A 72-year-old woman with chronic hypertension and diabetes mellitus type 2 presents with recurrent episodes of dizziness and near-syncope over the past week. Vital signs: BP 110/70 mmHg, HR 54 bpm. ECG shows a PR interval of 0.32 seconds. Rhythm strip shows: P wave, then a long PR interval, then QRS, then another P wave with a longer PR interval (0.40 seconds), then QRS, then a P wave followed by no QRS complex (dropped beat), then the cycle repeats. After the dropped beat, the PR interval resets to 0.28 seconds. What is the most likely diagnosis and the appropriate next step in management?

Explanation

## Diagnosis: Mobitz Type I Second-Degree AV Block (Wenckebach) ### ECG Pattern Recognition The **Wenckebach phenomenon** has a characteristic repeating cycle: 1. **Progressive PR prolongation**: 0.32 → 0.40 seconds 2. **Dropped QRS** (non-conducted P wave) after the longest PR interval 3. **PR reset**: After the dropped beat, the cycle restarts with a shorter PR interval (0.28 seconds) 4. **Repeating pattern**: The cycle then repeats **Mnemonic: "Long, Longer, Dropped"** — describes the progressive PR lengthening culminating in a dropped beat. ### Why This Is Mobitz I (Not Mobitz II) | Feature | Mobitz I (Wenckebach) | Mobitz II | |---------|----------------------|----------| | **PR interval pattern** | Progressive lengthening before dropped beat | Fixed PR in conducted beats; sudden dropped beat | | **Site of block** | AV node (usually) | Infranodal (His bundle, bundle branches) | | **Dropped beat frequency** | Usually every 3–5 beats | Unpredictable; often 2:1 or 3:1 | | **Escape rhythm if block progresses** | Junctional (40–60 bpm) | Ventricular (20–40 bpm) | | **Prognosis** | Benign; rarely progresses to complete block | Ominous; high risk of sudden complete block | | **Causes** | AV nodal ischemia, vagal tone, drugs (digoxin, beta-blockers, CCBs) | Acute MI, Lyme disease, infiltrative disease | | **Management** | Observation ± drug adjustment | Pacing | ### Clinical Context **Key Point:** Mobitz I is typically **benign and asymptomatic**. However, this patient has **symptomatic dizziness and near-syncope**, which indicates the block is causing hemodynamic compromise (likely due to loss of atrial contribution and slow ventricular rate during the dropped beats). **High-Yield:** The combination of chronic hypertension, diabetes, and age suggests **degenerative AV nodal disease**. Medications (beta-blockers, calcium channel blockers, digoxin) commonly cause or worsen Mobitz I. ### Management Strategy 1. **Telemetry monitoring** — assess frequency of dropped beats and symptoms 2. **Drug review** — discontinue AV nodal depressants (beta-blockers, non-dihydropyridine CCBs, digoxin) if possible 3. **Atropine trial** — if symptomatic, IV atropine (0.6 mg) may improve conduction by increasing AV nodal automaticity 4. **Pacing** — **temporary or permanent pacing is NOT routinely indicated** for asymptomatic Mobitz I; reserved for symptomatic cases unresponsive to drug withdrawal **Clinical Pearl:** Observation with telemetry is the **standard first-line approach** for Mobitz I, even if mildly symptomatic, because the block is usually **reversible** with drug adjustment or resolution of ischemia. Pacing is considered only if symptoms persist despite intervention. ### Why NOT Pacing Here? - Mobitz I has a **good prognosis** and rarely progresses to complete block - The block is **at the AV node** (proximal), which has intrinsic escape capability - **Temporary pacing** may be considered if symptoms are severe or if the patient is in acute MI, but this patient is stable (BP 110/70) - **Permanent pacing** is reserved for symptomatic Mobitz I refractory to medical management **Warning:** Do NOT confuse Mobitz I with Mobitz II — Mobitz II has a **fixed PR interval** in conducted beats and **no progressive lengthening**. Mobitz II is the ominous rhythm that demands pacing. [cite:Harrison 21e Ch 297]