Understanding Ecgs

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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:


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:


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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Understanding Ecgs

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