Understanding and Management Of ECG’s Mr Stuart Allen Technical Head Southampton General Hospital S Allen 2003

Contents What is an ECG Basic cardiac electrophysiology The cardiac action potential and ion channels Mechanisms of arrhythmias Tachyarrhythmias Bradyarrhythmias ECG in specific clinical conditions S Allen 2003

What is an ECG The clinical ECG measures the potential differences of the electrical fields imparted by the heart Developed from a string Galvinometer (Einthoven 1900s) S Allen 2003

The Electrocardiograph The ECG machine is a sensitive electromagnet, which can detect and record changes in electromagnetic potential. It has a positive and a negative pole with electrodes extensions from either end. The paired electrodes constitute a lead S Allen 2003

Lead Placements Surface 12 lead ECG Posterior/ Right sided lead extensions Standard limb leads Modified Lewis lead Right atrial/ oesphageal leads S Allen 2003

The Electrical Axis Lead axis is the direction generated by different orientation of paired electrodes S Allen 2003

The Basic Action of the ECG The ECG deflections represent vectors which have both magnitute and direction S Allen 2003

Time for intraatrial, AV nodal, and His-Purkinjie conduction P wave atrial activation Normal axis -50 to +60 PR interval Time for intraatrial, AV nodal, and His-Purkinjie conduction Normal duration: 0.12 to 0.20 sec QRS complex ventricular activation (only 10-15% recorded on surface) Normal axis: -30 to +90 deg Normal duration: <0.12 sec Normal Q wave: <0.04 sec wide <25% of QRS height S Allen 2003

Corrected to heart rate (QTc) QT interval Corrected to heart rate (QTc) QTc= QT / ^RR = 0.38-0.42 sec Romano Ward Syndrome S Allen 2003

represents the greater part of ventricular repolarization T wave ST segment represents the greater part of ventricular repolarization T wave ventricular repolarization same axis as QRS complex U wave uncertain ? negative afterpotential More obvious when QTc is short S Allen 2003

Clinical uses of ECG Gold standard for diagnosis of arrhythmias Often an independent marker of cardiac disease (anatomical, metabolic, ionic, or haemodynamic) Sometimes the only indicator of pathological process S Allen 2003

Limitations of ECG It does not measure directly the cardiac electrical source or actual voltages It reflects electrical behavior of the myocardium, not the specialised conductive tissue, which is responsible for most arrhythmias It is often difficult to identify a single cause for any single ECG abnormality S Allen 2003

Cardiac Electrophysiology Cardiac cellular electrical activity is governed by multiple transmembrane ion conductance changes 3 types of cardiac cells 1. Pacemaker cells SA node, AV node 2. Specialised conducting tissue Purkinjie fibres 3. Cardiac myocytes S Allen 2003

The Cardiac Conduction Pathway S Allen 2003

The Resting Potential SA node : -55mV Purkinjie cells: -95mV Maintained by: cytoplasmic proteins Na+/K+ pump K+ channels S Allen 2003

The Action Potential Alteration of transmembrane conductance triggers depolarization Unlike other excitatory phenomena, the cardiac action potential has: prominent plateau phase spontaneous pacemaking capability S Allen 2003

The Cardiac Action Potential 1 Membrane Potential Ca++ influx 2 -50 3 Na + influx K+ efflux 4 4 mV -100 S Allen 2003

The Transmembrane Currents Phase 0 Sodium depolarizing inward current (I Na) Calcium depolarizing inward current ( I Ca-T) Phase 1 Potassium transient outward current (I to) Phase 2 Calcium depolarizing inward current (I Ca-L) Sodium-calcium exchange (I Na-Ca) S Allen 2003

The Transmembrane Currents Phase 3 Potassium delayed rectifier current (I k) slow and fast components (Iks, Ikr) Phase 4 Sodium pacemaker current (I f) Potassium inward rectifier currents (I k1) S Allen 2003

Cardiac Ion Channels They are transmembrane proteins with specific conductive properties They can be voltage-gated or ligand-gated, or time-dependent They allow passive transfer of Na+, K+, Ca2+, Cl- ions across cell membranes S Allen 2003

Cardiac Ion Channels: Applications Understanding of the cardiac action potential and specific pathologic conditions e.g. Long QT syndrome Therapeutic targets for antiarrhythmic drugs e.g. Azimilide (blocks both components of delayed rectifier K current) S Allen 2003

Refractory Periods of the Myocyte Membrane Potential -50 Absolute R.P. -100 Relative R.P. S Allen 2003

Mechanisms of Arrhythmias: 1 Important to understand because treatment may be determined by its cause 1. Automaticity Raising the resting membrane potential Increasing phase 4 depolarization Lowering the threshold potential e.g. increased sympathetic tone, hypokalamia, myocardial ischaemia S Allen 2003

Mechanisms of Arrhythmias: 2 2. Triggered activity from oscillations in membrane potential after an action potential Early Afterdepolarization Torsades de pointes induced by drugs Delayed Afterdepolarization Digitalis, Catecholamines 3. Re-entry from slowed or blocked conduction Re-entry circuits may involve nodal tissues or accessory pathways S Allen 2003

Wide Complex Tachycardias Differential Diagnosis Ventricular tachycardia (>80%) Supraventricular tachycardia with (<20%) aberrancy preexisting bundle branch block accessory pathway (bundle of Kent, Mahaim) S Allen 2003

Wide Complex Tachycardias: Diagnostic Approach 1. Clinical Presentation Previous MI ( +ve pred value for VT 98%) Structural heart disease (+ve pred value for VT 95%) LV function 2. Provocative measures Vagal maneuvers Carotid sinus massage Adenosine (Not verapamil) S Allen 2003

Wide Complex Tachycardias: Diagnostic Approach 3. ECG Findings Capture or fusion beats (VT) Atrial activity (absence of 1:1 suggests VT) QRS axis ( -90 to +180 suggests VT) Irregular (SVT) Concordance QRS duration QRS morphology (?old) (? BBB) S Allen 2003

Ventricular Tachycardia with visible P waves S Allen 2003

Surpaventricular Tachycardia with abberancy S Allen 2003

Narrow Complex Tachycardias Differential Diagnosis Sinus tachycardia Atrial fibrillation or flutter Reentry tachycardias AV nodal Atrioventricular (accessory pathway) Intraatrial S Allen 2003

Narrow Complex Tachycardia: Atrial Flutter S Allen 2003

Narrow Complex Tachycardias: Diagnostic Approach 1. Look for atrial activity presence of P wave P wave after R wave AV reciprocating or AV nodal reentry 2. Effect of adenosine terminates most reentry tachycardias reveals P waves S Allen 2003

Management: the Unstable Tachycardic Patient Signs of the haemodynamically compromised: Hypotension/ heart failure/ end-organ dysfunction Sedate +/- formal anaesthesia (?) DC cardioversion, synchronized, start at 100J If fails, correct pO2, acidosis, K+, Mg2+, shock again Start specific anti-arrhythmics e.g. amiodarone 300mg over 5 - 10 min, then 300mg over 1 hour S Allen 2003

Ventricular Tachycardia >3 consecutive ventricular ectopics with rate >100/min Sustained VT (>30 sec) carries poor prognosis and require urgent treatment Accelerated idioventricular rhythm (“slow VT” at 60 - 100/min) require treatment if hypotensive Torsades de pointes or VT - difference in management S Allen 2003

Torsades or Polymorphic VT S Allen 2003

Accelerated Idioventricular Rhythm S Allen 2003

Ventricular Tachycardia: Management 1. Correct electrolyte abnormality / acidosis 2. Lidocaine 100mg loading, repeat if responds, start infusion 3. Magnesium 8 mmol over 20 min 4. Amiodarone 300 mg over 1 hour then 900 mg over 23 hours 5. Synchronized DC shock 6. Over-drive pacing S Allen 2003

Atrial Fibrillation: Management 1. Treat underlying cause e.g. electrolytes, pneumonia, IHD, MVD, PE 2. Anticoagulation 5-7% risk of systemic embolus if over 2 days duration (reduce to <2% with anticoagulation) 3. Cardiovert or Rate control Poor success rate if prolonged AF > 1 year, poor LV, MV stenosis S Allen 2003

Atrial Fibrillation: Cardioversion or Rate Control If < 2 days duration: Cardiovert amiodarone flecainide DC shock If > 2 days duration: Rate control first digoxin B blockers verapamil elective DC cardioversion S Allen 2003

Atrial Flutter Rarely seen in the absence of structural heart disease Atrial rate 250 - 350 / min Management DC cardioversion is the most effective therapy Digoxin sometimes precipitates atrial fibrillation Amiodarone is more effective in slowing AV conduction than cardioversion S Allen 2003

MULTIFOCAL ATRIAL TACHYCARDIA (MAT) At least 3 different P wave morphologies Varying PP and PR intervals Most common in COAD/ Pneumonia Managment Treat underlying cause Verapamil is treatment of choice (reduces phase 4 slope) DC shock and digoxin are ineffective S Allen 2003

Multifocal Atrial Tachycardia S Allen 2003

ACCESSORY PATHWAY TACHYCARDIAS WPW Mahaim pathway Lown-Ganong-Levine Syndrome Delta wave is lost during reentry tachycardia AF may be very rapid Management DC shock early Flecainide is the drug of choice Avoid digoxin, verapamil, amiodarone S Allen 2003

Bradyarrhythmias Treat if Symptomatic Risk of asystole Adverse signs Mobitz type 2 or CHB with wide QRS Any pause > 3 sec Adverse signs Hypotension, HF, rate < 40 Management Atropine iv 600 ug to max 3 mg Isoprenaline iv Pacing, external or transvenous S Allen 2003

Complete Heart Block and AF S Allen 2003

What is the cause of the VT? S Allen 2003

Hypokalaemia S Allen 2003

Electrical Alternans - ? Cardiac Tamponade S Allen 2003

Acute Pulmonary Embolism S Allen 2003

Acute Posterior MI (Lateral extension) S Allen 2003

Ventricular Tachycardia (Recent MI) S Allen 2003

Acute Pericarditis S Allen 2003

Thank you for listening S Allen 2003