Understanding Ecgs
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Transcript of Understanding Ecgs
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S Allen 2003
Understanding and Management
Of ECGs
Mr Stuart Allen
Technical HeadSouthampton General Hospital
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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 fieldsimparted 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 AxisLead 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:
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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 cardiacdisease (anatomical, metabolic, ionic, orhaemodynamic)
Sometimes the only indicator ofpathological 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 themyocardium, not the specialised conductivetissue, which is responsible for most
arrhythmias
It is often difficult to identify a single cause forany 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 (INa)
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 (INa-Ca)
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The Transmembrane CurrentsThe Transmembrane Currents
Phase 3
Potassium delayed rectifier current (Ik)
slow and fast components (Iks
, Ikr)
Phase 4
Sodium pacemaker current (If)
Potassium inward rectifier currents (I k1)
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Cardiac Ion ChannelsCardiac Ion ChannelsThey 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 delayedrectifier 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: 1Mechanisms 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 (
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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 TachycardiasDifferential Diagnosis
Sinus tachycardia
Atrial fibrillation or flutter
Reentry tachycardias
AV nodal
Atrioventricular (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 foratrial activity
presence of P wave
P wave after R wave
AV reciprocating or
AV nodal reentry
2. Effect ofadenosine
terminates most reentry tachycardias
reveals P waves
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Management: the UnstableManagement: 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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VentricularTachycardia >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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VentricularTachycardia:VentricularTachycardia:
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 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 ATRIALTACHYCARDIAMULTIFOCAL ATRIALTACHYCARDIA
(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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Electrical Alternans - ? Cardiac Tamponade
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Acute Pulmonary Embolism
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Acute Posterior MI (Lateral extension)
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Acute Pericarditis
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Thankyou for listeningThankyou for listening