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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. :)