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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 :)