Arrythmias

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Approach to Any Arrythmia

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ABC Patient Assessment and Management of Peri-Operative Cardiac Arrhythmias

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Tachyarrhythmias

A Simple Approach to Tachyarrhythmias

Regular, Narrow Complex

  • Sinus tachycardia
  • Ectopic atrial tachycardia
  • Atrial flutter
  • AV nodal re-entry (AVNRT)
  • AV re-entry (AVRT)

Irregular, Narrow Complex

  • Atrial fibrillation (AF)
  • Atrial flutter with variable block
  • Multifocal atrial tachycardia (MAT)

Regular, Broad Complex

  • Ventricular tachycardia
  • SVT with bundle-branch block
  • SVT with aberrant conduction
  • SVT with eccentric conduction
  • Ventricular pacemaker

Irregular, Broad Complex

  • AF with bundle-branch block
  • AF with aberrant conduction
  • AF with eccentric conduction
  • Multifocal ventricular rhythm
  • Torsade de Points

Monomorphic VT

Monomorphic VT_Calgary Guide

Definition:

  • A wide QRS complex tachycardia originating from the ventricles lasting > 30 seconds. Mechanisms include re-entry (e.g., scar-mediated) or increased automaticity.

Pathophysiology:

  • The sinoatrial node continues to depolarize the atria while the ventricles depolarize independently.
  • Re-entrant circuits or ectopic focus uniformly depolarize ventricular myocytes.

Mechanism and Symptoms:

  • Heart Rate > 100 beats/minute: Decreased ventricular filling time, preload, and stroke volume, leading to palpitations and hypotension.
  • Right Atrium: Contracts against a closed tricuspid valve causing Cannon A waves.

ECG Findings:

  • AV dissociation
  • Uniform morphology of QRS complexes
  • Wide QRS complexes (≥ 120 milliseconds)

Complications:

  • Inadequate organ perfusion, general malaise, chest pain, syncope, shortness of breath, hemodynamic collapse, and potentially sudden cardiac arrest or death.

Illustrated Flow:

  • Loss of coordination between atria and ventricles → AV dissociation → Capture beat/Fusion beat.
  • Symptoms: Palpitations, hypotension, Cannon A waves.
  • Organs affected: Muscles, heart, brain.

Outcome:

  • Inability to respond to increased cardiac demand, leading to severe complications, including death.

WPW

WPW_Calgary Guide

Pathophysiology:

  • Congenital Accessory Pathway: An alternative electrical conduction pathway from the atria to the ventricles.
  • Wolff-Parkinson-White Pattern: ECG findings showing isolated ventricular pre-excitation.
  • Wolff-Parkinson-White Syndrome: ECG findings associated with supraventricular arrhythmias.

Mechanism:

  • Impulse travels faster along the accessory pathway, shortening the time between atrial and ventricular depolarization (Short PR interval <0.12 sec).
  • Early ventricular depolarization (preexcitation) leads to wide QRS complex with a delta wave.
  • Altered ventricular repolarization results in ST and T-wave changes.

Arrhythmias:

  • Orthodromic AVRT: Narrow QRS complex tachycardia.
  • Antidromic AVRT: Wide QRS complex tachycardia.
  • Pre-excited Atrial Fibrillation: Wide, irregular QRS complex tachycardia.

Clinical Notes:

  • WPW pattern is more common than WPW syndrome.
  • Patients may also experience atrial flutter, AVNRT, ventricular tachycardia, and ventricular fibrillation.

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Management of Wolff-Parkinson-White Syndrome

Acute Management

  • Unstable: Synchronized DC shock.
  • Stable: Anti-arrhythmic to prolong the accessory pathway refractory period:
    • Sotalol
    • Amiodarone
    • Flecainide
    • Procainamide
  • Contraindicated Drugs:
    • Digoxin (shortens refractory period)
    • Verapamil and lignocaine (increase ventricular rate)
    • Beta-blockers (no effect on accessory pathway refractory period)

Long-term Management

  • Radio-frequency ablation

Atrial Flutter

Atrial Flutter_Calgory Guide

Atrial Flutter: Pathogenesis and Clinical Findings

Pathophysiology:

  • Causes: Rheumatic heart disease, idiopathic, LV dysfunction, iatrogenic (cardiac surgery).
  • Mechanism:
    • Spontaneous premature depolarization of atrial tissue
    • Depolarization wave propagates around atrial free-wall myocardium.
    • The “re-entry loop” electrical impulse circulates at a rate of 180-350/min, usually in the right atrium.
  • Electrical Conduction:
    • Tissue of the tricuspid valve annulus conducts the wave.
    • Conduction of depolarization wave through atrial septum.
    • AV node conducts only if not in a refractory state.
  • ECG Findings:
    • Saw-tooth P waves (waves inverted in leads II, III, and aVF).
    • Short PR interval (<0.12 sec).
    • 1 QRS complex per 2-5 atrial P waves.
  • Clinical Manifestations:
    • Heart Rate: Pulse of 60-200 bpm.
    • Symptoms: Dyspnea, presyncope, fatigue.
    • Carotid massage or vagal maneuvers decrease AV node conductivity, leading to transient decreases in ventricular rate.
    • If high ventricular rate decreases diastolic filling time, cardiac output decreases, leading to ineffective perfusion of body tissues.
  • Other Notes:
    • WPW pattern is more common than WPW syndrome, both rare (<1%).
    • Other arrhythmias can occur with WPW: atrial flutter, AVNRT, ventricular tachycardia, and ventricular fibrillation.
    • ST and T wave changes present in the opposite direction to the QRS complex and delta wave.

Torsade’s Des Points

Torsades_Calgary

Pathophysiology

  • Causes:
    • Acquired Long QT Syndrome: Drugs (Class 1A, Class III, TCAs, erythromycin), sinus bradycardia, AV block, metabolic abnormalities (hypo K+/Ca2+/Mg2+), primary heart disease (ischemic, congestive heart failure, cardiomyopathy).
    • Congenital Long QT Syndrome: Mutated cardiac ion channels, leading to decreased repolarizing current/increased depolarizing current in cardiomyocytes.
  • Mechanism: Prolonged ventricular action potential duration → Early after depolarization (EAD) → Triggering PVC → Functional re-entry.

ECG Findings

  • QTc Interval: Prolonged.
  • ECG Changes: Polymorphic ventricular tachycardia with shifting QRS morphology.

Clinical Manifestations

  • Non-sustained TdP: Asymptomatic, palpitations, syncope.
  • Sustained TdP: Degeneration to ventricular fibrillation (VF), sudden cardiac death.

Management

Unstable:
Defibrillation (200J biphasic)- may not be able to lock onto a QRS complex so may need to be unsynchronised.
Stable:
IV magnesium 2g over 15 mins, followed by 1g per hour.
Treat any hypokalaemia.
Stop all medications that prolong QT.
If refractory:
Speed up the heart:
Chemically: adrenaline infusion, dobutamine or isoproterenol.
Electrically: transcutaneous pacing.
Lignocaine 1-1.5mg/kg

Ventricular Fibrillation

VF_Calgary_guide

Pathophysiology

  • Channelopathies: Alterations in ion transport (e.g., Long QT or Brugada Syndromes).
  • Accessory Pathway: Alternatives for impulse conduction.
  • Structural Abnormalities: Congenital or acquired heart defects (e.g., cardiomyopathy, MI, cardiac surgery, ARVD).

Trigger Events

  • Acute myocardial infarction (AMI)
  • Dysrhythmias
  • Electrolyte abnormalities (K+, Mg2+, Ca2+)
  • Hypoperfusion
  • Hypothermia
  • Hypoglycemia
  • Trauma
  • Drugs

Mechanism

  • An acute trigger event can precipitate ectopic electrical activity and multiple micro-re-entry circuits.
  • Disorganized electrical activity interferes with normal conduction, causing uncoordinated ventricular contraction.

Clinical Findings

  • ECG: Disorganized without identifiable QRS or T waves.
  • Symptoms: Loss of consciousness, no palpable pulse, no heart rate (HR), no blood pressure (BP).
  • Complications: Clinical cardiac arrest, global hypoperfusion, multi-system organ failure, hypoxic brain, brain damage, brain death, death.
    Note: Ventricular fibrillation is a medical emergency requiring CPR and defibrillation.

Links

References:

  1. Hutchins, D. (2013). Peri-Operative Cardiac Arrhythmias: Part Two Ventricular Dysrhythmias. Anaesthesia Tutorial of the Week 285. World Federation of Societies of Anaesthesiologists. Retrieved from WFSA Resources.
  2. The Calgary Guide to Understanding Disease. (2024). Retrieved June 5, 2024, from https://calgaryguide.ucalgary.ca/
  3. FRCA Mind Maps. (2024). Retrieved June 5, 2024, from https://www.frcamindmaps.org/
  4. Anesthesia Considerations. (2024). Retrieved June 5, 2024, from https://www.anesthesiaconsiderations.com/

Summaries:

Copyright
© 2025 Francois Uys. All Rights Reserved.

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