Child Health - List A

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Child Health Assignment

Wolff-Parkinson-WhiteSyndrome

Student No. - z3332964

Date - 20/04/2013

Word count - 1299



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List A – Using Basic and Clinical Sciences

A critical analysis of diagnostic tests performed and the way in which their

results influence management



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Case Introduction

A 3.5 year old male presents to the emergency department (ED) with a 1 hour history of

heart palpitations and chest pain. The patient was tachypnoeic and dyspnoeic with anelevated heart rate of 200 bpm.

Prior to arriving at the hospital, the patient had complained to his mum regarding mild chest

pain and was noted to be quite short of breath. Following this, mum then got the patient to

perform vagal manoeuvres. This proved to be unsuccessful and hence the ambulance was

called.

A detailed history was taken from the mum and the patient was found to have Wolff-

Parkinson-White (WPW) syndrome. Two such episodes had occurred in the past. The first, a

year ago, resolved after vagal manoeuvres were performed. The second episode, 4 months

ago, resulted in admittance to ED after vagal manoeuvres failed and was given IV adenosine

and was brought back to a sinus rhythm.

Currently on 7mls of Sotalol twice-a-day.

The rationale for selecting the aforementioned perspective is that WPW syndrome presentswith interesting phenomenon on an electrocardiogram (ECG) and would allow for a critical

evaluation of significant and noteworthy features and how they factor into the management

of the patient.



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Diagnosis and Management of WPW Syndrome

The diagnosis of WPW syndrome usually only requires a surface ECG. This is typically

prompted by an ancillary finding on an ECG obtained for an unrelated clinical manifestation.Identifying a shortened PR interval, a wide QRS complex and a delta wave is often adequate

enough to confirm the diagnosis of WPW syndrome.

WPW syndrome is typically diagnosed in a patient with a pre-existing WPW pattern that can

be seen on an ECG, but then develops an arrhythmia which involves the accessory pathway

(Bundle of Kent). This diagnosis should always be considered in patients with an arrhythmia

and a very rapid ventricular rate, especially when a delta wave can be noted and in children

and adolescents who present with a paroxysmal arrhythmia (Wolff, Parkinson, & White,

2006).

Following admittance to the ED and eliciting a detailed history from the patient’s mum, a

series of ECG’s were conducted.

The first ECG was taken 10 minutes after his arrival, at 8:18AM [see ECG 1]



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ECG 1 A BDC



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Evaluation of ECG 1

Arrhythmias associated with WPW syndrome 1:

In WPW syndrome, tachycardias are classified into two subtypes – those which require an

accessory tract to initiate and propagate the tachycardia and those in which this accessory

tract merely acts as a “bystander” that provides a pathway of conduction from the site of

the tachycardia to other regions of the heart itself.

The following case is pertinent to tachycardias that require an accessory pathway to be

initiated and maintained, and as such will have a particular focus on it - Atrioventricular

reentrant tachycardia (AVRT) is a reentrant type tachycardia that has a conduction circuit

that is anatomically defined. It consists of two pathways, a normal conduction system

through the AV node and also an accessory pathway through the AV node. The two major

forms of this arrhythmia are orthodromic (anterograde) and antidromic (retrograde) AVRT

(Zachariah et al., 2013).

The above ECG is a classic presentation of orthodromic AVRT. Significant features that can

be noted on the ECG:

A – Narrow QRS complex (74 ms), which is defined as a narrow complex tachycardia (Heart

rate – 194 bpm). This suggests a very rapid activation of the ventricles via the normal His-

Purkinje system.

B – P waves buried in QRS complex. The re-entry circuit often stimulates impulses in both

directions and often a retrogradely conducted P-wave is buried within the QRS complex that

precedes it.

C – QRS alternans. Changes in the amplitude of the QRS complex as the forceful contraction

of the ventricles causes the heart to essentially wobble in the pericardial sac.

D – T-wave inversion. Is a benign finding and is normal for a child of his age.

(Gertsch, 2004)

Management

Narrow-complex AVRTs are managed by terminating acute episodes. This is done by

blocking the conduction of impulses through the AV node:

Vagal manoeuvres:

Valsalva – The patient is asked to hold their breath while exhaling forcefully. This works by

raising the pressure intra-thoracically and triggering the baroreceptors in the arch of the

aorta (Lim, Anantharaman, Teo, Goh, & Tan, 1998).



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Splashing cold water on the face – Triggers the mammalian diving reflex due to

parasympathetic action via the vagus nerve and resulting in bradycardia (Wildenthal, 1978).

These above manoeuvres proved to unsuccessful in this case. Consequently, the next step inthe management process is pharmacotherapy:

Adenosine – 3mgs of IV adenosine was then administered. This causes a transient block in

the AV node that is mediated by the A1 receptor: inhibition of adenylyl cyclase reduction

of cAMP increase efflux of K+ ions cell hyperpolarization (Mitchell & Lazarenko, 2008).

Following this, a second ECG was taken at 9:30 AM [see ECG 2]



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ECG 2

A

B C

D



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Evaluation of ECG 2

Arrhythmias associated with WPW syndrome 2:

AVRT is sometimes followed by atrial fibrillation (AF) in individuals with WPW, with one

report (Sung et al., 1977) suggesting that as many as 35% of episodes of AF were precededby AVRT. This is what happened in this case with the patient suddenly going into AF after

the administration of adenosine. However, the mechanisms by which AVRT precipitates AF

are not well understood, but increased stretching due to increased atrial pressure in atrial

myocardium due to reduced refractory period could play a role.

Characteristics features on the ECG:

A – No discernible P-wave due to uncoordinated atrial depolarisation resulting in

“fibrillations”.

B – Changes in shape and morphology of QRS-complexes. Note the notch in the R-wave as a

result of the ventricles contracting consecutively rather than simultaneously.

C – Exaggerated S-wave as a result of delayed ventricular depolarization due to improper

conduction of impulses through the AV node.

D – Broad complex AF (116 ms).

(Gertsch, 2004)

Management

In this particular case, the patient was managed supportively at this stage. The reason for

this being that, in the last such episode, the patient was noted to have gone into AF after

administering Adenosine and under observation returned to a sinus rhythm within the hour.

Following this, a final ECG was taken at 12:28 PM after the patient’s vital signs normalized

and had reverted to a sinus rhythm [see ECG 3]



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ECG 3 A BC D



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Evaluation of ECG 3

The accessory pathway present in WPW syndrome does not possess the rate slowing

properties of the normal AV node. As a result the electrical stimulus is conducted at asignificantly higher rate. This presents with quite interesting and notable features on an

ECG, namely:

A – Short PR-interval (86 ms), due to the aforementioned lack of rate limiting properties.

B – Broad QRS-complex with a slurred upstroke (delta wave). This is due to a slight delay

between the rapid arrival of impulse via the Bundle of His and depolarization of the

ventricles.

C – Dominant S-wave notable in the V1 lead. This is known as a type B sinus rhythm and is

indicative of a right sided accessory pathway (accessory tract between right atrium and rightventricle).

D – An interesting RSR’ pattern in V1-V2 that is a normal variant in children of this age.

(Gertsch, 2004)

Management

Following the patient’s return to a sinus rhythm, the management of his condition was of a

long-term perspective. The mainstay for the management of low risk individuals is oral

antiarrhythmic therapy. In this particular case, the patient was put on a Class III drug:

Sotalol –

β-blocker action – Binds to β1 and β2 adrenergic receptors prevents activation

decreased cAMP decrease in activity of Ca2+

channels. This results in:

1. Decreased electrical impulses for ventricular contraction

2. Decrease in strength and rate of contraction

Type III Antiarrhythmia Action

Acts on K channels, by inhibiting efflux of K+

ions, resulting in increased time before the

ventricular myocytes generate another impulse

The patient was then monitored overnight with no further complications. The nurses

described the patient as being as “happy and chatty” in the morning. He was then duly

discharged with a new regimen of 6mls of Sotalol, three times-a-day (Orczykowski et al.,

2008).



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Reflection

This assignment proved to be extremely fascinating and upon its conclusion I had a better

understanding as to the practicality and essentiality of ECG interpretation skills to a medicalstudent. To help me with the ECGs I had enlisted the help of the Cardiologist here at Griffith

Base and spent a significant amount of time analysing ECGs. I feel like I have become

moderately competent at a skill that not many of my peers would possess at this stage.

On a more personal note, I learned to approach the issue of medical management of

children with a more empathetic outlook. The fact that our young patient can’t live a

‘normal life’; as any stress, even playing with friends could possibly trigger a traumatic

tachycardic episodes, needs to be appreciated. We should cherish our normal, boring lives.



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References

Gertsch, Marc. (2004). The ECG: A Two-Step Approach to Diagnosis Springer.

Lim, S. H., Anantharaman, V., Teo, W. S., Goh, P. P., & Tan, A. T. (1998). Comparison of treatment of

supraventricular tachycardia by Valsalva maneuver and carotid sinus massage. Ann Emerg

Med, 31(1), 30-35.

Mitchell, J., & Lazarenko, G. (2008). Wide QRS complex tachycardia. Diagnosis: Supraventricular

tachycardia with aberrant conduction; intravenous (IV) adenosine. CJEM, 10(6), 572-573,

581.

Orczykowski, M., Szumowski, L., Szufladowicz, E., Bodalski, R., Zakrzewska-Koperska, J., & Walczak, F.

(2008). [Sotalol prevents atrio-ventricular tachycardia but not atrial fibrillation with rapid

ventricular response in a patient wiht WPW syndrome]. Kardiol Pol, 66(7), 800-804.

Sung, R. J., Castellanos, A., Mallon, S. M., Bloom, M. G., Gelband, H., & Myerburg, R. J. (1977).

Mechanisms of spontaneous alternation between reciprocating tachycardia and atrial

flutter-fibrillation in the Wolff-Parkinson-White syndrome. Circulation, 56(3), 409-416.

Wildenthal, K. (1978). Treatment of paroxysmal atrial tachycardia by diving reflex. Lancet, 1(8072),

1042.

Wolff, L., Parkinson, J., & White, P. D. (2006). Bundle-branch block with short P-R interval in healthy

young people prone to paroxysmal tachycardia. 1930. Ann Noninvasive Electrocardiol, 11(4),

340-353. doi: 10.1111/j.1542-474X.2006.00127.x

Zachariah, J. P., Walsh, E. P., Triedman, J. K., Berul, C. I., Cecchin, F., Alexander, M. E., & Bevilacqua,

L. M. (2013). Multiple accessory pathways in the young: the impact of structural heart

disease. Am Heart J, 165(1), 87-92. doi: 10.1016/j.ahj.2012.10.025

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