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Wednesday, 27 November 2013

Autumn5 - Hypercalcemia and the ECG

Autumn Term Case 5

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

You get as much history as possible from the daughter. 
This is an 80 yr old lady who is new the Practice, 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 a paramedic ambulance. 
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. 

The paramedics arrrive and start preparing to take her to hospital.
They do a 12 lead ECG before loading her into the ambulance:

ECG courtesy of M.Hammond

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
If you want to read more about junctional escape beat and rhythms click here

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 (thanks to Mark Hammonds @almalydan for providing, and teaching me, this!)  : 

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. 

Thank you. :)

Wednesday, 13 November 2013

Autumn4 - Full discussion

'Keeping  ECGs Simple' is an educational blog which runs alongside Twitter.

A new ECG case "quizz" is launched most Wednesday evenings in term time, via @ecgclass, and a conversation/discussion around the case evolves on #ECGclass during the course of the evening. Don't forget the follow the hashtag for the updates during the course of the evening!

Each term will be divided into 5 'classes' or 'cases' to discuss:



Cases are generally aimed at Primary Care.  All scenarios are completely fictitious, but based on commonly occurring presentations in General Practice. 
This is an educational site, intended for healthcare professionals and shouldn't be construed as patient advice. 

Please use the Hashtag #ECGclass on Twitter, if you want to ask the patient any questions, or request any further investigations. Alternatively, please join in discussion and leave comments below.

Remember there are no right or wrong answers!  

ECG interpretation is often open to debate, and will usually evolve and change as new information becomes available.  Everyone's opinion is valid, and useful for others, as the evolution process takes place.  Together we will try and form an interpretation based on the trace, and information, we have in front of us.  Don't worry if you disagree - shout up and share your thoughts - the diagnosis is often arguable on the basis of a 12 lead trace, and may only become more obvious when a longer rhythm strip is available. 

Please feel free to join in, but most important of all, have fun! :-)
So here goes.

Autumn Term (AT) Case 4 

A 88yr old lady comes in to see you. 

She complains that she's been getting more and more breathless recently. This seems to have been getting worse over several months, but now she's find it a struggle to do her housework without feeling quite exhausted.

You note from her records, that she has a history of an 'old MI' some 20years ago (diagnosed clinically and managed medically), but since then she has been very well, and symptom free. She denies ever having any chest discomfort. She has no family history of early IHD and although she smoked as a young adult, stopping in her late 50's. 

She diligently takes her secondary prevention in the form of aspirin and statin, but 20yrs ago, she was not offered a beta-blocker or an ACE-inhibitor. 

On examination, her pulse is irregular.
A manual BP is 128/76 and her heart sounds are normal with no murmurs or basal creps. She has no oedema anh her JVP doesn't appear to be raised.
Respiratory examination is normal with no wheeze, and normal peak flow.

Recent annual bloods for CHD monitoring were all normal, including U&Es, eGFR, glucose, TFTs and FBC.  

In view of her symptoms and irregular pulse, you decide to ask the practice nurse to do an ECG there and then:

This ECG throws up a few different things.

Toether, we need to come up with a next stage management plan, and perhaps some possible diagnoses.

So let's start simple as usual.

Q1.  Is it Regular?  What's the Rate?  Can you see P waves?

Q2.  Focussing now on the QRS complexes.  What do you think of their amplitude? Duration? Orientation? 

Q3. What about the T waves?

Q4. What is the axis on this ECG?


Update 1. Rate and rhythm

This is an irregular rhythm. 

Remember how to calculate the rate of an irregmular rhythm? Assuming standard paper speed of 25mm/sec, then count the number of complexes within 30 large squares (ie 6 secs) and multiply by 10. Taking the long lead II on this trace, there are about 7 complexes between 30 of the larger squares (depends slightly from which end you start measuring!) but the approximate rate is 70 bpm.

P waves are ceratinly not easy to see if at all, and there is no regularity to the irregular rhythm. By definition, this is AF. 

Update 2.  QRS

Voltage amplitude first.
In leads I and aVL, the amplitude of the R wave, meets the Voltage criteria for LVH. An ECHO would be needed to confirm this. The QRS amplitude in the precordial leads is normal, but this doesn't rule out possible LVH as these leads are more affected by body habitus, and apparent voltage amplitude can be reduced by anything that comes between the electrical impulse and the electrode (excess air, fat, fluid etc. in the thorax). 

The duration of the QRS complexes all appear within normal limits (0.06-0.11ses, or 1-5 to 2.5 small squares)

Q waves
The deep Q waves in leads III, aVF, V1 and V2 look pathological, and would ceratinly be consistent with a history of old MI. 

Update 3.  T waves

T waves are normally upright in all leads except V1 and aVR. 
(It is not uncommon, for T waves to be negative in lead Lead III also).

In this ECG The T waves are inverted in leads I, avL, V4, V5 and V6, with a biphashic pattern to them in V-3. This may suggest ischaemia 

Update 4.  Axis.

What is the axis?  

Look at the limb leads only and choose the most isolecetic lead. In this case, lead II.
To record an isoelectric trace, the impulse in lead II must be travelling at right angles to the cardiac impulse. (Any doubts about this, the refresh your axis knowledge with the Cardiac axis for 4yr olds)

Now, if you grab your ready made axis-ready-reckoner which we all keep in our pockets, look and see which lead the impulse must be travelling along (ie which lead is at 90deg right angle - to lead II?)

Yep.... It's travelling along avL.

But which way? 

Well, if the cardiac impulse was travelling towards aVL - the QRS deflection in Avl will be +ve; and if it's travelling away from avL - the QRS defelction in aVL will be negative. So which is it?

Yes - QRS is positive in lead aVL on this ECG so we now know that the cardiac impulse travelling along the myocardium towards aVL.  

All you have to do now is look back at the diagram and read off the axis associated with that direction = -30 degrees. (Just to say within normal, quite leftward, agreed, but normal).

So in Summary, this ECG shows:

1. AF 
2. Old MI 
3. Inverted T waves 
4. Possible LVH  - will be confirmed at ECHO. 

At this stage management needs to be a balance of timely accurate diagnosis, and symptomatic control. 

Q 5How shall we manage this lady in the next few days/hours?

Update 5 - Management

  • Think Stroke Protection first and foremost, and get her anticoagulated! (Consider adding oral anticoagulation for CVA protection, to her antiplatelet regime for her IHD protection. see below.)
  • Think QOF register second ;) 
  • Her rate control is reasonable, but a small dose of beta-blocker might be a wise choice (see below). She's obviously quite a busy 88yr old and we don't know what her rate does on exercise. 

Heart Failure?
(Old MI + new onset breathlessness) 
  • Assume LVSD until proven otherwise - in any patient with previous MI, and suspicious symtpoms of heart failure, Refer to Heart Failure team for urgent ECHO within 2 weeks. (but see below comment also).
  • You could do a serum BNP, but this should not delay referral for urgent ECHO. Interestingly, the ESC guidelines place almost equal emphasis on the role of the ECG and serum BNPin heart failure diagnosis. The ECG not only identifies potential causes of heart failure, but is also necessary for treatment decisions, eg rate control and anticoagulation for AF, or pacing for bradycardia. A normal ECG makes LVSD unlikely (negative predictive value of 98%).
  • Consider adding furosemide for symptomatic benefit in the meantime.
  • Keep ACE in mind, for next step treatment.

(SOBOE + Inverted T waves) 

  • RACPC referral? We need to keep her possible angina in mind when considering her management. Had this lady presented with more typical anginal symptoms, rather than breathless, a RACPC would have been the obvious most appropriate route. Given both possibilities, referral choice will depend on local pathway preferences and access.
  • Given her AF and apparently stable LVSD a low dose of Bisoprolol (1.25mg) would be a good option to consider. 

The AF is definite. That much we know.

Whilst the LVSD and Angina are both likely, as yet they are unconfirmed.
Treatment and management needs to reflect the symptoms and information we have in front of us. 


Initially, this lady was referred for an urgent (2 week) ECHO. 
However, within 1 week she returned complaining of chest pains on bending and on trivial house work. As her ECHO appointment had not yet arrived, her referral was amended to RACPC, with request for an ECHO on arrival. 

Ar RACPC, ECHO confirmed an old anterolateral myocardial infarct, a mildly dilated left atrium and moderate LVSD.  
There was no significant LVH. 

She went on to have a strongly positive ETT in stage one, with subsequent PCI and stent to a severe stenosis of the Left Anterior Descending coronary artery. 
Given her AF, IHD and PCI+Stent, she was discharged on aspirin + clopidogrel + warfarin (+PPI!) - to a nervous GP! 

Given her AF, she will need lifelong oral anticoagulation therapy, but hopefully her dual antiplatelet therapy would only need be for 3 months post PCI.

Aspirin vs Anticoagulation in peolpe with combined IHD and AF is a  complex therapeutic area. 
The European Heart Rhythm Association (EHRA) have published a Practical Guide on the use of the new oral anti-coagulants in patients with non-valvular AFThe view of EHRA is that stable CAD patients should receive anticoagulants depending on their CHADSVASc score without additional antiplatelet agents (section 12.4 of the guide).  
It is also felt likely that the advantages of NOACs over warfarin, are preserved in CAD patients who have AF.

She was also started on Bisoprolol. :)

Thanks for your time and input. 
Hope you managed to pick up on a few of the points on this ECG! 

Discussion summary will be shared next week on Storify. :)

Wednesday, 23 October 2013

Autumn3 - Digoxin and The Heart

#ECGclass - Autumn Term  Case 3

A "well" 83yrs lady attends surgery for her ‘annual review’. 
As part of this review a routine ECG is done by the practice nurse, which shows the following:

The nurse shows the ECG to the duty GP. 

Q1. What chronic condition is being monitored at her Annual review? 
Q2. What is she taking for this condition?
Q3. What action should the GP take now? 

You note she had her annual bloods taken the week before, in readiness for her annual review with the CHD nurse.   Her FBC, U&E's, Glucose, TFTs were all normal. 

As the nurse had already explained, you re-establish that she feels quite well. She's a relatively inactive 83yr old, who resides in the neighbouring residential home. The staff there haven't noticed any problems.  She tells you her appetite is good, and she denies andy nausea, dizziness, chest pains or breathlessness on routine daily activity, albeit minimal. She's "perfectly happy, thank you very much doctor".  

Examination is unremarkable, other than an irregular pulse, consistent with the ECG. 
She's normotensive with normal heart sounds and no added sounds.


Q1 .

Ignore the funny shaped ST segments for the time being. Start as always, by checking the background rhythm. Are there P waves present? Are the QRS complexes regular? 
As most of you worked out, the answer to both is ‘no”.
This ECG shows an underlying rhythm of AF with a good rate control (around 80 bpm ventricular response). 
The ‘quick’ way to measure rate on an irregular rhythm is by counting the number of complexes in 6 seconds (30 large squares) and multiplying by 10.
In this ECG, looking at the long lead II strip, there are 8 complexes in 30 large squares. So 8x10 = 80bpm. 
So, this lady was attending for her annual AF review. As AF is a precursor to many other cardiac conditions, an annual ECG helpful; but arguable. Annual pulse rate check is bear minimum. 
So far so good. 


This lady is taking Digoxin. 
The ST-T complexes here are “scooping” – consistent with Digitalis ‘effect’. 

For the Digitalis effect, remember Salvador Dali:  

In the Digitalis effect, the ST segments are often likened to a ‘reverse tick” or to shape of Dali’s moustache! Never to be forgotten again. 

The important learning point here, is that the digitalis ‘effect’ does not necessarily mean toxicity...and ECG features can often be seen when digoxin levels are in the therapeutic range. 
So, ECG changes with Digoxin can be either:

1. Therapeutic (Also known as the Digitalis “Effect”) 

  • ST segment depression resembling a ‘reverse tick’
  • Reduced T wave
  • Shortening of the QT interval

2. Toxic
  • T wave inversion
  • Arrhythmias


This lady appears clinically well and denies any untoward symptoms. Given the changes seen on her ECG, we can probably assume that this is simply a digitalis ‘effect’ and no treatment or adjustment to her medication is necessary. It wouldn’t harm to check her Digoxin levels (and while you’re on K+ - just in case!) for reassurance, but this isn’t necessarily essential.
  • In summary - Treat the patient, not the ECG 
    No action necessary. 

    Well done all! 


Foxglove (Digitalis Purpurea) 
Digoxin, derived from Digitalis lantana, was first described by William Withering in 1785. It is sometimes used to increase cardiac contractility (positive ionotrope) and as an antiarrhythmic agent to control heart rate, for example in fast AF. But superior rate-limiting agents, such as beta-blockers, have superseded it’s use as a first-line agent. It’s role remains important in AF associated with heart failure. 

Symptoms of Digoxin Toxicity 
Nausea and vomiting
Diarrhoea and abdominal pain
Visual disturbances, hallucinations and delirium
Severe headache
Almost any dysrhythmia may occur except sinus tachycardia, SVT and rapid AF. 

Below is an ECG after Digitalis overdose, in a very unwell patient with all above symptoms and digoxin levels of 4.7ug/L (Therapeutic range 1-2 ug/L) : 

ECG by kind permission ATurley Via MHammond        

Note the irregular bradycardia, AV block and T-wave inversion. Hopefully, the history and examination would be clues here! 

Thank you! 

Wednesday, 9 October 2013

Autumn2 - Pericarditis

#ECGclass: AT class2

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

He's complaining of 2 days ‘sharp’ central chest pain, without  radiation. His main complaint is breathlessness, and malaise, following his recent URTI which started 4 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. 
You note he's an infrequent  attender, with no significant past medical history, so you guess he really doesn't feel very well. 

What are you thinking?
Any more questions you'd like to ask?

Update i

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)

Update ii

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"). Never heard a rub? Listen here. 
CRP is usually significantly raised (normal CRP pretty much excludes pericarditis)
ECHO may reveal small pericardial Effusion.

For a summary on different patterns of ST elevation you might find this previous blog link useful. 

Once again, thanks to all who took part in tonights discussion, and for all your useful titbits and contributions. . As usual the whole conversation thread will be uploaded onto in the next  week. 

See you next week.
H :)

Wednesday, 11 September 2013

Autumn1 - Electrical Alternans

Welcome back to a new term of #ECGclass!
Hope you've all had a restful summer break, and a big welcome to all all newcomers.

Next week, for the benefit of all the newcomers, we're going to start the new term properly with some back to basics stuff. But first, to whet everyone's appetite, we're going to kick of with something a bit more interesting.....

Autumn Term - Case 1

It's Monday morning surgery and your 4th patient arrives at your door. She's a 30yrs old lady who is not well known to you, but at first glance she's visibly unwell. She's breathless at rest. 

Before she came into the room, you'd scanned her medical notes. No significant past history. No asthma. Her only attendances have been to see the practice nurse for the contraceptive pill. Her BP has always been fine and she's had no children. She's a slim, non-smoker. 

She tells you that she been very breathless on trivial exertion over the past couple of weeks but this has been steadily getting worse. Over the last 24hrs, she has become breathless at rest. She's also feeling dizzy and faint. Overnight she's been troubled by a tight pressure discomfort in her chest and has had to sit up all night to get comfortable.  She's been feeling generally more tired than usual for the past few weeks, such that she had been thinking about coming to see you, but little else to report. She denies any cough or prodromal illness.

On examination she's quite tachypnoeic with a peripheral Oxygen saturation of 97%. Her lung fields sound clear, but quiet.  She's has a tachycardia and her pulse feels weak. Her heart sounds are muffled. Her BP is on the low side, at  90/56, but her systolic is usually only around 100mmHG. 

You are quite concerned, and want her admitting for an urgent CXR. 
She certainly isn't well enough to travel by herself, so you arrange an urgent ambulance admission, to collect her from surgery.  When the paramedics arrive they do a 12-lead ECG whilst preparing her for the journey:

ECG provided with thanks to M.Hammond

Let's take it step by step...

Q1. What is the rate?

Q2. Are there any P waves and are they regular?  (Are they uniform and consistent?)

Q3. Are the QRS complexes seen? Are they of normal, narrow morphology? Are they uniform and consistent?

Q4. Are there any ST changes associated with her tight, nocturnal chest pressure discomfort?

Q5. Does the ECG help you predict what the CXR will show?

As usual please use the hashtag  #ECGclass  to tweet and questions, or thoughts, so that we can all share in each others thinking, and hopefully link the conversation in a summary at the end. :)


The ECG shows a regular sinus tachycardia with a rate of just over 100 bpm.

The P waves are present with normal consistent morphology and a normal PR interval.

There are no diagnostic ST segment changes.

But take a close look at the QRS complexes.
Yes they are of normal, narrow morphology, and follow each P wave, but note how within a single lead view they change in amplitude? (Seen perhaps most clearly in Leads II, III and V5).
This shouldn't happen.  How could it?  What determines the amplitude of the QRS?
Well, two things we know play a role in QRS amplitude are ventricular muscle mass (LVH) and thoracic impedance (body habitus) - neither should change beat-to-beat.

The ECG above shows Electrical Alternans.

Basically, in electrical alternans, the QRS amplitude - or even axis - alternates between beats.  This is seen in cardiac tamponade and severe pericardial effusion.  This results from changes in the ventricular electrical axis as the heart just 'swings' and wobbles about in a fluid filled sac.

Below is an example of the QRS complex not just changing amplitude - but it completely changes axis from one beat to the next (see leads V3, 4 & 5):

Image thanks to


The 30yr in the case above, has basically presented to you in heart failure.

She would have likely had a raised JVP and pulsus paradoxus if you'd checked, too.  You might have heard a pericardial friction rub (scratching noise, heard best on expiration with the patient sitting upright a forward). On arrival at hospital her CXR is likely to show a large globular cardiac shadow.

Thoracic malignancy, or potentially treatable infectious causes, of pericardial effusion need to be searched for as a matter of urgency in this lady. The commonest cause of malignant pericardial effusions is metastatic lung cancer in men, and breast cancer in women. Other causes of malignant pericardial effusions include haematological malignancies such as Leukaemia, Hodgkins, and non-Hodgins lymphoma. Infectious causes include HIV, TB, Cocksackie A and B and Hepatitis, amongst a whole host of other bacteria and parasites.

In the setting of the GP surgery, the ECG wouldn't necessarily have been the first test that would spring to mind here.  The diagnosis would have been made by CXR and subsequent ECHO.  Had the presentation been less acute, and admission not required, the ECG may have helped clinch things.

Well done all - and thanks for all your input.
Hope you found it interesting.

See you next week. :)

Welcome to #ECGclass Autumn Term 2013

Autumn Term 2013

Welcome back everyone to another term of interactive ECG learning. 
I hope you've all enjoyed the unusually long hot summer and feel suitable relaxed and refreshed as we head into Autumn.

Over the the last few months, I'm delighted to welcome many new-comers to the @ECGclass Twitter feed and hope you find it helpful and relevant. 

For the benefit of those who are new, below is brief outline of how the two component sites weave in together. 

1. This blog Forum

2. Twitter Account @ECGclass leading interactive discussion thread under #ECGclass

Keeping ECG's Simple

The aim of this blog is to improve confidence in ECG interpretation, and to encourage more doctors,  GP's in particular,  to 'have-a-go'. We need to keep the art of ECG interpretation alive and kicking, and remember always, how unreliable digital machine analysis can be.  
Keep it simple. But safe.

There is already a wealth of excellent blogs and social media outlets, for the more acute-care ECG interpretation (all that really clever stuff ). The intention is to keep this site purely for those every-day-ECG's which are thrown in front of us in General Practice, by our diligent Practice nurses.
Which of those "incidental" ECG's do we need to action?

The blog assumes a basic knowledge about heart anatomy, its conducting system, and the views obtained by a 12 -lead ECG.

So what is #ECGclass all about?

#ECG Class is an educational blog which runs alongside Twitter @ECGclass.
A new ECG "quizz" is launched most Wednesday evenings, in term time.
On alternate weeks, a summary of the previous week's interactive Twitter discussion is archived on for reflection and review (links provided after each case). Of course, the blog is always available for future reference also.  

Cases are generally aimed at Primary Care.  All scenarios are completely fictitious, but based on commonly occurring presentations in General Practice. 
This is an educational site, intended for healthcare professionals and shouldn't be construed as patient advice. 

Please use the Hashtag #ECGclass on Twitter, if you want to ask the patient any questions, or request any further investigations. Alternatively, please join in discussion and leave comments below.

Remember there are no right or wrong answers!  

ECG interpretation is often open to debate, and will usually evolve and change as new information becomes available.  Everyone's opinion is valid, and useful for others, as the evolution process takes place.  Together we will try and form an interpretation based on the trace, and information, we have in front of us.  Don't worry if you disagree - shout up and share your thoughts - the diagnosis is often arguable on the basis of a 12 lead trace, and may only become more obvious when a longer rhythm strip is available. 

Please feel free to join in, but most important of all, have fun! :-)


If you feel confident enough to join in, that's fantastic, but equally its great if you just prefer to watch and learn quietly.

Please feel free to leave any comments on the blog - It's really helpful to know how many people are 'out there', finding this class useful.

Enjoy. :)