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Understanding and Management Of ECG’s
- 1. S Allen 2003 Understanding and Management Of ECG’s
- 2. S Allen 2003 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
- 3. S Allen 2003 What is an ECGWhat 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)
- 4. S Allen 2003 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
- 5. S Allen 2003 Lead PlacementsLead Placements • Surface 12 lead ECG • Posterior/ Right sided lead extensions • Standard limb leads • Modified Lewis lead • Right atrial/ oesphageal leads
- 6. S Allen 2003 The Electrical AxisThe Electrical Axis Lead axis is the direction generated by different orientation of paired electrodes
- 7. S Allen 2003 The Basic Action of the ECGThe Basic Action of the ECG The ECG deflections represent vectors which have both magnitute and direction
- 8. S Allen 2003 • 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: <0.12 sec • Normal Q wave: <0.04 sec wide <25% of QRS height
- 9. S Allen 2003 • QT interval – Corrected to heart rate (QTc) • QTc= QT / ^RR = 0.38-0.42 sec Romano Ward Syndrome
- 10. S Allen 2003 • 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
- 11. S Allen 2003 Clinical uses of ECGClinical 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
- 12. S Allen 2003 LimitationsLimitations of ECGof 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
- 13. S Allen 2003 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
- 14. S Allen 2003 The Cardiac Conduction PathwayThe Cardiac Conduction Pathway
- 15. S Allen 2003 The Resting PotentialThe Resting Potential • SA node : -55mV • Purkinjie cells: -95mV • Maintained by: – cytoplasmic proteins – Na+/K+ pump – K+ channels
- 16. S Allen 2003 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
- 17. S Allen 2003 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
- 18. S Allen 2003 The Transmembrane CurrentsThe 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)
- 19. S Allen 2003 The Transmembrane CurrentsThe 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)
- 20. S Allen 2003 Cardiac Ion ChannelsCardiac 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
- 21. S Allen 2003 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 delayed rectifier K current)
- 22. S Allen 2003 Refractory Periods of the Myocyte 0 -50 -100 Membrane Potential Absolute R.P. Relative R.P.
- 23. S Allen 2003 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
- 24. S Allen 2003 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
- 25. S Allen 2003 Wide Complex TachycardiasWide Complex Tachycardias Differential Diagnosis Ventricular tachycardia (>80%) Supraventricular tachycardia with (<20%) aberrancy preexisting bundle branch block accessory pathway (bundle of Kent, Mahaim)
- 26. S Allen 2003 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)
- 27. S Allen 2003 Wide Complex Tachycardias:Wide Complex Tachycardias: Diagnostic ApproachDiagnostic Approach • 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)
- 28. S Allen 2003 Ventricular Tachycardia with visible P waves
- 29. S Allen 2003 Surpaventricular Tachycardia with abberancy
- 30. S Allen 2003 Narrow Complex TachycardiasNarrow Complex Tachycardias Differential Diagnosis Sinus tachycardia Atrial fibrillation or flutter Reentry tachycardias AV nodal Atrioventricular (accessory pathway) Intraatrial
- 31. S Allen 2003 Narrow Complex Tachycardia: Atrial Flutter
- 32. S Allen 2003 Narrow Complex Tachycardias:Narrow Complex Tachycardias: Diagnostic ApproachDiagnostic 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
- 33. S Allen 2003 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
- 34. S Allen 2003 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
- 35. S Allen 2003 Torsades or Polymorphic VT
- 36. S Allen 2003 Accelerated Idioventricular Rhythm
- 37. S Allen 2003 Ventricular Tachycardia:Ventricular Tachycardia: 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
- 38. S Allen 2003 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
- 39. S Allen 2003 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
- 40. S Allen 2003 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
- 41. S Allen 2003 MULTIFOCAL ATRIAL TACHYCARDIAMULTIFOCAL ATRIAL TACHYCARDIA (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
- 42. S Allen 2003 Multifocal Atrial Tachycardia
- 43. S Allen 2003 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
- 44. S Allen 2003 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
- 45. S Allen 2003 Complete Heart Block and AF
- 46. S Allen 2003 What is the cause of the VT?
- 47. S Allen 2003 • Hypokalaemia
- 48. S Allen 2003 • Electrical Alternans - ? Cardiac Tamponade
- 49. S Allen 2003 • Acute Pulmonary Embolism
- 50. S Allen 2003 • Acute Posterior MI (Lateral extension)
- 51. S Allen 2003• Ventricular Tachycardia (Recent MI)
- 52. S Allen 2003 • Acute Pericarditis
- 53. S Allen 2003 • Thank you for listeningThank you for listening