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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