s allen 2003 understanding and management of ecg’s
TRANSCRIPT
S Allen 2003
Understanding and Management Of ECG’s
S Allen 2003
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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• Thank you for listeningThank you for listening