Arrhythmia Recognition and Management

Cardiac arrhythmias represent abnormalities in heart rate, rhythm, or electrical conduction that can range from benign to life-threatening conditions. Understanding the pathophysiological mechanisms underlying arrhythmias is crucial for proper recognition and management.

Mechanisms of Arrhythmogenesis:

1. Abnormal Automaticity: Enhanced automaticity occurs when pacemaker cells depolarize faster than normal, or when non-pacemaker cells acquire automaticity. This can result from increased sympathetic stimulation, electrolyte imbalances (hypokalemia, hypomagnesemia), or ischemia.

2. Triggered Activity: This mechanism involves afterdepolarizations that reach threshold potential. Early afterdepolarizations (EADs) occur during phase 2-3 of the action potential and are associated with QT prolongation and torsades de pointes. Delayed afterdepolarizations (DADs) occur after complete repolarization and are linked to calcium overload states.

3. Reentry: The most common mechanism in clinical arrhythmias, reentry requires three conditions: (a) two functionally distinct pathways, (b) unidirectional block in one pathway, and (c) slow conduction allowing recovery of the blocked pathway. This mechanism underlies atrial fibrillation, AVNRT, AVRT, and ventricular tachycardia.

Classification Systems:

Arrhythmias are classified by anatomical origin (supraventricular vs. ventricular), rate (bradycardia <60 bpm, tachycardia >100 bpm), and regularity. Supraventricular arrhythmias originate above the bundle of His and typically produce narrow QRS complexes (<120 ms), while ventricular arrhythmias originate below the bundle of His and produce wide QRS complexes (≥120 ms).

Clinical Significance:

The hemodynamic impact of arrhythmias depends on ventricular rate, underlying cardiac function, and duration. Extremely fast rates (>150-180 bpm) compromise ventricular filling, while very slow rates (<40-50 bpm) may inadequately perfuse vital organs. Loss of atrial contraction in atrial fibrillation reduces cardiac output by 15-25%, which can be particularly problematic in patients with diastolic dysfunction.

Atrial fibrillation (AF) is the most common sustained arrhythmia in clinical practice, affecting 2-3% of the population. The pathophysiology involves multiple reentrant wavelets in the atria, with the AV node acting as a filter for ventricular response.

Diagnostic Criteria:

• Irregularly irregular rhythm
• Absence of discrete P waves
• Variable R-R intervals
• Undulating baseline (fibrillatory waves)

Classification by Duration:

• Paroxysmal: Self-terminating within 7 days (usually <48 hours)
• Persistent: Sustained >7 days or requiring intervention
• Long-standing persistent: Continuous AF >12 months
• Permanent: Accepted long-term AF

Acute Management Algorithm:

AF with Hemodynamic Instability ↓ Immediate synchronized cardioversion (100-200J biphasic) ↓ Consider anticoagulation if duration >48 hours or unknown

AF with Hemodynamic Stability ↓ Rate Control vs Rhythm Control Strategy ↓ Rate Control (Target: 80-110 bpm at rest)

• Beta-blockers: Metoprolol 25-100mg BID
• Calcium channel blockers: Diltiazem 120-360mg daily
• Digoxin: 0.125-0.25mg daily (elderly, heart failure)

Rhythm Control ↓ Duration Assessment ↓ <48 hours: Cardioversion without anticoagulation

48 hours or unknown: TEE or 3-week anticoagulation before cardioversion

Anticoagulation Considerations: The CHA₂DS₂-VASc score guides anticoagulation decisions:

• Score 0 (males) or 1 (females): No anticoagulation
• Score 1 (males) or 2 (females): Consider anticoagulation
• Score ≥2 (males) or ≥3 (females): Anticoagulation recommended

Direct oral anticoagulants (DOACs) are preferred over warfarin due to improved safety profile and convenience. Contraindications include mechanical heart valves, severe mitral stenosis, or CrCl <15 mL/min.

Supraventricular tachycardia (SVT) encompasses several arrhythmias originating above the ventricles, most commonly atrioventricular nodal reentrant tachycardia (AVNRT) and atrioventricular reentrant tachycardia (AVRT).

Differential Diagnosis of Regular Narrow-Complex Tachycardia:

Acute Management of SVT:

Hemodynamically Unstable SVT ↓ Synchronized cardioversion (50-100J, then 100-200J)

Hemodynamically Stable SVT ↓ Vagal Maneuvers

• Valsalva maneuver (15 seconds)
• Carotid sinus massage (if no carotid bruits)
• Diving reflex (cold water on face) ↓ If unsuccessful: Adenosine 6mg IV push (central line preferred) ↓ If no response: Adenosine 12mg IV push ↓ If still unsuccessful: Adenosine 12mg IV push (repeat) ↓ Alternative agents:
• Verapamil 2.5-5mg IV
• Metoprolol 2.5-5mg IV q5min (max 15mg)
• Diltiazem 0.25mg/kg IV

Adenosine Administration:

• Use large-bore IV in antecubital fossa or central line
• Give rapid IV push followed immediately by 20mL saline flush
• Warn patient about transient chest discomfort and feeling of impending doom
• Contraindications: Asthma, COPD, sick sinus syndrome, 2nd/3rd degree AV block
• Half-life: <10 seconds

Long-term Management: For recurrent SVT, options include:

• Beta-blockers or calcium channel blockers for prophylaxis
• Radiofrequency catheter ablation (cure rate >95% for AVNRT/AVRT)
• Patient education on vagal maneuvers

Special Considerations:

• Pregnancy: Adenosine is safe; avoid verapamil
• WPW syndrome: Avoid AV nodal blocking agents if AF/flutter present
• Pediatric patients: Weight-based adenosine dosing (0.1mg/kg, max 6mg)

Ventricular arrhythmias represent potentially life-threatening emergencies requiring immediate recognition and intervention. These arrhythmias originate from ventricular myocardium and typically present with wide QRS complexes (≥120 ms).

Ventricular Tachycardia (VT) Classification:

• Monomorphic VT: Uniform QRS morphology, suggests single focus or circuit
• Polymorphic VT: Varying QRS morphology
  • Torsades de pointes: Polymorphic VT with prolonged QT interval
  • Polymorphic VT with normal QT: Usually ischemia-related

Diagnostic Criteria for VT:

• Wide QRS tachycardia (≥120 ms)
• Rate typically 150-250 bpm
• AV dissociation (when present, highly specific for VT)
• Capture beats or fusion beats (pathognomonic for VT)

VT vs SVT with Aberrancy - Key Differentiating Features:

Management Algorithm for Wide-Complex Tachycardia:

Wide-Complex Tachycardia ↓ Hemodynamically Unstable? ↓ YES Synchronized cardioversion 100J → 200J → 300J → 360J (monophasic) 120-200J (biphasic)

↓ NO Regular or Irregular? ↓ REGULAR:

• Assume VT if unclear
• Amiodarone 150mg IV over 10 min
• Alternative: Procainamide 20-50mg/min
• Avoid verapamil/diltiazem

IRREGULAR:

• Likely AF with aberrancy or pre-excited AF
• If pre-excited AF: Procainamide or amiodarone
• Avoid AV nodal blockers

Torsades de Pointes Management:

• Immediate: Magnesium sulfate 1-2g IV over 5-15 minutes
• Correct underlying causes: Hypokalemia, hypomagnesemia
• Discontinue QT-prolonging medications
• Temporary pacing if bradycardia-induced
• Isoproterenol if pacing unavailable

Ventricular Fibrillation (VF):

• Immediate defibrillation with unsynchronized shock
• Follow ACLS protocol
• Energy: 120-200J (biphasic), 360J (monophasic)
• CPR between shocks, minimize interruptions
• Epinephrine 1mg IV q3-5 minutes
• Consider amiodarone 300mg IV after 3rd shock

Heart blocks represent conduction abnormalities between the atria and ventricles, classified by the degree of conduction impairment and anatomical location within the AV conduction system.

First-Degree AV Block:

• Definition: Prolonged PR interval >200 ms with 1:1 AV conduction
• ECG findings: Consistent prolonged PR interval in all conducted beats
• Clinical significance: Usually benign, may progress in elderly
• Management: Observation, identify reversible causes (medications, electrolytes)

Second-Degree AV Block:

Type I (Wenckebach/Mobitz I):

• Pattern: Progressive PR prolongation until a P wave is not conducted
• Location: Typically AV node (narrow QRS)
• Prognosis: Generally benign
• Management: Observation unless symptomatic

Type II (Mobitz II):

• Pattern: Fixed PR interval with intermittent non-conducted P waves
• Location: Infranodal (often wide QRS)
• Risk: High risk of progression to complete heart block
• Management: Pacemaker indicated

Third-Degree (Complete) AV Block:

• Definition: Complete AV dissociation with independent atrial and ventricular rhythms
• Escape rhythms:
  • Junctional: 40-60 bpm, narrow QRS
  • Ventricular: 20-40 bpm, wide QRS
• Management: Temporary pacing, permanent pacemaker

Management Algorithm for Symptomatic Bradycardia:

Bradycardia with Symptoms (Chest pain, SOB, altered mental status, hypotension, syncope) ↓ IMMEDIATE INTERVENTIONS: Atropine 0.5mg IV (may repeat q3-5min, max 3mg) ↓ If inadequate response: TRANSCUTANEOUS PACING

• Rate: 60-70 bpm
• Start at 70mA, increase until capture
• Sedation/analgesia as needed

↓ IF TRANSCUTANEOUS PACING FAILS: DOPAMINE INFUSION

• 2-10 mcg/kg/min titrate to effect
• Alternative: Epinephrine 2-10 mcg/min

↓ DEFINITIVE MANAGEMENT: Transvenous pacing if:

• Hemodynamically significant bradycardia
• High-grade AV block
• Failed medical therapy

Atropine Considerations:

• Dose: 0.5mg IV (avoid doses <0.5mg - may paradoxically worsen bradycardia)
• Mechanism: Blocks muscarinic receptors, increases SA node firing
• Contraindications: Hypothermic patients, complete heart block with wide QRS
• May be ineffective in: Infranodal blocks, transplanted hearts

Permanent Pacemaker Indications:

• Class I (Definite):
  • Third-degree AV block
  • Second-degree Mobitz II
  • Alternating bundle branch block
  • Symptomatic sinus node dysfunction
• Class IIa (Reasonable):
  • Asymptomatic third-degree AV block with ventricular rate <40 bpm
  • Asymptomatic second-degree Mobitz II with wide QRS
• Class IIb (May be considered):
  • First-degree AV block with symptoms and long PR >300 ms

Electrical cardioversion and defibrillation are critical interventions for managing life-threatening arrhythmias. Understanding proper technique, indications, and contraindications is essential for safe and effective treatment.

Synchronized Cardioversion: Used for organized rhythms (atrial fibrillation, atrial flutter, SVT, stable VT) to avoid delivering shock during vulnerable period of cardiac cycle.

Technique:

1. Sedation: Procedural sedation with propofol, etomidate, or midazolam
2. Synchronization: Ensure sync button activated - look for sync markers on R waves
3. Pad placement:
   • Anterolateral: Right parasternal, left mid-axillary line
   • Anteroposterior: Anterior chest, left infrascapular
4. Energy selection: Start low and escalate as needed

Energy Recommendations (Biphasic):

• Atrial fibrillation: 100-200J initially
• Atrial flutter/SVT: 50-100J initially
• Ventricular tachycardia: 100J initially
• Increase by 50-100J if unsuccessful

Unsynchronized Defibrillation: Used for pulseless rhythms (VF, pulseless VT) where immediate defibrillation is priority.

ACLS Defibrillation Protocol:

• Energy: 120-200J (biphasic), 360J (monophasic)
• CPR: 2 minutes between shocks
• Medications: Epinephrine 1mg q3-5min, amiodarone 300mg after 3rd shock
• Reversible causes (H's and T's): Hypoxia, hypovolemia, H+, hypo/hyperkalemia, hypothermia, toxins, tamponade, tension pneumothorax, thrombosis

Pre-cardioversion Checklist:

BEFORE CARDIOVERSION: □ Patient consent obtained □ NPO status confirmed (≥6 hours for elective) □ Baseline labs: CBC, BMP, PT/PTT, TSH □ Digoxin level if applicable □ Anticoagulation status assessed □ Emergency medications available □ Anesthesia/sedation plan □ Defibrillator checked and sync verified □ "All clear" protocol established

Anticoagulation for Cardioversion:

• <48 hours duration: Can proceed without anticoagulation
• >48 hours or unknown duration:
  • Option 1: 3 weeks therapeutic anticoagulation before cardioversion
  • Option 2: TEE to exclude thrombus, then heparin + cardioversion
• Post-cardioversion: Continue anticoagulation ≥4 weeks (atrial stunning)

Complications and Management:

• Thromboembolism: Risk 1-2%, highest in first 24-48 hours
• Arrhythmias: Transient bradycardia, VT/VF (rare)
• Skin burns: Proper pad placement, adequate gel/paste
• Aspiration: NPO requirements, appropriate sedation

Special Considerations:

• Implanted devices: Place pads ≥8cm from device, interrogate post-procedure
• Pregnancy: Safe when indicated, fetal monitoring recommended
• Digoxin toxicity: Avoid cardioversion, may precipitate lethal arrhythmias
• Hyperkalemia: Correct before cardioversion attempt

Rapid recognition and systematic approach to arrhythmia management can be life-saving. This section provides integrated decision-making algorithms for common emergency scenarios.

Universal Arrhythmia Approach:

ARRHYTHMIA RECOGNITION ↓

1. ASSESS HEMODYNAMIC STABILITY
   • Blood pressure
   • Mental status
   • Signs of shock
   • Chest pain severity ↓
2. IDENTIFY RHYTHM
   • Heart rate (<60, 60-100, >100 bpm)
   • QRS width (<120 ms vs ≥120 ms)
   • Regularity (regular vs irregular)
   • P wave relationship ↓
3. IMMEDIATE MANAGEMENT
   • Unstable: Cardioversion/pacing
   • Stable: Specific algorithm

Tachycardia with Pulse Algorithm:

Tachycardia (>100 bpm) with Pulse ↓ SYMPTOMS: Hypotension, altered mental status, chest pain, heart failure? ↓ YES SYNCHRONIZED CARDIOVERSION

• Sedate if conscious
• AF/Flutter: 100-200J
• SVT: 50-100J
• VT: 100J

↓ NO (STABLE) WIDE QRS (≥120 ms)? ↓ YES REGULAR? ↓ YES: Assume VT

• Amiodarone 150mg IV/10min
• Alternative: Procainamide ↓ NO: Irregular wide complex
• Likely AF with aberrancy
• Consider expert consultation

↓ NO (NARROW QRS) REGULAR? ↓ YES

• Vagal maneuvers
• Adenosine 6mg → 12mg → 12mg
• If refractory: β-blocker or CCB ↓ NO
• Likely AF
• Rate control vs rhythm control
• Anticoagulation consideration

Bradycardia Algorithm:

Bradycardia (<60 bpm) ↓ SYMPTOMS: Hypotension, altered mental status, chest pain, heart failure? ↓ NO OBSERVE AND MONITOR

↓ YES ATROPINE 0.5mg IV (may repeat q3-5min, max 3mg) ↓ ADEQUATE RESPONSE? ↓ NO TRANSCUTANEOUS PACING OR DOPAMINE 2-10 mcg/kg/min OR EPINEPHRINE 2-10 mcg/min ↓ CONSIDER TRANSVENOUS PACING CONSIDER PERMANENT PACEMAKER

Critical Decision Points:

1. Hemodynamic Instability Indicators:

   • Systolic BP <90 mmHg
   • Altered mental status
   • Ongoing chest pain
   • Heart failure signs
   • Shock

2. When to Avoid Certain Medications:

   • Adenosine: Asthma, COPD, 2nd/3rd degree block
   • Verapamil/Diltiazem: Wide complex tachycardia, heart failure
   • Beta-blockers: Severe asthma, cocaine intoxication

3. Consultation Triggers:

   • Refractory arrhythmias
   • Hemodynamic instability
   • Suspected drug toxicity
   • Need for invasive procedures

Post-Resuscitation Care:

• 12-lead ECG and continuous monitoring
• Electrolyte correction (K+ 4.0-5.0 mEq/L, Mg2+ >2.0 mg/dL)
• Identify and treat precipitating factors
• Consider cardiology consultation
• Evaluate need for long-term antiarrhythmic therapy or device placement