Interesting Case Rounds Alyssa Reed R1 Emergency Medicine

CASE #1 16F presenting with 2 syncopal episodes over the last two days PMHx: chiari malformation, chronic back pain Meds: Naprosyn Vitals at Triage: 80 16 106-60 96% 5.5 Q: What else would you like to know? Q: What is your approach to this patient?

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

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........

Dx???

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%)

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 22500 showed .25% had pattern but only 1.8% of these had a documented arrhythmia sudden death: 0-.39% annually

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?

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????

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

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

**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

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%

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

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

Irregular, Wide complex Tachycardia

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

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

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

** 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

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?

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

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

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

QUESTIONS?