I've done a presentation on these ECGs before. One of my young doctors asked if I could make an ECG of them. Here it is. It's just over 12 minutes and a bit of fun. Enjoy and hope to see you at the Cardiac Bootcamp Live Course.

The arrhythmia from Hell! Everyone stresses about wide complex tachycardias(WCT). In the Cardiac Bootcamp Course we make it simple.
A recent article in JAMA Internal Medicine looked at the ECG features that differentiated VT from SVT.
In the course you learn my 120CRAM rule. Let's see what this paper found.

Cerantola M et al. Diagnostic Approach to Wide Complex Tachycardia. JAMA Intern Med 2021 Sep 1;181(9):1231-1233
A few points of summary from this article. 90% of patients with a WCT and a history of myocardial infarction, will be in Ventricular Tachycardia(VT).
We know that about 80% of WCT is VT, so it is a safe assumption. But there are a few other things to take into account.
The ECG factors that were associated with VT included:
A.  AV Dissociation, Capture and Fusion Beats
B.  Positive QRS in aVR
C.  QRS Concordance in the precodial leads
D.  QRS duration > 160ms
E.  A deflection in the initial portion of the QRS

There are really only a few causes of Wide Complex Tachycardia:

1. VT
2. Sinus + Bundle Branch Block
3. SVT with Aberrancy
4. Hyperkalaemia
5. Na Channel Blocker
6. Paced Rhythm
7. Ischaemia

120: This is a critical number. The rate must be faster than 120bpm and wider than 120ms. However BEWARE, if the QRS is too wide always think of HYPERKALAEMIA.
C: Concordance
R: Dominant R wave in aVR
A: AV dissociation
M: Morphology which includes capture and fusion beats and an Rsr pattern in V1 and a QS in V6 ( refer to the section on Wide Complex Tachycardia in the Course)

​Below is a slide from the course.

Do you have a simple failsafe approach to arrhythmias?
You must have your own simple approach. Members can go to the 'Narrow Complex Tachycardias' section to view my simple algorithm approach to the fast and slow rhythms.
An old boss of mine used to have what he called 'The 2am in the morning' approach to airway drug doses, so that it was simplified and minimised errors, when you were called in at that time.
It's important to have a similar simple approach to arrhythmias.
Here is my approach.

It comes back to some simple questions. 
If the rhythm is fast (>100 bpm) there are some critical questions to ask.
Is it Narrow? If Yes:

• Is it regular?

If it's narrow and regular then, what are the differentials?

• Sinus tachycardia
• SVT
• If it's irregular make sure it is irregularly irregular as we don't want to miss sinus arrhythmia. If it is irregularly think of:
  • Atrial fibrillation- irregularly irregular
  • Multifocal atrial tachycardia- very irregular as 3 different atrial foci

Is it wide? If Yes:
What are the causes of wide complex tachycardia:

1. Ventricular Tachycardia
2. SVT with Bundle Branch Block
3. Ischaemia
4. Na channel blockade
5. Hyperkalaemia
6. Pacing

That's about it. Sure, we can have some WPW abnormalities, like AF with WPW, but for most cases, these are the diagnoses.
Given that 80% of wide complex rhythms are Ventricular Tachycardia(VT), we can settle on that for most patients. However there are a few things to remember about VT:

• Monomorphic VT is exquisitely regular, so if you have an irregular wide complex tachycardia, it's isn't monomorphic VT.
• It really must be faster than 120bpm to be VT
  • If it's not faster than 120bpm check:
    • The potassium as it could be hyperkalaemia
    • Ensure there is no Na channel blocker overdose
    • That is not a reperfusion accelerated idioventricular rhythm

Below is the fast portion of the algorithm and a couple of examples from the course to try.

This is WPW with Atrial Fibrillation. The rate in some areas is 300 bpm. If you have any rate faster than 250bpm in an adult, there must be an accessory pathway. It is irregularly irregular. Some complexes are wide and others are narrow, as some pass through the AV node and others via the accessory pathway. See below:

How do we manage this condition?
If we used Procainamide, that would be fine, as it preferentially blocks the accessory pathway. What we cannot use, is an AV nodal blocker, such as a beta or calcium channel blocker, or Amiodarone. If we did this all the impulses would be conducted down the accessory pathway and the heart would go into ventricular fibrillation.

What if we applied the simple algorithm approach?
​We don't need to know what the diagnosis is.... that's the benefit of having an approach like this. Just follow the flow....

Let's try one more, then you can go to the course and do a bundle of examples.
What is the diagnosis of the ECG below?

It is a fast, narrow complex tachycardia. It is AVN re-entry tachycardia. What if you weren't sure of what to do? What would the algorithm say?

Remember to develop your own approach or just use mine. It's very satisfying when you have a simple approach. You can then add all the other learnings to this.

​Join me for an a fun approach to really understanding  arrhythmias, when I cover 'Rule the Arrhythmia'  at the Cardiac Bootcamp on the Gold Coast  on January 18 2022, 

A 79 yo male presents with palpitations. He is haemodynamically stable with a BP of 138/68. His ECG is shown below. What does it show?

ECG: A narrow complex regular tachycardia with a ventricular rate of 145, but no visible P waves.
You think it's some type of SVT, so you try vagal manoeuvres including the new REVERSE Vagal Manoeuvre. However there is no response.
You decide to give Adenosine.
Your colleague asks "Are you sure you want to give adenosine?"
Your response is: "It's a regular narrow complex, so Adenosine should be fine. If it were irregular ie., atrial Fibrillation and there were wide complexes indicating it might be atrial fibrillation with WPW, then I wouldn't give it. We should be OK". (members go to ECG's, when giving the wrong drug can kill your patient)
​You give Adenosine and the following ECG is taken. What does it uncover?

As the ventricular beats are blocked, the p waves become evident and the underlying atrial tachycardia is uncovered. We can sometimes use the LEWIS LEAD to make p waves more prominent, however the rate may make that difficult to do here.

It is a type of supraventricular tachycardia that can occur in both normal hearts and in congenital heart disease.
The ECG usually has the following characteristics:

• Rate > 100bpm
• If seen the P waves have an atypical morphology
• There is a narrow QRS

We think of Atrial tachycardias as falling into 3 groups:

1. Focal Atrial Tachycardia
   1. It is REGULAR
   2. Localised to one atrial focus
   3. There are discrete P waves
   4. Usually caused by catecholamines/stimulants, digoxin and alcohol.
2. Multifocal Atrial Tachycardia(MAT)
   1. It is IRREGULAR because because of multiple foci firing at different times
   2. There are 3 different P wave morphologies
3. Re-Entrant Atrial Tachycardia
   1. Usually persistent
   2. Occur after cardiac surgery or ablation

MANAGEMENT

• These atrial tachycardias are usually self terminating and except for some cases of congenital heart disease are usually not life threatening.
• Focal atrial tachycardias may respond to cardioversion, however MAT DOES NOT.
• Class Ia and Ic anti-arrhythmics such as Flecainide, have some effectiveness, however we have to be sure that there are no structural abnormalities (ie., ECHO is needed) as they can be arrhythmogenic.
• Class III drugs such as Amiodarone and Sotalol, although not effective in terminating the arrhythmia are good for maintaining a sinus rhythm.
• If the patient has a re-entry atrial tachycardia, AV nodal blockers are unlikely to terminate, however cardioversion is appropriate in unstable patients.

OTHER INVESTIGATIONS
What other investigations may be appropriate?
LABS

• Electrolytes,
• Haemoglobin,
• Digoxin levels

RADIOLOGY

• CXR, looking for COPD,
• CTPA if suspicious for a PE
• ECHOCARDIOGRAPHY to look for structural heart disease, left atrial size and pulmonary arterial pressure.