Kitty Chan School of Nursing,The Hong Kong Polytechnic University

1. Basic Clinical Electrocardiography Kitty Chan School of Nursing,The Hong Kong Polytechnic University Email:hskittyc@inet.polyu.edu.hk Date: 2005

2. Objectives Upon completion of the session, the students should: • have developed a basic understanding of anatomy and of the physiology of cardiac conduction in relation to ECG interpretation; • have developed a systematic and pragmatic approach to ECG interpretation; • appreciate the clinical significance of ECG interpretation.

3. Indicative Readings • Wiegand, L-M D. J. & Carlson, K. K. (Eds.) (2005). American Association of Critical-Care Nurses AACN Procedure Manual for Critical Care. (5th ed.). Philadelphia: W B Saunders. Section 8 • Huszar, R. J. (2002). Basic Dysrhythmias: Interpretation & Management. (3rd Ed.). St Louis: Mosby.

4. Introduction The electrocardiogram [ECG] is a helpful in diagnosing cardiac & non-cardiac illnesses. It is also used to monitor the effects of therapeutic treatment. Cardiac monitoring, or telemetry provides a continuous and real-time observation of the client’s cardiac rhythm. A single-strip ECG gives a prompt identification of life-threatening rhythms. In addition, abnormalities that are detected can serve as a basis for 12-Lead ECG or other investigations. 12-Lead ECG imparts more information, such as ischaemia and myocardial infarction. The above two aspects will be the main focus of this module. Of course, interpreting axis deviation & hypertrophies or other abnormalities is highly recommended.

5. Introduction Electrical activities produce current that transmit through the heart conduction system. This is sensed and transformed into ECG waveforms. Depolarization and repolarization occurs in a precise sequence. Normally, mechanical heart contraction follow to generate the cardiac output. However, when disturbances arise, cardiac contraction may not be effective, and there may even be no contractions. Therefore, always match the ECG rhythm with the patients’ clinical manifestation and complains. Before we start interpreting ECG, the anatomy, cardiac cycle and electrophysiology are reviewed

6. Five Phases of the Depolarization-Repolarization Cycle

7. Myocardial Transmembrane Potentials Early Repolarization   Action Potentials Rapid Depolarization Rapid Repolarization Mechanical Contraction  Potential milivolts Threshold Potentials Resting State  Relative Refractory Period Outside cell - - - - - + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - Cell membrane + + + + + Absolute Refractory Period Restoration of Balance K+ Cardiac cell K+ K+ 0 - - - - - - - - - - - - - - - - - - - - - - - - - Cell membrane Na+ + + + + + + + + + + + + + + + + Ca++ + + + + + + + + + + + + + + Na+ Outside cell Na+ Sodium Pump Plateau Fast Sodium Influx Slow Calcium channel open  Plateau

8. Properties of Cardiac Cells

9. Automaticity of Cardiac Cells

10. Pacemaker Action Potentials & Automaticity + 10mV Action Potential Membrane Potential Threshold Potential -60mV -90mV Resting Membrane Potential Time (Second) 0.8 2.4 1.6 0 Pacemaker Potential: Spontaneous Depolarization Automaticity in cardiac muscles: • a gradual  in K+ permeability  resting potential  Transmembranous Potential [TMP] reaches a threshold  Spontaneous depolarization occurs • SA node - shortest phase 4  dominates impulse generation

11. Pacemaker Action Potentials & Automaticity + 10mV Action Potential Membrane Potential Steeper Slope: Automaticity Increase Threshold Potential -60mV -90mV Resting Membrane Potential Time (Second) 0.8 2.4 1.6 0 Pacemaker Potential: Spontaneous Depolarization

12. Pacemaker Action Potentials & Automaticity + 10mV Action Potential Membrane Potential Slope Decreases: Automaticity Decreases Threshold Potential -60mV -90mV Resting Membrane Potential Time (Second) 0.8 2.4 1.6 0 Pacemaker Potential: Spontaneous Depolarization

13. + 10mV Action Potential Membrane Potential Threshold Potential -60mV -90mV Resting Membrane Potential Bigger Difference Time (Second) 0.8 2.4 1.6 0 RMP TP Effect of Change in RMP RMP Decreases (More Negative): • Cells are less excitable  Stronger stimulus required for depolarization  contractility weakens • This occurs in HYPOKalaemia

14. + 10mV Action Potential Membrane Potential Threshold Potential -60mV -90mV Resting Membrane Potential Time (Second) 0.8 2.4 1.6 Closer to TP 0 RMP TP Effect of Change in RMP RMP Increases (Less Negative): • Cells are easily excitable  Depolarization occurs with a very weak stimulus contractility slow & ineffective • This occurs in HYPERKalaemia

15. + 10mV Action Potential Membrane Potential Threshold Potential -60mV -90mV Resting Membrane Potential Time (Second) 0.8 2.4 1.6 Closer to RMP 0 RMP TP Effect of Change in TP TP Decreases: • Closer to RMP, the cells are more excitable  Depolarization occurs with a very weak stimulus contractility slow & ineffective • This occurs in HYPOCalaemia  HYPERCALCAEMIA is a Positive Inotrope since it sustains & strengthens cardiac contractions

16. Electrical Conduction System Sinoatrial (SA) Node Interatrial conduction tract (Bachmann Bundle) Atrioventricular (AV) Node AV Junction Bundle of His Internodal atrial conduction tract Left Bundle Branch Left posterior fascicle Left anterior fascicle Purkinje fibres Right Bundle Branch

17. Wave Deflection & Current Direction

18. Cardiac Depolarization & Electrical Current 1 4 2 R 3 1.Atrial Depolarization 2.Septal vector 3. Apical vector & both ventricles 4. Remainder of the left ventricle R. Resultant Cardiac Vector • A positive deflection (upstroke) Λis recorded as depolarization proceeds towards the particular electrode & vice versa.

19. Lead I + + + Einthoven’s Equilateral Triangle Lead III Lead II Limb Leads: Frontal Plane of the HeartStandard Bipolar Leads Inferior

20. Lead aVL Lead aVR Null Reference Point x Lead aVF Limb Leads: Frontal Plane of the HeartThe Augmented Unipolar Leads Null Reference Point: the negative reference for leads aVR, aVL, aVF & the precordial leads V1 - V6 (calculated from the right & left arm and right & left leg electrodes)

21. -900 -1200 -600 aVL -300 aVR -1500 LAD Indeterminate I00 +1800 NORMAL RAD +1500 +300 III +1200 II+600 aVF+900 Hexaxial Reference Circle For determining frontal plane axis deviation

22. 12-Lead Electrode Placement Mid-Clavicular Line Anterior Axillary Line Mid-Axillary Line V2 V5 V3 V6 V1 V4 Lateral Leads Septal Leads Anterior Leads V1 to V6: Corresponding sites for monitoring of MCL1 to MCL6 ✼Precordial Leads are useful in detecting ST Changes & Aberrant Ventricular Conductions i.e., Electrode Placement at V6 equivalent of MCL6 Paul S & Hebra J D 1998 The Nurse’s Guide to Cardiac Rhythm Interpretation: Implications for patient care. Philadelphia: Saunders.

23. Mid-Clavicular Line Anterior Axillary Line Mid-Axillary Line V2R V3R V6R V5R V4R Right-sided Chest Electrode Placement

24. Posterior Chest Electrode Placement V9 V6 V7 V8 Left Paraspinal Line Posterior Axillary Line Mid-Axillary Line Wiegand & Calrson, 2004, p. 426

25. Cardiac Monitoring & Lead Placement • 3-Lead-Wire system: • limited to leads I, II, III & • modified chest leads (MCL1-6) • For single-lead ECG monitoring, unless a specific part of the heart is under scrutiny, Lead II is usually chosen since both the positive & negative vectors are travelling in the same direction of cardiac impulse conduction, producing upright P & QRS complexes.

26. Cardiac Monitoring & Lead Placement • 5-Lead-Wire system: • 4 standardized electrodes corresponding to limbs leads I, II, III, aVR, aVL & aVF • placement of 5th chest leads provides 7 precordial lead options V1-V6 (1 at a time)

27. 1 Large Square 1 Small Square 1mm tall = 0.1mV of amplitude 5mm across = 0.2 second 1mm across = 0.04 second *Sweep speed of ECG & paper dispense @ 25mm per second 5 Large Squares = 1 Second

28. Lead II R R ST Segment T P U S PR Interval S Q Q QT Interval Normal ECG/EKG Waveform ST Segment T P U PR Interval QT Interval

29. Normal ECG Waveforms & Configurations

30. P wave: Atrial Depolarization P PR INTERVAL • P: • rounded & symmetrical • 0.06- 0.10 sec • amplitude: 0.5-2.5mm • positive in Lead I, II, aVF & V4-V6 • PR Interval: • 0.12-0.20 sec Paul S & Hebra J D 1998 The Nurse’s Guide to Cardiac Rhythm Interpretation: Implications for patient care. Philadelphia: Saunders.

31. P QRS QRS: Ventricle Depolarization • QRS: • Q waves is small & nonsignificant in leads I, II, III, aVL, V4-V6 • R wave progressively higher in amplitude from V2-V4/V5 gradually diminish to V6 • 0.06- 0.12 sec • amplitude: >5mm in limb leads; >10mm in Chest leads Paul S & Hebra J D 1998 The Nurse’s Guide to Cardiac Rhythm Interpretation: Implication for patient care. Philadelphia: Saunders

32. J Point P QRS ST SEGMENT ST Segment: Isoelectric Line • ST: • Curves gently into the proximal limb of the T wave • Isoelectric in ALL Leads • elevation <1mm • depression <0.5mm • J Point: • The junction of QRS complex & the J point of the ST segment • deviates from the isoelectric line if an ST elevation/ depression exist Paul S & Hebra J D 1998 The Nurse’s Guide to Cardiac Rhythm Interpretation: Implications for patient care. Philadelphia: Saunders.

33. T wave: Ventricular Repolarization T P QRS QT • T: • slightly rounded & symmetrical • positive in leads I, II, V3-V6 • inverted in aVR • amplitude <5mm in limb leads & <10mm in chest leads • QT: ventricular refractory period • 0.30-0.44sec • *0.12-0.20 sec (<½ preceding RR) • U wave:delayed repolarization of the purkinje system Paul S & Hebra J D 1998 The Nurse’s Guide to Cardiac Rhythm Interpretation: Implications for patient care. Philadelphia: Saunders.

34. Sinus Rhythm Sinus Rhythm

35. 6Seconds P P P P P P P P Normal Sinus Rhythm [NSR]

36. 6 Seconds P P P P P QRS Complex Sinus Bradycardia

37. Sinus Dysrhythmias

38.  Atrial Dysrhythmias

39.  6Seconds F F F F F F F F F F QRS Complex Identical undulating SAW-TOOTH FLUTTER WAVES Atrial Flutter

40. 6 Seconds Atrial Fibrillation [Fine AF]

41. 6 Seconds Atrial Fibrillation [Coarse AF]

42.         P’ P’ P’ P’ P’ Atrial Dysrhythmias • MAT (multifocal atrial tachycardia) • Various P morphologies originate from multiple atrial ectopic foci • *(3 or more pacemaker sites) • Rate = 160-240bpm

43. 6 Seconds QRS Complex Juntional Rhythm 

44. Junctional Dysrhythmias 1o pacing from the AV node

45. Re-Entry Phenomenon [1] Non-uniform recovery from refractory period leading to re-entry circuit: 1. Slow conduction of impulses at a refractory zone → Unidirectional Block→Detouring of Impulse 2. Activation & transmission of impulse via accessory pathway 3. Subsequent activation of impulse through the previously refractory zone (now recovered) 4. The reentry & activation of new impulses occur in a circuitry manner

46. Re-Entry Phenomenon [2] Normal Impulse NOT yet fired from SAN ∴ AV Node NOT Reactivated • Unidirectional Block & Delayed Conduction within the circuit • Original impulse emerges & reenters the adjacent tissue (just recovered) • Recycles within the circuit Paul S & Hebra J D 1998 The Nurse’s Guide to Cardiac Rhythm Interpretation: Implications for patient care. Philadelphia: Saunders.

47. Ventricular Pre-excitation AVNRT (AV Node Re-entry Tachycardia) Micro-Circuits: At cellular level within the AV node with unidirectional block & the Purkinje fibers Paul S & Hebra J D 1998 The Nurse’s Guide to Cardiac Rhythm Interpretation: Implication for patient care. Philadelphia: Saunders

48. Classic Ventricular Pre-excitation delta wave (slurred upstroke) Wolf-Parkinson-White Syndrome: pre-excitation via a Bundle of Kent without delay at the AV node Depolarization occurs with AV impulse after normal delay AVRT (AV Re-entry Tachycardia)- Macro-Circuits:Antegrade travel through the AV node & retrograde across an accessory pathway Paul S & Hebra J D 1998 The Nurse’s Guide to Cardiac Rhythm Interpretation: Implication for patient care. Philadelphia: Saunders

49. *It is useful to capture the beginning of the PSVT to identify the re-entry loop, especially when aberrant conduction occurs & a wide bizarre QRS exists PSVT (Paroxysmal Supraventricular Tachycardia)

50. Atrioventricular Blocks(Heart Block)