1. Interesting Case Rounds
Alyssa Reed
R1 Emergency Medicine

2. CASE #1 16F presenting with 2 syncopal episodes over the last two days
PMHx: chiari malformation, chronic back pain
Meds: Naprosyn
Vitals at Triage: %
Q: What else would you like to know?
Q: What is your approach to this patient?

3. Syncope DDx Other CNS Dysfunction
Focal Hypoperfusion of CNS Structures
SAH
Hyperventilation
Systemic Hypoperfusion Resulting in CNS Dysfunction
Outflow Obstruction
CHD
valve stenosis
Reduced Cardiac Output
WPW
SVT
Tachycardias
Bradycardias
Long QT syndrome
Aortic dissection
Cardiomyopathy
Vasomotor
Other CNS Dysfunction
Hypoglycemia
Seizure
Toxic

4. Findings O/E: AVSS, no significant findings
N S1S2, no murmurs, no extra sounds, no JVD, no pulse delays, pressure same both arms, normal neuro exam
Labs: CBC, Lytes, Ca, Mg, PO4 normal
CXR: no cardiomegaly
ECG

5. Dx???

6. WPW
Definition: a preexcitation of the ventricles through an accessory pathway- the Bundle of Kent- which provides an abnormal pathway of electical communication between the atria and the ventricles
WPW Pattern: ECG abormalities
WPW Syndrome: ECG abnormalities and associated arrhythmia
AVRT (80%)
Atrial Fibrillation (15-30%)
Atrial Flutter (5%)

7. Prevalence WPW Pattern 0.15-0.25% in general population
0.55% among first-degree relatives of affected patients
in one large study it was 2x more prevalent in males
WPW Syndrome
approx 1% with pattern have arrhythmia
review of showed .25% had pattern but only 1.8% of these had a documented arrhythmia
sudden death: 0-.39% annually

8. CASE #2
8F presenting with several episodes of “black-outs” that she remembers dating back to when she was two. None witnessed.
PMHx: healthy, no meds
FHx: mom has some unknown heart condition- she was treated with something that ends in “lol”
O/E: no significant findings
Q: would you do an ECG?

10. Familial WPW
WPW syndrome- 3.4% have 1st degree relative with preexcitation syndrome
much lower than I expected
Usually inherited as autosomal dominant trait
Can also be associated with a familial hypertrophic cardiomyopathy
- so my ECG yield in this 8yo was pretty low, but it is such a benign test why not do it????

11. Pathophysiology/ECG
Bundle of Kent is a muscle fiber accessory pathway that directly connects the atria and the ventricles
conduction down this pathway is faster allowing ventricular activation earlier but occurs at a slower speed
Q: What are the basic ECG findings in sinus WPW?
1. PR is short
2. Delta wave
3. Wide QRS

12. 1. Short PR
due to rapid conduction through the accessory pathway and bypass of the AV node
2. Delta Wave
upstroke slurred because of slow muscle fiber-to-muscle fiber conduction
- longer refractory period in AV node so it goes down accessory pathway more quickly but the depolarization is slower because muscle fibers not as good as the normal bundles
3. Wide QRS
fusion between early ventricular activation and the normal activation through the normal pathway

13. **the more rapid the conduction along the accessory pathway, the greater the amount of myocardium depolarized via the accessory pathway, resulting in a more prominent or wider delta wave, and longer QRS

14. 10% 10% 50% 30% - looking down on the heart
- all pass through the AV valve plane
- left result in tall R wave in V1-3
- right result in no R in v1-3
10%
50%
30%

15. Arrhythmias PSVT/AVRT Orthodromic AVRT* Antidromic AVRT
Atrial Fibrillation
Atrial Flutter
*most common

16. - antegrade conduction down the AV node then retrogradely up the accessory path to atria
- Antegrade down accessory path then retrograde up the AV node

17. Irregular, Wide complex Tachycardia

18. Management Who to treat? patients with WPW syndrome
Options for treatment?
Pharmacologic
Antiarrhythmics
Nonpharmacologic
Radiofrequency ablation

19. Pharmacologic Mx Indications
patients who are not candidates for ablation
well-tolerated arrhythmias
Choice depends on the ECG/electrophys testing and want it directed at the “weak link” in the conduction pathway
Acute termination vs chronic prevention

20. OAVRT Weak link is the AV node (antegrade conduction)
Acute Termination
Vagal maneuvers
IV verapamil (Class IV)
IV adenosine
Chronic Prevention
Class IC (flecainide, propafenone)
Beta blockers
- so you want to lengthen the AV nodal refractoriness and depress its conduction
- IV= Calcium channel blockers
IC= marked block of Na channels
BB= AV nodal specific activity

21. ** put circles around vagal stim, bb, verapimil, adenosine, flecainide, propafenone
- as you can see, you could also use amio but common adverse effects, and could use sotalol but increased risk of torsade in long-term use

22. AAVRT Weak link is retrograde conduction through AV node
BUT this should not be targeted unless you are 100% sure this is AAVRT
Q: Why?
Q: What drugs should be avoided?

23. Management WCT Avoid the ABCDs! Adenosine Beta Blockers
DDX
1. VTach
2. SVT with Aberrrancy
- Antidromic WPW
-WPW with AFib
- MAT
- A flutter
- AVNRT
Avoid the ABCDs!
Adenosine
Beta Blockers
Calcium Channel Blockers
Digoxin
Stable vs Unstable
Unstable- cardiovert
Stable- procainamide
* slow conduction through AV node, but not through accessory pathway and can actually SHORTEN refractory period of accessory pathway THEREFORE, can speed conduction and precipitate faster ventricular rates leading to HD instability
- IA: Na channel blocker

24. - put circle around procain
- IA agent that slows conduction through the AV node and the accessory pathway and is a moderate Na channel blocker

25. Non-Pharm Mx Ablation of Accessory Pathway Catheter Surgical
Indications
Symptomatic tachyarrhythmias
Occupations in which development of Sxs would put themselves or others at risk
Selected asymptomatic patients

26. QUESTIONS?