Arrhythmias
GENERAL
An approach to arrhythmia
- fast or slow?
- ventricular or supraventricular?
- compromised or not?
- does arrhythmia need management?
- what is underlying substrate predisposition?
- what is trigger?
- will arrhythmia recur?
BRADYCARDIA
- blocks and bradycardia are caused by impaired automaticity or conduction
- if one pacemaker fails another generally takes over at a lower rate
TACHYCARDIA
General
- reentrancy
- automaticity (increased/abnormal)
- triggered activity
Reentrancy
- impulse reaches a point where it can go two ways (A or B) -> if A is blocked then impulse can only go down B.
- however, when impulse reaches a point where A and B re-join -> impulse may be retrogradely conducted up path A until it reaches the beginning and travels down path A creating a reentry loop.
- the block that leads to rentry is often transient and timing dependent.
- sometimes they do not even occupy a fixed anatomical location (ie. some forms of AF)
Automaticity
- increased: normal spontaneous depolarisation is increased for some reason (adrenergic stimulation)
- abnormal: local ischaemia, hypokalaemia, drugs
Trigger Activity
- = ‘after depolarisation’ where normal action potential suddenly swings positive again allowing another depolarisation to occur abnormally.
- early after depolarisations: occur before repolarisation has finished (partial blockade of Ik)
- delayed after depolarisations: occur after membrane potential has returned to normal (from raised intracellular Ca2+)
FACTORS CONTRIBUTING TO ARRHYTHMOGENESIS
Structural
- MI
- hypertrophy
- myopathic ventricle
- ischaemia
- congenital defects
Systemic
- hypoxia
- acidosis
- electrolytes
- catecholamines
Drugs
- catecholamines
- proarrhythmic drugs
- anti-arrhythmics in certain situations:
- -> toxicity (increased dose or reduced clearance)
- -> severe LVF -> digoxin
- -> brachycardia
VAUGHAN-WILLIAMS CLASSIFICATION OF ANTI-ARRHYTHMICS
- Simple, but problematic as many drugs fall into multiple classes
Class 1 – inhibit fast Na+ channels
- inhibit fast voltage sensitive sodium channels during depolarisation (phase 0) of cardiac action potential -> decreased depolarization & conduction velocity.
-> membrane stabilisers
1a – Prolonged AP duration
- decrease rate of phase 0 depolarisation -> reducing the excitability of the non-nodal regions in the heart which are important for propagation of the action potential.
- lengthen duration of action potential
- ie. quinidine, procainamdie
1b – Shortened AP duration
- decrease rate of spontaneous phase 4 outside the atria -> decreases automaticity
- ie. lignocaine, phenytoin
1c – No change in AP duration
- potent Na+ channel blockers -> decrease in rate of phase 0 depolarisation and speed of conduction of cardiac impulses.
- little effect on the duration of cardiac action potential & effective refractory period in ventricular myocardial cells
- shortens the duration of the action potential in Purkinje fibres.
- ie. flecanide, encainide
Class II – decrease rate of depolarisation (beta blockers)
- beta-adrenoceptor antagonists
- increase effective refractory period of AV node & decreased automaticity, decreased QT duration
-> decrease HR & O2 consumption - ie. metoprolol, esmolol, propanolol
Class III – inhibit K+ ion channels
- prolong the refractory period
block K+ channel -> prolong cardiac depolarisation, action potential duration & effective refractory period.
-> decrease the time in which the cardiac muscle cells are excitable. - ie. amiodarone, sotalol, bretylium
- amiodarone has some class I ( Na channel), II (beta-blocker), III (K+ channel) & IV effects (Ca2+ channel)
Class IV – inhibit slow Ca2+ channels
- inhibit inward slow calcium ion currents that may contribute to development of VT
- block L type Ca2+ channels -> impair SA node pacemaker activity.
- decrease duration of action potential but no effect on automaticity
- ie. verapamil, diltiazem, nifedipine
VIDEO
Mannik MD’s medical rap for learning about anti-arrhythmic drugs
References and Links
Introduction to ICU Series
Introduction to ICU Series Landing Page
DAY TO DAY ICU: FASTHUG, ICU Ward Round, Clinical Examination, Communication in a Crisis, Documenting the ward round in ICU, Human Factors
AIRWAY: Bag Valve Mask Ventilation, Oropharyngeal Airway, Nasopharyngeal Airway, Endotracheal Tube (ETT), Tracheostomy Tubes
BREATHING: Positive End Expiratory Pressure (PEEP), High Flow Nasal Prongs (HFNP), Intubation and Mechanical Ventilation, Mechanical Ventilation Overview, Non-invasive Ventilation (NIV)
CIRCULATION: Arrhythmias, Atrial Fibrillation, ICU after Cardiac Surgery, Pacing Modes, ECMO, Shock
CNS: Brain Death, Delirium in the ICU, Examination of the Unconscious Patient, External-ventricular Drain (EVD), Sedation in the ICU
GASTROINTESTINAL: Enteral Nutrition vs Parenteral Nutrition, Intolerance to EN, Prokinetics, Stress Ulcer Prophylaxis (SUP), Ileus
GENITOURINARY: Acute Kidney Injury (AKI), CRRT Indications
HAEMATOLOGICAL: Anaemia, Blood Products, Massive Transfusion Protocol (MTP)
INFECTIOUS DISEASE: Antimicrobial Stewardship, Antimicrobial Quick Reference, Central Line Associated Bacterial Infection (CLABSI), Handwashing in ICU, Neutropenic Sepsis, Nosocomial Infections, Sepsis Overview
SPECIAL GROUPS IN ICU: Early Management of the Critically Ill Child, Paediatric Formulas, Paediatric Vital Signs, Pregnancy and ICU, Obesity, Elderly
FLUIDS AND ELECTROLYTES: Albumin vs 0.9% Saline, Assessing Fluid Status, Electrolyte Abnormalities, Hypertonic Saline
PHARMACOLOGY: Drug Infusion Doses, Summary of Vasopressors, Prokinetics, Steroid Conversion, GI Drug Absorption in Critical Illness
PROCEDURES: Arterial line, CVC, Intercostal Catheter (ICC), Intraosseous Needle, Underwater seal drain, Naso- and Orogastric Tubes (NGT/OGT), Rapid Infusion Catheter (RIC)
INVESTIGATIONS: ABG Interpretation, Echo in ICU, CXR in ICU, Routine daily CXR, FBC, TEG/ROTEM, US in Critical Care
ICU MONITORING: NIBP vs Arterial line, Arterial Line Pressure Transduction, Cardiac Output, Central Venous Pressure (CVP), CO2 / Capnography, Pulmonary Artery Catheter (PAC / Swan-Ganz), Pulse Oximeter
Critical Care
Compendium
Chris is an Intensivist and ECMO specialist at The Alfred ICU, where he is Deputy Director (Education). He is a Clinical Adjunct Associate Professor at Monash University, the Lead for the Clinician Educator Incubator programme, and a CICM First Part Examiner.
He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives. He was one of the founders of the FOAM movement (Free Open-Access Medical education) has been recognised for his contributions to education with awards from ANZICS, ANZAHPE, and ACEM.
His one great achievement is being the father of three amazing children.
On Bluesky, he is @precordialthump.bsky.social and on the site that Elon has screwed up, he is @precordialthump.
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