1. Understanding and Management Of ECG’s
Mr Stuart Allen
Technical Head
Southampton General Hospital
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2. 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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3. 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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4. 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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5. 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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6. The Electrical Axis
Lead axis is the direction generated by different orientation of paired electrodes
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7. The Basic Action of the ECG
The ECG deflections represent vectors which have both magnitute and direction
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8. Time for intraatrial, AV nodal, and His-Purkinjie conduction
P wave
atrial activation
Normal axis to +60
PR interval
Time for intraatrial, AV nodal, and His-Purkinjie conduction
Normal duration: 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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9. Corrected to heart rate (QTc)
QT interval
Corrected to heart rate (QTc)
QTc= QT / ^RR = sec
Romano Ward Syndrome
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10. represents the greater part of ventricular repolarization T wave
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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11. 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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12. 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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13. 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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14. The Cardiac Conduction Pathway
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15. The Resting Potential SA node : -55mV Purkinjie cells: -95mV
Maintained by:
cytoplasmic proteins
Na+/K+ pump
K+ channels
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16. 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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17. The Cardiac Action Potential1
Membrane Potential
Ca++ influx 2
-50 3
Na + influx
K+ efflux 4 4 mV
-100
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18. 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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19. 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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20. 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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21. 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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22. Refractory Periods of the Myocyte
Membrane Potential
-50
Absolute R.P.
-100
Relative R.P.
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23. 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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24. 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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25. 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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26. 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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27. Wide Complex Tachycardias: Diagnostic Approach
3. ECG Findings
Capture or fusion beats (VT)
Atrial activity (absence of 1:1 suggests VT)
QRS axis ( -90 to suggests VT)
Irregular (SVT)
Concordance
QRS duration
QRS morphology (?old) (? BBB)
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28. Ventricular Tachycardia with visible P waves
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29. Surpaventricular Tachycardia with abberancy
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30. Narrow Complex Tachycardias
Differential Diagnosis
Sinus tachycardia
Atrial fibrillation or flutter
Reentry tachycardias
AV nodal
Atrioventricular (accessory pathway)
Intraatrial
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31. Narrow Complex Tachycardia: Atrial Flutter
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32. 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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33. 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 min, then 300mg over 1 hour
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34. 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 /min) require treatment if hypotensive
Torsades de pointes or VT - difference in management
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35. Torsades or Polymorphic VT
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36. Accelerated Idioventricular Rhythm
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37. 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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38. 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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39. Atrial Fibrillation: Cardioversion or Rate Control
If < 2 days duration: Cardiovert
amiodarone
flecainide
DC shock
If > 2 days duration: Rate control first
digoxin
B blockers
verapamil
elective DC cardioversion
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40. Atrial Flutter Rarely seen in the absence of structural heart disease
Atrial rate / 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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41. 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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42. Multifocal Atrial Tachycardia
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43. 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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44. Bradyarrhythmias Treat if Symptomatic Risk of asystole Adverse signs
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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45. Complete Heart Block and AF
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46. What is the cause of the VT?
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47. Hypokalaemia
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48. Electrical Alternans - ? Cardiac Tamponade
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49. Acute Pulmonary Embolism
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50. Acute Posterior MI (Lateral extension)
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51. Ventricular Tachycardia (Recent MI)
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52. Acute Pericarditis
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53. Thank you for listening
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