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Eduovisual

Cardiovascular

Supraventricular tachycardia: acute termination and chronic prevention

Clinical Overview and When to Suspect SVT

AVNRT (60%): dual AV nodal pathways, reentry within the node; most common in young women

AVRT (30%): accessory pathway (e.g., WPW with bundle of Kent); orthodromic (narrow) vs antidromic (wide)

Atrial tachycardia (10%): ectopic atrial focus; often in structural disease, COPD, digoxin toxicity (MAT variant)

— Sudden-onset, sudden-offset palpitations ("on/off switch") with neck pounding (frog sign from cannon A waves in AVNRT)

— Rate >150 bpm regular, no clear P waves or retrograde P after QRS

— Triggered by caffeine, alcohol, stress, exercise, pregnancy, hyperthyroidism, stimulants (cocaine, decongestants, albuterol)

Definition: Supraventricular tachycardia (SVT) = narrow-complex tachycardia (QRS <120 ms) with rate typically 150–250 bpm originating at or above the AV node, excluding sinus tachycardia and atrial fibrillation/flutter in most board usage.
Mechanism categories (must distinguish for chronic prevention):
When to suspect SVT in ambulatory or ED setting:
Demographics: AVNRT peaks 20–40s, female predominance 2:1; AVRT presents earlier (teens–young adult); atrial tach common in older patients with heart disease.
Step 3 management: First clinical decision in any tachyarrhythmia is hemodynamic stability, not rhythm subtype. Unstable (hypotension, AMS, ischemic chest pain, pulmonary edema) → synchronized cardioversion regardless of mechanism. Stable narrow-complex regular → vagal maneuvers, then adenosine.
Board pearl: "Paroxysmal" SVT = abrupt start/stop pattern; this single historical feature differentiates SVT from sinus tachycardia (which warms up/cools down gradually) and is the highest-yield history clue on Step 3 stems. Always ask about onset speed when palpitations are described.
Hyperthyroidism and pulmonary embolism must be considered as provokers even after rhythm termination — failure to evaluate for these on outpatient follow-up is a common Step 3 trap.
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Presentation Patterns and Key History

— Sudden-onset palpitations ("racing," "fluttering"), often felt in the neck

— Lightheadedness, dyspnea, chest discomfort, diaphoresis, anxiety

— Polyuria post-episode (ANP release from atrial stretch — highly specific for SVT)

— Syncope is uncommon but suggests rapid rates, accessory pathway, or structural disease

Onset: abrupt vs gradual; what was patient doing (exertion, bending over, Valsalva)

Duration: seconds to hours; episodes terminated by Valsalva, breath-holding, cold water suggest reentrant SVT

Frequency and trend: escalating frequency warrants ablation referral

Triggers: caffeine, ethanol ("holiday heart"), cannabis, cocaine, methamphetamine, OTC sympathomimetics, energy drinks

Medications: theophylline, albuterol, levothyroxine overreplacement, digoxin (atrial tach with AV block)

Comorbidities: WPW family history, prior MI, valvular disease, hyperthyroidism, pheochromocytoma, anxiety/panic

— Syncope during episode → suspect WPW with rapid pathway conduction

— Known WPW + new AF → preexcited AF, life-threatening

— Anginal symptoms in patient with CAD → demand ischemia

Classic symptom cluster:
History elements to extract (CCS-style data gathering):
Red flag history requiring escalation:
Step 3 management: In ambulatory follow-up after an ED visit for SVT, document episode burden (frequency, duration, impact on work/driving) — this drives the shared decision between chronic AV nodal blockade and catheter ablation referral (Class I for symptomatic recurrent AVNRT/AVRT).
Key distinction: Panic attack vs SVT — both cause palpitations and dyspnea, but SVT typically has rate >150 with abrupt cessation and post-episode polyuria; panic has gradual buildup, rate usually <130, and prominent paresthesias/derealization. A rhythm strip or event monitor during symptoms is diagnostic.
Ask about driving and occupation (pilots, commercial drivers) — affects urgency of definitive therapy.
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Physical Exam Findings and Hemodynamic Assessment

— HR typically 150–220 bpm, regular

— BP may be normal, low, or borderline; reassess after each intervention

— RR may be elevated from anxiety or pulmonary congestion

— SpO2 usually preserved unless heart failure develops

— Rapid regular rhythm without respiratory variation (vs sinus tach)

Cannon A waves in jugular venous pulse from atria contracting against closed tricuspid valve — pathognomonic for AVNRT (atria and ventricles contract simultaneously)

Frog sign: visible rapid neck pulsations the patient may have noticed at home

— Variable S1 intensity suggests AV dissociation (favors VT, not SVT)

— SBP <90 with end-organ hypoperfusion

— Altered mental status

— Ischemic chest pain with ECG changes

— Acute pulmonary edema (rales, hypoxia)

Valsalva (40 mmHg pressure × 15 sec) — termination rate ~17%

Modified Valsalva (REVERT trial): supine repositioning with leg raise after strain — termination ~43%, now preferred

Carotid sinus massage — avoid if carotid bruit, recent TIA/stroke, or age >65 without prior auscultation

Vital signs first — this drives the entire algorithm:
Cardiac exam:
Signs of hemodynamic instability (mandate immediate synchronized cardioversion):
Pulmonary exam: Clear lungs typical; crackles suggest tachycardia-mediated cardiomyopathy or precipitating HF.
Provocative bedside maneuvers (both diagnostic and therapeutic):
CCS pearl: Always order continuous telemetry and place defibrillator pads on the patient before giving adenosine — transient asystole, AF induction, and bronchospasm can occur. Have a working IV in the antecubital fossa or more proximal for adenosine push (peripheral hand IVs fail due to half-life <10 seconds).
Document neuro exam and peripheral perfusion before/after intervention — Step 3 stems test recognition of subtle hypoperfusion (cool extremities, delayed cap refill) as instability criteria.
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Diagnostic Workup — ECG and Initial Labs

Narrow QRS (<120 ms), regular, rate 150–250 → SVT spectrum

AVNRT typical (slow-fast): retrograde P buried in QRS or producing pseudo-R' in V1, pseudo-S in II/III/aVF

AVRT (orthodromic): retrograde P after QRS, RP <70 ms typical, often visible in inferior leads

Atrial tachycardia: distinct P wave preceding QRS with abnormal axis; long RP interval

Atrial flutter: sawtooth flutter waves, ventricular rate often 150 (2:1 block)

Delta wave + short PR (<120 ms) + wide QRS = WPW (preexcitation); changes management — avoid AV nodal blockers chronically

— Look for prior MI, LVH, long QT, Brugada pattern

Electrolytes (K, Mg, Ca) — hypokalemia/hypomagnesemia provoke

TSH — hyperthyroidism is a reversible precipitant

CBC — anemia exacerbates symptoms

Troponin only if ischemic symptoms or prolonged tachycardia (rate-related troponin leak common and nondiagnostic)

β-hCG in reproductive-age women before meds/imaging

Tox screen if stimulant use suspected

12-lead ECG is the cornerstone — obtain during tachycardia AND after termination:
Post-conversion sinus rhythm ECG — critical:
Initial labs (focused, not shotgun):
CXR: if dyspnea, suspected HF, or to rule out PE precipitant; otherwise not routine.
Board pearl: A wide-complex regular tachycardia is VT until proven otherwise in patients >35 or with structural heart disease — do not assume SVT with aberrancy. Brugada criteria help, but when in doubt, treat as VT (amiodarone or cardioversion); adenosine is safe diagnostically in stable wide-complex regular tachycardia per ACLS but contraindicated in preexcited AF.
Step 3 management: Always print and save the tachycardia tracing — electrophysiology consultation depends on it for ablation planning.
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Diagnostic Workup — Advanced and Confirmatory Studies

24–48 hr Holter: for daily symptoms

14–30 day event monitor / patch (Zio): for weekly symptoms — highest yield for typical SVT

Implantable loop recorder: for syncope of suspected arrhythmic origin, episodes <1/month

Smartphone/wearable ECG (Apple Watch, KardiaMobile): increasingly accepted; print tracings for documentation

— Indicated in all patients with newly diagnosed SVT to assess structural heart disease, LV function, Ebstein anomaly (associated with WPW), and rule out tachycardia-mediated cardiomyopathy

— Repeat after rate/rhythm control if LV dysfunction was present — often reversible

— Definitive diagnosis of SVT mechanism

— Combined with catheter ablation in same session

— Class I indication: symptomatic recurrent AVNRT, AVRT, focal AT, and any preexcitation with symptoms or high-risk features

— Exercise stress test: abrupt loss of delta wave at higher HR suggests low-risk pathway

— EP study with isoproterenol to measure shortest preexcited RR interval (SPERRI) — <250 ms = high risk, ablation indicated

— Terminates AV-nodal-dependent SVT (AVNRT, AVRT)

— Unmasks flutter waves or atrial tach by producing transient AV block

— Avoid in known/suspected preexcited AF

Ambulatory rhythm monitoring (outpatient workup of paroxysmal palpitations without captured episode):
Echocardiogram (TTE):
Electrophysiology (EP) study:
Risk stratification of asymptomatic WPW:
Adenosine as diagnostic tool:
Key distinction: Tachycardia-mediated cardiomyopathy presents as new HF with reduced EF in a patient with chronic incessant SVT or rapid AF — EF typically recovers within 3–6 months after rate/rhythm normalization. Always reassess EF before labeling a patient with permanent HFrEF.
Genetic testing for familial WPW (PRKAG2) reserved for clusters; not routine.
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Risk Stratification and Acute Management Algorithm

— Unstable (hypotension with hypoperfusion, AMS, ischemic chest pain, acute HF) → synchronized cardioversion 50–100 J biphasic, escalate as needed

— Sedate if time permits (etomidate, midazolam) — but do not delay cardioversion in extremis

Vagal maneuvers first (modified Valsalva preferred, ~43% success)

— If fails → Adenosine 6 mg rapid IV push via proximal vein with 20 mL saline flush; if no conversion in 1–2 min, 12 mg, may repeat 12 mg once

— If adenosine fails or contraindicated → IV diltiazem or verapamil (calcium channel blockers), OR IV metoprolol/esmolol (beta-blockers)

— Rate control with diltiazem or beta-blocker; treat underlying cause for MAT (correct hypoxia, Mg)

— Assume VT; if suspected SVT with aberrancy, may try adenosine cautiously

— Procainamide preferred over amiodarone for hemodynamically stable VT (PROCAMIO trial)

Preexcited AF (irregular wide complex, rate >200, varying QRS morphology): AVOID adenosine, CCB, beta-blockers, digoxin — they enhance accessory pathway conduction → VF. Use procainamide or ibutilide, or cardiovert

— Severe asthma/COPD with active bronchospasm (relative)

— Heart transplant (denervation hypersensitivity — use 1 mg starting dose)

— Preexcited AF

— High-grade AV block without pacemaker

Step 1 — Stability check:
Step 2 — Stable, narrow regular SVT:
Step 3 — Stable, narrow irregular (likely AF/aflutter with variable block or MAT):
Step 4 — Wide-complex regular tachycardia (stable):
Contraindications to adenosine:
CCS pearl: Document a continuous rhythm strip during adenosine administration — capturing the moment of AV block reveals the underlying atrial mechanism and is often the diagnostic gold for atrial tach vs flutter vs AVNRT. Warn the patient about transient chest pressure, flushing, and "sense of doom" lasting ~10 seconds.
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Pharmacotherapy — Chronic Suppression

Beta-blockers: metoprolol succinate 25–200 mg daily, atenolol, nadolol — preferred in CAD, HFrEF, hypertension, pregnancy (metoprolol/labetalol)

Non-dihydropyridine CCBs: diltiazem CD 120–360 mg daily, verapamil ER — preferred in asthma/COPD; avoid in HFrEF

Flecainide or propafenone (class Ic) — effective for AVNRT/AVRT, can use "pill-in-pocket" 200–300 mg flecainide at episode onset in selected outpatients

— Requires structurally normal heart (no CAD, no LV dysfunction) — CAST trial showed increased mortality post-MI

— Often combined with AV nodal blocker to prevent 1:1 conduction if atrial flutter develops

Sotalol or dofetilide (class III) — reserved for refractory cases, QT monitoring required (inpatient initiation for dofetilide)

Avoid AV nodal blockers (digoxin absolutely contraindicated; beta-blockers/CCBs relative)

Catheter ablation is first-line definitive therapy

— If ablation declined: flecainide or propafenone

— Treat underlying cause (digoxin toxicity, COPD, ischemia)

— Beta-blocker or CCB; ablation for focal AT

— Treat underlying pulmonary disease/hypoxia; correct Mg and K

— Verapamil or metoprolol if needed; avoid beta-blockers in severe bronchospasm

— Cardioversion ineffective (not reentrant)

Goal: reduce symptomatic episode frequency in patients not pursuing ablation or as bridge to EP.
First-line chronic agents (AV-nodal slowing, for AVNRT and orthodromic AVRT without preexcitation on baseline ECG):
Second-line / refractory:
WPW-specific chronic therapy:
Atrial tachycardia chronic management:
MAT (multifocal atrial tach):
Step 3 management: When prescribing chronic AV nodal blockade, screen the post-conversion sinus ECG for delta waves before discharge — missing WPW and discharging on diltiazem is a tested error. Document the ECG review in the chart.
Educate on Valsalva self-termination technique at home for mild recurrences.
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Catheter Ablation and Procedural Management

AVNRT: slow pathway modification in Koch's triangle; success >95%, AV block risk <1%

AVRT/WPW: accessory pathway ablation; success 93–95%

Focal atrial tachycardia: mapping and ablation of focus; success 80–90%

Typical atrial flutter: cavotricuspid isthmus ablation; success >95%

— Symptomatic recurrent SVT despite or intolerant of medical therapy

— Patient preference for definitive therapy as first-line (especially young patients, athletes, pregnancy planning, pilots/CDL drivers)

— Symptomatic WPW, asymptomatic WPW with high-risk features (rapid pathway, high-risk occupation)

— Tachycardia-mediated cardiomyopathy

— TTE, baseline ECG, basic labs, pregnancy test

— Hold antiarrhythmics ≥5 half-lives before EP study (allows induction)

— Anticoagulation continued for left-sided ablations

— Femoral venous (± arterial) access; transseptal puncture for left-sided pathways

— RF energy or cryoablation (cryo preferred near AV node for AVNRT in young patients — reversible cooling allows testing before permanent lesion)

— Vascular access (hematoma, pseudoaneurysm): 1–2%

— Cardiac tamponade: <1%

— Complete heart block requiring pacemaker: <1% (higher near AV node)

— Stroke for left-sided procedures: <0.5%

— Death: <0.1%

— Bed rest 4–6 hours; ambulate, discharge same day or next morning

— No heavy lifting × 1 week; resume normal activity in 2–3 days

— Follow-up in 4–6 weeks with ECG; event monitor if symptoms recur

Catheter ablation = definitive cure for most reentrant SVTs:
Indications (2015 ACC/AHA/HRS guideline, Class I):
Pre-procedure workup:
Procedure:
Complications (quote for informed consent):
Post-procedure:
Board pearl: For pregnant patients with refractory symptomatic SVT, ablation can be performed in second trimester with minimal/no fluoroscopy using 3D electroanatomic mapping (CARTO/Ensite) — preferred to chronic antiarrhythmic exposure when feasible.
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Special Populations — Elderly and Renal/Hepatic Impairment

— Higher prevalence of atrial tachycardia and atypical AVNRT vs young AVNRT predominance

— Coexisting CAD, HFrEF, conduction disease alter drug choice

— Polypharmacy increases interaction risk (especially with verapamil/diltiazem + beta-blockers → bradycardia, heart block)

— Increased fall risk with rate-slowing agents and postural hypotension

— Carotid sinus massage requires pre-massage auscultation for bruits; avoid if recent TIA/stroke, MI <3 months

Sotalol: renally cleared; reduce dose for CrCl 40–60 mL/min, avoid if <40

Dofetilide: strict renal dosing, contraindicated if CrCl <20

Digoxin: narrow therapeutic index; reduce dose, monitor levels; toxicity manifests as atrial tachycardia with AV block (paradoxical)

Atenolol, nadolol: renally cleared; prefer metoprolol in CKD

Adenosine: no renal adjustment (RBC-metabolized, t½ <10 sec)

Diltiazem, verapamil: hepatically metabolized; reduce dose in cirrhosis

Metoprolol, propranolol: hepatic metabolism; titrate carefully

Amiodarone: hepatotoxic; check LFTs at baseline and q6 months

Flecainide: hepatic and renal; caution in mixed dysfunction

— Avoid non-dihydropyridine CCBs (negative inotropy worsens HF)

— Avoid flecainide and propafenone (proarrhythmic in structural heart disease)

— Acceptable: beta-blockers (carvedilol, metoprolol succinate, bisoprolol), amiodarone, dofetilide, ablation

Elderly considerations:
Drug dose adjustments — renal impairment:
Drug dose adjustments — hepatic impairment:
HFrEF-specific considerations:
Step 3 management: In elderly patients with new "SVT," always re-examine the ECG for atrial flutter at 150 bpm with 2:1 block — this is more common than true AVNRT in this group and changes therapy toward rate control + anticoagulation assessment using CHA₂DS₂-VASc.
Reassess driving safety after symptomatic episodes; counsel per state law.
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Special Populations — Pregnancy and Pediatrics

— SVT incidence increases due to elevated blood volume, sympathetic tone, and estrogen-mediated changes

— Preexisting SVT often worsens, especially in second/third trimester

Acute termination: vagal maneuvers first; adenosine is safe in all trimesters (Category C but extensive safety data, does not cross to fetus appreciably)

Synchronized cardioversion safe in pregnancy if unstable; fetal monitoring during procedure

Chronic prophylaxis: metoprolol or propranolol preferred (avoid atenolol — IUGR association); verapamil acceptable

Avoid: amiodarone (fetal hypothyroidism, neurodevelopmental effects), atenolol, dronedarone

— Flecainide and sotalol acceptable if refractory; flecainide also used for fetal SVT

— Ablation deferrable to postpartum; if essential, perform in 2nd trimester with minimal fluoroscopy

AVRT more common than AVNRT under age 12 (opposite of adults)

— Neonatal SVT often presents with poor feeding, irritability, tachypnea, pallor — not classic palpitations

— Heart rate thresholds: infants >220 bpm, children >180 bpm

Vagal maneuvers: ice to face (diving reflex) in infants; Valsalva via blowing through a straw in older children

Adenosine dosing: 0.1 mg/kg (max 6 mg) first dose, then 0.2 mg/kg (max 12 mg)

Cardioversion: 0.5–1 J/kg, escalate to 2 J/kg

Chronic prevention: propranolol or atenolol; digoxin historically used but contraindicated in WPW

— Ablation safe and effective in children >15 kg; deferred when possible until older if asymptomatic

Pregnancy:
Pediatrics:
Board pearl: Fetal SVT detected on obstetric ultrasound (rate >200 with hydrops risk) is treated with maternal transplacental digoxin, flecainide, or sotalol — a classic Step 3 obstetrics-cardiology crossover question.
Key distinction: WPW + AF in adolescent presenting with syncope — emergent cardioversion and procainamide; AV nodal blockers and digoxin are contraindicated.
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Complications and Adverse Outcomes

Hemodynamic collapse: rare in structurally normal heart; common with rapid preexcited AF (degeneration to VF — sudden cardiac death risk)

Demand ischemia / NSTEMI: in patients with underlying CAD

Syncope: from rapid rates or transition to AF

Acute pulmonary edema: in patients with diastolic or systolic dysfunction

— Chronic incessant SVT (often atrial tach in adults, permanent junctional reciprocating tachycardia in children) → progressive LV dilation and dysfunction

— Reversible: EF typically recovers within 3–6 months after rhythm restoration

— Underdiagnosed; consider in any new HFrEF with frequent ectopy or persistent tachycardia

— Adenosine: transient asystole, AF induction (~12%), bronchospasm, chest discomfort

— Beta-blockers/CCBs: bradycardia, hypotension, AV block; combined use risky

— Flecainide/propafenone: ventricular proarrhythmia in structural disease; flutter with 1:1 conduction

— Amiodarone: thyroid dysfunction (hyper- and hypo-), pulmonary fibrosis, hepatotoxicity, corneal microdeposits, blue-gray skin

— Sotalol/dofetilide: torsades from QT prolongation

— AV block requiring permanent pacemaker (highest near septal/AV nodal substrate)

— Cardiac tamponade, vascular access injury, stroke (left-sided), phrenic nerve injury, pulmonary vein stenosis (for atrial procedures)

— Anxiety, panic, avoidance behaviors are common; screen and address

— Many patients restrict caffeine, exercise unnecessarily — counsel reasonably

Acute complications of SVT episodes:
Tachycardia-mediated cardiomyopathy (TMC):
Complications of pharmacotherapy:
Complications of ablation:
Psychological burden:
CCS pearl: Order a follow-up TTE 3 months after rhythm control in any patient who presented with concurrent reduced EF — if EF normalizes, the diagnosis is tachycardia-mediated cardiomyopathy and they do NOT need lifelong HF therapy (but should remain on beta-blocker for SVT prevention and recurrence surveillance).
Driving restrictions vary by state after syncope; counsel per AHA/HRS 2015 statement.
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When to Escalate Care — ICU, Consult, and Triage

— Hemodynamic instability requiring cardioversion

— Preexcited AF (WPW + AF) — high VF risk

— SVT in setting of acute MI, decompensated HF, or hypoxia

— Refractory SVT not terminating with adenosine + two AV nodal blockers

— Tachycardia-mediated cardiomyopathy with acute HF

— Drug initiation requiring monitoring (dofetilide always inpatient; sotalol typically inpatient initiation)

— Any preexcitation on resting ECG (delta wave) — even if asymptomatic ablation discussion

— Recurrent symptomatic SVT despite AV nodal blocker

— Syncope associated with documented SVT

— Wide-complex tachycardia of uncertain mechanism

— Pregnancy with recurrent SVT

— Athletes and high-risk occupations (pilots, drivers, military)

— First episode, structurally normal heart, asymptomatic post-conversion, no preexcitation → discharge home with outpatient cardiology follow-up in 1–2 weeks, event monitor, TTE

— Recurrent episodes, established diagnosis, responsive to home Valsalva → discharge, ensure rate-control prescription and EP referral if not yet evaluated

— Slow conversion, ongoing symptoms but stable

— Initiation of rate-control medication with monitoring

Indications for immediate ED → ICU/CCU admission:
Cardiology / EP consultation triggers:
Disposition from ED — stable patient after termination:
Observation unit appropriate for:
Step 3 management: A patient discharged after first SVT episode needs three concrete arrangements before leaving: (1) cardiology outpatient appointment, (2) ambulatory rhythm monitor if recurrent symptoms suspected, (3) clear return precautions (syncope, chest pain, episode >30 min unresponsive to vagal maneuvers). Documentation of all three is a quality measure and a Step 3 testable item.
Coordinate with PCP for medication reconciliation — particularly removing offending agents (decongestants, stimulants, excess thyroid replacement).
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Key Differentials — Other Tachyarrhythmias

— Gradual onset and offset (warm-up/cool-down)

— Rate usually 100–150, rarely >170 except with severe physiologic stress

— Visible upright P waves before each QRS in II, III, aVF

— Treat the cause (pain, fever, hypovolemia, anemia, hyperthyroidism, PE, sepsis), NOT the rhythm

— Persistent sinus tachycardia at rest without identifiable cause, often young women

— Diagnosis of exclusion; treat with ivabradine or beta-blocker

— Irregularly irregular, no discrete P waves

— Rate control + anticoagulation by CHA₂DS₂-VASc

— Distinct from SVT in management; do NOT use adenosine if preexcited

— Sawtooth flutter waves (negative in II/III/aVF for typical CCW flutter)

— Ventricular rate commonly 150 with 2:1 conduction — frequently mistaken for AVNRT

— Adenosine unmasks flutter waves diagnostically

— Treatment: rate control, anticoagulation, CTI ablation curative

— ≥3 distinct P-wave morphologies, rate >100

— Associated with COPD exacerbation, theophylline, hypoxia

— Treat underlying disease; verapamil or metoprolol; cardioversion ineffective

— Narrow QRS, no P or retrograde P, rate 70–130

— Causes: digoxin toxicity, post-cardiac surgery, ischemia

— Wide complex, regular; assume VT in patients with prior MI or HF

— AV dissociation, fusion/capture beats, QRS >140 ms favor VT

Sinus tachycardia:
Inappropriate sinus tachycardia (IST):
Atrial fibrillation:
Atrial flutter:
Multifocal atrial tachycardia (MAT):
Junctional tachycardia:
Ventricular tachycardia mimicking SVT with aberrancy:
Key distinction: Regular narrow-complex tachycardia at exactly 150 bpm = atrial flutter with 2:1 block until proven otherwise. Always assess for flutter waves with vagal maneuvers or adenosine before labeling AVNRT.
Board pearl: Digoxin toxicity classically produces atrial tachycardia WITH AV block — a near-pathognomonic combination on Step 3.
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Key Differentials — Non-Arrhythmic Mimics

— Gradual onset palpitations, paresthesias, derealization, hyperventilation

— Rate usually 110–130, not >170

— Capture ECG during episode — if sinus, treat anxiety, avoid unnecessary cardiology workup

— Persistent sinus tachycardia, weight loss, heat intolerance, tremor, hyperreflexia, lid lag

— Check TSH in any patient with new tachyarrhythmia, including SVT

— Treat thyroid disease; beta-blockers (propranolol) for symptom relief

— Paroxysmal tachycardia + hypertension + headache + diaphoresis

— Check plasma free metanephrines if suspected

— Never give beta-blocker before alpha-blocker (unopposed alpha → hypertensive crisis)

— Cocaine, methamphetamine, MDMA → tachycardia, hypertension, chest pain

— Avoid beta-blockers in acute cocaine intoxication (unopposed alpha vasoconstriction)

— Use benzodiazepines + nitroglycerin first-line; phentolamine for refractory HTN

— Alcohol withdrawal: tachycardia with tremor, sweating, hallucinations — benzodiazepines

— Sinus tachycardia is the most common ECG finding (more common than S1Q3T3)

— Always consider PE in unexplained tachycardia, especially with dyspnea or hypoxia

— Compensatory sinus tachycardia; treat underlying condition

— Beta-blockade is harmful when sinus tachycardia is compensatory

— Albuterol, theophylline, decongestants, ADHD stimulants, levothyroxine overreplacement, dobutamine, sympathomimetic eye drops

— HR rise ≥30 bpm within 10 min of standing (≥40 in adolescents), without orthostatic hypotension

— Treat with volume expansion, compression stockings, ivabradine, low-dose beta-blocker

Anxiety/panic disorder:
Hyperthyroidism:
Pheochromocytoma:
Substance use / withdrawal:
Pulmonary embolism:
Hypovolemia / sepsis / anemia:
Medication-induced:
POTS (postural orthostatic tachycardia syndrome):
Step 3 management: A patient labeled "SVT" who actually has compensatory sinus tachycardia from sepsis, PE, or GI bleed can decompensate catastrophically with beta-blockade or CCB. Always rule out hypovolemia and hypoxia before pharmacologic rate control.
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Secondary Prevention and Discharge Planning

— Rate-control agent if recurrent: metoprolol succinate or diltiazem CD daily

— "Pill-in-pocket" flecainide 200–300 mg or propafenone 450–600 mg for selected outpatients with infrequent well-tolerated episodes and structurally normal heart (after first dose given under monitoring)

— Discontinue offending agents: pseudoephedrine, energy drinks, excessive caffeine (>400 mg/day), illicit stimulants, smoking, OTC weight-loss supplements

— Optimize thyroid replacement (target TSH within range, not suppressed)

— Treat OSA — apnea-induced sympathetic surges trigger SVT/AF

— Moderate alcohol (≤1 drink/day women, ≤2 men); abstinence if episodes alcohol-triggered

— Exercise is encouraged — not restricted — in absence of preexcitation/structural disease

— Hydration, sleep, stress management

— Teach modified Valsalva for home use

— Symptomatic recurrent SVT despite medication or patient preference for cure

— All symptomatic WPW

— Tachycardia-mediated cardiomyopathy

— Pregnancy planning in symptomatic patients (curative before conception)

— Not indicated for AVNRT, AVRT, or focal AT (no embolic risk)

— Required for atrial flutter and AF per CHA₂DS₂-VASc, even if confused with SVT initially

— Mechanism (AVNRT vs AVRT vs AT) on discharge summary

— Presence/absence of preexcitation on resting ECG

— Medications avoided and why (e.g., "AV nodal blockers contraindicated due to WPW")

Discharge medication checklist after first or recurrent SVT:
Lifestyle counseling:
Ablation referral:
Anticoagulation:
Document for transitions of care:
Board pearl: Asymptomatic WPW pattern incidentally found on ECG in a low-risk occupation adult does NOT mandate ablation — risk-stratify with exercise stress testing or EP study based on shared decision-making (2015 ACC/AHA/HRS). Sudden cardiac death risk in asymptomatic WPW is ~0.1%/year.
Ensure PCP and cardiology share the plan via care summary.
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Follow-Up, Monitoring, and Counseling

— Post-ED visit: cardiology in 1–2 weeks with rhythm monitor data

— Post-ablation: ECG at 4–6 weeks; clinical follow-up at 3 and 12 months

— On chronic antiarrhythmic: every 3–6 months initially, annually once stable

Beta-blockers / CCBs: HR, BP, fatigue, depression, peripheral edema (CCB)

Flecainide / propafenone: ECG for QRS widening (>25% from baseline = reduce/stop), exercise stress test to assess for exercise-induced proarrhythmia

Sotalol: QTc (stop if >500 ms), renal function, ECG q6 months

Dofetilide: QTc 2 hr after first 5 doses inpatient; outpatient renal function and QTc q3 months

Amiodarone: TSH, LFTs, CXR baseline and q6 months; pulmonary function tests if respiratory symptoms; ophthalmologic exam yearly; skin and neuro exam

— Event monitor or patch for breakthrough episodes despite therapy

— Wearable ECGs (Apple Watch, Kardia) helpful for documenting infrequent episodes — counsel on appropriate use vs anxiety amplification

— Recognize episode triggers and avoid

— Teach Valsalva self-termination (blow into thumb with closed glottis ×15 sec, then lie back and elevate legs)

— Seek emergency care for: syncope, chest pain, episode >30 min not responsive to vagal maneuvers

— Driving and pregnancy planning — discuss explicitly

— Screen for anxiety/PTSD-like symptoms after frightening episodes; consider CBT referral

— Avoid SSRIs that prolong QT (citalopram >20 mg) in patients on QT-prolonging antiarrhythmics

Routine follow-up cadence:
Monitoring by drug:
Ambulatory rhythm assessment:
Counseling pearls:
Cardiac rehab: not standard for isolated SVT, but encourage structured exercise; aerobic fitness reduces sympathetic tone.
Mental health:
Step 3 management: At each visit, reassess episode burden, medication adherence and side effects, ECG changes, and ablation candidacy — patients often defer ablation initially but become candidates as episode frequency or medication intolerance evolves. Document shared decision-making each visit.
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Ethical, Legal, and Patient Safety

— Disclose AV block requiring pacemaker (~1%), tamponade (<1%), vascular injury, stroke (left-sided procedures), and mortality (<0.1%)

— Discuss alternative of chronic medication and risk of breakthrough episodes

— Use teach-back to confirm understanding; document

— Risk of sudden cardiac death is low (~0.1%/yr) but devastating

— Especially in children, athletes, and high-risk occupations, EP risk stratification offers definitive guidance — patient (or pediatric assent + parental consent) must weigh procedural risk vs lifetime SCD risk

— AHA/HRS 2015 statement: private drivers may resume after symptom-free interval (varies by state, generally 6 months); commercial drivers face stricter limits

— Physician duty to counsel; mandatory reporting laws vary by state (CA, OR, NV, NJ, PA require)

— Document counseling explicitly in chart — failure-to-warn liability

— Pilots (FAA), commercial drivers (DOT), military, law enforcement, transit operators — diagnosis affects certification

— Catheter ablation often required for return to duty

— Discharge after SVT without confirming sinus-rhythm ECG review for delta waves — risk of inappropriate AV nodal blockade in undiagnosed WPW

— Failure to communicate "avoid digoxin and verapamil" in WPW patients to PCP/pharmacy

— Use structured handoff (SBAR, discharge summary with explicit drug avoidance list)

— Verify drug-drug interactions: amiodarone + warfarin (INR↑), amiodarone + digoxin (level↑), CCB + beta-blocker (bradycardia)

— Pharmacy MTM consult for polypharmacy in elderly

— Adolescents should participate meaningfully in ablation decisions

— Document assent for patients age 7+

Informed consent for ablation:
Asymptomatic WPW — shared decision-making:
Driving safety after syncope:
Occupational disclosure:
Transition-of-care risks (Step 3 high-yield):
Medication safety:
Pediatric assent and parental authority:
CCS pearl: When patient declines recommended ablation, document specific risks discussed, alternatives offered, and acknowledgment of recurrence risk — this protects both autonomy and provider; reassess preference at each visit as circumstances change.
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High-Yield Associations and Rapid-Fire Facts
AVNRT = most common SVT (60%); slow-fast type; pseudo-R' in V1, pseudo-S in inferior leads
AVRT = WPW physiology; orthodromic narrow, antidromic wide; delta wave on baseline ECG
WPW + AF = preexcited AF; AVOID adenosine, beta-blockers, CCBs, digoxin; use procainamide, ibutilide, or cardioversion
Adenosine half-life = <10 seconds; give via proximal IV with fast saline flush
Adenosine + heart transplant = use 1 mg (denervation hypersensitivity)
Adenosine contraindications = preexcited AF, severe asthma flare, high-grade AV block without pacer
Atrial tachycardia with AV block = digoxin toxicity until proven otherwise
MAT = ≥3 P-wave morphologies, COPD/theophylline; treat hypoxia, give Mg, verapamil
Atrial flutter ventricular rate 150 = think 2:1 conduction; vagal maneuvers/adenosine unmask flutter waves
CAST trial = flecainide/encainide ↑ mortality post-MI → contraindicated in structural heart disease
PROCAMIO trial = procainamide superior to amiodarone for stable VT
REVERT trial = modified Valsalva (supine + leg raise) ~43% conversion vs 17% standard
Polyuria post-SVT = ANP release from atrial stretch
Cannon A waves / frog sign = AVNRT (simultaneous atrial-ventricular contraction)
Ebstein anomaly = associated with WPW and accessory pathways
PRKAG2 = familial WPW gene
Pregnancy first-line acute SVT = vagal → adenosine → metoprolol → cardioversion
Pregnancy avoid = amiodarone (fetal hypothyroidism), atenolol (IUGR), dronedarone
Fetal SVT = maternal transplacental digoxin, flecainide, or sotalol
Pediatric SVT first-line acute = ice to face → adenosine 0.1 mg/kg
Tachycardia-mediated cardiomyopathy = reversible HFrEF; EF recovers 3–6 months after rhythm control
Asymptomatic WPW SCD risk = ~0.1%/year; risk-stratify with stress test or EP study
CTI ablation = curative for typical atrial flutter, success >95%
Board pearl: Memorize the 150-bpm rule — regular narrow tachycardia at exactly 150 = atrial flutter with 2:1 block; this single fact saves many Step 3 ECG questions.
Sotalol/dofetilide → torsades risk; check QTc; renal dosing critical
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Board Question Stem Patterns

— 28-year-old woman with sudden palpitations, rate 180, narrow regular QRS, pseudo-R' in V1

— Next step: vagal maneuvers, then adenosine 6 mg IV push

— Long-term: discuss beta-blocker vs ablation

— Young patient with syncope, ECG shows irregular wide-complex tachycardia with varying QRS morphology, rate 220

— Next step: synchronized cardioversion (unstable) or IV procainamide/ibutilide (stable)

— Trap answers: adenosine, diltiazem, metoprolol, digoxin — all WRONG (enhance pathway conduction)

— 60-year-old man with palpitations, rate 150 regular, ECG shows possible AVNRT

— Adenosine reveals sawtooth flutter waves; next step is rate control + anticoagulation assessment with CHA₂DS₂-VASc

— Elderly woman with renal impairment on digoxin presents with nausea, visual halos, rate 130 with regular atrial activity but variable AV block

— Diagnosis: atrial tachycardia with AV block; treat with digoxin Fab

— Middle-aged patient with new HFrEF (EF 30%) and chronic SVT or rapid AF

— Manage rhythm → reassess EF in 3–6 months → likely recovery

— 28-week pregnant patient with recurrent SVT

— Acute: vagal → adenosine (safe)

— Chronic: metoprolol (not atenolol); avoid amiodarone; consider 2nd-trimester ablation if refractory

— Pre-participation ECG shows delta wave; manage with EP study or exercise stress test for risk stratification; ablation if high-risk pathway

— Address vascular access care, ECG at 4–6 weeks, return precautions, gradual return to activity, no driving restriction in absence of syncope

— Irregular rhythm with ≥3 P morphologies; treat hypoxia and bronchospasm; verapamil if rate persistent; avoid cardioversion

Stem 1 — Classic AVNRT presentation:
Stem 2 — WPW + AF (preexcited AF):
Stem 3 — Atrial flutter masquerading:
Stem 4 — Digoxin toxicity:
Stem 5 — Tachycardia-mediated cardiomyopathy:
Stem 6 — Pregnancy SVT:
Stem 7 — Asymptomatic WPW in athlete:
Stem 8 — Post-ablation discharge:
Stem 9 — MAT in COPD exacerbation:
Step 3 management: Each stem hinges on mechanism identification → stability → correct first drug or procedure → avoidance of contraindicated agents. Practice the WPW-AF stem repeatedly — it's the most commonly tested high-stakes scenario.
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One-Line Recap

Supraventricular tachycardia management hinges on rapid identification of mechanism, hemodynamic stability assessment, and avoiding AV nodal blockers in preexcited rhythms — with vagal maneuvers and adenosine as acute first-line, AV nodal blockers or class Ic agents for chronic suppression in structurally normal hearts, and catheter ablation as definitive curative therapy for symptomatic recurrent SVT or any preexcitation.

Acute, stable, regular narrow: modified Valsalva → adenosine 6 mg → 12 mg → IV diltiazem or beta-blocker; unstable → synchronized cardioversion 50–100 J.
Preexcited AF (WPW + irregular wide tachycardia): procainamide or ibutilide or cardioversion; never adenosine, CCB, beta-blocker, or digoxin — they accelerate accessory pathway conduction and can precipitate VF.
Chronic prevention: identify and remove triggers (caffeine, stimulants, hyperthyroidism, OSA), prescribe beta-blocker or non-DHP CCB, consider pill-in-pocket flecainide for selected structurally normal hearts; refer all symptomatic patients and all WPW for EP evaluation and ablation.
Transitions of care priorities: post-conversion sinus ECG review for delta waves, TTE to exclude structural disease, ambulatory rhythm monitor for breakthrough symptoms, cardiology follow-up within 1–2 weeks, explicit return precautions for syncope or sustained episodes, and shared decision-making documentation regarding ablation vs lifelong medication.
Board pearl: Three SVT facts that win exams — (1) regular narrow tachycardia at exactly 150 bpm = atrial flutter with 2:1 block until proven otherwise; (2) atrial tach with AV block = digoxin toxicity; (3) WPW + AF = no AV nodal blockers, ever — use procainamide or cardioversion. Master these and you will answer the majority of Step 3 SVT items correctly.
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