Understanding and Management Of ECG’s

Understanding and Management Of ECG’s

1. S Allen 2003
Understanding and Management
Of ECG’s

2. 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 ECG
The 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 (I
ks
, I
kr
)
•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
+
, Ca
2+
, 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%)
aberrancy
preexisting bundle branch block
accessory 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 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 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 pO
2
, acidosis, K
+
, Mg
2+
, 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)

51. S Allen 2003•Ventricular Tachycardia (Recent MI)

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•Acute Pericarditis

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•Thank you for listeningThank you for listening