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Monday, 10 December 2012

Complete Heart Block with Narrow QRS escape Rhythm


This ECG educational blog runs alongside Twitter.
A new ECG is launched most Monday nights, in term time. Cases are generally aimed at Primary Care. 

Please use the Hashtag #ECGclass if you want to ask the patient any questions, or request any further investigations. 

Remember there are no right or wrong answers!  ECG interpretation is often open to debate, and will usually evolve as new information becomes available. Everyone's opinion is valid, and useful to others, towards this evolution process. 

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

#ECGclass Case 19
Today's case is adapted from old ECGclass, from the early (pre-blog) days. 
So those of you who were in from the beginning have no excuses! :)

A 74yrs gentleman comes to see you with funny turns. His wife describes him as having brief episodes of transient 'faint-like' attacks, when he seems unresponsive for a moment, and looks very pale. On one occasion he actually collapsed, but came round moments later. 

Obviously - you want an ECG - this is #ECGclass after all!
So here it is:


Q1. Is the rhythm Regular or Irregular? 

Q2. Can you see P-waves? 

Q3. What is the rate? (Atrial? and Ventricular?)

Q4. Does the P-QRS morphology look normal, or abnormal?

Update 1

So far, having answered Questions 1 to 4, you can already make the following comments (Remember the art of ECG bluffing - July blog) :

This is a 12 lead ECG, on which electrical activity can be seen.
The gain calibration is noted and normal, but no paper-speed is noted. For calculation purposes, we will assume standard paper speed of 25mm/sec.

When mapped out, the ventricular rate is regular at 50 beats per minute. (6 large squares between complexes = 300/6). The Atrial rate is also regular at around 85 beats per  minute. (somewhere between 3 and 4 large squares between complexes = 300/3.5)

P waves, which are usually best seen in V1 and V2 , are not clearly seen in these leads, but can be clearly seen in other leads.

Morphology and amplitude:
The P and QRS morphology both appear normal in shape. 

There are large R wave amplitude deflections in Lead I and the chest leads, consistent with voltage criteria for left ventricular hypertrophy (LVH).  The ST segments in the infero-lateral leads, also show typical down-sloping "strain" pattern often seen with LVH. 

The P waves, where seen, are normal in duration (2-3 small squares) and height (<3mm high), and consistency (same appearance throughout). 

That all sounds like quite impressive banter, and not bad at all, considering you haven't even had to plump for a diagnosis yet! 
All you've done so far is 'describe what you see". 

So now let's concentrate on something else...

Q5. What is the relationship between the P waves and the QRS? Can you calculate the PR interval? Does it alter? (Should be 3-5 small squares)

Update 2
The P-R interval does alter, making it impossible to calculate.
As far as I can see the relationship is chaotic. (Has anyone else spotted any pattern that i've missed?)
When there is no relationship between the atrial and ventricular depolaristions, they must occurring independently, from separate pace-maker sites. 
In other words, Atrioventricular dissociation is present.
This ECG shows complete heart block. 

But what about the QRS Morphology?  We've said it's normal. 
This ECG shows a narrow QRS complex escape rhythm. 

The QRS complexes often seen in ventricular 'escape' beats are broad, and oddly shaped in appearance. This is because of the abnormal spread of the depolarisation from the 'make-shift' safety-net pacemaker, as it misses the usual conductive tissue pathways.
If, however, that abnormal pacemaker focus just happens to be very high, close to the original one, and is situated proximal to the bifurcation of the Bundle of His, then it is a junctional pacemaker and the QRS complexes will be close to normal morphology.

The symptoms described by the patient are classical of Stoke-Adams Attacks and result from a sudden drop in cardiac output, and therefore cerebral perfusion. Recovery is rapid when the cardiac rhythm is restored. 
This patient is at high risk of sudden death and should be admitted for a permanant pacemaker insertion.


Complete Heart Block (CHB)Otherwise known as Third degree heart block.


Complete heart block is a potentially life threatening arrhythmia. 
ABCDE guidelines should be instigated in a symptomatic patient and  The Resuscitation Council UK 2010 Guidelines for "Adult Bradycardia" should be followed. 

In CHB the Sino-Atrial node functions normally so atrial contraction is normal, and P waves are present and normal.
But...the electrical impulses are blocked at the Atrioventricular node, so NO beats are conducted to the ventricles. 
To compensate for this, in order to maintain cardiac output, the ventricles are excited by a 'slow escape' mechanism from a depolarising focus within the ventricular myocardium. 

As a result, in CHB:

  • There is no relationship between the P and the QRS waves. 
  • The atrial rate is NORMAL
  • The Ventricular rate is SLOW.   

If you ever see slow QRS complexes without associated P waves, you can generally assume a Ventricular escape rhythm.
The QRS complex is often, but not always, abnormal in shape (for the reasons discussed above).

Causes of complete heart block

  • ACUTE. Myocardial infarction (MI). CHB may also be transiently seen during an MI.
  • CHRONIC.
    1. Fibrosis or scarring around the Bundle of His
    2. A block of BOTH Bundle branches at the same time (i.e. LBBB plus RBBB = CHB)

CHB versus Atrioventricular Dissociation (AV Dissociation)

As discussed above, CHB gives rise to a slow ventricular escape rhythm, and the atrial rate is faster than the ventricular rate.

AV Dissociation which is not due to a complete heart block, sometimes arises during an excessive sinus bradycardia. To compensate for long bradycardic pauses between beats, a faster 'escape' rhythm than the background sinus rate kicks in.  This escape rhythm arises from the AV junction or ventricles. As a result, the ventricular rate is faster than the Atrial rate. ;-)

This rate difference helps differentiate between AV dissociation of excessive bradycardia and Complete heart block. 

Complete Heart Block. In a Nutshell. :)

Enjoy a beautiful Christmas Everyone. 
See you back at #ECGclass in the New year.
Thanks
H. 










#ECGclass Case 19


#ECG Class is an educational blog which runs alongside Twitter.


A new ECG "quizz" is launched most Monday evenings, in term time. 
Cases are generally aimed at Primary Care. 
All scenarios are completely fictitious and theoretical, 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! :-)


#ECGclass Case 19

Today's case is adapted from old ECGclass, from the early (pre-blog) days. 
So those of you who were in from the beginning have no excuses! ;)

A 74yrs gentleman comes to see you with funny turns. His wife describes him as having brief episodes of transient 'faint-like' attacks, when he seems unresponsive for a moment, and looks very pale. On one occasion he actually collapsed, but came round moments later. 

Obviously - you want an ECG - this is #ECGclass after all!
So here it is:



Q1. Is the rhythm Regular or Irregular? 

Q2. Can you see P-waves? 

Q3. What is the rate? (Atrial? and Ventricular?)

Q4. Does the P-QRS morphology look normal, or abnormal?



Update 1

So far, having answered Questions 1 to 4, you can already make the following comments (Remember the art of ECG bluffing - July blog) :

This is a 12 lead ECG, on which electrical activity can be seen.
The gain calibration is noted and normal, but no paper-speed is noted. For calculation purposes, we will assume standard paper speed of 25mm/sec.

When mapped out, the ventricular rate is regular at 50 beats per minute. (6 large squares between complexes = 300/6). The Atrial rate is also regular at around 85 beats per  minute. (somewhere between 3 and 4 large squares between complexes = 300/3.5)

P waves, which are usually best seen in V1 and V2 , are not clearly seen in these leads, but can be clearly seen in other leads.

Morphology and amplitude:
The P and QRS morphology both appear normal in shape. 
There are large R wave amplitude deflections in Lead I and the chest leads, consistent with voltage criteria for left ventricular hypertrophy (LVH).
The P waves, where seen, are normal in duration (2-3 small squares) and height (<3mm high), and consistency (same appearance throughout). 

That all sounds like quite impressive banter, and not bad at all, considering you haven't even had to plump for a diagnosis yet! 
All you've done so far is 'describe what you see". 

So now let's concentrate on something else...

Q5. What is the relationship between the P waves and the QRS? Can you calculate the PR interval? Does it alter? (Should be 3-5 small squares)

When you've had a go,  you'll find the full discussion on the next blog!
Thank you. :)

Monday, 3 December 2012

Sino-Atrial Node Dysfunction and Sino-Atrial Block


This ECG educational blog runs alongside Twitter.
A new ECG is launched most Monday nights, in term time. Cases are generally aimed at Primary Care. 
Please use the Hashtag #ECGclass if you want to ask the patient any questions, or request any further investigations. 

Remember there are no right or wrong answers, and everyone's opinion is valid. 
Do feel free to join in, but most important of all, have fun! :-)

Case 18

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.

You obtain the ECG below:




Q1 What's going on?
What is the rate?
What is the rhythm?
Can you see P-waves?
Anything else you want to know?

Please use the hashtag #ECGclass for any thoughts and questions.
Updates coming later.

Update 1
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?


Update 2
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.


Update 3
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.
Just one more #ECGclass before the Christmas break. :)
H.






#ECGclass Case 18


This ECG educational blog runs alongside Twitter.
A new ECG is launched most Monday nights, in term time. Cases are generally aimed at Primary Care. 
Please use the Hashtag #ECGclass if you want to ask the patient any questions, or request any further investigations. 

Remember there are no right or wrong answers, and everyone's opinion is valid. 
Do feel free to join in, but most important of all, have fun! :-)

Case 18

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.

You obtain the ECG below:



Q1 What's going on?
What is the rate?
What is the rhythm?
Can you see P-waves?
Anything else you want to know?


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?
Would any other investigations be helpful here?


Update 2
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.


When you've had a go,  you'll find the full discussion on the next blog!

Tuesday, 27 November 2012

The NICE Chest Pain Guidelines


The NICE Chest Pain Guidelines.

There is a lot of understandable confusion over the NICE chest pain guidelines.

It is true that when the 2010 guidelines were first launched, they created quite a stir, even amongst cardiologists, who struggled to agree on their interpretation.

Possibly, the biggest mistake NICE made, was to launch the "Management of New Onset Chest Pain Guidelines" almost 18 months before they updated the  "Management of Stable Angina" guidelines. These two guidelines are clearly designed to be interpreted in conjunction, and this delay led to considerable confusion.

The second mistake, was not to recognise the importance of 'prognostic' information in patients with angina, such as can be gained from an exercise ECG.


To clarify - there are two relevant Guidelines which need to be considered in conjunction.

1.  The Management of Chest Pain of Recent Onset - CG95 March 2010

2. The Management of Stable Angina CG126 - Updated July 2011

Diagnosing Angina

The first guideline (CG95) is all about diagnosis, in a patient presenting with new onset chest pain.

Pages 1-9 deal mainly with "unstable" chest pain (such as may occur at rest, without any triggers) and is suggestive of Acute Coronary Syndromes, and the management thereof.
Pages 10 onwards, deal with the management of newly presenting, but "stable", chest pain - i.e. the patient is well at the time of presentation and the symptoms are often predictable, short-lived and well-tolerated.  This is the section we will deal with here.

The guideline stresses that in many cases, a diagnosis of angina can be made clinically.
In these circumstances, exercise ECG's are not required to make the 'diagnosis'.  So, for example, those with classical symptoms, and a Coronary Artery Disease risk (CAD risk) likelihood of  >90% don't need further diagnostic tests. You can be pretty confident that they have angina.
But...The guidelines fail to point out, that an Exercise ECG can offer very important prognostic information, and help stratify that risk. For example, an exercise tolerance of >6 minutes of the Bruce protocol, before being limited by pain or ST changes, puts a patient with angina in a very good prognostic/low risk group.

According to NICE CG95 (The Management of Chest pain of recent onset) a diagnosis of angina can be excluded if the pain does not fulfil any of the following 3 criteria:

1. A constricting discomfort in the front of the chest, neck, shoulders, jaw or arms
2. Precipitaed by physical exertion
3. Relieved by rest - or GTN if tried - in under 5 minutes.

NICE goes on to define:
  • Typical Angina - as a pain which fulfils all three criteria (3/3)
  • Atypical Angina - as a pain that fulfils two of the three criteria (2/3)
  • Non-Angina - as a pain that fulfils one, or none, of the criteria. (0-1 /3)
The management of patients who only fulfil 0-1 of these criteria, no longer needs to follow the above guidelines. In other words, a pain which is "continuous or prolonged at rest, unrelated to activity, aggravated by breathing, or associated with other symptoms" is unlikely to be angina, and other causes should be considered.  

If 2 or more of these criteria are fulfilled, then we should go on to calculate a % CAD risk score (see below) to tell us the likelihood that this patient's symptoms are the result of significant underlying coronary disease.  Usually, this risk assessment is calculated at the RACPC, where patients can then be directed onwards to the most appropriate investigations. 

The RACPC

There are two common conditions worth mentioning, which often pop up at the RACPC as a cause  of chest pain.

Anaemia? 
When referring a patient to RACPC, it's always worth checking their FBC, renal function and lipid profile results before they get there.  Nothing more awkward than a patient arriving in clinic and looking up their FBC to find an Hb on 7g/dl and explaining that is the cause of their chest pain and no further cardiac tests are indicated.  

Aortic Stenosis?
Also - always check for murmurs in patients presenting with chest pain.  Aortic stenosis as a cause for angina should not be missed.  The management of this condition is completely different to that of coronary artery disease.  Any murmur should be clearly mentioned in the referral letter so that arrangements can be made for an ECHO on arrival, as part of the assessment. 


At the RACPC, the patient will be assessed with the following considerations in mind

1.  The history
2.  The risk factors
3.  Is the pain angina or not? (If not - what's the cause?) Can the diagnosis be made on clincial grounds, or are more tests needed?
4.  Is there any underlying IHD (if so - what's the prognosis? ) Consider further functional/anatomical tests.
4.  Who should be considered for revascularisation? (based on 3 + 4)

Don't be disheartened, as a GP, if your patient attends the RACPC and is discharged with a diagnosis of "non-cardiac chest pain".  It's not meant as an insult!
Firstly, don't forget, as GP's we have under 10 minutes to take a detailed history, examination, check risk factors, arrange tests, consider all the implications, share all that with the patient, and finally, read code every aspect of the consultation.
In the RACPC, the clinician has team of cardiac technicians, and sometimes up to 45 mins per patient, to establish a detailed history. Also, patient's stories do sometimes change! (Tell me about it - I have seen that with my own patients, whom I later felt embarrassed to have referred when assessed again by myself at RACPC!).

Secondly, The RACPC does have an another important role.  A number of clearly non-cardiac patients, need enhanced level reassurance to enable them to move forward, thus preventing the ongoing psychological morbidity associated with worry. Not to mention, repeated emergency admissions with non-cardiac chest pain.

At the RACPC  a % CAD score is calculated, but only those with chest pain which sounds suggestive of ischaemia.  Based on this score,  further tests of cardiac function are then offered to clarify any uncertainty in diagnosis.

Assessing Risk - What is the CAD risk score?

The CAD risk score estimates the percentage of people estimated to have Coronary Artery Disease according to age, sex, risk factors and typicality of symptoms.

Once the risk is assessed, the CAD score table (provided in the NICE guidelines) is used to assess the PRE-TEST likelihood of CAD.  A web-based alternative to using this numeric CAD scoring chart has been kindly provided by Dr Mark Dayer of The West Hertfordshire Hospitals:  Coronary Risk Assessment Dukes Score .
This on-line Tool is so quick and easy to use, most cardiologists find it far preferable to the numeric chart. 

  • If CAD risk <10% - Easy. Consider other causes of chest pain, or, if symptoms are classically angina, then consider other (non ischaemic) causes of angina  e.g. HOCM
  • If CAD risk >90% - Easy.  The guidelines state "Treat as stable angina without need for further diagnostic tests".  In other words, you've successfully made the diagnosis clinically, and continue to treat in accordance with the NICE Management of Stable Angina Guidelines (CG127).    True.  But they may still benefit from a prognostic test (see below).
  • If CAD risk is between 10-90% then other diagnostic tests many be indicated. This section is then divided into 3 further sub-groups. (see below)

For %CAD risk is between 10 and 90% The patients are subdivided into 3 groups:

          CAD risk 10-29%  - Offer CT calcium Scoring
          CAD risk 30-60%  - Offer non-invasive functional imaging (Stress ECHO/MIBI etc)
          CAD risk 61-90% -  Offer angiography, if acceptable, and if PCI is being considered.

This is not rocket science. Anyone can calculate the CAD risk score. True, if a GP has a confident grasp of the chest pain guidelines, and has open access to all the available cardiac imaging tests, then perhaps they could confidently manage all patients appropriately without the need to refer, until surgical intervention is required.  In reality, I don't think many GP's have open access for these tests, nor have the time or resources to take on this role from secondary care.

Arguably, those patients who would not chose to accept any surgical intervention, if offered, (PCI or CABG), and are well controlled on medical therapy, don't really need referral either. Like any health discussion, this is a decision which needs to be taken together, with their GP, after appropriate counselling and knowledge-sharing. It may be an entirely reasonable choice.
Would you want an angiogram/PCI even if all your symptoms are controlled on medication?
Some will. Some won't.


A word of note. The CAD % risk is a predictive score only. 
(It is based on a small research study of only 1030 patients between 1983 and 1985, at Dukes University Medical Centre, USA.  Of the 1030 patients, 168 underwent Angiography.)

What's more, the NICE risk score does not include other factors such as HDL, FH and ethnicity and in many ways this is disappointing. 


So Why Do An Exercise ECG?

NICE Say: "Do not use an exercise ECG to diagnose or exclude stable CAD"

But ... nothing stops us from choosing to use it once we've made a clinical diagnosis, yet want some prognostic information.


ETT are useful to
  • Assess or trigger symptoms (arrhythmias, valvular heart disease)
  • Assess exercise capacity
  • Provide prognostic information - e.g for DVLA
A sensible report from the RACPC might read something like this:

"Thank you for referring this 49yrs gentleman with a clinical diagnosis of atypical angina (i.e. Short-lived constricting left chest and arm pain, which has an inconsistent relationship to exertion). He managed 9 minutes of the Bruce protocol today before developing symptoms. There were no ST segment changes. If he does indeed have angina, today's test puts him in a good prognostic group. 
I note his various risk factors for IHD. 
His CAD risk score calculated  today is 45%.  In accordance with NICE guidelines, to help clarify the diagnosis, we will arrange another non-invasive test of cardiac function, such as a stress ECHO, and write with the results. 
In the meantime, he has been advised about lifestyle choices and the use of GTN/999 for prolonged symptoms".

Who needs Intervention?

Once angina has been diagnosed, the second guideline, Management of Stable Angina (CG126) comes into play.

According to NICE CG126, if a patient on optimal therapy (Note: This is defined as being on only one, or two, anti-anginal medications) and is still getting symptoms, then further intervention (PCI or CABG) should be considered.
So - even if you confidently diagnose Angina clinically in GP land, and start a beta-blocker of your choice -  unless symptoms are completely controlled, they may still need some further input via the RACPC.

In practice, when patients arrive at RACPC with classical ischaemic symptoms, they have often already been started, quite appropriately, on anti-anginal therapy by their GP. The RACPC therefore, is already in a position to consider if their symptoms are well controlled on treatment, or if further intervention may be required.

So, in summary, The Acute Trusts should not be selling all their Treadmills.  Not just yet anyway.

Simple?

Hope that helps, and that I haven't confused everyone even more.
H :-)


Acronym Guide:
NICE National Institute of clinical excellence
CG Clinical Guideline
ACS Acute Coronary Syndrome
CAD Coronary Artery Disease
RACPC Rapid Access Chest Pain Clinic