Friday 10 September 2010

MRCP revision battle 7.1: cardiac action potentials

I've got that Friday feeling so I've decided to indulge in a cardiology fest.  Today's revision battles will therefore be:

MRCP revision battle 7.1: cardiac action potentials
MRCP revision battle 7.2: the Vaugham-Williams classification system
MRCP revision battle 7.3: long QT
MRCP revision battle 7.4: adenosine
MRCP revision battle 7.5: cause of the broad complex tachycardia

Now I know that may look like a lot but quite a few of the battles are short and almost sweet, so lets get stuck in!

MRCP revision battle 7.1: cardiac action potentials

Understanding the basics of the cardiac action potential is essential to grasp how antiarrhythmic drugs work.  The basic cardiac action potential looks like this:

                                                                                                            thanks to for the image

In stage 0, there is a rapid influx of sodium
Stage 1 is then an efflux of potassium, followed by
Stage 2, which is an influx of calcium.  Finally in
Stage 3 the efflux of pottasium continues, terminating the action potential.

Try and keep this image in mind as we move on to the fabulous world of Vaughan-Williams classification...

MRCP revision battle 7.2: The Vaughan Williams Classification

The Vaughan-Williams classification is a way of dividing anti-arrhythmic drugs into groups based on their mechanism of action.  It was devised in the 1970s, and like some other inventions of that era (such as flares) it has a few flaws.  The main flaw is that many anti-arrhythmics actually work in several different ways, so although they can be put into a class based on their main mechanism of action this grouping only tells you part of how they work.

However, understanding it a) makes you seem clever (most consultants would have forgotten it within hours of passing MRCP) and b) helps you answer MRCP questions correctly.  So lets ignore its faults and embrace it whole-heartedly...

The original classification had groups I, II, III and IV.  A 'catch all' group of V has now been added for awkward drugs who just didn't fit in anywhere originally.  Lets look at each class in turn:

Class Ia:
  • works by blocking sodium channels - called a 'membrane stabiliser'
  • distinguishes itself from the other class Is by having intermediate association/dissociation with the sodium channels --> end result longer action potential
  • members include disopyramide, quinidine and procainamide

Class Ib:
  • works by blocking sodium channels - called a 'membrane stabiliser'
  • distinguishes itself from the other class Is by having fast association/dissociation with the sodium channels --> end result shorter action potential
  • members include lidocaine and phenytoin

Class Ic:
  • works by blocking sodium channels - called a 'membrane stabiliser'
  • distinguises itself from the other class Is by having slow association/dissociation with the sodium channels --> end result same action potential
  • members include flecanide and propafenone

Class II:
  • are beta blockers 
  • I'm sure you don't really need examples but think atenolol, bisoprolol, misoprolol...

Class III:
  • works by blocking potassium channels
  • this results in prolonged repolarisation
  • members include amiodarone and sotolol

Class IV:
  • works by blocking calcium channels
  • members include verapamil and diltiazem

(Class V: = last minute 'catch all', includes digoxin and adenosine)

Thats rather a lot to try and remember; understanding and linking it to the cardiac action potential makes it a bit easier to understand, then a bit of word-play might clarify things further:

To remember the broad classes of drugs, try recalling 'Sodium Blocks Potassium Channels' (just substitute calcium for channels and you have the 4 mechanisms of action)

To remember the members of each class, think "Double quarter pounder, lemonade please, fries please... and salt uh oh vomiting and diarrhoea..."

Got it?  Good, cos you'll need in for battle 7.3, long QT.

MRCP revision battle 7.3: long QT

The QT interval is that sneaky part of the ECG measured from the start of the QRS complex to the end of the T way.  I call it sneaky as as clinicians we rarely pay it much attention, then it just happens to get a bit on the long side and oh whoopsie we have a ventricular arrhythmia on our hands.

The first thing to learn about the QT interval is that it decreases as heart rate increases.  It is therefore necessary to correct it, which is achieved by using either Bazetts or Fridericas formula.

Bazetts = corrected QT = QT/square root of heart rate
Fridericas = corrected QT = QT/cube root of heart rate

Upper limit of normal is generally taken to be 450ms in a man and 470ms in a woman (for some bizarre reason I remember 450 by singing the song 'brimful of asha on the 45' then just remember that females are 20 more)

There are multiple causes of long QT:

  1. familial
    • Romano-Ward Syndrome (to be covered tomorrow)
    • Jervell-Lange-Nielson Syndrome (also to be covered tomorrow)
  2. metabolic
    • low Mg/Ca/K
    • low temp
    • low thyroid (also known as hypothyroidism.. :) )
  3. drugs
    • class I and III antiarrhythmics (which after the last revision battle you should be able to name)
    • erythromycin
    • TCA/haloperidol/risperidone/SSRIs
    • cocaine
    • organophosphates
    • antihistamines
  4. other
    • MI
    • myocarditis
    • SAH

Treatment is possibly beta blockers, possibly ICD.

Now on to revision battle 7.4, to meet a drug that fell into class V...

MRCP revision battle 7.4: Adenosine

Adenosine is a purine nucleoside which clinically is used to try and terminate SVTs/expose the underlying rhythm.  While doing so it has the potential to cause cardiac standstill, so it can have a unique dual action of increasing the adminstering doctor's heart rate in proportion to how much it decreases the receiving patients heart rate.

It's half life is 8 to 15 seconds, and it works by activating potassium channels which decreases AVN conduction.

The effect of adenosine is increased by dipridamol and carbamezepine.
The effect of adenosine is decreased by aminophylline.

A positive of adenosine is that it has no significant negatively inotropic effects.

Risks associated with its use include:
  • enhancing conduction through the accessory pathway in Wolff-Parkinson-White
  • causing a dangerously fast ventricular response in pre-excited AF/flutter

The side effects include:
  • anxiety
  • chest tightness
  • bronchospasm (avoid in asthma)
  • facial flushing
  • nausea

The usual dosing regime is 6mg, then if unsuccessful 12mg 2 mins later and if still unsuccessful another 12mg 2 mins after that.  Ensure cardiac monitoring is in place when it is given (it can cause cardiac standstill) and remember that given its short halflife it must be given as a rapid bolus, flushed instantly with saline.

So to the final revision battle of the day, with that most feared ECG pattern: the broad complex tachycardia.

MRCP revision battle 7.5: broad complex tachycardia

At some point an ECG will be shoved under your nose which shows an unnerving broad complex pattern going at a fast rate.  If in doubt, these must always be regarded as VT.  However, there are a few less scary possibilities, such as:
  • AF with LBBB
  • orthodromic tachycardic WPW
  • ventricular paced rhythm

Essentially the main call is whether the broad complex tachycardia is superventricular or ventricular in origin, and the features the MRCP exam expects you to pick up on to differentiate these two are:

  • AV dissociation - suggests VT
  • fusion/capture beats - suggest VT
  • positive QRS concordance in chest leads - suggests VT
  • marked left axis deviation - suggests VT
  • history of IHD - more likely VT
  • QRS>140ms - suggests VT
  • no response to adenosine/massage - suggests VT

Well thats if for today.  A quick test of yesterdays topics is available here if you still have the energy.

MRCP questions: War 6

As with previous 'wars' after 'battles' these are just a few quick questions to see if your brain cells have retained the information provided in battles 6.1 to 6.5.

Jot your answers down on a piece of paper then compare them to the answers here

Question 1:
Which HLA is ankylosing spondylitis associated with?

Question 2:
List 5 symptoms/signs associated with acute iritis

Question 3:
What is the correct term for sterile pus in the anterior chamber of the eye?

Question 4:
List 7 infections associated with reactive arthritis

Question 5:
Name and describe a dermatological condition associated with reactive arthritis

Question 6:
What is reiters syndrome?

Question 7:
Define Light's criteria
    Question 8:
    List 5 possible causes of transudates and 5 possible causes of exudates

    Question 9:
    Which 5 causes of pleural effusion would cause a low pH (<7.3)?

    Question 10:
    List 3 associations of yellow nail syndrome

    answers here