# Clinical Cases: Cardiac Electrophysiology

## Case 1: Wolff-Parkinson-White Syndrome with SVT

### Patient Presentation
**Demographics:** 24-year-old male

**Chief Complaint:** Sudden onset rapid heartbeat and near-syncope

**History of Present Illness:**
A 24-year-old previously healthy male presents to the emergency department with sudden onset rapid, regular palpitations that began 45 minutes ago while playing basketball. He reports lightheadedness, mild chest discomfort, and feels like his heart is "racing out of his chest." He has had similar but shorter episodes in the past that resolved spontaneously. No prior cardiac history.

**Physical Examination:**
- Vital Signs: BP 95/62 mmHg, HR 210 bpm (regular), RR 22/min, SpO2 96% on room air
- General: Anxious, diaphoretic
- Cardiovascular: Tachycardic, regular rhythm, no murmurs
- Lungs: Clear bilaterally

### Workup
- **ECG during tachycardia:** Narrow complex regular tachycardia at 210 bpm, no visible P waves
- **ECG after conversion:** Short PR interval (100 ms), delta wave (slurred upstroke of QRS), wide QRS complex (140 ms)
- **Echocardiogram:** Normal LV function, no structural abnormalities
- **Electrophysiology study:** Left lateral accessory pathway identified

### Diagnosis
**Wolff-Parkinson-White syndrome with orthodromic atrioventricular reentrant tachycardia (AVRT)**

*Electrophysiology Correlation:* WPW syndrome occurs due to an accessory pathway (Bundle of Kent) that bypasses the AV node, creating an anatomical circuit for reentry. The accessory pathway has faster conduction than the AV node and lacks decremental conduction properties. During orthodromic AVRT, the impulse travels down the AV node (anterograde) and returns via the accessory pathway (retrograde), creating a macro-reentrant circuit. The delta wave on resting ECG represents ventricular pre-excitation via the accessory pathway.

### Treatment
**Acute management:**
1. Vagal maneuvers (Valsalva, carotid massage) - attempted, unsuccessful
2. Adenosine 6 mg IV push - converted to sinus rhythm
3. Avoid AV nodal blockers if atrial fibrillation develops (can accelerate conduction down accessory pathway)

**Long-term management:**
1. Catheter ablation of accessory pathway (definitive treatment)
2. High success rate (>95%) with low complication risk
3. Avoidance of triggers (caffeine, alcohol)

### Clinical Image
![WPW ECG Pattern](case_01_image.jpg)

**Image Description:** 12-lead ECG demonstrating Wolff-Parkinson-White pattern with characteristic short PR interval (<120 ms) and delta wave (slurred upstroke of QRS complex) representing ventricular pre-excitation through the accessory pathway.

**Source:** Wikimedia Commons - WPW syndrome ECG
**License:** CC BY-SA 3.0
**URL:** https://commons.wikimedia.org/wiki/File:WPW_ECG.png

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## Case 2: Complete Heart Block (Third-Degree AV Block)

### Patient Presentation
**Demographics:** 72-year-old female

**Chief Complaint:** Syncope and fatigue

**History of Present Illness:**
A 72-year-old female with history of hypertension presents after a witnessed syncopal episode while sitting in a chair. She lost consciousness for approximately 30 seconds without seizure activity and regained consciousness spontaneously. Over the past 2 weeks, she has noted progressive fatigue and dizziness. She denies chest pain or shortness of breath.

**Physical Examination:**
- Vital Signs: BP 140/85 mmHg, HR 35 bpm (regular), RR 14/min, SpO2 98% on room air
- General: Alert, no acute distress
- Cardiovascular: Bradycardic, regular rhythm, variable intensity S1 (cannon A waves in JVP), no murmurs
- Neurological: No focal deficits

### Workup
- **ECG:** Complete AV dissociation with atrial rate 80 bpm and ventricular rate 35 bpm; narrow QRS escape rhythm; P waves bear no relationship to QRS complexes
- **Labs:** Troponin negative, electrolytes normal, TSH normal
- **Echocardiogram:** Normal LV function, no structural abnormalities
- **Telemetry:** Persistent complete heart block

### Diagnosis
**Complete (third-degree) atrioventricular block with junctional escape rhythm**

*Electrophysiology Correlation:* Third-degree AV block occurs when no atrial impulses conduct to the ventricles, resulting in complete AV dissociation. The escape rhythm depends on where the block occurs:
- Block at AV node → junctional escape (narrow QRS, 40-60 bpm)
- Block below AV node (infranodal) → ventricular escape (wide QRS, 20-40 bpm)

This patient's narrow QRS escape suggests the block is at the AV node level. The variable S1 intensity occurs because of changing timing between atrial and ventricular contraction. Cannon A waves occur when the atrium contracts against a closed tricuspid valve.

### Treatment
1. Temporary transcutaneous pacing standby
2. Atropine (limited efficacy for complete heart block)
3. **Permanent pacemaker implantation** (definitive treatment)
   - Dual-chamber pacemaker (DDD) indicated for AV block with sinus node function
4. Hold any AV nodal blocking medications

### Clinical Image
![Complete Heart Block ECG](case_02_image.jpg)

**Image Description:** ECG rhythm strip showing complete heart block with AV dissociation. P waves (atrial activity) occur regularly but independently of QRS complexes (ventricular activity). The ventricular rate is slow with a junctional escape rhythm.

**Source:** Wikimedia Commons - Third-degree AV block
**License:** CC BY-SA 4.0
**URL:** https://commons.wikimedia.org/wiki/File:Third_degree_heart_block.png

---

## Case 3: Long QT Syndrome with Torsades de Pointes

### Patient Presentation
**Demographics:** 18-year-old female

**Chief Complaint:** Cardiac arrest during swimming

**History of Present Illness:**
An 18-year-old female was found unresponsive at the bottom of a swimming pool during swim practice. Bystander CPR was initiated immediately. Upon EMS arrival, the cardiac monitor showed polymorphic ventricular tachycardia (torsades de pointes). She was defibrillated once with return of spontaneous circulation. She had experienced several "fainting spells" over the past 2 years, including one episode while startled by a loud noise. Her maternal uncle died suddenly at age 25 during exercise.

**Physical Examination (post-resuscitation):**
- Vital Signs: BP 105/65 mmHg, HR 68 bpm, RR 14/min (intubated), Temp 36.2°C
- General: Intubated, sedated
- Cardiovascular: Regular rhythm, no murmurs
- Neurological: Purposeful movements to stimulation

### Workup
- **ECG:** Sinus rhythm with markedly prolonged QTc interval (520 ms), notched T waves in lateral leads
- **Echocardiogram:** Normal LV function, no structural abnormalities
- **Labs:** Electrolytes normal (K+ 4.0, Mg 2.1, Ca 9.2)
- **Genetic testing:** KCNQ1 mutation identified (LQT1)
- **Family screening:** Mother has prolonged QTc (480 ms)

### Diagnosis
**Congenital Long QT Syndrome Type 1 (LQT1) with aborted sudden cardiac death due to torsades de pointes**

*Electrophysiology Correlation:* Long QT syndrome results from mutations in cardiac ion channels that prolong repolarization. LQT1 is caused by mutations in KCNQ1 gene encoding the IKs potassium channel (slow delayed rectifier). Prolonged repolarization creates heterogeneity in refractoriness and increases risk of early afterdepolarizations (EADs), which can trigger torsades de pointes. LQT1 is characteristically triggered by exercise, especially swimming, and emotional stress (catecholamine-mediated).

The action potential prolongation is due to:
- Reduced IKs current → delayed phase 3 repolarization
- EADs during plateau phase → triggered activity
- Dispersion of refractoriness → reentry

### Treatment
1. **Beta-blocker therapy** (nadolol preferred for LQT1) - reduces catecholamine triggers
2. **ICD implantation** (indicated after cardiac arrest)
3. Avoid QT-prolonging medications (www.crediblemeds.org)
4. Avoid strenuous exercise, especially swimming
5. Family screening with ECG and genetic testing
6. Magnesium repletion and potassium optimization

### Clinical Image
![Torsades de Pointes](case_03_image.jpg)

**Image Description:** ECG showing torsades de pointes, a polymorphic ventricular tachycardia characterized by QRS complexes that appear to twist around the isoelectric baseline. The characteristic "twisting of the points" pattern with undulating axis is visible.

**Source:** Wikimedia Commons - Torsades de pointes ECG
**License:** CC BY-SA 3.0
**URL:** https://commons.wikimedia.org/wiki/File:Torsades_de_Pointes.svg