1.4 Supraventricular Tachycardias, Ventricular Arrhythmias & Bradycardias
Key Takeaways
- Conduction defects, bradyarrhythmias, tachyarrhythmias and cardiac resuscitation are all enumerated under the dysrhythmias blueprint subsection.
- AV-nodal blocking agents are contraindicated in pre-excited atrial fibrillation because they accelerate conduction down the accessory pathway.
- Mobitz II and third-degree AV block are infranodal, do not respond reliably to atropine, and require pacing.
- Asymptomatic bifascicular block without syncope or higher-grade block does not require a pacemaker.
- Channelopathies such as long QT and Brugada syndrome present with syncope or arrest in structurally normal hearts and are diagnosed from the resting ECG.
1. Supraventricular Tachycardias (SVT)
AV Nodal Reentrant Tachycardia (AVNRT)
- Mechanism: Dual AV nodal pathways (slow pathway with short refractory period; fast pathway with long refractory period) creating a micro-reentrant circuit within the AV node.
- ECG: Regular narrow-complex tachycardia (140-220 bpm) with P waves buried within or immediately following the QRS complex (pseudo-r' in lead V1, pseudo-S in inferior leads).
- Acute Treatment: (1) Vagal maneuvers (modified Valsalva with supine leg elevation); (2) IV Adenosine (6 mg rapid IV push through large antecubital vein followed by 20 mL saline flush; if no response within 1-2 min, administer 12 mg IV); (3) IV Diltiazem or Metoprolol if adenosine fails; (4) Synchronized cardioversion if unstable.
- Definitive Treatment: Radiofrequency catheter ablation of the slow pathway (curative in >95% of cases).
AV Reentrant Tachycardia (AVRT) & Wolff-Parkinson-White (WPW) Syndrome
- Mechanism: Congenital extranodal accessory pathway (Bundle of Kent) connecting atrium and ventricle, bypassing the AV node.
- Baseline ECG Triad: Short PR interval (<120 ms), slurred QRS upstroke (delta wave), and widened QRS (>120 ms).
- Orthodromic AVRT (90%): Conduction travels anterograde down the AV node and retrograde up the accessory pathway -> Regular narrow-complex tachycardia. Treat identical to AVNRT (vagal maneuvers, IV Adenosine).
- Antidromic AVRT (10%): Conduction travels anterograde down the accessory pathway and retrograde up the AV node -> Regular wide-complex tachycardia.
- Pre-Excited Atrial Fibrillation (AF + WPW):
- ECG: Irregularly irregular, wide-complex tachycardia with bizarre, polymorphous QRS morphology and extremely rapid ventricular rates (>250-300 bpm).
- CRITICAL BOARD CONTRAINDICATION: AV nodal blocking agents ("ABCD": Adenosine, Beta-blockers, Calcium channel blockers [Diltiazem/Verapamil], Digoxin) are STRICTLY CONTRAINDICATED. Blocking the AV node diverts 100% of electrical impulses down the accessory pathway, which has a very short refractory period, precipitating ventricular fibrillation and cardiac arrest.
- Treatment: Hemodynamically stable -> IV Procainamide (or IV Ibutilide) which prolongs the refractory period of the accessory pathway. Hemodynamically unstable -> Emergency Synchronized Direct-Current Cardioversion.
- Definitive: Catheter ablation of the accessory pathway.
2. Ventricular Arrhythmias & Channelopathies
Monomorphic Ventricular Tachycardia (VT)
- Defined as >=3 consecutive ventricular beats at a rate >100 bpm with identical QRS morphology. Wide QRS complex (>120 ms).
- ECG Signs of VT vs. SVT with Aberrancy:
- AV Dissociation: P waves marching independently of wide QRS complexes (pathognomonic).
- Capture Beats & Fusion Beats: Normal narrow QRS (capture) or hybrid hybrid QRS (fusion) demonstrating dual supraventricular and ventricular activation.
- Concordance: Uniformly positive or uniformly negative QRS complexes across leads V1-V6.
- Brugada Sign: Interval from onset of R wave to deepest nadir of S wave >100 ms in any precordial lead.
- Management:
- Pulseless VT: Immediate CPR + Defibrillation (unsynchronized 200 J biphasic) + Epinephrine + Amiodarone/Lidocaine.
- Unstable with Pulse: Synchronized cardioversion (100-200 J).
- Stable with Pulse: IV Amiodarone (150 mg over 10 min, then 1 mg/min for 6 hours) or IV Procainamide (20-50 mg/min until arrhythmia suppressed, hypotension ensues, or QRS widens >50%).
Polymorphic VT & Torsades de Pointes (TdP)
- Torsades de Pointes: Polymorphic VT characterized by QRS complexes continuously twisting around the isoelectric baseline, occurring in the setting of prolonged baseline QT interval (QTc >500 ms).
- Causes of Prolonged QTc:
- Electrolytes: Hypokalemia, Hypomagnesemia, Hypocalcemia.
- Drugs: Antiarrhythmics (Sotalol, Dofetilide, Procainamide), Psychotropics (Haloperidol, Citalopram, Methadone), Antimicrobials (Macrolides, Fluoroquinolones, Azole antifungals), Antiemetics (Ondansetron).
- Congenital Long QT Syndromes (LQTS): Romano-Ward (autosomal dominant), Jervell and Lange-Nielsen (autosomal recessive with sensorineural deafness).
- Acute Management of Torsades de Pointes:
- IV Magnesium Sulfate: 2 grams IV push over 1-2 minutes, repeated if necessary, regardless of baseline serum magnesium level.
- Withdraw all QT-prolonging medications and vigorously recheck/correct potassium to >4.0-4.5 mEq/L.
- Overdrive Transvenous Pacing or Isoproterenol Infusion: Increases heart rate to 100-110 bpm, which shortens ventricular repolarization and eliminates pauses that trigger TdP.
- Unsynchronized defibrillation if degenerates to VF or hemodynamic collapse.
3. Bradycardias and Conduction Blocks
Sinus Node Dysfunction (Sick Sinus Syndrome)
- Manifests as persistent sinus bradycardia, sinus pauses/arrest (>3 seconds), or Tachycardia-Bradycardia Syndrome (paroxysms of AF alternating with severe sinus pauses). Permanent Pacemaker (PPM) is indicated when bradycardia is symptomatic.
Atrioventricular (AV) Blocks & Pacing Indications
| AV Block Type | Site of Block | ECG Findings | Clinical Behavior | Permanent Pacemaker (PPM) Indication? |
|---|---|---|---|---|
| First-Degree AV Block | AV Node (usually) | PR interval > 200 ms (constant); every P wave is followed by a QRS | Benign; asymptomatic | NO (except rare symptomatic "pacemaker syndrome" with PR >300 ms) |
| Second-Degree Mobitz Type I (Wenckebach) | AV Node (above His bundle) | Progressive PR prolongation culminating in a non-conducted P wave; grouped beating | Usually benign; physiological in young athletes; low risk of progression | NO if asymptomatic. PPM only indicated if chronically symptomatic. |
| Second-Degree Mobitz Type II | Infranodal (His-Purkinje system) | Constant PR interval with intermittent, unpredictable dropped QRS complexes; wide QRS common | High risk of sudden progression to complete heart block and asystole | YES — Class I Indication for PPM in all patients, even if asymptomatic. |
| Third-Degree (Complete) AV Block | Infranodal or AV Node | Complete AV dissociation; regular P-P intervals and regular R-R intervals; escape rate 30-40 bpm (wide QRS) or 40-60 bpm (narrow QRS) | Severe bradycardia, syncope (Stokes-Adams attacks), heart failure, sudden death | YES — Class I Indication for PPM in all patients (unless transient due to reversible Lyme carditis, hyperkalemia, or medication toxicity). |
Acute Symptomatic Bradycardia Protocol:
- Atropine: 1 mg IV push q3-5min (max 3 mg total). Note: Atropine is effective for AV nodal block (Mobitz I), but is INEFFECTIVE for infranodal block (Mobitz II / wide-QRS complete block).
- If atropine fails or is contraindicated: Transcutaneous Pacing or IV Chronotropic Infusions (Dopamine 5-20 mcg/kg/min or Epinephrine 2-10 mcg/min).
- Emergent Transvenous Temporary Pacing while preparing for permanent pacemaker implantation.
A 71-year-old woman with a history of hypertension and osteoarthritis presents to the clinic for a routine checkup. She is completely asymptomatic. A 12-lead ECG is obtained which demonstrates normal sinus rhythm at 72 bpm, a constant PR interval of 160 ms, and intermittent non-conducted P waves with dropped QRS complexes occurring in a 3:2 pattern without any preceding PR prolongation. Her QRS duration is 138 ms with a right bundle branch block pattern. Physical exam and laboratory tests are normal. What is the most appropriate management?
A 28-year-old man presents to the emergency department with sudden-onset palpitations and lightheadedness. His blood pressure is 114/72 mmHg and pulse is 210 bpm. The 12-lead ECG demonstrates an irregularly irregular rhythm with wide, bizarre, polymorphous QRS complexes ranging in rate from 190 to 280 bpm. A baseline ECG from 6 months ago showed a PR interval of 100 ms and a delta wave in lead II. What is the most appropriate acute pharmacologic intervention?