01Approach to the Critical Patient/attcp22

Immediate Stabilization

›Hemodynamic instability triggers

›Hypotension (SBP <90 mmHg), altered mental status, or signs of shock

›Irregular wide-complex tachycardia (preexcited AF) with any instability

›Heart rate >250 bpm with hemodynamic compromise

›Immediate synchronized DC cardioversion

›50-100 J biphasic initial energy for all unstable tachyarrhythmias

›Sedate if time permits; do not delay cardioversion for IV access in pulseless or near-pulseless patients

›If VF results, immediate unsynchronized defibrillation at 200 J

›Resuscitation bay activation criteria

›Cardiac arrest or aborted SCD presentation

›Preexcited AF with hemodynamic compromise

›Wide-complex tachycardia with collapse

Contraindicated Drug Alert

›AVOID in any wide-complex or preexcited tachycardia with WPW

›Adenosine — may precipitate AF and accelerate ventricular rate via accessory pathway

›Verapamil and diltiazem — block AV node without prolonging AP refractoriness; risk of VF

›Digoxin — shortens accessory pathway refractory period; risk of VF

›IV amiodarone — contraindicated in preexcited AF

›IV beta-blockers — may accelerate accessory pathway conduction in preexcited AF

Monitoring and Access

›Continuous cardiac monitoring and defibrillator at bedside

›12-lead ECG to characterize tachycardia morphology

›IV access with resuscitation equipment immediately available

›Oxygen supplementation for SpO2 <94%

02History/hx30

Presenting Symptoms

›Palpitations

›Sudden-onset, rapid, regular racing or fluttering sensation

›Abrupt onset and offset (paroxysmal) distinguishing AVRT from sinus tachycardia

›Episode duration and frequency

›Syncope or presyncope

›Independent predictor of adverse outcomes and high-risk pathway

›Syncope during exertion raises concern for preexcited AF or VF

›Associated symptoms

›Chest discomfort or dyspnea during episodes

›Exercise intolerance or fatigue

Alarm Features

›High-risk historical features

›Cardiac arrest or aborted SCD — may be the sentinel event, especially in children (65% of pediatric life-threatening events)

›Irregular palpitations suggesting preexcited AF

›Family history of sudden cardiac death in a young relative

›Male sex and age <30 years — SCD risk higher in children (1.93/1000 person-years) vs adults (0.86/1000 person-years)

Triggers and Exposures

›Episode precipitants

›Exercise, emotional stress, catecholamine surges

›Caffeine, alcohol, or stimulant use (energy drinks, pre-workout supplements)

›Medication history

›Prior adenosine, verapamil, or diltiazem administered for tachycardia

›Prior antiarrhythmic drug use (procainamide, flecainide, propafenone, sotalol)

Past Medical and Family History

›Prior arrhythmia history

›Previous SVT, AF, or cardiac arrest episodes

›Prior ED visits or cardioversions

03Physical Exam/exam16

Cardiovascular Examination

›Vital signs during tachycardia

›Heart rate and regularity — regular in AVRT, irregular in preexcited AF

›Blood pressure for hemodynamic compromise

›Jugular venous pressure

›Cannon A waves during AVRT (simultaneous atrial and ventricular contraction)

›Cardiac auscultation

›Tricuspid regurgitation murmur or widely split S1 suggesting Ebstein anomaly

›Systolic murmur at left lower sternal border suggesting HCM

Inter-episode Examination

›Baseline findings

›Often entirely normal between episodes

›Signs of heart failure if tachycardia-induced cardiomyopathy is present

›Hepatomegaly or developmental delay suggesting glycogen storage disease

Hemodynamic Assessment

›Shock assessment

›Altered mental status, diaphoresis, cool extremities

›Capillary refill >2 seconds

›Hypotension with tachycardia — immediate cardioversion threshold

04Differential Diagnosis/ddx26

Supraventricular Tachycardias

›AVNRT (atrioventricular nodal reentrant tachycardia)

›Most common SVT; narrow-complex, no delta wave in sinus rhythm

›Pseudo-R' in V1 or pseudo-S in inferior leads during tachycardia

›Responds to vagal maneuvers and adenosine

›Atrial flutter with rapid conduction

›Regular wide-complex tachycardia at ~150 bpm if 2:1 conduction via AP

›Flutter waves visible in inferior leads

›Preexcited atrial fibrillation

›Irregular wide-complex tachycardia — hallmark finding

›Can mimic polymorphic VT; potentially lethal if treated with AV nodal blockers

Wide-Complex Tachycardia Mimics

›Ventricular tachycardia

›Antidromic AVRT produces wide-complex tachycardia morphologically similar to VT

›When in doubt, treat as VT — avoid AV nodal blocking agents

›Mahaim fiber tachycardia

›Atriofascicular pathway producing LBBB-morphology wide-complex tachycardia

›Left-axis deviation, rate typically 150-250 bpm

›Lown-Ganong-Levine syndrome

›Short PR without delta wave — enhanced AV nodal conduction, not true preexcitation

Benign Mimics and Structural Associations

›Fasciculoventricular pathway

›Mimics WPW pattern on ECG but does not participate in reentrant circuits

›Benign — does NOT require ablation

›Hypertrophic cardiomyopathy

›Can produce pseudo-preexcitation patterns on ECG

›Septal hypertrophy may create Q-wave changes mimicking delta waves

›Bundle branch block

05Laboratory Tests/lt19

Metabolic and Electrolyte Panel

›Basic metabolic panel

›Serum potassium — hypokalemia lowers VF threshold and promotes arrhythmia

›Serum magnesium — hypomagnesemia potentiates atrial and ventricular arrhythmias

›Target K+ 4.0-5.0 mmol/l and Mg2+ >1.0 mmol/l in acute arrhythmia management

›Thyroid-stimulating hormone

›Hyperthyroidism as a trigger for AF/SVT

›Indicated in new-onset tachyarrhythmia without prior diagnosis

Cardiac Biomarkers

›Troponin

›Indicated for chest pain, prolonged tachycardia, or hemodynamic compromise

›Elevation may reflect demand ischemia from sustained tachycardia

›BNP or NT-proBNP

›Indicated if concern for heart failure or tachycardia-induced cardiomyopathy

›Elevated in chronic cardiomyopathy from right-sided AP dyssynchrony

Additional Testing

›Complete blood count

›Anemia as a contributing trigger for palpitations and exercise intolerance

›Genetic testing

›Indicated when WPW is combined with HCM and/or progressive conduction disease

›PRKAG2 gene testing for WPW + HCM + conduction disease triad

›Not routinely indicated for isolated WPW without associated cardiomyopathy

06Diagnostic Tests/dt44

Scoring Systems

›WPW risk stratification tools

›No validated clinical scoring system equivalent to HEART or Wells exists for WPW

›Risk stratification relies on clinical features, EP study, and exercise testing

›High-risk features: syncope, multiple APs, shortest RR interval <250 ms in preexcited AF

›Low-risk features: loss of preexcitation during exercise testing (intermittent preexcitation)

›ACC/AHA/HRS 2015 SVT Guideline risk categories

›Class I indication for EP study in symptomatic patients to guide ablation decision

›Class IIa for EP study in asymptomatic patients in high-risk occupations (pilots, competitive athletes)

›Invasive EP study is gold standard for AP refractory period measurement

MRI

›Cardiac MRI indications

›Evaluation for structural heart disease not adequately assessed by echocardiography

›Assessment of ventricular function in suspected tachycardia-induced or dyssynchrony-related cardiomyopathy

›Characterization of HCM phenotype when WPW + HCM present

›MRI findings in associated conditions

›Ebstein anomaly — apical displacement of tricuspid valve, right atrial enlargement

›HCM — asymmetric septal hypertrophy, late gadolinium enhancement pattern

›MRI not used to identify accessory pathways directly

CT

›CT indications in WPW

›CT angiography for structural evaluation if echocardiography is non-diagnostic

›Coronary CT angiography if ischemia is suspected as a contributing factor

›CT not a primary diagnostic tool for WPW arrhythmia evaluation

›Pre-procedural CT

›CT of pulmonary veins and left atrium before complex ablation procedures

›3D anatomical reconstruction to aid catheter ablation planning

07Disposition/dispo18

Admission Criteria

›Indications for inpatient admission

›Hemodynamic instability or cardiac arrest presentation

›Preexcited AF requiring monitoring after acute cardioversion

›Recurrent tachycardia refractory to acute treatment

›New diagnosis with syncope or high-risk features pending EP consultation

›Tachycardia-induced cardiomyopathy requiring inpatient management

Discharge Criteria

›Safe for discharge when

›Stable orthodromic AVRT that converts with vagal maneuvers or adenosine

›Known WPW with brief self-limited episode and established cardiology follow-up

›Asymptomatic WPW pattern discovered incidentally with outpatient EP referral arranged

›Normal ECG, normal vital signs, and no high-risk features at time of discharge

Referral and Consultation

›Electrophysiology consultation

›All patients with WPW pattern or syndrome should be referred to electrophysiology

›Urgent EP consultation for syncope, cardiac arrest, or preexcited AF

›Class I indication: EP referral for all symptomatic WPW patients for ablation consideration

›Pediatric electrophysiology

›All children with WPW pattern regardless of symptoms require pediatric EP referral

›SCD risk in children 1.93/1000 person-years versus 0.86/1000 person-years in adults

08Treatment/t56

Hemodynamically Unstable — Any Rhythm

›Synchronized DC cardioversion

›Initial energy 50-100 J biphasic

›Sedate with IV midazolam 1-2 mg or propofol 0.5-1 mg/kg if time and hemodynamics permit

›Repeat at higher energy (200 J) if initial attempt fails

›Unsynchronized defibrillation 200 J for VF or pulseless VT

Orthodromic AVRT — Narrow-Complex, Hemodynamically Stable

›Step 1: Vagal maneuvers

›Modified Valsalva maneuver — strain for 15 seconds then supine leg raise

›Carotid sinus massage — avoid if carotid bruit present

›Success rate of modified Valsalva ~43% for SVT termination

›Step 2: Adenosine IV

›Initial dose 6 mg IV rapid push followed by 20 mL saline flush

›Second dose 12 mg IV if no response after 1-2 minutes

›Third dose 12 mg IV if needed

›Effective in 90-95% of AVRT cases

›Caution: may precipitate AF — have defibrillator at bedside before administration

›Use only when no preexcitation on resting ECG (i.e., confirm narrow complex)

›Step 3: AV nodal blocking agents (only if no preexcitation on baseline ECG)

›IV diltiazem 0.25 mg/kg over 2 minutes (max 25 mg), then 0.35 mg/kg if needed

›IV metoprolol 2.5-5 mg over 2 minutes, up to 3 doses

›IV verapamil 5-10 mg over 2 minutes

Preexcited AF — Wide-Complex Irregular, Hemodynamically Stable

›IV procainamide

›Loading dose 10-15 mg/kg IV at 25-50 mg/min

›Maximum infusion rate 50 mg/min

›Slows AP conduction and may terminate AF

›Monitor BP and QRS width during infusion; stop if QRS widens >50%

›IV ibutilide (alternative)

›1 mg IV over 10 minutes; repeat once if needed for patients >60 kg

›0.01 mg/kg IV for patients <60 kg

›Monitor for QT prolongation and torsades de pointes post-infusion for 4 hours

›STRICT avoidance in preexcited AF

›Adenosine — may precipitate VF via accelerated AP conduction

›Verapamil, diltiazem — block AV node, accelerate AP conduction, precipitate VF

›Digoxin — shortens AP refractory period, increases risk of VF

›IV amiodarone — contraindicated in preexcited AF

›IV beta-blockers — contraindicated in preexcited AF

Antidromic AVRT — Wide-Complex Regular, Hemodynamically Stable

›Preferred antiarrhythmic agents

›IV procainamide 10-15 mg/kg at 25-50 mg/min

›IV ibutilide as per preexcited AF dosing above

›Synchronized cardioversion if pharmacotherapy fails or hemodynamics deteriorate

Definitive Treatment — Catheter Ablation

›Radiofrequency (RF) ablation

›Class I recommendation for symptomatic WPW syndrome

›Success rate >90%; major complication rate <1%

›Risk of AV block requiring permanent pacemaker 0.3%

›RF ablation recurrence ~11.6% over ~37 months for septal pathways

›Ablation reduces arrhythmic events by 92% (RR 0.08) in high-risk patients over 5 years

›Cryoablation

›Preferred for anteroseptal and midseptal pathways to reduce AV node injury risk

›Lower long-term success rate than RF but safer profile near His bundle

Chronic Pharmacotherapy — Ablation Deferred or Failed

›Oral antiarrhythmics for AP conduction

›Flecainide 50-150 mg twice daily — Class IC; avoid in structural heart disease

›Propafenone 150-300 mg three times daily — Class IC; avoid in structural heart disease

›Sotalol 80-160 mg twice daily — Class III; monitor QTc

›Amiodarone 100-200 mg daily (maintenance) — reserve for refractory cases given toxicity

›Pediatric pharmacotherapy

›Propranolol 1-4 mg/kg/day divided three times daily — first-line in young children not yet eligible for ablation

›Atenolol 0.5-1 mg/kg/day — alternative beta-blocker option

09Special Populations/sp36

Pregnancy

›Physiologic changes affecting WPW

›Increased blood volume and cardiac output elevate arrhythmia susceptibility

›Estrogen and progesterone effects may increase AP conduction velocity

›SVT incidence increases in pregnancy, particularly in third trimester

›Acute management in pregnancy

›Vagal maneuvers and adenosine are safe in all trimesters (Class I)

›DC cardioversion is safe in all trimesters; does not induce fetal arrhythmia at standard energies

›Procainamide acceptable for acute preexcited AF if cardioversion deferred

›Chronic management in pregnancy

›Flecainide and propafenone — limited data; use only if benefits outweigh risks

›Beta-blockers (metoprolol, propranolol) — generally considered safe after first trimester; monitor for neonatal bradycardia

›Catheter ablation — defer until postpartum if possible; if required, perform after 16 weeks with lead shielding and minimizing fluoroscopy

Geriatric

›Altered arrhythmia presentation

›Atypical presentation — dyspnea, fatigue, or falls rather than palpitations

›Higher prevalence of comorbidities (coronary artery disease, diastolic dysfunction) that increase hemodynamic impact of tachycardia

›Drug considerations in elderly patients

›Adenosine — use with caution; may cause prolonged AV block or bronchospasm in COPD

›Verapamil and diltiazem — increased risk of hypotension; use minimum effective dose

›Procainamide — reduce dose by 25-50% for reduced renal clearance; monitor QRS and QT

›Ablation in elderly patients

›Catheter ablation remains effective and safe in appropriately selected elderly patients

›Higher risk of vascular access complications and periprocedural events

›Lower recurrence rate per person-year due to higher background mortality

Pediatrics

›Age-specific risk profile

›SCD risk highest in children: 1.93/1000 person-years vs adults 0.86/1000 person-years

10Background/b43

Epidemiology

›Prevalence and incidence

›WPW ECG pattern prevalence 0.1-0.3% in the general population

›WPW syndrome (preexcitation + symptoms/arrhythmias) affects a subset of those with the ECG pattern

›Male sex predominance; risk highest in first two decades of life

›~3% of affected individuals have a symptomatic first-degree relative

›Sudden cardiac death risk

›Lifetime SCD risk approximately 2-4%

›SCD can be the first manifestation in ~50% of cases

›Pediatric SCD rate 1.93/1000 person-years; adult rate 0.86/1000 person-years

›Risk is front-loaded in young patients and highest in first two decades of life

›Complication rates

›Catheter ablation success rate >90%; major complication rate <1%

›RF ablation septal pathway recurrence ~11.6% at ~37 months

›Tachycardia-induced cardiomyopathy reversible with restoration of sinus rhythm

Pathophysiology

›Accessory pathway anatomy

›Anomalous muscular connection between atria and ventricles bypassing the AV node

›Short AP refractory period (<250 ms) is the key determinant of high-risk pathway

›Multiple accessory pathways present in a subset, increasing arrhythmia risk

›Tachycardia mechanisms

›Orthodromic AVRT — anterograde conduction via AV node, retrograde via AP; produces narrow-complex tachycardia

›Antidromic AVRT — anterograde conduction via AP, retrograde via AV node; produces wide-complex tachycardia

›Preexcited AF — AF with rapid anterograde conduction via AP bypassing rate-limiting AV node; rates >300 bpm possible; can degenerate to VF

›ECG basis

›Short PR interval <120 ms due to AP bypassing AV nodal delay

›Delta wave from slow accessory pathway depolarization of ventricular myocardium

›QRS widening from fusion of AP and AV nodal ventricular activation

11Patient Discharge Instructions/pdi24

copy discharge instructions

›What you were diagnosed with

›Wolff-Parkinson-White (WPW) syndrome is a heart condition where an extra electrical pathway (accessory pathway) connects the upper and lower chambers of the heart, bypassing the normal electrical relay station (AV node)

›This extra pathway can cause your heart to beat very fast (tachycardia), sometimes dangerously fast

›Your heart rhythm was restored today; you will need specialist follow-up for further treatment

›Medications to avoid

›Do NOT take verapamil, diltiazem (Cardizem), or digoxin unless specifically cleared by your cardiologist

›Inform any treating physician or emergency provider that you have WPW before receiving any heart rhythm medications

›Carry a medical alert card or wear a medical alert bracelet noting WPW and listing contraindicated medications

›Activity and lifestyle

›Avoid caffeine, energy drinks, pre-workout supplements, and alcohol — these can trigger fast heart rhythms

›Avoid stimulant-containing medications (cold remedies with pseudoephedrine, diet pills)

›Do not restrict normal activity unless advised by your specialist; competitive sports discussion is required with your cardiologist

›Self-management during an episode

›If you feel your heart racing: try the Valsalva maneuver (bear down as if having a bowel movement for 15 seconds, then lie flat and raise your legs)

›If the episode does not stop within 1 minute of trying the maneuver, call 911

›Follow-up required

›Cardiology or electrophysiology referral appointment within 1-2 weeks is mandatory

›Catheter ablation may be recommended; this procedure has a >90% success rate and is the definitive treatment

›Return to the emergency department immediately if

›Fainting, near-fainting, or loss of consciousness

›Chest pain or severe shortness of breath

›Heart rate feels very fast, irregular, or does not stop with self-management

›Sensation of pounding or fluttering that is different from previous episodes

›Any episode lasting more than 5 minutes without self-termination

12References/r16

Guidelines and Key Sources

›Primary guidelines

›Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia. Heart Rhythm. 2016. https://linkinghub.elsevier.com/retrieve/pii/S1547-5271(15)01189-3

›Writing Committee Members, Joglar JA, Chung MK, et al. 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation. J Am Coll Cardiol. 2024. https://pubmed.ncbi.nlm.nih.gov/38043043

›January CT, Wann LS, Alpert JS, et al. 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation. J Am Coll Cardiol. 2014. https://pubmed.ncbi.nlm.nih.gov/24685669

›Lampert R, Chung EH, Ackerman MJ, et al. 2024 HRS Expert Consensus Statement on Arrhythmias in the Athlete. Heart Rhythm. 2024. https://doi.org/10.1016/j.hrthm.2024.05.018

Supporting Evidence

›Key studies and reviews

›Peng G, Zei PC. Diagnosis and Management of Paroxysmal Supraventricular Tachycardia. JAMA. 2024. https://jamanetwork.com/journals/jama/fullarticle/10.1001/jama.2024.0076

›Al-Khatib SM, Arshad A, Balk EM, et al. Risk Stratification for Arrhythmic Events in Patients With Asymptomatic Pre-Excitation. J Am Coll Cardiol. 2016. https://pubmed.ncbi.nlm.nih.gov/26409260

›Nielsen JC, Lin YJ, de Oliveira Figueiredo MJ, et al. EHRA/HRS/APHRS/LAHRS Expert Consensus on Risk Assessment in Cardiac Arrhythmias. Heart Rhythm. 2020. https://doi.org/10.1016/j.hrthm.2020.05.004

›Wilde AAM, Semsarian C, Marquez MF, et al. EHRA/HRS/APHRS/LAHRS Expert Consensus Statement on Genetic Testing for Cardiac Diseases. Heart Rhythm. 2022. https://linkinghub.elsevier.com/retrieve/pii/S1547-5271(22)01697-6

›Coban-Akdemir ZH, Charng WL, Azamian M, et al. Wolff-Parkinson-White syndrome: De novo variants and evidence for mutational burden in genes associated with atrial fibrillation. Am J Med Genet. 2020. https://onlinelibrary.wiley.com/doi/10.1002/ajmg.a.61571

›Erickson CC, Salerno JC, Berger S, et al. Sudden Death in the Young: Information for the Primary Care Provider. Pediatrics. 2021. https://publications.aap.org/pediatrics/article-lookup/doi/10.1542/peds.2021-052044

›William J. Brady. Wolff-Parkinson-White Syndrome. The Electrocardiogram in Emergency and Acute Care. 2023. https://onlinelibrary.wiley.com/doi/10.1002/9781119266938.ch20

›Ganz LI, Friedman PL. Supraventricular Tachycardia. N Engl J Med. 1995. https://www.nejm.org/doi/full/10.1056/NEJM199501193320307

›Krumerman A. Abandoning Non Invasive Risk Stratification in WPW: There Is no Such Thing as a Free Lunch. J Cardiovasc Electrophysiol. 2025. https://onlinelibrary.wiley.com/doi/10.1111/jce.70085

›Finocchiaro G, Westaby J, Sheppard MN, Papadakis M, Sharma S. Sudden Cardiac Death in Young Athletes: JACC State-of-the-Art Review. J Am Coll Cardiol. 2024. https://pubmed.ncbi.nlm.nih.gov/38199713

Evidence & Review

Evidence & Review