimiately linked to each other and relate to the depolarisation of the ventricle, many concepts refer to the "QRS complex"
This is simply defined as from the initiation of the Q wave, to the end of the S wave.
Don't make the common error of correctly referring to the initial downwards pointy bit as the Q wave (remembering that it might not exist, dependent upon lead!)
but then incorrectly measure the QRS complex from this pointy bit.
Measure it from when this downwards pointy bit begins.
A 2D object
Any 2D image will have a width, and a height.
the QRS complex is no different.
We begin with it's height, or more appropriately it's "amplitude"
The "amplitude" of a QRS complex refers to the most positive (highest) to the most negative (lowest).
It is worth reinforcing this specific detail - the amplitude does not refer to a specific component/wave of the ECG.
The reason for this can be demonstrated as below:
As we have established prior, there should be no Q waves in the anterior leads.
Thus, whereas in the above example in V2 there is (and this is therefore abnormal), in V3 there isn't.
Likewise, in the above example V3 has an R wave, but V2 does not
Therefore, anchoring a definition to bits of an entity that may or may not exist and thereby making them Schrödinger's ECG is generally not optimal for day to day operations.
Whilst talking about amplitude, it is worth discussing at this point how as a general rule, it is normal for these to get bigger as we towards middle age (30-40) and then tail off again.
It is also worth a brief detour into why there seems to finally be a shift in cardiology from arbitrary values, to ones measured against itself.
To better explain this concept, I present the following:
If we took an ECG of these two patients, we would expect the complexes to be large for the chap on the left, and small for the guy (?) on the right.
This phenomenon is due to "impedence."
Harking back to the very beginning of this series, recall how an ECG is a recording of a summation of electrical activity, not the actual heartbeat itself.
This inconvenient detail is relevant because the more distance you have between the heart and your leads, the less said leads are going to detect, and vice versa.
To demonstrate this point, one only has to refer to the entity known as "Left Ventricular Hypertrophy".
Whenever I see one of my colleagues comment "Left ventricular hypertrophy" based purely upon the fact the voltages are large, the voices in my head start whisphering sweet symphonies.
These symphonies can be summarised as follows:
(NB: other causes include amyloid/sarcoid, and because exams demand an endocrine reason - hypothyroidism can also cause this.
(No, i don't know how. Ask an endocrinologist.)
The width
This has basically been covered in section 5 - rate.
The key cutoff, especially for exam purposes, is 0.12s
This value was chosen as the acceptable tradeoff between sensitivity vs specificity, and has been established in essentially all cardiology guidelines since the 1970's.
Of interest, in Einthoven's original work, he found the values of 0.08-0.10 were most common.
Likewise, in large population studies (such as the revered Framingham study), 95-99% distribution had 0.11s as their upper limit.
(This does lend itself to a conundrum to nerds like myself, when faced with an obvious LBBB morphology ECG but the QRS is not >0.12s.
Given human beings are not copy pasted, and patients do not read textbooks - is this not a failure of ourselves to label what is individually pathophysiologically wrong, but instead we are pleasing arbitrary dogma?)
Anyway - for revision's sake, we say hello to an old image
With regards to how to calculate/discern the various bundle branch block patterns which can occur - i cover this in part 2 of my lecture series.
Click for the next part:
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