Understanding and Management Of ECGs

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Understanding and Management Of ECGs

• Mr Stuart Allen
• Technical Head
• Southampton General Hospital

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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

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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)

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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

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Lead 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 Axis
Lead axis is the direction generated by different
orientation of paired electrodes
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The 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 lt0.12 sec
• Normal Q wave lt0.04 sec wide lt25 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 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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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

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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

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The Cardiac Conduction Pathway
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The Resting Potential

• SA node -55mV
• Purkinjie cells -95mV
• Maintained by
• cytoplasmic proteins
• Na/K pump
• K channels

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The 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 Potential
1
Membrane Potential
Ca influx
0
2
0
-50
3
Na influx
K efflux
4
4
mV
-100
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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)

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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)

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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
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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)

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Refractory Periods of the Myocyte
Membrane Potential
0
-50
Absolute R.P.
-100
Relative R.P.
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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 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 Tachycardias
Differential Diagnosis Ventricular
tachycardia (gt80) Supraventricular
tachycardia with (lt20) aberrancy preexisting
bundle branch block accessory pathway (bundle
of Kent, Mahaim)
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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)

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Wide Complex Tachycardias Diagnostic Approach

• 3. ECG Findings
• Capture or fusion beats (VT)
• Atrial activity (absence of 11 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 Tachycardias
Differential Diagnosis Sinus tachycardia Atrial
fibrillation or flutter Reentry
tachycardias AV nodal Atrioventricular (acces
sory pathway) Intraatrial
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Narrow Complex Tachycardia Atrial Flutter
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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

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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

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Ventricular Tachycardia

• gt3 consecutive ventricular ectopics with rate
  gt100/min
• Sustained VT (gt30 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 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

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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 lt2 with anticoagulation)
  
• 3. Cardiovert or Rate control
• Poor success rate if prolonged AF gt 1 year, poor
  LV, MV stenosis

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Atrial Fibrillation Cardioversion or Rate Control

• If lt 2 days duration Cardiovert
• amiodarone
• flecainide
• DC shock
• If gt 2 days duration Rate control first
• digoxin
• B blockers
• verapamil
• amiodarone
• elective DC cardioversion

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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

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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

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Multifocal Atrial Tachycardia
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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

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Bradyarrhythmias

• Treat if
• Symptomatic
• Risk of asystole
• Mobitz type 2 or CHB with wide QRS
• Any pause gt 3 sec
• Adverse signs
• Hypotension, HF, rate lt 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 listening