3.4 WPW Sydrome Flashcards
What are the causes of palpitations?
- Anxiety
- Exercise
- Panic attacks
- Caffeine, alcohol
- Drugs:
Thyroxine, cocaine, beta 2 agonists
- Drugs:
- Cardiac:
MI, arrthymias, ectopics, AF, flutter, VT, reentry tachyarrhythmia
- Cardiac:
- Endocrine:
hyperthyroidism, hypoglycaemia, phaeochromocytoma
- Endocrine:
Why do arrthymias occur?
- Reentry circuits
- Enhanced automaticity
- Triggered activity
What investigations would you
like her to have?
- History and examination is paramount
- ECG: 12-lead, 24-hour, ambulatory
- Cardiac electrophysiological study
- Bloods, to rule out endocrine causes
Figure 3.2 illustrates her ecG.
comment on the positive findings.
What is the diagnosis?
Rate: 75/min
Sinus rhythm
Normal axis
PR interval: 3–4 small squares (not very short)
Initial slow upstroke of QRS but later becomes normal complexes
Presence of delta waves
explain to me what Wolff–Parkinson-White (WPW) syndrome is.
- Presence of faster accessory pathway
(bundle of Kent)
between atrium and ventricle
(accessory AV pathway)
- Presence of faster accessory pathway
- This pathway conducts impulses
faster than the normal AV node
- This pathway conducts impulses
- Electrical signals traveling down
this abnormal pathway may stimulate
the ventricles to contract prematurely,
resulting in a unique type of
supraventricular tachycardia
- Electrical signals traveling down
What are the characteristics of ecG in WPW?
- Sinus, normal axis, short PR interval
- Presence of delta waves
What is a delta wave?
- Accessory pathway conducts impulse faster than AV node,
resulting in short PR interval
- Accessory pathway conducts impulse faster than AV node,
- The initial depolarization takes place
in ventricular muscle;
hence, the slow and slurred delta wave
- The initial depolarization takes place
- Later, when the impulse arrives at the AV node,
bundle of His and
Purkinje carries the impulse,
which is normal and faster than ventricular
wave; hence, the rest of the QRS is normal
- Later, when the impulse arrives at the AV node,
What are the treatment options for patients with WPW syndrome?
- Risk stratification to exclude patients
who are at risk of sudden death.
This is done with the presenting symptoms of syncope,
etc., and with invasive electrophysiological studies
- Pharmacological therapy for stable
tachyarrhythmias and cardioversion
for decompensated patients - Drugs:
Commonly used drugs are amiodarone and procainamide.
Some avoided
- Ablation:
Definitive treatment is by
radiofrequency ablation of the
accessory pathway
What drugs are contraindicated WPW
Drugs such as
- adenosine,
- diltiazem,
- verapamil,
- beta blockers
are avoided due to the risk of slowing the heart’s normal conduction and favouring accessory conduction leading to unstable dysrhythmias
What are the implications of WPW for anaesthesia?
- There is a tendency to
paroxysmal supraventricular tachycardia in the
perioperative period and
there may be associated congenital cardiac abnormality
- Unmasking of WPW syndrome
under either general or regional anaesthesia
has been reported,
which means the patient was asymptomatic
with normal ECG preoperatively and
under anaesthesia re-entrant arrhythmia
gets unmasked with clinical symptoms.
- Anaesthetic drugs tend to change the physiology of AV conduction.
If the patient is asymptomatic,
then risk of perioperative arrhythmias is much less.
What are the implications of WPW for anaesthesia?
- General anaesthesia
- Avoid light planes of anaesthesia and drugs
that can precipitate tachycardia
(like atropine, glycopyrrolate, ketamine)
resulting in paroxysmal supraventricular tachycardia
or atrial fibrillation.
- Opioids, such as fentanyl,
and benzodiazepines,
including midazolam,
have been found to have no effect
on the accessory pathway.
- Agents - Induction
There are references showing disappearance
of delta waves after propofol administration,
making it the drug of choice for induction. - Agents - Maintenance
Isoflurane and sevoflurane have been found to have no effect
on AV node conduction,
making these agents preferable
for maintenance of cardio-stability.
- Muscle relaxant
Short acting nondepolarizing muscle relaxant
without histamine release would be an acceptable choice
as reversal of neuromuscular blockade
using neostigmine and glycopyrrolate is not required.
Regional anaesthesia
There is significant advantage over general anaesthesia
as multidrug administration,
laryngoscopic stimulation,
intubation, and light planes
leading to sympathetic stimulation are avoided.
What are the common types of tachyarrhythmias that can develop in the perioperative period?
There are two common life-threatening arrhythmias
that occur in patients with WPW.
- Atrial fibrillation leading to ventricular fibrillation
- Circuit re-entrant tachycardia
causing ventricular or paroxysmal supraventricular tachycardias.
Ventricular tachycardias are very difficult to
treat and may even be life threatening
How would you manage intraoperative tachyarrhythmias?
After taking all precautions, if arrhythmias develop, the patient is treated after
a careful ABC assessment..
Atrial fibrillation
* The treatment principle is to prolong the
anterograde refractory period of the accessory pathway
relative to the AV node.
This slows the rate of impulse transmission
through the accessory pathway and, thus,
the ventricular rate.
This is in direct contradiction to the goal of treatment of
non-WPW atrial fibrillation,
which is to slow the refractory period of the AV node
Paroxysmal supraventricular tachycardia
- Vagal manoeuvres initially
- Haemodynamically stable:
Lignocaine, adenosine, disopyramide, and
procainamide can be used.
These drugs block transmission via the accessory pathway
by blocking fast sodium channel
- Haemodynamically unstable:
Synchronized DC cardioversion at 25–50 J
may be needed for atrial fibrillation.
Digitalis and verapamil are strictly contraindicated in patients
with pre-excited atrial fibrillation or flutter with
rapid conduction over an accessory pathway
Treat possible triggers:
hypoxia,
hypercarbia,
acidosis,
Electrolyte imbalance
