This ECG shows an atrial tachycardia with atrial rate of 120bpm. The p waves are inverted in III and aVF, which is abnormal. This is a unifocal atrial tachycardia. It can occur in structurally normal and abnormal hearts. it arises from a particular part of the atrium and its location can be diagnosed by the axis of the p waves.
Below is another example:

This is someone at a rate of 120bpm. Notice the inverted p’s in lead III. Again, this is unifocal atrial tachycardia.
Clinical Presentation
The usual presentation is one of palpitations, but may be that of syncope, or cardiac failure if the patient has been in the rhythm long enough.
Workup
An ECG and electrolytes to ensure no abnormalities and a full blood count to exclude anaemia.
Very few other investigations are needed in the emergency department. Perhaps a chest xray if lung pathology is suspected. The patient should have an echocardiogram, to look for structural abnormalities, but this can be as an outpatient.
Management
The unifocal atrial tachycardia can be treated like an SVT.
The general treatment for this condition is:

1. Pharmacological
   1. Beta blockers
   2. Calcium channel blockers
2. Cardioversion

In this case we gave the patient his usual dose of Sotalol and waited, however it was clear that there was not going to be resolution, so we proceeded to cardiovert.

Introduction
When we assume that every wide complex tachycardia is Ventricular Tachycardia(VT) our sensitivity for picking up VT is 100%. In the emergency department setting, this is a must! We use electricity on all of these patients because it is safe and effective. We can try adenosine, in case it’s a supra ventricular tachycardia(SVT) but only if it’s a regular rhythm.
Our specificity in this scenario lags, however in our favour, is that fact that 80% of WCT is VT. If we wanted to determine if an ECG is showing VT, we have a range of rules at our disposal,  including Brugada and Vereckei, that give a respectable specificity, but it’s still in the mid 80%.
A new validated rule
The VT Score, uses 7 criteria, some of which we already use, to diagnose VT.  A specificity of 100% is reached when 4 or more criteria are satisfied(1).

The Seven Criteria are as follows:
NOTE: Before we start I would add that the rate should be greater than 120 beats per minute for us to start considering VT.
1. Dominant Initial R wave in V1. This can be notched(the original rabbit’s ear) provided the notch is on the descending limb.

LETS MAKE IT EASIER TO REMEMBER:

1. Rate must be > 120bpm to be VT
2. Concordance in V1-V6
3. AV Dissociation
4. Josephson’s Sign in V1 -V2
5. Look at V1 for a FAT INITIAL R wave (r>40ms) this could be the rabbits ear
6. Look at aVR for a FAT Wave to begin with
7. Look at lead II RWPT > 50ms- again a big R wave.

References

1. Jastrzebski M et al. The ventricular tachycardia score: a novel approach to electrocardiographic diagnosis of ventricular tachycardia. Europace. 2016 Apr;18(4):578-84
2. Vereckei A et al. Application of a new algorithm in the differential diagnosis of wide QRS complex tachycardia. Eur Heart J 2007.28:589-600
3. Brugada P. et al. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation 1991:83:1649-1659

​The Case
​A 40 yo is brought to the emergency department with the following vitals:

• GCS 4
• SBP 70mmHg
• HR 140
• RR 50
• T 39C

There are no signs of injury. Heart sounds are dual and no extra sounds.  There are reduced breath sounds and crepitations in the left base. The abdomen is soft and the patient appears to have peripheral cyanosis.
The patient has a known history of IVDU and has been found in a chair, not rousable.
She has fluids and inotropes and antibiotics and she has the ECG shown.
What are your differential diagnoses for this patient? What is the most likely diagnosis? 
The computer says acute AMI. Could it be?
Let’s look at the ECG

Rate 106
Is it sinus?– P waves are upright in II and inverted in aVR; Yes
Is there a P for every QRS? Yes
QRS:
Is it tall/small?: It’s about right, there is no hypertrophy.
Is it wide/narrow? It’s narrow
Is it of abnormal morphology ie., delta wave? No
Is it clumped?(just incase we miss a Mobitz- but it’s not slow enough) No
ST-T
Remember the baseline is the T-P line
If we look we see that there is some ST elevation in some areas of the ECG of about 1mm, although this is difficult to gauge as the T wave goes straight into the p wave.
The most visible abnormality is the inverted T waves.
What causes inverted T waves?As this is an adult patient we can overlook the T wave inversion of childhood. Other prominent causes are:

• Acute Myocardial Infarction
• Ventricular Hypertrophy( not present on this ECG)
• Pulmonary Embolism
• Raised Intracranial Pressure( I would usually expect them to be deeper)

PR and QT Intervals
The PR is normal and the QT is very prolonged.
PACING Spikes: None.
Putting it all together, what would seem the most probable diagnosis?Before we look at the most likely diagnoses. One differential to entertain is an overdose, however there are no signs of classic QRS widening of Na channel blockade, or a terminal R wave in aVR.
It might be an AMI, there is no evidence of hypertrophy, the patient is not behaving like they have a PE, but they may have raised intracranial pressure given the decreased conscious state. The decreased conscious state may be simply due to low blood pressure.
The patient is also febrile. Why? Remember this patient has a history of IVDU, so infective endocarditis is a consideration. The patient may also have meningitis. The fever may also be secondary to stroke as we know that about 50% of stroke develop a fever, which in itself is a marker of severity and marker of mortality.
Let’s narrow it down to 2 causes, AMI and raised intracranial pressure. Raised intracranial pressure ECG’s have deep T wave inversion and a prolonged QT. I’m thinking this is an intracranial event, especially if the fever is due to this.
Echo showed a myocardium, not contraction properly, with clean valves, so it may be AMI. However the CT gave the diagnosis with large subarachnoid haemorrhage.
This is a neurocardiogenic phenomenon when the heart is affected by deranged autonomic supply coming from a stroke. A fascinating case mixed with electrolyte abnormalities etc. I hope you enjoyed it.

A 31 yo female presents to the emergency department with pleuritic chest pain. The patient is 19/40 gestation and no medical conditions. The history of the event is that the patient was sitting on the couch and developed left shoulder and then left chest pleuritic chest pain. There was no history of trauma, or fevers, cough or wheeze and the patient had no history of a DVT.
Clinical examination was normal.
Basic blood tests were done that showed:
CRP 4
D-Dimer 0.71 mg/L
Na 134/ K 4.1/ HCO3 19/ Creat 61/ eGFR 90
WCC 10.4/ Neut 6.3/
High sensitivity troponin 3
Vitals were HR 80bpm, BP 122/70 SpO2 100% on RA.
​What is your working diagnosis so far?
​An ECG was done as shown below. The resident reported it as normal. What does it show and what is your diagnosis?

Take Part in the Poll

What did the YEARS Study tell us?
In 2017, we were given a new approach to looking at PE and the D-dimer(2)
They used a clinical decision rule which consisted of 3 items:

1. Clinical Signs of Deep Venous Thrombosis
2. Haemoptysis
3. Is Pulmonary Embolism the Most Likely Diagnsosis?

The flow diagram is shown below, but in summary it says:
In the non-pregnant patient:

• If no criteria can rule out PE with d-dimer of <1000 ng/mL
• If criteria can rule out PE with a D-dimer of <500ng/mL

In the pregnant patient:

• If no criteria can rule out PE if D-dimer is < 1000 ng/mL 
• If criteria can rule out PE if D-dimer is <500 ng/mL

OVERALL

• In any patient with NO CRITERIA a D-dimer of <1000 ruled out PE
• In any patient WITH CRITERIA a D-dimer of < 500 rule out PE

The Pregnancy Adapted algorithm from 2019(3) is shown below:

It was decided that although pleuritic chest pain was all that the patient had, there was nothing else to explain the symptom. The D-dimer was > 500, so the patient was sent for a CTPA. It was negative. The patient was discharged for GP followup.

References

1. Marchick M.R. et al. 12 Lead ECG Findings of Pulmonary Hypertension occur more frequently in Emergency Department patients with Pulmonary Embolism than in patients without Pulmonary Embolism. Annals of Emergency Medicine. Vol 55, Issue 4, April 01, 2010; pp 331-335
2. Van der Hulle T et al. Simplified diagnostic management of suspected pulmonary embolism (the YEARS study): a prospective, multicentre, cohort study. Lancet. 2017; 390:289-297.
   
3. Van der Pol L.M et al. Pregnancy-Adapted YEARS Algorithm for Diagnosis of Suspected Pulmonary Embolism.N Engl J Med 2019; 380:1139-1149
   

This week I have 4 questions for you. 3 are ECGs you must know and the fourth is a simple question on what you should look for in the QRS complex, when reading the ECG. Enjoy. Hope to see you at the Live Cardiac Bootcamp Course on the Gold Coast in January 2022. Congratulations to everyone who has purchased the Online Cardiac Course and thank you for all the great comments. New sections added regularly..

A 69 year old woman presents with dyspnoea. Her ECG is shown below. Describe the ECG and interpret the changes by giving your most likely diagnosis.

In my ECG in 20 seconds method, what are the 4 things to look for when looking at the QRS?

A 54 yo male presents with chest pain, that radiates into his jaw. He has a previous history of an AMI 10 years previously and also has hypertension, diabetes and hypercholesterolaemia. An ECG is done. Does this patient need to go to the Cath lab? What is the 'sign' seen here?

A 64 yo male presents with chest pain. What are the important ECG changes and what other ECGs would you perform?

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.

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.