Download Understanding ecgs

Understanding and Management
Of ECG’s
S Allen 2003
Contents
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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
1
0
2
0
Na +
influx
-50
4
mV
-100
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Ca++
influx
3
K+
efflux
4
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.
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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
(>80%)
Supraventricular tachycardia with
(<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
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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
(VT)
(absence of 1:1 suggests VT)
( -90 to +180 suggests VT)
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(SVT)
Irregular
Concordance
QRS duration
QRS morphology
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(?old) (? BBB)
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
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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
• >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:
Cardiovert
• amiodarone
• flecainide
• DC shock
• 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
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– Atropine iv 600 ug to max 3 mg
– Isoprenaline iv
– Pacing, external or transvenous
Complete Heart Block and AF
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What is the cause of the VT?
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• S 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)
2003
• Acute Pericarditis
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• Thank you for listening
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