A 60 yo male is brought into the Emergency Department following collapsing at work.
On arrival he is alert and oriented with a heart rate of 20bpm, BP of 105/70 and a respiratory rate of 16.
He has no chest pain or other concerning features.
His past history includes:

• Atrial Fibrillation (on Sotalol and a NOAC)
• Hypercholesterolaemia

His ECG is shown below. After looking at his ECG, what would you do?
​
(a) Increase his heart rate using pharmacology
(b) Do nothing as you might cause harm and his BP is acceptable and he is alert.
(c) Defibrillate
(d) Give Magnesium or an extra dose of Sotalol

 ATROPINE
Muscurinic Acetylcholine Receptor Antagonist
t1/2 = 3-4 hours
Indication: AV nodal blockade. It works by decreasing vagal tone, so may not be effective in high degree AVN block.
Dose: Start at 0.5 mg-1mg (max of 3mg) Lower doses may cause a reflex bradycardia
Beware:

•  Patients with coronary artery disease as can increase myocardial demand​
• Acute angle closure glaucoma
• Bowel obstruction
• Cardiac transplant patients- may result in asystole.

Atropine may be the first line to use whilst you are getting set up for the definitive drug ie Isoprenaline. Atopine may not work on all patients or if it does work, beware, as it can wear off fairly rapidly.

ISOPRENALINE
Beta adrenoreceptor agonist 
t1/2 = 5 minutes, but immediate onset of action
Dose: If given centrally start at 0.5-1 mcg/min and titrate. It is also safe for peripheral infusion and can be started at 5mcg/min then titrate up or down. Usual range is 2-10 mag/min, however higher doses have been used.
Beware: Hypotension, tachycardia, angina. May not be tolerated by the patient longer term as can cause headaches and trembling.

ADRENALINE
​Non-selective adrenergic agonist Beta 1 > alpha 1 and Beta 2
t1/2 = 5 minutes. Acts within a minute and lasts for 5-10 minutes.
Dose: This can be used peripherally. Start dose at 1 mcg/min. Usual dose is 1-10 mcg/min. Higher doses may be needed.
It has a wide range of effect, being a chronotrope and inotrope.
Beware: ​Tachycardia and arrhythmias, narrow angle glaucoma, Phaeochromocytoma

​.........MEMBERS can go to the new section titled Managing Bradycardia and read further about Transcutaneous and Transvenous Pacing

He responded well to Isoprenaline..perhaps too well, becoming a little tachycardia. However given that isoprenaline has such a rapid turnoff effect, it was weaned. The patient was discussed with cardiology and was referred for a pacemaker.

It is a mimic. Pseudo-Wellens’, is a similar pattern to Wellens’, but results from other ECG abnormalities such as  abnormal T waves, due to left ventricular hypertrophy(LVH). We cannot diagnose Wellens' Syndrome in a patient with left ventricular hypertrophy. The biphasic waveforms are a direct result of the left ventricular hypertrophy, and represent a T wave change associated with the enlarged heart.
So if there is LVH we cannot diagnose Wellens’ Syndrome on ECG. The patient may however still have ischaemia, so beware. One more thing that is different in Pseudo-Wellens’, is that the changes are more lateral i.e.., V3-V6, whereas in true Wellens’ they are at V2-V3.
The ECG below is a very good example of the ‘pseudo’ pattern.  The biphasic waveforms are due to left ventricular hypertrophy. They are also more lateral than the true Wellens. 

Substance abuse such as cocaine and other stimulants as well as cannabis can also result in a mimic pattern. Examples of these mimics are shown below.
Even though we may consider them as mimics, our first priority always is to rule out ischaemia first. The diagnosis of a pseudo-Wellens' is a diagnosis of exclusion.

A patient presenting after taking cocaine and showing the pseudo-Wellens' pattern:

A patient with excessive cannabis use, showing a pseudo-Wellens' pattern:

A 90 yo patient with multiple co-morbidities and mild dementia presents with chest pain.
The patient is haemodynamically stable. 
An ECG is done and there is concern over the rate. 
Look at the ECG. What is the diagnosis?

Is it SVT? Is it Torsades? What do you do next?
.........Move away from the patient..... ie., do nothing. Let's see why.
Let's go back to the clinical picture.
The patient is haemodynamically stable and looks well.
Now back to the ECG: It is a narrow complex EXTREME tachycardia.
Notice lead III. It is not the same as the others. One lead cannot refuse to show the tachycardia whilst all the others are. In fact lead III here is the underlying rhythm. The rest of the ECG is artifact.
Remember that if the ventricle is beating at above 300 beats per minute in an adult patient, it will very soon convert to ventricular fibrillation.
Clinically at a rate of 350 or so, the patient will not be stable, as the ventricle doesn't have time to fill properly, so the blood pressure will be impaired. 

What is the artifact caused by?
Artifacts can be external, relating to line current. They can also be internal relating to tremor or shivering. They can also be caused by other devices such as deep brain stimulators ( which are usually there to control tremor).

​An ECG was redone and is shown below. The artifact is gone and the patients underlying rhythm is there.

Don't be fooled by the mimics.
To read more on this and see more examples like the one below go to the blog on 'A Patient with Wide Complex Tachycardia'