Lesson 13

Posted Posted in August
A new ECG is launched most Monday evenings. 

Cases are generally aimed at healthcare students and professionals. 
All scenarios are completely fictitious and theoretical, but based on commonly occurring presentations in  practice. 

This is an educational site, intended for healthcare professionals and shouldn’t be construed as patient advice. 

A 22-year-old male presents with agitation and delirium after smoking an unknown substance that an equally unknown person on the street offered him. You note a rapid radial pulse at around 150 bpm and attach him to the cardiac monitor:


Well now we’re in a tough spot. It’s difficult to tell whether the ECG shows sinus tachycardia or some non-sinus narrow-complex tachycardia (we’ll use the colloquial shorthand of “SVT” to include all those other options on the differential, including AVNRT, AVRT, ectopic atrial tachycardia, junctional tachycardia, etc…). If it is indeed sinus tach, then the requisite P-waves must be those upright deflections in II and III and superimposed on the T-waves.

Is there something we could do to see if those really are P-waves buried in the T-waves?

Lesson 12

Posted Posted in August
A new ECG is launched most Monday evenings. 

Cases are generally aimed at healthcare students and professionals. 
All scenarios are completely fictitious and theoretical, but based on commonly occurring presentations in  practice. 

This is an educational site, intended for healthcare professionals and shouldn’t be construed as patient advice. 

This 64 year old woman presented intoxicated with nausea and vomiting and epigastric pain, with no chest pain. She has a history of a stent, but unknown in which artery. She stopped taking clopidogrel 2 weeks ago because she ran out. Here is the initial ECG; there was no previous ECG for comparison.

before pseudonormalization

Lesson 11

Posted Posted in July

A man in his 60’s presented after 4 days of chest pain, with some increase of pain on the day of presentation.  Exact pain history was difficult to ascertain.  There was some SOB.  He had walked into the A&E (did not use the ambulance).  He was in no distress and vital signs were normal.  Here is his ECG:


First ECG 4 days after onset of pain

What is your interpretation?  Obviously there is MI.  How acute is it?

There is atrial fibrillation at a rate of 95.  There is Right Bundle Branch Block with a QR particularly noted in V1-V3 (no rSR’, because there is an initial Q-wave; this is diagnostic of infarction in the anterior wall and septum).  The Q-waves extend to V5 and are very wide (80 ms in V2).  There are also inferior Q-waves which can mimic a left anterior fascicular block, as they result in left axis deviation.  There is rather massive ST elevation, and this is not only anterior but inferior (see analysis below).

First ECG 4 days after onset of pain-arrows

The end of the QRS is best seen in lead V1 (and results in a QRS duration of 176 ms).  If one draws a line down to lead II across the bottom, one can find the end of the QRS in lead II.  From there, one can find the end of the QRS in all leads.  This analysis shows that there is ST elevation after the end of the QRS in lead II, III, and aVF, and reciprocal ST depression in aVL.  Thus, this is BOTH an anterior and inferior STEMI in the setting of RBBB.

How old is this antero-inferior STEMI? 

Could it be acute (vs. subacute or days old)?  Although the patient has had pain for 4 days, could the artery have fully occluded only within hours?  Very unlikely.  Although acute anterior STEMI frequently has narrow QR-waves within one hour of onset (1. Raitt et al.), such Q-waves are associated with larger MI and worse outcomes (2. Armstrong et al.), the presence of such well developed, wide, anterior Q-wave suggests completed transmural STEMI.

So this patient likely has a several day old infarction, with persistent ST elevation and persistently upright T-waves.

The wide Q-waves suggest “transmural” MI (completed MI with infarction of the entire thickness of the ventricle).  This was common in the days before reperfusion of STEMI, but still happens in patients who present late and therefore do not get timely reperfusion therapy.  When there is MI extending all the way to the epicardium (transmural), that infarcted epicardium is often inflamed (postinfarction regional pericarditis, or PIRP).

What complication is the patient with post-infarction regional pericarditis at risk for?

The patient was taken to the cath lab emergently and a 100% mid LAD occlusion was opened but opening resulted in no flow.  The initial troponin I was 23.7 ng/ml and was falling, confirming infarction days ago.

Case Continued

2 days later the patient became increasingly tachycardic, hypotensive, clammy (in cardiogenic shock) and had a new murmur.  This was the 12-lead ECG.

2 days later more STE upright T

Not much change, except a slightly faster ventricular response at 110bpm.  No resolution of ST elevation.  The T-waves are persistently positive.  This remains consistent with PIRP, as was the first ECG.  Notice also how easy it is to diagnose ST elevation in the PVC.

An echocardiogram showed no hemopericardium, but Doppler showed a new small ventricular septal defect with left to right shunting.  This was in addition to a large septal, anterior, and apical wall motion abnormality, and moderately severely decreased LV function.

An intra-aortic balloon pump was placed, and the patient was taken for immediate surgical repair but did not survive.



When there is full thickness infarction, there is epicardial inflammation (post-infarction regional pericarditis), and the myocardium is at risk of “rupture.”  The term “rupture” makes it sound like some sort of explosion or massive blowout, but it is usually a small, slow leak that, over time, can cause tamponade and death.  Rupture can be either free wall rupture (causing tamonade) or septal rupture, causing ventricular septal defect with left to right flow and resulting pulmonary edema and shock.  If detected early by ultrasound, the patient can be saved.  Our own Dave Plummer of HCMC reported on survival of 2 of 6 patients with STEMI who had free wall myocardial rupture diagnosed by presence of hemopericardium on bedside ultrasound in the ED.(3)

Oliva et al. (4) strongly associated myocardial rupture with postinfarction regional pericarditis (PIRP), and associated PIRP with persistent upright T-waves.  He found 2 ECG patterns of atypical T-wave development in PIRP:
1) persistently positive (upright) T-waves 48 hours after AMI onset. 
2) premature, gradual reversal of inverted T waves to positive (upright) deflections by 48 to 72 hours after MI onset in the presence of well formed Q-waves.


1. Well formed Q-waves with persistent ST elevation, especially in a patient with prolonged pain, should alert to transmural MI with possible post-infarction pericarditis. One should be on the alert for myocardial rupture.
2. In the case of septal MI, as here, be on the alert for development of a ventricular septal defect.
3. Bedside echo may detect these in a timely way.
4. Additionally, these patients have a high incidence of LV aneurysm with mural thrombus.
5. Although rupture has a high mortality, it is not uniformly fatal




1.  Raitt MH, Maynard C, Wagner GS, Cerqueira MD, Selvester RH, Weaver WD. Appearance of abnormal Q waves early in the course of acute myocardial infarction: implications for efficacy of thrombolytic therapy. J Am Coll Cardiol 1995;25(5):1084-8.

2.  Armstrong PW et al.   Baseline Q-wave surpasses time from symptom onset as a prognostic marker in ST-segment elevation myocardial infarction patients treated with primary percutaneous coronary intervention.  J Am Coll Cardiol 53(17):1503-9. Apr 28, 2009.

3. Plummer D.  Dick C. Ruiz E. Clinton J. Brunette D. Emergency department two-dimensional echocardiography in the diagnosis of nontraumatic cardiac rupture.  Ann Emerg Med 1994; 23(6):1333-42.
4. Oliva PB, Hammill SC, Edwards WD. Electrocardiographic diagnosis of postinfarction regional pericarditis: ancillary observations regarding the effect of reperfusion on the rapidity and amplitude of T wave inversion after acute myocardial infarction. Circulation 1993;88(3):896-904.


5. Oliva PB.  Hammill SC.  Edwards WD.  Cardiac rupture: a clinically predictable complication of acute myocardial infarction: report of 70 cases with clinicopathologic correlations.  J Am Coll Cardiol 1993;22(3):720-6



Lesson 10

Posted Posted in July

You are called urgently out of the ECG room. The receptionists have taken an elderly lady straight into a side room, when she was brought in to the hospital by her daughter.

You get as much history as possible from the daughter.

This is an 80 yr old lady who is new the clinic, and you have never met her before. The daughter explains she has become increasingly worried about her mother’s in recent months and has brought her to live nearer.

In the last few weeks she seems to have been getting generally weaker, and has been complaining of headaches and nausea. Her daughter has felt she was more low in mood, and more confused than usual. She was planning to book her an appointment to see you soon, but had been putting her decline down to her recent move, and was waiting to see if she picked up first.

On visiting her this morning, she found her quite ‘out-of-sorts’ and almost ‘vacant’ at times.

On examination she looks quite unwell. A thin, frail lady, who appears to be confused and has started vomiting.

She denies any chest pain.

You make a quick assessment and call the on call cardiac registrar.

Meanwhile cardiovascular and abdominal examination are unremarkable other than a bradycardia. Her BP is 100/60. She’s had no recent blood tests.

Her daughter tells you she has taken Atenolol ‘for many years’ for blood pressure.  Other than that only some weekly ‘bone strengthening’ tablets and calcium/VitD supplements.

You do a 12 lead ECG:



What do you notice?

Q1. Can you see P waves? Is it regular?  What is the rate?

What is the likely explanation?

Q2. Comment on the QRS complexes, ST segments and QT interval. (Hint: just describe what    you see)




Q1. The heart rate is between 42-50 bpm (calculated crudely, by counting squares).  This is of course assuming standard paper speed of 25mm/sec (not stated).


There are between 6 and 7 large squares between each QRS complex. So the rate is between 300÷6 and 300÷7


Using a rate-ruler, it’s 42 bpm 😉


So it’s a bradycardia.


I can’t make out any P waves, but the rhythm is regular.

This is most likley a junctional escape rhythm.

The Atenolol won’t be helping!



Q2.  Firstly, the QRS complexes are a little wide (more than 1.5 small squares, but not > 3 small squares – as needed to define a bundle branch block). This suggests an intraventricular conduction defect. On it’s own, this can often be seen on ECGs, and may be of no signicicance.


More interesting, are the ST segments and QT interval.


This ECG has a very short QT interval, with hardly any ST segment. This is the classic ECG picture of Hypercalcaemia.


Normal QT interval range:  0.36 -0.44 seconds (9-11 small squares)

On this ECG:


Corrected QT (QTC) = Bazett’s Formula = QT Interval / √ (RR interval).


Measured QT interval (ms) = 400

HR = 42

RR Interval (60 ÷ HR)       = 1.4

√ RR                              = 1.2


QTC   334.7ms (0.33 sec)




Mild hypercalcaemia may have no symptoms or signs.

Symptoms of hypercalcaemia are more common at high serum calcium levels (12.0 mg/dL or 3 mmol/l). They include:


  • Nausea & vomiting
  • Alterations of mental status / lethargy / depression / headache/confusion
  • Abdominal or flank pain
  • Weakness and vague muscle/joint aches
  • Polyuria, polydipsia, nocturia

Causes include

  • Malignancy (via caused by increased osteoclastic activity within the bone)
  • Primary hyperparathyroidism.
  • Vit D toxicity (rare but recognised – see below)



Severe hypercalcaemia (above 15–16 mg/dL or 3.75–4 mmol/l) is considered a medical emergency, and cardiac arrest can result.


Electrolyte changes and the ECG can be remembered by recalling this simple sketch:

twave kplus

The T wave generally goes up and down with K+ level

The QT interval generally lengthens & shortens opposite to  Ca2+ levels

Hypercalcaemia produces classical ECG changes of short ST segment, and a short QT interval. Sometimes the T wave is widened.


Hypocalcaemia gives the opposite effect, that is, a long ST segment and long QT interval.


Hyper- and Hypokalaemia – Generally, the amplitude of the T wave is proportional to the serum K+ level.

Is it possible, that this mildly confused lady, has been taking accidental overdoses of her calcium supplements, or even taking over the counter cod-liver oil in addition to her prescribed medication……???

Vitamin D Toxicty causing Hypercalcaemia with ECG changes.

This Pubmed link from July 2013 highlights the rare, but potentially fatal complication of Vitamin D3 (cholecalciferol) toxicity.


Severe hypercalcemia can sometimes mimic an acute Myocardial Infarction on ECG.   This earlier Pubmed article, of 2003, presented a case of Vitamin D intoxication which mimicked acute myocardial infarction.


Hypercalcaemia can also mimic hypothermia, giving an ECG appearance of the Osborne wave.

Food for thought as more and more people become aware of the potential benefits of Vitamin D supplements.


See you next week.

Lesson 9

Posted Posted in July

#Pulsemdx is an educational blog which runs alongside Twitter.
A new ECG “quizz” is launched every Monday evening. 
Any discussions generated with be archived for summary and reflection, on the following interim @Pulsemdx

A 56yrs man who rarely attends, but he woke in the small hours of the night with ‘indigestion’. The pain hasn’t got any worse, but it’s niggled on for several hours now, so his wife booked the appointment and insisted he came down to have an ECG before work.
He’s never really suffered with indigestion before, but has no cardiac history or risk factors.

He looks a little unsettled and restless, but nothing else of note. Apart from a slight tachycardia, his pulse is normal, and BP borderline elevated (he’s visibly a bit anxious).

The ECG shows:



What does the ECG show? (Stick to describing the ST changes only).

The ECG shows 2-3mm of horizontal/downsloping ST depression in leads V1-4

At first glance I would have felt this showed anterior ischaemia.

But, bear in mind, he has ongoing pain, at rest.   This has to be assumed to be Acute Coronary Syndrome until proven otherwise.

In accordance with NICE Guidelines for new onset chest pain, and in order appropriate to the circumstances, offer:

  • Pain relief
  • Aspirin
  • Other Therapeutic interventions
  • Pulse oximetry (supplement O2 only if % SAO2 indicates)
  • Monitor until ambulance arrives (GP) or diagnosis confirmed (Hospital)

On arrival at A&E, serial troponins were taken, and the posterior ECG leads (V7-9) were monitored. 

A subsequent diagnosis of Posterior MI was made.
Posterior Myocardial Infarction

With Acute MI, the presence of persistent ischaemic pain, indicates that still viable areas of ischaemic and injured myocardium are in danger of necrosis.

It is outwith the concept of this forum, to go into management of Acute Coronary Syndrome (ACS) in any detail, but everyone should make themselves familiar with the NICE Guideline “Chest Pain of Recent Onset” (CG95).  

Pages 1-9 of the Quick reference guide linked above, deals with ACS, whereas pages 10 onwards, deal with stable angina.

In STEMI, the ECG leads which are orientated to the area supplied by the affected coronary artery will reveal the ST elevation. And so, the area of infarction can be determined by which leads of the ECG are affected:


And it follows, that the coronary artery affected in Acute Myocardial Infarction, is determined by the location of the MI :



Of course, reliance on ST elevation to diagnose STEMI, assumes we are viewing the affected myocardium from the front. What if the ST elevation is in the posterior myocardial wall?

If ST depression is present in leads V1-V3, with ongoing chest pain, then recording of the posterior leads (V7,V8,V9) will be invaluable. 

The posterior leads are placed on the posterior chest wall:

Lead place

Of course,the recordings from the 3 posterior leads will therefore be a mirror-image of V1-3 :



And so, the posterior ST elevation becomes obvious.

Posterior MI is often a bit of an enigma to GP’s and students, and I’m sure we all recall been told to flip the ECG paper upside down, and view form the back. When lacking precious time/ability to monitor the posterior leads, this method can still be invaluable – it’s just remembering to think of it!


Hope that helps a little.
Looking forward to any more gems of education on posterior MI’s (for me) from anyone who’d like to add a comment! 🙂

Thank you.

Lesson 8

Posted Posted in July

All cases are generally aimed at healthcare students and professionals. 

All scenarios are completely fictitious and theoretical, but based on commonly occurring presentations in  practice. 

This is an educational site, intended for healthcare professionals and shouldn’t be construed as patient advice. 
So. This delightful 84yrs old man has been referred to clinic for an ECG. Amongst other things, he mentions some chest pains. His symptoms are a bit vague and non-specific. He’s been having them for 6yrs. They don’t sound cardiac, but he has a history of IHD.
He’s not a fit man, but on the other hand, he’s not clinically unwell today.


A long with his known IHD and CKD5, he’s also pretty immobile from his osteoarthritis and obesity. He seems a bit breathless today.
You think this could be anything….! He has a lot of potential problems.


You note from his recent annual review blood checks that he has chronic stable anaemia (Hb10.5ish for many yrs) secondary to his CKD. His renal function is stably poor (eGFR is 10-12).

Lets look at the ECG methodically and see if it helps. All ECG’s can be analysed with a few simple rules. If in doubt, just describe what you see.



The rate has already been calculated for you at 52bpm. If not a quick ready reckoner is as follows: 
For regular rhythms: Rate = 300 divided the number of large squares between 2 complexes. 
For irregular rhythms: Rate = The number of complexes in 30 large squares (ie

6 seconds) multiplied by 10 

Comment – Is this a regular or an irregular rhythm? 
It’s regular. Best seen by studying the QRS complexes in long lead II in this case. 
If there is no rhythm strip on a 12 lead ECG, you may only have 3 complexes to study. If so, regularity can be very difficult/impossible to determine. 

Are there any P waves? Are they obvious – or perhaps hidden in other waves, or non-existent? How do they appear (Morphology? Orientation? Size?) Do they have a consistent appearance? Do they have a consistent relationship with the QRS? 
I can just to say see P waves in the chest leads v1-6 but they are subtle! Because of poor quality baseline, I can’t see them in the limb leads or rhythm strip. (It may be impossible to see on your social media device – may need to zoom in or print a large copy) 
(Cheats tip: If you’re not sure about seeing complexes – get a repeat ECG with the ‘gain’ increased to magnify the complexes. This is the second ECG I took on this man – you may have noticed the comment on the top right of the ECG: “non Standard lead gain”). 
On his standard ECG I couldn’t be sure if he had P-waves or not. If there were no P-waves, then this would be a ventricular escape rhythm ie. No atrial activity seen, and the ventricles have helpfully responded by setting up their own pacemaker focus somewhere within them. 
Of the few P-waves we can see, their shape is uniformly round. They appear to be upright in V1 but possibly inverted in v2-6. Not important for purposes of this lesson. 

The P-waves we can see appear to have a consistent relationship with the following QRS complexes, HOWEVER, this is prolonged… 
The normal PR interval (start of P wave to the first deflection of the QRS complex) should be 3-5 small squares (0.11 to 0.20 seconds). In this case the PR interval is between 8-9 small squares. (>0.32 seconds) 


QRS Complexes. 
Now we need to study the QRS complexes.
We’ve already decided they are regular.
We can’t really comment on the size, because we now know that the gain has been increased. So there’s no point thinking about LVH on this ECG. 
We can consider their shape. Are they consistent in all leads? What about their orientation?
Is there any axis deviation? 
(If you need help with calculating axis and normal conduction orientation, then refer back to link on previous #ECGclass – or search “ECG Teacher-Axis video” on You Tube!) 
What is their duration?
(A normal QRS complex should be no wider than 1 and half to 2 and half small squares (0.06 – 0.11 seconds). 


In a heart with a healthy conduction system, once the impulse passes through the AV node, it travels through bundle of His, and down the Left and Right Bundle branches. As long as there is no delay in this conduction, this gives rise to a narrow QRS complex (less than 3 small squares). 
If, however, after the impulse reaches the Bundle of His, there is any delay in the conduction, through either the Left or Right bundle branch, then the QRS complex will be widened. 

LBBB usually gives rise to a wider QRS complex than RBBB. In LBBB, the width of the QRS is > 120ms (MORE than 3 small squares) whereas RBBB is often ≤ 3 small squares.

LBBB = Left chest leads (I, V5 and V6) show RSR pattern (remember: WiLLiaM 
RBBB = Right chest leads (V1 and 2) show RSR pattern. (remember MaRRoW) 

If we go back to the ECG in Case 4, we notice that the QRS complexes are slightly broad, with RBBB formation. 


But, that’ s not all….

If you have successfully worked out the cardiac axis, you will also see that there is 

Left Axis Deviation here. RBBB alone would not normally alter the cardiac axis. 
Two common causes of LAD are:
1. Left ventricular Hypertrophy 

2. Inferior MI
3. May be normal variant in obese or stocky habitus

A none of these situations apply here, so we know something else must be going on. 

The Left Bundle branch divides into two – the Anterior fascicle, and the Posterior fascicle. If both fascicles are blocked, then it becomes a full LBBB, but if only one fascicle is blocked, this is known as a “Hemiblock” or “Fasicular” block. 

A Left Anterior Hemiblock (Left fasicular block), will always cause a LAD. 
If you ever see RBBB + LAD, on an ECG, then you almost certainly have a LEFT ANTERIOR HEMIBLOCK. 

In fact, he is relying entirely on his small posterior fascicle, of the left bundle branch for ventricular conduction. If that fails him, he’s in trouble. 

Unsurprisingly, an ECHO revealed severely reduced LV systolic function. He needs a full cardiology assessment and consideration for pacing. 

Lesson 7 Summary thus far

Posted Posted in June

Question 1

A 35 year old man presents with palpitations. He has been drinking heavily with friends over the weekend. This is his ECG. Present your findings and give a diagnosis.

Assessment 2-1


Question 2

A 45 year old business man presents with a feeling that his heart is racing. He also has some shortness of breath.

This is his ECG. Present your findings and give a diagnosis.

Assessment 2-2


Question 3

A 75 year old man with a history of COPD presents with fever and increased sputum production. An ECG is taken in the emergency department. What does it show?

Assessment 2-3


Lesson 6

Posted Posted in June

A 22yrs man, previously fit and well, comes to see you holding an ECG.

He explains he is a medical student. He, and few fellow students, were practicing doing ECG’s on each other. He became worried when he discovered the ‘machine analysis’ on his own ECG mentioned a variety of abnormal features.

He denies any symptoms of chest pain/tightness, or palpitations. He has no significant past history, and has never been in hospital apart from a handful of A&E attendances with rugby injuries.

Apart from being a little overweight, with slightly quiet heart sounds, examination is unremarkable.





Clue: Remember, If you are ever baffled by and ECG, go back to first principals, and work through it systematically.

Start with the axis, then the P waves.

What is the axis on this ECG? 

Can you describe the P waves in each lead?


Remember the normal ECG axis?

This ECG unusually shows Right Axis deviation of the P wave (the P wave is Negative in aVL and lead I) and Right axis deviation of the QRS complex (between +90 and +120 degrees).

There is also very low voltage/amplitude  in the precordial leads, V4 to V6 . 
Whilst this could be down to patient habitus impeding the electrical reading, or a pericardial effusion, if this was so you would expect to see low amplitude in all chest leads.

A normal ECG shows ‘progression of the R wave’ in the precordial leads. In other words the relative size of the R wave to the s wave increases gradually from V1 to V5. (V5 is often remains taller than V6 because of the attenuating affects of the lungs).

Look at Lead aVR. It appears more like we would expect lead aVL to look……

In short, voltage and axis deflections are not as we would expect.

This ECG shows dextrocardia.


Classical Features of Dextrocardia on ECG:


  • Right axis deviation
  • aVR often shows Positive QRS complexes (with upright P and T waves) – 
  •      admittedly, not clearly demonstrated in the above example.

  • Lead I: inversion of all complexes, (inverted P wave, negative QRS, inverted T wave)  
  • Absent R-wave progression in the chest leads (dominant S waves throughout), often with smaller amplitude complexes in the left sided chest leads (V4-6)

A similar ECG picture would be obtained in the limb leads, if the Right and Left limb leads electrodes had been accidentally reversed on placement.  If this was the case, the chest leads would still appear normal showing natural progression of the R wave (maximum amplitude in V3-V4).

Lesson 5

Posted Posted in June

A 64yr old lady comes to see you, complaining of breathlessness on minimal exertion over the past 6months. She denies any chest tightness or discomfort.
She has no past cardiac history, and has always enjoyed a healthy lifestyle.
She takes no medication.

Examination in unremarkable. She appears slim and healthy, is normotensive, with a regular pulse rate of 80 bpm, and no murmurs.

You arrange some routine bloods, which are normal, and an ECG. Her serum BNP comes back at 38.

Her ECG is below. The digital ECG machine interpretation reports :

Sinus rhythm
Multifocal ventricular extrasystoles
Run of ventricular extrasystole
Inferior myocardial infarct, age undetermined.

#ecgclass case23


What do you think?

Lets take each of these statements in turn.

Q1.  Is this sinus rhythm? (Can you see P waves, and if so are they regular and associated with every QRS?)

Yes. We’re happy with the machine’s analysis that this is Sinus rhythm, because for every P wave there is a QRS complex.

Q2. Can you see the multifocal ventricular extrasystoles, or the run of ventricular extrasystoles?

  As far as the first statement goes, there are no isolated dysmorphic beats that resemble a ventricular ectopic.  As for the “Run of ventricular extrasystoles” – this is of course, it’s referring to lead V6. But what about this?
Remember, that each ‘column’ on an ECG trace, records the heart rate at the same moment in time for all 3 leads in that column. So the first column simultaneously records the view from the limb leads (I, II and II). The recording will then switch to the second column, which in turn records simultaneous beats in the Augmented limb leads (AvR, aVL, avF). The third column records V1, V2 and V3 simultaneously, and the fourth records V4,V5 and V6.

Whilst the heart rate and rhythm might well change between columns, within each of the columns it should always remain the same.

So, how could a run of VE’s appear in V6 but not in V4 and V5?
It couldn’t!

The only explanation for the anomaly in V6 is artefact. Mostly likely the V6 badge was knocked, or lost contact. We are not concerned about this pattern at all!

Q3.  Is this ECG consistent with an Inferior MI? 

Aha.  We have now reached the real point of this ECGclass.

How often do we see a computer generated report “Inferior infarct cannot be ruled out”  or “possible anterior infarct, aged undetermined”.
This is a very common reason for otherwise well patients, or those with clearly non-cardiac chest pain, to be referred for a cardiology opinion. This can cause unnecessary alarm for the patient.

In short, no, this ECG is not suggestive of an old MI. 
In this lady, once I’d ruled out possible angina (by taking a more detailed history), I’d be looking for other, non-cardiac,  causes of her breathlessness.

So lets talk about Q waves….. 

Pathological Q waves – or not?

When are the Q waves pathological?


A pathological Q wave is a result of absence of electrical activity, following myocardial damage. They generally take several hours to develop after an MI, and usually persist indefinitely.
The exception to this is if seen during an acute MI, but the myocardial tissue is reperfused early by Primary PCI  (Percutaneous Coronary Intervention). The myocardial tissue can then recover, and the pathological Q waves disappear.

To be pathological there are a couple of simple rules of thumb:

  • The depth of the Q wave should be at least 25% of the depth of the associated R wave
  • The pathologically deep Q wave should appear in at least 2 contiguous leads (An isolated Q wave to lead III is a very common normal variant)
  • Any Q wave in leads V1- V3 with a duration of >0.02seconds is likely to be pathological.
  • Many ‘apparently’ pathological Q-waves, often infact have a tiny R-deflection preceeding them – this can be so small it may need searching closely for. (seen in example 1 above).
  • A pathological Q wave may also be broad, in appearance, but again, must be seen in two contiguous leads. 

There are many more detailed criteria suggested for Pathological Q waves, if you are interested, search for either the ESC classification; the Minnesota Code Classification System; or the Novacode system.

Lesson 4

Posted Posted in June

A 40yrs old man comes in to see you in clinic.

He’s complaining of 2 days ‘sharp’ central chest pain, without  radiation. His main complaint is breathlessness, and malaise, following his recent upper respiratory tract infection (URTI) which started 8 days earlier.

On taking further history you discover his pain worse on inspiration, but also on chest wall pressure. At a glance, he looks a little unwell, and has slightly clammy skin.  He’s has no significant past medical history, so you guess he really doesn’t feel very well.

What are your thought?
Which other questions would you like to ask?

Questions people asked answered below:

He’s a slim, muscular, non-smoker, on no medication.

His father had an MI aged 68yrs.

No other family history of IHD or vascular disease.
He’s never had any bloods taken, so his cholesterol is unknown. 
He’s not previously reported/noted any exertional chest discomfort. 

He has had a slight irritant, dry cough since his URTI, but no sputum and haemoptysis, and no history of recent travel.

On examination he’s normotensive, and CVS examination is normal with normal heart sounds and no added sounds. He has a low grade pyrexia and mild tachycardia, in keeping with his reported URTI.
His peripheral O2 sats are 99%. Indeed he has costal tenderness over the anterior chest wall.

He admits he’s worried about his heart.

His history and clinical appearance doesn’t seem suggestive of acute coronary syndrome requiring a 999 admission, so you agree with him to get an ECG, there and then.

Here it is.

Quick check –

  • Is it regular?


  • Can you see P waves? (if unclear in one leads, just check the others – they’re either there or not). If present, quick check – is their morphology normal and consistent? Same for their relationship with the QRS?


  • What about the ST segments? How would you describe them? (Take it lead by lead if necessary)

Yes. It appears to be regular doesn’t it, and despite being slightly tachycardic when you examined him, his rate has settled down to around 60bpm.

P waves can clearly be seen and their morphology looks pretty normal and consistent.  There is a strange scooping seen after some of them – most notably in the inferior leads. Take a look at lead II, III and aVF – see the slight depression of the baseline between the P and the QRS waves. In contrast – this same PR segment looks to be elevated in avR.

So now to the ST segments. There is widespread (non-localised) ST elevation in all but a couple of leads (V1, III and aVR I think are spared?)
The elevation seen might be described as scooped, or saddle-backed.

So where are you at with your diagnosis?
Are there any other tests you’d like to arrange in Primary care?
Or do you think he needs admitting? 


Pericarditis is a cause of ST elevation which often throws us.  As it is an inflammation of the pericardium it can lead to ST elevation in almost all leads. This is an important distinguishing feature from myocardial infarction, which has ST elevation localised to the region of infarct. MI also presents more acutely.

If faced with uncertainty, in patients who are not unwell enough to warrant admission, and in whom the chest pain history does not suggest an acute coronary syndrome, then the most helpful test to support the ECG, is a serum CRP (CRP is rarely normal in pericarditis).

Patients with pericarditis are often younger, with a lingering history of onset of symptoms, and frequently present to GP. (Some are inevitably admitted via the paramedic 999 service, having presented with chest pains and an abnormal ECG).

Key Points:

  • ST segment elevation is widespread across multiple leads (not localised as in STEMIs) and there is no reciprocal ST segment depression
  • Scooped or saddle-shaped ST segments, Often notched.
  • Associated PR segment depression – that is depression between the end of the P wave and the start of the QRS. (usually elevated in aVR).


The chest pain is often associated with viral prodrome – such as a bad cold with aching joints. (Hence inflammatory markers are usually raised)

Longer-lasting symptoms than acute MI.

Pain can be eased sitting forward, and may be worse when laying back.


Sometimes associated pericardial friction rub is noted on auscultation (“footsteps in the snow”).

CRP is usually significantly raised (normal CRP pretty much excludes pericarditis)

ECHO may reveal small pericardial Effusion.

Thank you to all who joined in.