89. Wolff–Parkinson–White syndrome Flashcards
A 22-year-old woman is admitted for a routine hysteroscopy. She has a
history of being admitted to casualty six months ago with palpitations.
This is her ECG at the time of admission to casualty. What does it
show?
The ECG shows a supraventricular tachycardia. The rate 190 beats per
minute.
What would be suitable initial management if her blood pressure was
stable?
ABC, oxygen
Check electrolytes (including Mg2+).
Carotid sinus massage.
Adenosine –
caution in asthma and if taking dipyridamole (prolongs half-life).
This is her resting ECG. What does it show?
It shows sinus rhythm at a rate of 74 bpm.
The axis is normal.
The P-R interval is shortened (normal is 110 – 210 ms)
and there are delta waves present.
diagnosis is Wolff–Parkinson–White syndrome.
ventricular complex is predominantly positive in lead V1
suggesting Type-A WPW syndrome.
(Type-B has predominantly negative ventricular complex in lead V1.)
What is the ‘delta wave’?
There is an accessory atrio-ventricular pathway
(formerly called the bundle of Kent),
which conducts the atrial impulse to the ventricles much faster than the A–V node.
This results in the start of ventricular depolarisation sooner than
normal, hence the short P–R interval.
That initial ventricular depolarisation takes place
in normal ventricular tissue (i.e. not specialised conducting tissue).
The initial rate of depolarisation is therefore slower,
hence the slurred, delta wave.
When the rest of the impulse finally arrives through the A–V node, the
specialised conducting tissue continues, the ventricular depolarisation as
normal, so the rest of the QRS complex looks normal.
What are the implications for anaesthesia?
These patients may develop paroxysmal tachyarrhythmias during anaesthesia.
Patients who have a history suggestive of frequent arrhythmias should
ideally be investigated by a cardiologist and put on appropriate therapy.
Those with infrequent episodes may not require any treatment.
What types of arrhythmia do they develop?
There are two common arrhythmias in WPW.
These are atrial fibrillation (AF)
and A-V nodal re-entrant tachycardia.
Atrial fibrillation
Patients with WPW who develop atrial fibrillation are at
risk of very rapid ventricular responses as the accessory pathway does not
provide any ‘protective delay’ like the A-V node. This may result in heart
failure or may even deteriorate into ventricular fibrillation. In AF, most
conducted impulses reach the ventricles via the accessory pathway, so delta
waves are seen on the ECG.
Re-entrant tachycardia
A re-entry circuit is set up. After transmitting an
atrial impulse, the A–V node usually recovers before the accessory pathway.
If an atrial ectopic occurs at the right time, it will transmit through the A–V
node while the accessory pathway is still refractory. By the time it has done
this, the accessory pathway may have recovered and the impulse will then
pass through it back into the atria. As the impulses are all reaching the
ventricles via the A–V node and not the accessory pathway, there are no
delta waves on the ECG.
How would you manage an intra-operative tachycardia?
Treat possible triggers of rhythm disturbance such as hypoxia, hypercarbia,
acidosis, electrolyte disturbance or any cause of sympathetic stimulation.
Assess the degree of cardiovascular compromise
Assess the degree of cardiovascular compromise. If there was significant
compromise, then synchronised DC cardioversion starting at 25–50 J would
be the treatment of choice. If the blood pressure was stable, then the
management would depend on the rhythm.
Pharmacological therapy
Pharmacological therapy: For re-entrant tachycardia, adenosine would be
the first choice. Class 1a drugs such as procainamide (5–10 mg/kg) and
disopyramide prolong the refractory period, decrease conduction in the
accessory pathway and may terminate both re-entrant tachycardia and AF.
More conventional drugs such as amiodarone, sotalol and other
beta-blockers such as esmolol may also be useful
Are there any drugs you should not use?
Verapamil and digoxin are contra-indicated as they both preferentially block
A–V conduction thereby increasing conduction through the accessory
pathway.
Although verapamil could, in theory, be used to terminate a
re-entrant tachycardia, its use is not advisable, because these patients may
then revert to AF or flutter.
A further hazard with verapamil is that a
tachyarrhythmia that looks like re-entrant tachycardia may actually be VT.
Adenosine would preferentially block the A–V node and therefore should
not be used in AF.
