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Cardiac Rhythm Disturbances - Emergency Medicine PG Guide

Source: Tintinalli's Emergency Medicine, Chapter 18 (Brady & Glass)

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PART 1 - THE EMERGENCY FRAMEWORK

The Two Questions That Drive Every Decision

1. Is the patient STABLE or UNSTABLE?
2. Is the QRS narrow or wide? Is the rhythm regular or irregular?

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PART 2 - RECOGNIZING INSTABILITY

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PART 3 - INITIAL APPROACH (ALL ARRHYTHMIA PATIENTS)

For Stable Patients

• Focused history: presenting complaints, medications (especially new ones or dose changes), herbal/recreational drugs, caffeine
• Check for hyperthyroidism symptoms
• Family history of sudden death or syncope (raises risk)
• Physical examination
• Continuous cardiac rhythm monitoring
• 12-lead ECG
• Review rhythm strip

For Unstable Patients

• IV access immediately
• Cardiac rhythm monitoring
• 12-lead ECG
• Be ready for drug OR electrical therapy without delay

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PART 4 - BRADYDYSRHYTHMIAS

Definition

• Ventricular rate < 60 bpm in adults
• Below age-appropriate rate in children

Categories

1. Sinus bradycardia - intrinsic sinus node slowing
2. Conduction system disease - AV nodal or infranodal block
3. Junctional/escape rhythms - intrinsic pacemaker takes over

Causes (the reversible ones - treat these first)

• Medications: beta-blockers, calcium channel blockers, digoxin, amiodarone
• Electrolytes: hyperkalemia (the great mimicker)
• Hypothyroidism
• Increased vagal tone (vasovagal, inferior MI)
• Ischemia: inferior STEMI (RCA territory - supplies SA and AV node)
• Hypothermia
• Increased ICP (Cushing reflex)

AV Blocks - The Hierarchy

• PR interval > 200 ms (0.20 sec) - just prolonged, every P conducts
• ECG: regular P waves, regular QRS, long PR
• No treatment needed in isolation
• Watch for medications causing it (digoxin toxicity, beta-blockers)

• Progressive PR prolongation until a P wave is dropped (non-conducted)
• ECG: "longer, longer, longer, drop - then you have a Wenckebach"
• Block is at the AV node level
• Often benign, may be vagally mediated, can be seen in inferior MI
• Treatment: only if symptomatic (atropine)

• Fixed PR interval with sudden non-conducted P waves (no warning)
• Block is infranodal (His-Purkinje level)
• QRS often wide (bundle branch block pattern)
• HIGH RISK - can progress suddenly to complete heart block
• Urgent pacemaker consultation regardless of symptoms

• No relationship between P waves and QRS complexes (AV dissociation)
• P rate and QRS rate are independent
• ECG: P waves "march through" at their own rate, QRS at slow escape rate
• QRS morphology tells you the escape source:
  • Narrow QRS (~40-60 bpm) = junctional escape (AV node level block, more stable)
  • Wide QRS (~20-40 bpm) = ventricular escape (infranodal block, unstable - needs pacemaker urgently)
• Critical pitfall: Complete block in the setting of inferior MI may respond to atropine (vagally mediated); complete block with anterior MI is usually infranodal and will NOT respond to atropine - transcutaneous pacing immediately

Treatment Ladder for Symptomatic Bradycardia

• Dose: 0.5 mg IV every 3-5 min, max total 3 mg
• Works by blocking vagal tone at the AV node
• Does NOT work for infranodal (Mobitz II, wide-complex complete block, post-anterior-MI block)

• Use if atropine fails or contraindicated
• Set rate 60-80 bpm
• Increase current until electrical capture (QRS follows spike)
• Verify mechanical capture (pulse)
• Painful - sedate the conscious patient (fentanyl + midazolam)
• Bridge therapy - arrange transvenous pacing

• Dopamine 2-10 mcg/kg/min
• Epinephrine 2-10 mcg/min
• Isoproterenol (for torsades or beta-blocker toxicity)

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PART 5 - TACHYDYDYSRHYTHMIAS

The Classification Grid - YOUR MENTAL MODEL

                    REGULAR              IRREGULAR
NARROW QRS        SVT, AVNRT, AVRT      Atrial Fibrillation
(<120 ms)         Atrial Flutter        MAT (multifocal AT)
                  Sinus Tachycardia     Atrial Flutter (variable)

WIDE QRS          VT (monomorphic)      VF
(≥120 ms)         SVT with aberrancy    VT (polymorphic)
                  Pre-excited rhythms   Torsades de Pointes

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PART 6 - NARROW COMPLEX TACHYCARDIAS

Sinus Tachycardia

• Rate: 100-180 bpm
• Each P wave looks normal (upright in I, II, aVF), before every QRS
• ALWAYS treat the cause - it is a symptom, not a dysrhythmia
• Causes: fever, pain, hypovolemia, sepsis, PE, thyrotoxicosis, anemia, anxiety, sympathomimetics
• Never cardiovert sinus tachycardia

Supraventricular Tachycardia (SVT) - AVNRT & AVRT

• Rate: 150-250 bpm, usually around 160-180 bpm
• ECG: narrow QRS, regular, P waves hidden in QRS (AVNRT) or just after QRS (AVRT)
• Sudden onset and termination ("paroxysmal")

1. Vagal maneuvers first (Valsalva, carotid sinus massage)
   • Modified Valsalva (patient bears down, then legs raised to 45°) - most effective, 40-50% conversion
   • Do NOT do carotid massage if carotid bruit present, recent stroke, or hypersensitivity
2. Adenosine (drug of choice)
   • 6 mg IV rapid push in large antecubital vein, flush immediately with 20 mL NS
   • If no response in 1-2 min: 12 mg rapid push (can repeat 12 mg once more)
   • Warn the patient: "You will feel like you're dying for about 10 seconds" - chest tightness, sense of doom, flushing
   • Half-life: 10-15 seconds - extremely short
   • Contraindicated in pre-excited AF (can precipitate VF), severe asthma, 2nd/3rd degree AV block
   • Give higher dose if patient on theophylline (blocks adenosine receptor); give lower dose if on dipyridamole or carbamazepine (potentiates it)
   • Diagnostic value: if tachycardia continues after adenosine but AV block transiently occurs, look for flutter waves - this unmasks atrial flutter
3. Calcium Channel Blockers (if adenosine fails or recurs)
   • Diltiazem 15-20 mg IV over 2 min, repeat 25 mg in 15 min
   • Verapamil 5-10 mg IV over 2 min
   • Contraindicated with wide-complex tachycardia (unless definitively SVT) and with IV beta-blockers
4. Beta-Blockers (alternative to CCBs)
   • Metoprolol 5 mg IV every 5 min x3
   • Esmolol (short-acting, useful if unsure about tolerance)
5. Synchronized cardioversion if unstable or drugs fail: 50-100 J (biphasic)

Atrial Flutter

• "Sawtooth" flutter waves at 300 bpm (250-350 bpm range) - best seen in II, III, aVF, V1
• Classic: 2:1 block → ventricular rate ~150 bpm
• Rule: Heart rate of exactly 150 bpm = think flutter until proven otherwise
• QRS narrow unless aberrant conduction
• Can have variable block (3:1, 4:1, variable → irregular QRS)

• Rate control: diltiazem or beta-blockers (same as AF)
• Rhythm conversion: ibutilide 1 mg IV over 10 min (most effective for flutter), or electrical cardioversion 50-100 J
• Anticoagulation: same principles as AF (flutter carries equal thromboembolic risk)

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PART 7 - ATRIAL FIBRILLATION (THE BIG ONE)

ECG Features

• Irregularly irregular rhythm (the hallmark)
• No distinct P waves - replaced by chaotic fibrillatory baseline (f waves)
• QRS narrow (unless aberrant conduction or pre-excitation)
• Rate: ventricular response 100-180 bpm in uncontrolled AF

Classification (Clinically Relevant)

The Two Critical Management Decisions in the ED

Decision 1 - UNSTABLE AF → Immediate Synchronized Cardioversion

• 150-200 J biphasic
• Do NOT delay for anticoagulation
• Do NOT waste time on rate control medications

Decision 2 - STABLE AF → Rate Control vs. Rhythm Control

• Goal: resting ventricular rate < 100 bpm
• First line: Diltiazem 0.25 mg/kg IV over 2 min (typical adult: 15-20 mg), repeat 0.35 mg/kg (25 mg) in 15 min if needed
• Alternative: Metoprolol 5 mg IV q5min x3, or esmolol infusion
• If refractory: IV amiodarone or IV procainamide
• Contraindication to diltiazem/beta-blockers: pre-excitation (WPW) - can accelerate accessory pathway → VF

• Pharmacologic cardioversion:
  • Flecainide or propafenone ("pill-in-the-pocket") - only in patients with no structural heart disease
  • IV procainamide (preferred in Canada/some centers, good for AF + WPW)
  • IV amiodarone (slower conversion, good for AF with LV dysfunction)
  • Ibutilide 1 mg IV (effective but risk of torsades - monitor post-dose for 4+ hours)
• Electrical cardioversion: 150-200 J biphasic (synchronized)

Anticoagulation in AF - The ED Decision

• AF confirmed <48 hours AND hemodynamically stable → can cardiovert without prior anticoagulation OR after heparin
• Still start anticoagulation afterwards (4 weeks minimum post-cardioversion, continued long-term based on risk)

• Do NOT cardiovert without 3 weeks of therapeutic anticoagulation OR transesophageal echo (TEE) to rule out LA appendage thrombus
• Exception: if TEE negative for thrombus, can cardiovert with heparin bridge

• Score 0 (male): no anticoagulation
• Score 1 (male) or 2 (female): consider anticoagulation
• Score ≥2 (male) or ≥3 (female): anticoagulate

• AV nodal blockers (adenosine, diltiazem, verapamil, digoxin, beta-blockers)
• All of these can accelerate conduction via the accessory pathway → extremely rapid ventricular rates → VF
• Use: IV procainamide (drug of choice), or electrical cardioversion

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PART 8 - WIDE COMPLEX TACHYCARDIAS

Approach: Wide Regular Tachycardia

ECG Clues Favoring VT (Brugada Criteria)

1. No RS complex in any precordial lead (all negative deflections) - VT
2. RS interval > 100 ms in any V lead - VT
3. AV dissociation - VT (P waves march through independently, unrelated to QRS)
4. Morphology criteria in V1 and V6 (specific LBBB/RBBB morphology patterns)

• Fusion beats (normal and abnormal beat partially fuse)
• Capture beats (sinus P captures ventricle momentarily - produces a normal narrow QRS within the wide-complex tachycardia) - pathognomonic for VT

• Typical RBBB or LBBB morphology
• Very narrow initial QRS deflection
• Responds to adenosine

Monomorphic Ventricular Tachycardia

• Unstable (hypotension, chest pain, altered mental status): Synchronized cardioversion immediately - 100-200 J biphasic
• Stable VT:
  • IV Amiodarone 150 mg IV over 10 min, then 1 mg/min x6h, then 0.5 mg/min x18h (drug of choice for stable monomorphic VT)
  • IV Procainamide 15-17 mg/kg at 25-50 mg/min (effective but watch for hypotension)
  • IV Lidocaine 1-1.5 mg/kg IV bolus (older option, less effective, still used in ischemia-related VT)
  • Never use verapamil for wide complex tachycardia (can cause hemodynamic collapse if it's VT)

Polymorphic VT and Torsades de Pointes

Polymorphic VT (without QT prolongation)

• Associated with acute myocardial ischemia
• Treat underlying ischemia
• Amiodarone if needed

Torsades de Pointes (TdP) - VT with QT prolongation

• ECG: "twisting of the points" - QRS axis rotates around the baseline
• Long QT before the run of tachycardia is the key feature

• Drugs: Class IA antiarrhythmics (quinidine, procainamide), Class III (amiodarone, sotalol), antipsychotics (haloperidol, droperidol, quetiapine), antibiotics (azithromycin, fluoroquinolones), methadone, ondansetron
• Electrolytes: Hypokalemia, hypomagnesemia, hypocalcemia
• Congenital: Romano-Ward, Jervell-Lange-Nielsen syndromes
• Bradycardia (pause-dependent TdP)

1. IV Magnesium sulfate 2 g IV over 1-2 min (drug of choice - terminates TdP even with normal Mg levels)
   • Repeat 2 g if recurs
   • Works mechanically - shortens QT, stops early afterdepolarizations
2. Correct electrolytes: K⁺ to 4.5-5 mEq/L, correct Ca²⁺
3. Remove causative drug - essential
4. Increase heart rate to shorten QT: isoproterenol infusion 2-10 mcg/min OR overdrive pacing (rate 90-110 bpm) - both prevent the pauses that trigger TdP
5. Defibrillate if degenerates to VF
6. Do NOT use amiodarone or other drugs that prolong QT

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PART 9 - VENTRICULAR FIBRILLATION AND PULSELESS VT

Management

1. CPR immediately - high-quality chest compressions (100-120/min, 5-6 cm depth, allow full recoil)
2. Defibrillation - unsynchronized shock (because there is no organized QRS to synchronize to)
   • Biphasic: 120-200 J (manufacturer-specific, use highest if unknown)
   • Monophasic: 360 J
3. Resume CPR immediately after shock (2 min before rhythm check)
4. Epinephrine 1 mg IV every 3-5 min (first dose as soon as IV access)
5. Amiodarone 300 mg IV bolus for shock-refractory VF/pVT (second dose 150 mg)
   • Alternative: Lidocaine 1-1.5 mg/kg IV
6. Look for reversible causes (H's and T's)

H's and T's (Reversible Causes of Cardiac Arrest)

• Synchronized cardioversion: for organized rhythms with QRS complexes (AF, flutter, SVT, monomorphic VT with pulse)
• Defibrillation (unsynchronized): for VF, pulseless VT, polymorphic VT (no organized QRS to sync to)

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PART 10 - JUNCTIONAL RHYTHMS

• Rate: 40-60 bpm (junctional escape) or 60-100 bpm (accelerated junctional) or >100 bpm (junctional tachycardia)
• QRS narrow (unless aberrant conduction)
• P waves: absent, inverted before QRS, or inverted after QRS (retrograde conduction)

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PART 11 - JUNCTIONAL AND IDIOVENTRICULAR (ESCAPE) RHYTHMS

Accelerated Idioventricular Rhythm (AIVR)

• Rate: 40-120 bpm, wide QRS (>120 ms), no P waves, regular
• Reperfusion rhythm: commonly seen after successful thrombolysis or PCI for MI
• Usually benign and self-limiting
• Do NOT treat with lidocaine or antiarrhythmics (suppressing it can cause asystole if no other pacemaker)

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PART 12 - SPECIAL SITUATIONS IN THE ED

Pre-Excitation Syndromes (WPW)

• Short PR interval (<120 ms)
• Delta wave (slurred upstroke of QRS)
• Wide QRS (≥120 ms)
• Secondary ST-T changes

• IV Procainamide (slows accessory pathway, drug of choice)
• IV Flecainide (if available)
• Electrical cardioversion

• Adenosine, verapamil, diltiazem, beta-blockers, digoxin - all block the AV node and preferentially channel conduction to the accessory pathway → ultra-rapid ventricular rate → VF

Digoxin Toxicity

• Increased automaticity: PVCs (bigeminy, trigeminy), accelerated junctional rhythm, VT
• Increased block: AV block (any degree)
• "Regularized AF" - any regular rhythm in a patient known to have AF = think dig toxicity

• Digoxin-specific Fab antibody fragments (Digibind/DigiFab) - indications: hemodynamic instability, life-threatening dysrhythmia, K⁺ > 5.5 mEq/L in acute toxicity

Hyperkalemia - The Great Cardiac Mimicker

1. Peaked, tall, narrow ("tented") T waves (K⁺ ~5.5-6.5)
2. PR prolongation, widening QRS (K⁺ ~6.5-7.5)
3. Loss of P waves, "sine wave" pattern (K⁺ ~7-8)
4. VF, asystole

1. Calcium gluconate (or CaCl) - membrane stabilization (buys 30-60 min, does not lower K⁺)
2. Sodium bicarbonate (in metabolic acidosis)
3. Insulin + dextrose - shifts K⁺ intracellularly (onset 15-30 min)
4. Albuterol nebulized (synergistic with insulin)
5. Kayexalate/patiromer (for elimination, slower)
6. Dialysis (definitive for severe/refractory cases)

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PART 13 - ELECTRICAL THERAPY QUICK REFERENCE

Synchronized Cardioversion - Energy Doses (Biphasic)

Defibrillation (Unsynchronized)

Key Rules

• Always sedate before synchronized cardioversion in conscious patients (midazolam + fentanyl or propofol)
• Never put pads directly over a pacemaker or ICD generator (place at least 8 cm away)
• In a patient with an ICD: if ICD is firing but not converting, you may need to cardiovert/defibrillate externally (ICD may be shocked-out or threshold too low)

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PART 14 - ANTIARRHYTHMIC DRUGS QUICK REFERENCE

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PART 15 - THE PG PEARL SUMMARY

1. Unstable patient + any tachyarrhythmia = synchronized cardioversion now
2. Wide complex regular tachycardia = VT until proven otherwise. Never give verapamil.
3. Rate 150 bpm = think atrial flutter 2:1 until proven otherwise
4. AF with WPW = do NOT give AV nodal blockers. Use procainamide or cardiovert.
5. Torsades = IV magnesium 2 g. Remove the offending drug. Increase the heart rate.
6. Atropine does not work for infranodal blocks (Mobitz II, complete heart block with wide QRS). Pace.
7. Adenosine unmasksflutter waves when it fails to convert - a diagnostic tool
8. AIVR after MI = reperfusion rhythm. Do not suppress it.
9. Any regular rhythm in a known AF patient = think digoxin toxicity
10. AF > 48 hours (or unknown duration) = do NOT cardiovert without anticoagulation or TEE

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