A 9 yo girl is brought into the emergency department, following an episode of syncope. She has a current viral illness and looks miserable. She was walking into the Emergency Department with her mother, when she collapsed. She recovered quickly with no post-ictal component but has no memory of the event, although the event was preceded by ‘dizziness’ and diaphoresis.  Her past medical history is ADHD, for which she is on no medication.
You review her in the triage room as the department is filled to capacity. The vitals are all normal but the child looks tired and has some coryza symptoms. You ask the resident to get the rest of the story and show you an ECG.
The resident brings you the ECG shown below. What is your comment on this ECG?

ECG Interpretation
At first glance: There is T wave inversion in anterior leads but you would expect this in a young girl. There are however T waves inverted in the lateral leads…….STOP. Let’s go over the ECG in a systematic fashion.
Is it sinus rhythm? For it to be sinus, the p wave in II must be upright and the p wave in aVR inverted. This is not the case. Now look at lead I, The p waves are inverted and they should be upright.
Two things give you this pattern:

1. Limb lead reversal and
2. Dextrocardia

This ECG is the result of limb lead reversal.
You have the ECG redone. The ECG is shown below. How would you comment on this?

For quite some time I've been less than eager to calculate axis on all ECGs. The one exception that I made is, when there was a RBBB on the ECG, as I would then look for a Fascicular Block.
However I have found it more useful than I thought.
In this Blog we will look at how to calculate axis and refer you back to the section in the course on ECG Axis to do this in more detail and we will further look at some of the uses.

There are many ways to calculate axis;

• the quadrant method,
  
• the 3 lead method,
  
• the degree method and more.
  

The difference is in the preciseness with which you wish to calculate the axis ie., are you happy to say it's normal or it's leftward, or do you need to know that this axis is not only rightward, but that it is 95 degrees.

There was a case we covered in a prior blog of a 70 yo male who presents to the emergency department following a collapse at home. There is no prodrome and he does not remember the incident.
​His ECG is shown below. What is the diagnosis?

This was an incomplete triphasicular block, with:

• RBBB
• First degree block
• left axis ie LAFB

Read the section on fascicular blocks to find out more.

The next case is one of an amphetamine overdose. Can the axis help us here?
​The patient has been in a sinus tachycardia and now he has a wide complex.

• Is it VT?
  
• Is it Na channel Blockade?
  
• Is it RBBB?

It is a wide complex tachycardia. It has a rate > 120, so it qualifies to continue with my 120CRAM formula for diagnosing VT. It has some of the elements of VT.
First thing to say is that amphetamines DO NOT cause Na channel blockade, so it can't be that.
What is the axis? It looks like a right axis. Right axis can be cause by ventricular ectopy ie VT. So it can be VT.
RBBB doesn't tend to cause a right axis. BUT HyperK+ does and this patient was hyperkalaemic. After being shocked with no result, the patient was treated with bicarb and Ca++ and sinus rhythm was obtained.
Axis can help.

HOW TO QUICKLY CALCULATE AXIS: Let's use the Quadrant Method
We will use leads I and aVF
Here is how to perform this:

• Assign Lead I to your LEFT ARM
• Assign Lead aVF to your RIGHT ARM

Now look at the leads and raise the arm belonging to the positive lead and lower the arm belonging to the negative lead. The arm left upward will be the axis if Left or right.
Let's practice on the ECG below:
Using the Quadrant Method the left arm goes up as lead I is positive and the right arm is downas aVF is negative. The resultant positive arm is the left so it is a LEFT AXIS. 

For a Video on how to do this and a bit of fun with Donald Trump showing us how to calculate axis, go to the Basic ECG Section.

That's all I've got for you this week....

A 22 yo male presents to the emergency department with a history of lethargy, fatigue and palpitations. He has no chest pain or SOB.
There is no past medical history.
The patient believes he feels like this, as he had a big gym workout today.
An ECG is done because of the history of palpitations. What is your interpretation?

Sinus Rhythm at rate of 98bpm
Normal QRS width
Widespread ST depression I, II, aVL aVF V1-V6 with abnormal ST segments due to?
Intervals: PR is prolonged, Is that a long QT?

1. What is the diagnosis?​
2. What is the potential cause in this patient?
3. If this patient went into Torsades de Pointes, following cardioversion with electricity, would you treat with:​
   1. Amiodarone or
   2. ​Magnesium?
4. What are the causes generally?​
5. What conditions is this ECG pattern mistaken for?

​....answers are below.

This is the classic ECG of hypokalaemia. It has the 4 classic changes:

1. ST segment Depression
2. Inverted T waves
3. Large U waves
4. Prolonged PR Interval

Beware here as there is no prolonged QT, but a long QU due to the prominent U waves.
​See the ECG Below for these changes. The patient's potassium was 1.1 mmol/L

This patient has Hypokalaemic Periodic Paralysis. It is characterised by muscle weakness of the shoulders and hips associated with hypokalaemia.
Proximal Weakness is usually greater than distal weakness. The respiratory muscles are usually spared, although they may not be.
The conditions presents with first attacks in childhood and adolescence. A first attack in someone older than 25 years is almost never this condition, unless it is associated with thyrotoxic periodic paralysis.
It has an autosomal dominant inheritance.
Attacks are precipitated by:

• High carbohydrate meal
  
• Rest following Exercise
  
• High Na Content Foods
  
• Sudden Change in Temperature

Clinical Diagnosis is made by:

• Episodes of Paralysis
  
• Low K during attacks but normal between
  
• Triggers
  
• Familial History

Patients tend to develop a progressive myopathy over time.

Obviously we would need to treat the hypokalaemia. However rapid correction of hypokalaemia can result in ventricular arrhythmias and asystole.
Usually patients with hypokalaemia also have hypomagnesaemia. Magnesium is modulator of K+ ion transport.
​Therefore GIVE MAGNESIUM.

Go to the Hypokalaemia section of the cardiac Course and see more cases, causes and what it is mistaken for.

Perhaps we can now see some ST elevation in I and aVL and even in V2. Perhaps the ST depression in III is a little reduced.
The TIMI Score has now increased to 4 and predicts about a 20% chance of MI or ischaemia or all-cause mortality.

The patient was taken to the cath lab and an occluded Diagonal artery was found, for which he had successful PCI.

So the question here is is, without the 6 hour troponin and the fact that there is no ST elevation in contiguous leads, this might be one of those ECG we miss. We need to look at this particular pattern in the ECG. ​

An 80 yo woman presents to the emergency department with the complaint of feeling her legs give way. There has been no syncope, no injuries and the patient had no other clinical symptoms or signs, just the leg weakness. There was no headache, no palpitations, no chest pain, no shortness of breath, or abdominal pain ( review The SYNCOPE PLUS RULES).
An ECG was done as shown below, with an initial concern of ischaemia.
What does the ECG show?

Using the ECG in 20 seconds approach the following are obvious:

• Irregularly irregular ie atrial fibrillation
• ST depression in I, II, aVL, V3-V6

What question do you want to ask next?

• "Are these changes old or new?"
• "Is the patient on digoxin?" 

As it turns out the changes are old and the patient is on digoxin.
The changes on this ECG are not of classic morphology, so lets look at it a little more closely.

Digoxin has a very narrow therapeutic index. It is used frequently and has positive inotropic and negative chronotropic effects. It decreases heart rate due to increased vagal activity, whilst shortening the action potential by increasing intracellular Calcium

T WAVE CHANGES
The T wave can be inverted or flattened or biphasic(usually in V4-6). It can look upright in its terminal portion however in most cases this is a U wave.

QT CHANGES
There is usually QT shortening

It is important to remember that the changes seen on ECG are due to the patient being on digoxin. They do not necessarily indicate toxicity.

The ECG of athletes can pose a challenge, in distinguishing pathological changes from those physiological changes, that are associated with physical training and cardiac remodelling. We don’t want to erroneously attribute heart disease to those with normal variants and more importantly, we don’t want potentially life threatening cardiac conditions being erroneously dismissed as normal variants.
The changes we see are related to:

1. Increased vagal tone
2. Enlarged cardiac chamber size

Those athletes that participate in endurance sports experience a volume load on all heart chambers, whereas those that participate in strength training experience a pressure overload on the heart, secondary to increased systemic vascular resistance(1).
In 2010, The European Society of Cardiology produced recommendations for ECG interpretation in athletes. In 2015, a meeting of sports physicians and sports cardiologists produced the most up to date set of criteria for determining normal and abnormal ECGs in athletes. These were the Seattle Criteria(2).
​
A CASE of an incidental finding in an ECG of an athlete
A 23 year old male who is training for a triathlon presents with a history of a mechanical fall. He trains over 8 hours per week and today whilst running tripped and fell. He has had a head strike, but no loss of consciousness. He complains of a small amount of midline neck pain. He is in bed with a cervical collar in-situ. There are no other injuries. He has full memory of the event and feels well. The nurse does as ECG and hands it to you.
This is the ECG. What do you think?

Transient ST segment changes post cardioversion are well described. Their significance is uncertain.
Hypotheses for the ST segment changes include:

1. Coronary Artery Spasm- Although the time it takes for the spasm to occur and the time it takes for changes appear don't seem to coincide ie., the changes occur much earlier.
2. Acute Myocyte necrosis- Cardiac Troponin levels are not necessarily raised.
3. Potential differences between depolarised and non-depolarised parts of the membrane

Regardless of the reason that they occur, these changes are transient, and thought to be of little consequence.
However, given that Brugada patterns predispose to ventricular arrhythmias, it may be prudent to monitor these patients for a period of time.
Read more on Brugada Syndrome and How to diagnose both Type I and Type II in the Cardiac Bootcamp Course.
References
1. Abdalla K et al Transient appearance of Brugada-like Type 1 electrocardiogram pattern immediately after biphasic synchronised electrical cardioversion for atrial fibrillation: a case series. ​European Heart Journal - Case Reports, Volume 3, Issue 4, December 2019, Pages 1–8