Hello, I'm Gary Dhillon. I'm a board-certified Pediatric Cardiologist
and a current Clinical Fellow in Critical Care Medicine
at the Department of Anesthesiology, Critical Care, and Pain Medicine at Boston Children's
Hospital at the Harvard Medical School. And today, we'll be discussing Wolff-Parkinson-White,
referred to as WPW syndrome, and pearls for the anesthesiologist and intensivist.
I have no disclosures for this presentation. This lecture is purely for educational purposes,
and the information provided in this lecture should not be used as a replacement
for the expertise advice of cardiology, anesthesiology, and intensive care consultations.
The objectives for this talk will be threefold. We will discuss WPW syndrome,
review electrocardiogram examples of this syndrome, and also provide a brief review of
perioperative considerations in patients with Wolff-Parkinson-White. Wolff-Parkinson-White
is due to the anatomic presence of an accessory conduction pathway that allows for reentrant
SVT. This accessory pathway represents an abnormal fibromuscular connection into
the ventricular myocardium and remains after incomplete atrioventricular separation.
The prevalence of this syndrome is 0.1% to 3.1% in the general population,
higher in males. Symptoms in patients with Wolff-Parkinson-White include palpitations,
presyncope, and syncope. It can even include sudden cardiac death.
This syndrome accounts for upwards of approximately 1% of sudden cardiac death
in athletes. This population is at risk for supraventricular tachycardia due to the presence
of this accessory conduction pathway. And the characteristic ECG findings that we'll review
include three main factors-- the presence of a short PR interval, a delta wave,
which is a slurring of the P wave into the QRS, and a widening of the QRS complex.
It's also important to note, that WPW can be associated with specific congenital heart lesions,
which is why one of the important diagnostic workups in this syndrome is an echocardiogram.
Three high-yield CHD lesions that are known to be associated with WPW are Ebstein anomaly, which is
an abnormal development of the tricuspid valve, hypertrophic cardiomyopathy, and L-transposition
of the great arteries, also known as congenitally corrected transposition or ventricular inversion.
In WPW, intermittent pre-excitation on ECG or loss of pre-excitation in a single beat
on exercise stress testing is associated with the presence of a low-risk accessory pathway,
and thereby a low-risk of ventricular arrhythmias, which is why, along with echocardiograms, ECGs,
Holter testing, and exercise stress testing become important as diagnostic workups.
From the standpoint of evaluation of patients either with diagnosed or suspicion for WPW, a very
thorough personal history and family history, as well as physical exam also becomes very important,
alongside diagnostic imaging and ECG workup. Treatments, commonly, are beta blockade for
symptomatic patients, activity restriction in certain population-- i.e., those with concern for
high-risk pathways, and electrophysiologic studies with potential ablation of accessory pathways.
As you can see here, I have provided a characteristic EKG
of patients with Wolff-Parkinson-White. And you can see the three things that are commonly seen
in patients with Wolff-Parkinson-White. First and foremost, you'll see here a short PR interval.
As you can see, unlike normal EKGs, where you generally tend to have a P wave followed by a
return a baseline and then the QRS complex, this P wave blends right into the QRS.
Secondly, that delta wave that, in this EKG, can be seen in the pre-cordial leads and in
lead 1 in particular, you can see that that P wave slurs into the QRS complex.
And then lastly, the widened QRS, which, in general, does vary depending on the
age and size of the patient, with normative values already present in the literature,
and in adolescents and adults would be greater than 120 milliseconds.
Pre-operative considerations in patients presenting for surgeries
who have Wolff-Parkinson-White-- if they are already on anti-arrhythmic treatment,
consider continuing those pre-operatively unless the patient is presenting for EP study,
in which case it may behoove to not continue those anti-arrhythmics because the goal of the
study would be to elicit the abnormal rhythm to identify and map it for ablation purposes.
Anticipate using agents that don't result in stimulation of the sympathetic system,
which we'll discuss more as far as why in the next slide. Confirm the ECG, Holter, and echo
data in patients with Wolff-Parkinson-White pre-operatively, i.e., to identify whether or
not there are associated underlying congenital heart defects that require the clearance
and presence of cardiovascular anesthesiology, and also to consider cardiology and cardiovascular
anesthesiology consultation to determine a safe anesthetic management plan in this population.
Intra-operative considerations-- consider adequate induction doses of anesthetic medications
to suppress the sympathetic response of laryngoscopy. High sympathetic tone in
this population can effectively increase the ability for that accessory pathway to conduct
at faster rates, which can thereby also increase the risk of life-threatening arrhythmias. So
the suppression of that high sympathetic tone during laryngoscopy can become very important.
Propofol can be considered appropriate for use as an anesthetic agent
in Wolff-Parkinson-White for both EP study and non-EP study procedures. Volatile anesthetics
can interfere with cardiac conduction properties. If to be used, isoflurane is preferential,
as it can prolong the accessory pathway refractory period, thereby decreasing tachycardia risk.
Nitrous oxide has not been reported to have adverse events in this population.
Fentanyl and remifentanil can be used safely but can interfere with conduction properties,
while sufentanil has less conduction interference. Etomidate is known to
have cardiovascular stability in patients with WPW. Ketamine, on the other hand,
consider avoiding that medication due to its sympathomimetic effects. Both depolarizing and
non-depolarizing neuromuscular blockers have been used safely in Wolff-Parkinson-White.
However, one must be wary with the reversal of these non-neuromuscular blockades with
neostigmine, atropine, or glycopyrrolate, as they can result in tachyarrhythmias due to
depression of the AV node and facilitating accessory pathway conduction. Sugammadex
can be considered as a reversal alternative when neuromuscular blockade is used.
Monitor intra-operatively also for tachyarrhythmias,
and considering things like having pads available, as well as adenosine.
Considering the use of short-acting esmolol may be beneficial if the patient is high risk
for triggered SVT. And being watchful for the presence of irregular wide-complex tachycardia
in this population is important. And we'll discuss that shortly.
Post-operative considerations include minimizing sympathetic stimulation with
emergence with an airway and considering deep extubation in this population,
monitoring for arrhythmias in the early post-operative period,
and considering observation with telemetry in Wolff-Parkinson-White patients post-operatively.
As we discussed briefly, monitoring for irregular wide-complex tachycardia is important
in Wolff-Parkinson-White, as it could be a finding consistent with pre-excited atrial fibrillation.
If a patient has an accessory pathway that is able to conduct rapidly, that would place this patient
at risk for a life-threatening ventricular arrhythmia. If that patient also has atrial
fibrillation that is conducting down that accessory pathway, the presence of its conduction
down an accessory pathway instead of the AV node will result in a wide QRS. The presence of it
being atrial fibrillation that is conducting down the accessory pathway will result in an irregular
pattern. And that combination will be seen here as an irregular wide-complex tachycardia.
As you can see on this EKG strip, if this were clear ventricular tachycardia,
ventricular arrhythmias tend to be very consistent in their rates,
like a metronome. And this wide-complex tachycardia is not as consistent. Some QRS
complexes have shorter R-to-R intervals than others. And this period, this area in the box,
highlights that irregular wide-complex tachycardia as a sign of pre-excited atrial fibrillation.
This rhythm becomes important, because use of AV nodal blocking agents is not indicated
with this arrhythmia. The blocking down of the AV node could result in rapid one-to-one conduction
of atrial fibrillation down the accessory pathway,
resulting in life-threatening ventricular arrhythmias, i.e., ventricular fibrillation.
Takeaway points for this brief discussion-- Wolff-Parkinson-White is associated with the
presence of a short PR interval, delta wave, and widened QRS. The presence of
this accessory conduction pathway allows for a reentrant supraventricular tachycardia,
predisposing to cardiac symptoms and ventricular arrhythmias, and even sudden cardiac death.
Patients with these findings that are consistent with Wolff-Parkinson-White
warrant expert cardiology consultation, a diagnostic workup that includes echocardiogram,
exercise stress testing, and possibly intra-cardiac studies and ablation of
accessory pathways. Medical treatments-- first line of therapy are beta blockade.
And be watchful for the presence of irregular wide-complex tachyarrhythmias in this population.
Beta-blockade, while used to prevent recurrent SVT in neonates and toddlers,
is a 2b adult recommendation only for those that refuse ablation or are not candidates
for ablation. The concern is that the chronic AV nodal blockade, from use of beta blockers,
could enhance accessory pathway conduction during an episode of atrial fibrillation.
Additionally, as stated earlier in this talk, AV nodal blocking agents,
such as adenosine, calcium channel blockers, and beta blockers,
are absolutely contraindicated in patients with an irregular wide complex tachycardia.
Thank you.