Hello Everyone
As the dust settles from the last EMCORE Conference e and as we start to prepare for the next ones in Singapore, London, Bali and Fiji, there is one ECG we did not cover in the quiz, that is important to discuss.
​The ECG below was the last in the Quiz.
I did not give you a history at all, but that is the key here...diagnose with no history. I could add that this is a 67 yo patient with a presentation of SOB, chest tightness and palpitations.

What is the Diagnosis?
(a) Ventricular Tachycardia
(b) Hyperkalaemia
(c) Anterolateral MI
(d) SVT with Bundle Branch Block

Let's draw lines at where the QRS ends. This is the same process as we used in the 'Shark Fin' ECG (Blog coming next week).

When we do this we can see the ST elevation and the depression.
​With that marked, we see that it is an anterolateral MI. See below and watch the brief video.

A 62 yo male with a previous history of paroxysmal atrial fibrillation presents to the emergency department with a rapid irregular heart beat and a complaint of palpitations, that started 2 hours previously.
His ECG is shown below.

The patient is haemodynamically stable and is not greatly distressed by the palpitations. He  is not on any anticoagulation.
Here are some important questions to answer in relation to this patient:

1. Do we shock this patient now, or give the patient 24 hours to potentially self-revert?
2. We know that if we shock early, we are doing so, to a number of patients who would self revert. Should we send the patient home and get them to come back the next day?
3. Are there any risks in waiting  for 24 to 48 hours, or is the risk of stroke equal during the first 48 hours?

​Watch the video lecture below for all the answers (From Cardiac Bootcamp).

A 78 yo woman with known moderate coronary artery disease, (with no previous interventions) and a history of controlled atrial fibrillation, presents with left sided chest pain.
Previous history includes hypertension. She is on a DOAC, and metoprolol and Perindopril.
She is haemodynamically stable.
​The ambulance have given aspirin and topical GTN. On arrival she is pain-free.
Her ECG is shown below. 

Blood tests are essentially normal, however the high sensitivity troponin is 89 ng/L (normal is <14). Is this a type I or type II Myocardial Injury(MI)? Differentiating the two can sometimes be very difficult.
MI is now far easier to detect with high sensitivity troponin. Troponin are very specific for MI, however they do not really give us the cause.

Myocardial infarction is caused by coronary thrombus, however non-thrombotic causes also exist. Type II MI is due to a mismatch between oxygen supply and demand and is due to causes other than atherothrombosis including:

• Coronary artery spasm
• Coronary embolism
• Coronary artery dissection
• Other specific causes
  • hypoxaemia
  • anaemia
  • hypotension
  • severe hypertension
  • Brady/tachyarrhythmias.

Differentiating between subtypes, of which there are 5, according to the 4th universal definition of MI, can be challenging.

Mortality Outcomes
Both short and long term mortality is higher in type II rather than type I MI. Predictors of poor survival in those patients with type II MI include:

• Older age
• Female
• Heart failure
• Shock
• The presence of CAD

Troponin
Those patients with Type II MI usually have a lower peak troponin level.
A 20% change in Troponin differentiates between stable and dynamic troponin patterns.
There are some recommendations that a 50% change in troponin should be used for dynamic change and a 20% change used when the baseline value is substantially elevated.

Differentiating between Types I and II can be difficult, however in general, if there are signs and symptoms of ischaemia, type I MI should be diagnosed.

These patients should all be admitted.

Reference
DeFilippis A et al. Assessment and Treatment of Patients with Type 2 Myocardial Infarction and Acute Nonischemic Myocardial Injury. Circulation 2019;140:1661-1678

This week I wanted to ask you what you thought of an ECG. It was sent to me initially, with no past medical history for an opinion. It is of a 29yo with palpitations. That's all the info for now.
What does the ECG show?
What is the diagnosis? Is it VT or SVT?
Let me know what you think. Answers (plus more history) in next weeks blog, plus a simplified method of arrhythmia diagnosis.

My response to the ECG without any history was:
It is real ie not a mimic.
It is regular
The rate is faster than 120bpm, so we can consider VT. It is a little too fast perhaps at about 198, but can still be VT
The QRS width is just wider than 120ms ie., 124ms. It is a little borderline, but favours VT
There is no concordance
There is a dominant R wave in avR which favours VT
There is no AV dissociation that I can see
The morphology is RBBB with an Rsr which favours VT, also the R/S in V6 is <1 ( ie the QRS is entirely negative in V6)which favours VT.

Rx Cardioversion is probably safest. If not haemodynamically unstable, you could give adenosine. If VT, nothing would happen, if SVT will cause an AV block and may revert. (Adenosine is also safe to give as this is a regular rhythm,)
I would add to this that there is a borderline left axis deviation

The history at presentation was that the patient developed palpitations whilst running. There was a long history of SVT, for which he had an ablation several years previously.
The cardiac history was more significant in that the patient had had endocarditis some 14 years previously. As a consequence there had been an aortic and mitral valve repair. Several years after this, he had an aortic root replacement.

The patient had attempted valsalva manoeuvres, with no success.
He was haemodynamically stable.
The patient was treated with Magnesium 5mmol, 500ml of IV fluid stat and Metoprolol and reverted to sinus rhythm.
​His ECG was shown below. It shows atrial enlargement with some inverted p waves in V2.

What are your thoughts? The chances are that it was probably SVT. Could it have been idiopathic ventricular tachycardia. Cardiac Bootcamp Course members login to read all about this. This usually occurs in structurally normal hearts and doesn't respond to metoprolol, but to verapamil. 
​What would you have done?

I’ve presented the ‘Imposters’ before, Here is a case of a STEMI that’s not a STEMI.
At a recent Cardiac Bootcamp I spoke about the 4 things I look for in an ECG to help me determine if there are signs of ischaemia on the ECG.
 
4 Things I look for to RULE IN ischaemia on an ECG

1. If there is ST depression in any other lead except aVR and V1, it is ischaemia
2. ST elevation III>II is a STEMI
3. QR-T Sign or convex ST segment it is a STEMI
4. Are there Hyperacute T waves (“T wave towards over the QRS in V3 or V4): It is a STEMI  (check that it isn’t hyperkalaemia)

 
CASE 1(1)
A 57 yo male presents to the emergency department with central dull chest pain that started after going for a walk. There was no radiation but the patient had dyspnoea and fatigue. He had no past medical history and was on no medications.
He had a family history of his father having had a cerebrovascular event and mother a pulmonary embolism.
On examination he was afebrile, HR of 100bpm, BP of 102/60, respiratory rate of 22 and SaO2 of 95% on oxygen.
An ECG was done and is shown below:

What's your diagnosis?
 
The assumption was an acute antero-septal myocardial infarction and the patient was taken to the cath lab.
Coronary angiogram showed: Normal coronaries. There was a small separate conus artery arising from the aortic root with embolic occlusion. However this was too small to stent. (The conus artery is usually the first branch of the right coronary artery, but in up to 50% can arise from a separate ostium from the right aortic sinus.)
 
An echocardiogram demonstrated normal left ventricular function, enlarged right cardiac chambers, with paradoxical movement of the interventricular septum and a right heart pressure of 40mm Hg and thrombi were seen in both pulmonary arteries confirming pulmonary embolism. He was then treated for this.
Ultrasound of the lower limbs showed a DVT.
 
The ST segments in the ECG normalised however the patient developed T wave inversion in the inferior leads.
 
WHY DOES THIS MIMIC OCCUR?
The cause is not really known although ST elevation in leads V1-V4 has been reported in the literature (2,3,4,5).
 
There are two theories:

1. The right ventricle is very prone to ischaemia and doesn’t tolerate increased pressures very well. (read the Right Ventricular Spiral of Death). A pulmonary embolism results in sudden pressure increases in the right ventricle, that can result in both focal and global myocardia ischaemia. The ST elevation is due to epicardial or microvascular coronary vasospasm.
2. A second theory relates to a catecholamine surge occurring with acute pulmonary embolism. This results in increased myocardial work resulting in ischaemia.

 
Conus artery embolism has been shown to cause ST elevation(6). Hence the possibility of paradoxical embolism must also be considered, especially if there is communication between the venous and arterial systems.
 
CASE 2 ​(7)
A 57 yo male presents to the emergency department following a syncopal episode at home. There was no prodrome. On awakening the patient had central chest pain and shortness of breath. The patient had a significant coronary artery disease history with previous cardiac stents. Past medical history also included hypertension, hyperlipidaemia and renal impairment.
He was afebrile, HR of 111bpm, BP 123/80 SaO2 96%
The initial ECG is shown below:

What is your diagnosis now?

The patient was given GTN, following which the blood pressure dropped and the GTN was removed. Was this a clue that this could be right heart related?
 
An acute occlusion was suspected and the patient was taken to the cath lab.
Cardiac catheterisation demonstrated patent stents and no occlusive lesions.
Transthoracic echocardiography revealed right ventricular enlargement and displacement of the interventricular septum, with elevated right sided pressures and normal left ventricular function. Pulmonary embolism was suspected and a V/Q scan showed large bilateral ventilation-perfusion mismatches. The patient was treated for pulmonary embiolism.
 
 
CONCLUSION
We need to consider the diagnosis of acute pulmonary embolism in patients with ST elevation in the praecordial leads, especially if the history has elements relating to dyspnoea.

At Cardiac Bootcamp we look at ischaemia on ECG and go over how to differentiate it from Pericarditis or Benign Early Repolarisation.

Follow these 4 rules to increase your chances of picking up ischaemia. See the examples below.

A 38 yo patient presents with chest pain. The ECG is shown below.
​Is this ischaemia, pericarditis or benign early repolarisation(BER)?

Let's answer the 4 questions. This ECG is not a straight-forward rule in.

1. Is there ST depression in any lead other than aVR and V1
   1. There may potentially be some ST depression in III- This could be ischaemia
   2. There is also some PR depression, which may point to pericarditis
2. Is STE III>II
   1. No
   2. There is some STE in I, aVL, II, V4-V6- Too many territories to be ischaemia
3. Is there a QRT Sign or a convex segment
   1. No
4. Are there hyperacute T waves
   1. No

The diagnosis is pericarditis.

I've been emailed a few times about the ECG in 20 Seconds Method. This is an approach to reading the ECG, I put together years ago, mostly to help myself read the ECG and not miss things. There is nothing new and groundbreaking about this. It has the elements of the classic ECG approach. Some say it is too simple, but that's its greatest strength!......
What is special about this method, is that it allows us to learn a basic algorithm, that looks for the most important ECG findings. You won't pick up everything with this, but you will pick up those important ECG changes that will have the highest yield for your patient, like the sneaky ischaemia, differentiating a lethal from non-lethal arrhythmia. It gives you the confidence to read ECG's.
Why did I call it 'ECG in 20 Seconds'? Because it only takes 20 seconds to pick up the abnormalities in the algorithm. You can then sit down and spend a few minutes sorting them.
​Below are the basic elements. For a more detailed approach login and go to the ECG in 20 seconds page.

We look at a lot of ECG's and we do a lot of troponins, however the most important thing we are going to do in the patient who presents with chest pain is take a good history. Regardless of a normal troponin or a normal ecg, if the patient has a very good history for acute coronary syndrome, we have to admit that patient, or at least watch them and do serial testing. The low risk group that we clear with rapid rule-out criteria, are just that, low risk on history.

Here is an example of a patient who presents to the emergency department with chest pain. Please rank the following in terms of likelihood for predicting a myocardia infarction, or at least ischaemia.

• Left arm pain
  
• Right arm pain
  
• Indigestion pain

CASE
A patient presents to the emergency department with chest pain and you put a pre-test probability of x% on that chest pain being ischaemic. How does it change with the following? DOES IT INCREASE OR DECREASE THE CHANCE THAT THIS IS ISCHAEMIC PAIN?

Reference
Body R et al. ​The value of symptoms and signs in the emergent diagnosis of acute
coronary syndromes. Resuscitation 81 (2010) 281-286.

A 6 week old is brought to your rural emergency department with several days history of irritability and poor feeding.
On history there was poor/no antenatal care and the child was a home birth. On examination the child is afebrile, with a tachycardia and is haemodynamically stable. There is a 4/6 holosystolic  murmur on cardiac auscultation and bilateral lung crepitations.
An ecg is done and is shown below.  Please answer the following:

1. What does the ECG show?
2. What is the most likely diagnosis?
3. What investigations would you perform?

STEMI mimics(1) are important to understand, because in taking the time to investigate the mimic, we can miss opportunity for early treatment of the real disease. Unlike STEMI equivalents, which have been covered previously, some of the mimics are not as serious.
​Here are some examples.

This can be in 2 forms, where in both the ST segment is concave:

1. Male pattern: 1-3 mm STE in V1-V4
2. Female pattern: 1mm STE in V1-V4

The formal definition of a STEMI as per AHA/ACC(2) is:

• Men
  • < 40 yo: >2.5 mm ST-elevation in V2 or V3, 1 mm in any other lead
  • ​> 40 yo: >2.0 mm ST-elevation in V2 or V3, 1 mm in any other lead
• Women: >1.5 mm ST-elevation in V2 or V3, 1 mm in any other lead

​The ECG below is from a male who presents with chest pain. It is normal.

This condition is present in a younger population group and amongst athletes. There are three types:

1. Type 1: Pattern occurs in the lateral leads
2. Type 2: Pattern occurs in the inferior/inferolateral leads
3. Type 3: Pattern occurs throughout the whole ECG.

BER Pattern:
Point notch with elevation
STE with concave up morphology V2-V6, II, III, avF usually < 2mm
No reciprocal changes
​Symmetrical Concordant T wave
​STE/T-wave height <0.25 in V6

Benign Early Repolarisation may not be that benign, being associated with serious arrhythmias in some studies. 

Diffuse STE
ST/T-wave >0.25
There are 4 stages in pericarditis:

• Stage I: ST and PR changes
  • Diffuse concave up ST segment elevation,
  • Reciprocal ST depression in  aVR. 
  • PR elevation in lead AVR + V1
• Stage II: Normalisation of ST segments
• Stage III: T wave inversions.
• Stage IV: Normalisation of T waves

ST-T and QRS discordant.
​STE is concave and <5mm

Peaked T waves
​Downsloping ST segment.

Type I: Coved Pattern

• Leads V1-V2
• High take-off > 2mm and concave downscoping ST segment

Can present with STE in Precordial leads
A more common presentation of right ventricular injury is STE in V1-V3 and/or ST depression of V4-V6.
Theories for why STE occurs in the precordial leads include:

1. Paradoxical Embolism via atrial-septal defect or patent foramen ovale (5)
2. Myocardial ischaemia caused by a sudden pressure load on the right ventricle, which is unable to compensate.(5)
3. Hyperaemia from PE induces a catecholamine surge, increasing myocardial workload and ischaemia.(6)