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.

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.

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?

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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?

Discussion.
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)

 
Note:
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).

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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.

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.

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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

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).

Symptoms:

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.

Examination/Ix

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.

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Lesson 3

It is Tuesday morning at the clinic and your 6th patient arrives. 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:

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?

Discussion:

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.

Summary.

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.

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.

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A new ECG is launched most Monday and Wednesday 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. 

Remember to use the #pulsemdx

An 82yr old lady is brought to see you by her daughter.
She is complaining of intermittent dizzy spells.
On examination, the lady appears frail, but clinically well. Her BP is good and heart sounds are normal. Her pulse seems a bit irregular, but not fast.

See the ECG below:

The ECG shows a Sinus bradycardia, with a variable rate of around 50 beats per minute. (Remember how to calculate the rate of an irregular ECG?  Count the number of complexes in 6 seconds and multiple this by 10.  Assuming paper speed of 25mm/sec then 6 seconds = 30 large squares).   Now study the Lead II rhythm strip. There are P waves in front of every QRS complex, and the P waves appear morphologically constant and normal; as do the QRS complexes. Every P wave is conducted.   The PR interval is constant, but slightly prolonged (at just over the max. of 5 small squares, or 0.20 secs).   So a First degree AV block is present.   But that’s not all.

You also note a ‘pause’ on the long lead II.  No P wave (and no QRS complex) occurs when expected.  If this pause was interrupted by an odd looking QRS complex, this would be called an “escape” beat originating from an abnormal site within the ventricular wall.  However, no escape beats are seen, and the pause is terminated by a sinus beat.    You are concerned about the ECG and ask a bit more about her dizzy spells.
Her daughter is discloses that she is worried, that on at least one occasion, she thinks her mother may have transiently ‘blacked’ out.

Q2. What are you thinking now?

You decide to get a long lead II rhythm strip to help you:     What do you think of the pauses now?

This looks a bit more sinister. Far more pauses can be seen. The duration of each pause is double the basic R-R interval.   The ECG’s show Sino-Atrial block.   You may want to do ambulatory ECG recording to look for longer pauses (ie. failed conduction of several consecutive sinus beats, which will gives pause durations in multiples of the basic R-R interval). Given this lady’s symptoms of possible blackouts,  she probably needs admitting, or urgent referral, for permanent pacing.   Sino-atrial block is one form of Sino-Atrial Dysfunction, or Sick Sinus syndrome.
Others types include Sinus Pause, Sinus arrest, and Bradycardia-Tachycardia Syndrome.
SA Dysfunction is  a sign of diseased tissue around the sino-atrial node. This may be damage secondary to an MI , or to a degenerative ageing process affecting the node. Although  the sinus node depolarises normally, there is intermittent failure of that impulse being conducted through the atrial tissue.

Summary
The ECG above shows:
1. A Sinus Bradycardia
2. A First degree A-V block
3. A Sino-Atrial Block

Lessons:

1.  Be very suspicious if you ever suspect Sinus Arrhythmia in the elderly.  Sinus arrhythmia occurs with respiration in the young and healthy. The rise and fall of the heart rate is gradual with respiration.  In the elderly, sinus arrhythmia is rare. Study the R-R interval, if the distance is always in multiples of the basic rate, then a Sino-Atrial block is far more likely in this age group.

2.  Look very carefully for P-waves:

Atrioventricular (AV)Heart Blocks

A First degree AV heart block (prolonged PR interval) results when each wave is conducted from the Sino-Atrial node to the ventricles, but something slows it down.

A Second degree AV heart block would be present if all the P waves are normally conducted, but occasionally a wave is not conducted to the ventricles at the Atrio-ventrcular node; nor through the Bundle of His. (i.e. Not all P-waves are  followed by a QRS). 
There are 3 variations of second degree Heart Block:

• Mobitz Type I or Wenckebach (Usually benign)
• Mobitz Type II (may trigger a complete heart block)
• 2:1 or 3:1 Conduction type (May trigger a complete heart block)

A Third degree AV heart block
Atrial contraction is normal, but no beats are conducted to the ventricles.  To compensate, the ventricles are excited by a “slow escape” mechanism, starting from an abnormal focus within the ventricles. Thus the atrial rate is normal, but the ventricular rate is often very slow.
There is no relationship between the P waves and the QRS waves.

Sino-Atrial (SA) Heart Blocks
A Sinus Block occurs when there is complete failure of the sinus node to depolarise the atrium.  
In a sino-atrial block, the P-P interval remains regular (as in above ECG) but an entire PQRS complex will be occasionally missing.

Thank you for your time.

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