First things first… a bit of history!
Right lets get started with ECG theory!
Nice one everybody!
Now we all know what we can learn from an ECG, lets move onto interpreting it:
Nice one! Think we got there between us!
So, for those who need to revise their physiology:
1. The Sino-Atrial (SA) node is the 'pacemaker' of the heart. It spontaneously depolarises setting off a 'wave' of depolarisation.
2. This spreads through the atria (causing contraction, and a P wave on our ECG machine) but cannot cross the atrioventricular ring- except at the Atrio-Ventricular (AV) node.
3. The wave of depolarisation spreads through the AV node slowly, creating a delay (our P-Q interval) which allows the ventricles to fill.
4. From the AV node the wave of depolarisation is conducted down the bundle of His to the base of the heart, and from there to the left and right bundle branches. This is so that the wave of depolarisation (and therefore contraction) starts at the base of the ventricles, and pushes the blood up and out. This forms our QRS complex.
5. After each cell depolarises it must repolarise before it can conduct again- the atrial cells repolarise whilst the ventricles are depolarising (which can't be seen on an ECG as it is hidden in the QRS), and the ventricles repolarise straight after depolarisation (termed the "T wave").
Quick question ….
Well I never! So now we all feel as though we've learnt nothing at all in the last 5 years, lets carry on with the case!
Ok, so the first thing we need to talk about is the heart rate on the ECG.
Well that's definitely worth knowing! #UsefulTip
Great! I think we #NailedIt! Onto our first ECG:
Ok- so Venticular Premature Complexes (VPCs) are wide and bizzare (because they're ventricular in origin) and come before there would be a normal beat (so they're "premature"). If we have 4 or more in a row then we're looking at Venticular Tachycardia (VT).
Don't try to treat it unless it is causing a problem! Any antiarhythmic drug is potentially pro-arrhythmic, so in the abscence of clinical signs or markers of sudden death risk (high rate, prolonged VT, or R-on-T) then treating may be more of a risk than a benefit. Investigate the arrhythmia, don't reach for the drugs!
Here's another one to look at:
So in that last ECG we had a bit of R-on-T:
And we also had a bit of plain ol' ventricular tachycardia (VT). What do we treat VT with?
Nice one! So we can give some IV lidocaine and hope for conversion back to sinus rhythm.
Once the rhythm is converted to sinus after a bolus, we can put the patient on a lidocaine CRI and transition to oral antiarrhythmics, such as amiodarone or sotalol. Mexiletine, an oral antiarrhythmic from the same class as lidocaine, is no longer available in the UK or Europe, but can be obtained by special import on a named patient basis (a bit awkward in reality…)
So back to our R-on-T… and here it is looking a little wobbly….
Before it leads to this… #NameThatRhythm
Yes, well done all! Ventricular fibrillation (VF) is a common arrest rhythm, but appropriate CPCR and electrical defibrillation may be successful. It depends on why the patient has gone into VF… More investigation needed here!
Here's another one… #NameThatRhythm
Ok so that's a supraventricular premature complex (SVPC). You can tell because they're premature, but unlike the ventricular complexes the QRS is of a normal size and shape because the depolarisation through the ventricles is still normal. Note that the P waves, if not hidden within the T wave of the previous complex, may appear abnormal (e.g. negative) because they do not usually originate in the sinus node.
Next up…. #NameThatRhythm
Well done everybody, I'm loving all the right answers tonight- this is indeed Atrial Fibrillation (AF)! As you can see from the picture above, depolarisation occurs throughout the atria, bombarding the AV node, which conducts when and as normally as it can! So AF has that classic undulating baseline (from the random atrial depolarisations- often termed 'f' waves) and no P waves visible. It also has irregular R-R intervals (AV node conducting whenever it can) and the QRS has normal morphology because it is still conducting through the ventricles normally, but they may vary in amplitude.
At this point Lily jumped in with a bit of horse stuff, and we decided to electrically cardiovert our atrial fibrillation dog…
…which was luckily successful!
We then had a quick question about other types of conversion:
And another #NameThatRhythm
So like venticular premature complexes and ventricular tachycardia, we can let the odd SupraVentricular Premature Complex (SVPC) go- but once we have a collection of them, we're looking at SupraVentricular Tachycardia (SVT).
Ok we've got another one to look at now- a cat with a HR of 50:
Brilliant! For more on the 'Blocked Cat' please see past scenario here:
Just a quick word about escape rhythms:
Ventricular escape rhythms occurr when there is no depolarisation crossing to the AV node (for whatever reason). But it's ok, because the cells of the heart all depolarise spontaneously. Without the faster depolarisation being passed through the AV node, the heart falls back on the slower rate of depolarisation in the ventricles. This can come from the lower AV node or bundle branches, which produce a normal (but slow) QRS complex, or it can come from the Purkinje fibres producing an abnormal slow QRS complex. I.e the ventricles 'escape' the block and depolarise on their own!
Well done everybody!