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: Normal duration: Normal Q wave:
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-30 to +90 deg <0.12 sec <0.04 sec wide <25% of QRS height

 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

Membrane Potential
0

1 Ca++ 2 influx 0 Na + influx

-50

4
mV

3 K+ efflux

-100 2003 S Allen

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 timedependent They allow passive transfer of Na+, K+, Ca2+, Clions 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
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Relative R.P.

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 Supraventricular tachycardia with (>80%) (<20%)

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 Atrial activity QRS axis
Irregular Concordance QRS duration QRS morphology

(VT) (absence of 1:1 suggests VT) ( -90 to +180 suggests VT)

(SVT)

(?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 Intraatrial
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(accessory pathway)

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 S Allen 2003

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
>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: 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 <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: Cardioversion or Rate Control

If < 2 days duration:
amiodarone flecainide DC shock

Cardiovert

If > 2 days duration:

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Rate control first

digoxin B blockers verapamil amiodarone elective DC cardioversion

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 > 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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 S Hypokalaemia Allen 2003

 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) S Allen 2003

 Acute Pericarditis
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 Thank you for listening

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