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Understanding and Management Of ECG’s

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ContentsContents

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

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What is an ECGWhat 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)

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The ElectrocardiographThe 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

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Lead PlacementsLead Placements

• Surface 12 lead ECG

• Posterior/ Right sided lead

extensions

• Standard limb leads

• Modified Lewis lead

• Right atrial/ oesphageal leads

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The Electrical AxisThe Electrical Axis

Lead axis is the direction generated by different orientation of paired electrodes

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The Basic Action of the ECGThe Basic Action of the ECGThe ECG deflections represent vectors which have both magnitute and direction

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• 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

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• QT interval

– Corrected to heart rate (QTc)• QTc= QT / ^RR = 0.38-0.42 sec

Romano Ward Syndrome

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• 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

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Clinical uses of ECGClinical 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

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LimitationsLimitations of ECGof 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

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Cardiac ElectrophysiologyCardiac 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

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The Cardiac Conduction PathwayThe Cardiac Conduction Pathway

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The Resting PotentialThe Resting Potential

• SA node : -55mV

• Purkinjie cells: -95mV

• Maintained by:

– cytoplasmic proteins– Na+/K+ pump– K+ channels

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The Action PotentialThe Action Potential

• Alteration of transmembrane conductance triggers depolarization

• Unlike other excitatory phenomena, the cardiac action potential has:– prominent plateau phase– spontaneous pacemaking capability

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The Cardiac Action PotentialThe Cardiac Action Potential

0

-50

-100

Membrane Potential

4

0

1

2

3

Ca++ influx

K+ efflux

Na + influx

mV

4

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The Transmembrane CurrentsThe 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)

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The Transmembrane CurrentsThe 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)

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Cardiac Ion ChannelsCardiac 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

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Cardiac Ion Channels: Cardiac Ion Channels: ApplicationsApplications

• 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)

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Refractory Periods of the Myocyte

0

-50

-100

Membrane Potential

Absolute R.P.

Relative R.P.

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Mechanisms of Arrhythmias: 1 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

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Mechanisms of Arrhythmias: 2Mechanisms 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

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Wide Complex TachycardiasWide Complex Tachycardias

Differential Diagnosis

Ventricular tachycardia (>80%)

Supraventricular tachycardia with (<20%)

aberrancypreexisting bundle branch blockaccessory pathway (bundle of Kent, Mahaim)

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Wide Complex Tachycardias: Wide Complex Tachycardias: Diagnostic ApproachDiagnostic 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)

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Wide Complex Tachycardias: Wide Complex Tachycardias: Diagnostic ApproachDiagnostic 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)

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Ventricular Tachycardia with visible P waves

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Surpaventricular Tachycardia with abberancy

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Narrow Complex TachycardiasNarrow Complex Tachycardias

Differential Diagnosis

Sinus tachycardia

Atrial fibrillation or flutter

Reentry tachycardias

AV nodalAtrioventricular (accessory pathway)Intraatrial

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Narrow Complex Tachycardia: Atrial Flutter

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Narrow Complex Tachycardias: Narrow Complex Tachycardias: Diagnostic ApproachDiagnostic 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

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Management: the Unstable Management: the Unstable Tachycardic PatientTachycardic 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

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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

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Torsades or Polymorphic VT

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Accelerated Idioventricular Rhythm

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Ventricular Tachycardia: Ventricular Tachycardia: ManagementManagement

• 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

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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

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Atrial Fibrillation: Atrial Fibrillation: Cardioversion or Rate ControlCardioversion or Rate Control

• If < 2 days duration: Cardiovert• amiodarone• flecainide• DC shock

• If > 2 days duration: Rate control first• digoxin• B blockers• verapamil• amiodarone• elective DC cardioversion

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Atrial FlutterAtrial 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

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MULTIFOCAL ATRIAL TACHYCARDIA MULTIFOCAL ATRIAL TACHYCARDIA (MAT)(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

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Multifocal Atrial Tachycardia

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ACCESSORY PATHWAY TACHYCARDIASACCESSORY 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

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Bradyarrhythmias

• Treat if

• Symptomatic

• Risk of asystole– 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

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Complete Heart Block and AF

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What is the cause of the VT?

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• Hypokalaemia

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• Electrical Alternans - ? Cardiac Tamponade

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• Acute Pulmonary Embolism

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• Acute Posterior MI (Lateral extension)

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• Ventricular Tachycardia (Recent MI)

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• Acute Pericarditis

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