Presentation on theme: "Interesting Case Rounds"— Presentation transcript:
1Interesting Case Rounds Alyssa ReedR1 Emergency Medicine
2CASE #1 16F presenting with 2 syncopal episodes over the last two days PMHx: chiari malformation, chronic back painMeds: NaprosynVitals at Triage: %Q: What else would you like to know?Q: What is your approach to this patient?
3Syncope DDx Other CNS Dysfunction Focal Hypoperfusion of CNS StructuresSAHHyperventilationSystemic Hypoperfusion Resulting in CNS DysfunctionOutflow ObstructionCHDvalve stenosisReduced Cardiac OutputWPWSVTTachycardiasBradycardiasLong QT syndromeAortic dissectionCardiomyopathyVasomotorOther CNS DysfunctionHypoglycemiaSeizureToxic
4Findings O/E: AVSS, no significant findings N S1S2, no murmurs, no extra sounds, no JVD, no pulse delays, pressure same both arms, normal neuro examLabs: CBC, Lytes, Ca, Mg, PO4 normalCXR: no cardiomegalyECG
6WPWDefinition: 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 ventriclesWPW Pattern: ECG abormalitiesWPW Syndrome: ECG abnormalities and associated arrhythmiaAVRT (80%)Atrial Fibrillation (15-30%)Atrial Flutter (5%)
7Prevalence WPW Pattern 0.15-0.25% in general population 0.55% among first-degree relatives of affected patientsin one large study it was 2x more prevalent in malesWPW Syndromeapprox 1% with pattern have arrhythmiareview of showed .25% had pattern but only 1.8% of these had a documented arrhythmiasudden death: 0-.39% annually
8CASE #28F presenting with several episodes of “black-outs” that she remembers dating back to when she was two. None witnessed.PMHx: healthy, no medsFHx: mom has some unknown heart condition- she was treated with something that ends in “lol”O/E: no significant findingsQ: would you do an ECG?
10Familial WPWWPW syndrome- 3.4% have 1st degree relative with preexcitation syndromemuch lower than I expectedUsually inherited as autosomal dominant traitCan 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????
11Pathophysiology/ECGBundle of Kent is a muscle fiber accessory pathway that directly connects the atria and the ventriclesconduction down this pathway is faster allowing ventricular activation earlier but occurs at a slower speedQ: What are the basic ECG findings in sinus WPW?1. PR is short2. Delta wave3. Wide QRS
121. Short PRdue to rapid conduction through the accessory pathway and bypass of the AV node2. Delta Waveupstroke 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 bundles3. Wide QRSfusion 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
1410% 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 v1-310%50%30%
15Arrhythmias PSVT/AVRT Orthodromic AVRT* Antidromic AVRT Atrial FibrillationAtrial 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
18Management Who to treat? patients with WPW syndrome Options for treatment?PharmacologicAntiarrhythmicsNonpharmacologicRadiofrequency ablation
19Pharmacologic Mx Indications patients who are not candidates for ablationwell-tolerated arrhythmiasChoice depends on the ECG/electrophys testing and want it directed at the “weak link” in the conduction pathwayAcute termination vs chronic prevention
20OAVRT Weak link is the AV node (antegrade conduction) Acute TerminationVagal maneuversIV verapamil (Class IV)IV adenosineChronic PreventionClass IC (flecainide, propafenone)Beta blockers- so you want to lengthen the AV nodal refractoriness and depress its conduction- IV= Calcium channel blockersIC= marked block of Na channelsBB= 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
22AAVRT Weak link is retrograde conduction through AV node BUT this should not be targeted unless you are 100% sure this is AAVRTQ: Why?Q: What drugs should be avoided?
23Management WCT Avoid the ABCDs! Adenosine Beta Blockers DDX1. VTach2. SVT with Aberrrancy- Antidromic WPW-WPW with AFib- MAT- A flutter- AVNRTAvoid the ABCDs!AdenosineBeta BlockersCalcium Channel BlockersDigoxinStable vs UnstableUnstable- cardiovertStable- 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
25Non-Pharm Mx Ablation of Accessory Pathway Catheter Surgical IndicationsSymptomatic tachyarrhythmiasOccupations in which development of Sxs would put themselves or others at riskSelected asymptomatic patients