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Clinical Skills

Clinical Skills. Electrocardiogram (ECG). Cardiff and Vale ECG Department. Aims & Outcomes. The aim of this module is to produce a technically accurate, artefact free 12 lead ECG in accordance with AHA/ SCST guidelines. To be able to recognise the basic components of the ECG.

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Clinical Skills

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  1. Clinical Skills Electrocardiogram (ECG) Cardiff and Vale ECG Department

  2. Aims & Outcomes The aim of this module is to produce a technically accurate, artefact free 12 lead ECG in accordance with AHA/ SCST guidelines. To be able to recognise the basic components of the ECG. Learning Outcomes At the end of the session the student should be able to: Recognise the anatomy of the conduction system of the heart. Identify the waveforms of the cardiac cycle, as seen on the ECG. Calculate the heart rate from the ECG. Outline the equipment and specifications required for recording a 12 lead ECG. State and demonstrate the anatomical positions for electrode placement. Recognise and minimise interference patterns on an ECG. Identify Einthoven’s Triangle, and its uses in practical electrocardiography. Produce a technically accurate ECG. Aims & Outcomes

  3. What is an ECG? An ECG is a transthoracic interpretation of the electrical activity of the heart. A typical ECG tracing of the cardiac cycle (heartbeat) consists of a P wave, QRS complex, T wave and sometimes a U wave. William Einthoven chose the letters P,Q,R, S, T to identify the tracing. WHAT IS AN ECG?

  4. Conduction System The heart is influenced by the autonomic nervous system which can increase or decrease the heart rate in line with the requirements of the body. However, due to an intrinsic regulating system, called the conduction system it is possible for the heart to go on beating without any direct stimulus from the nervous system. This system is composed of specialised muscle tissue that generates and distributes the conduction that causes contraction of the cardiac muscle. These tissues are found in the sinus (or sinoatrial) node, atrioventricular node, bundle of His, bundle branches, and conduction myofibres. When stimulated by electrical activity, muscle fibres contract and produce motion. In the heart, this electrical activity is referred to asdepolarisation. The contraction causes the blood to be pumped around the body. Relaxation of the heart muscle is caused by electricalrepolarisation. Conduction System

  5. Conduction System DEPOLARISATION REPOLARISATION

  6. Principles of how the ‘ECG’ works In this example we are recording the potential difference between two points. As depolarisations (positive charge entering the cell from outside) move across the cell, the voltage difference increases. A movement of positive charges into a cell is recorded as a positive deflection and a movement of positive charges out of the cell is recorded as a negative deflection. Principle of how the ‘ECG’ works

  7. Principles of how the ‘ECG’ works Principle of how the ‘ECG’ works To understand the morphology of the ECG waveforms one needs to appreciate only one biophysical fact: if a wave front of depolarisation travels towards the electrode attached to the + input terminal of the ECG amplifier and away from the electrode attached to the – terminal, a positive-going deflection will result. If the waveform travels away from the + electrode towards the – electrode, a negative-going deflection will be seen. If the waveform is travelling in a direction perpendicular to the line joining the sites where the two electrodes are placed, no deflection or a biphasic deflection will be produced.

  8. Views of Depolarisation It can then be seen that the voltage recorded along a particular lead axis (the vector joining the - to the + electrode) at a particular time is obtained by taking a projection onto that axis of the vector representing the magnitude and direction of depolarization at that time.  Thus, when the lead axis in the figure alongside points from left to right, parallel to the direction of movement of depolarization, a positive-going complex results.  When the two directions are anti-parallel, a negative-going complex is produced. Views of Depolarisation

  9. Atrial Depolarisation The electrical activity of the heart originates in the sino-atrial node.  The impulse then rapidly spreads through the right atrium to the atrioventricular node.  It also spreads through the atrial muscle directly from the right atrium to the left atrium. The P-wave is generated by activation of the muscle of both atria. Atrial Depolarisation

  10. Septum Repolarisation The impulse travels very slowly through the AV node, then very quickly through the bundle of His,  then the bundle branches, the Purkinje network, and finally the ventricular muscle. The first area of the ventricular muscle to be activated is the interventricular septum, which activates from left to right.  This generates the Q-wave. Septum Repolarisation

  11. Ventricular Depolarisation Next, the left and right ventricular free walls, which form the bulk of the muscle of both ventricles, gets activated by an action potential from the bundles of His and begin to cause depolarisation from the septum towards the apex (bottom) of the ventricles.  This generates the R-wave on the ECG. Ventricular Depolarisation

  12. Late Ventricular Depolarisation A few small areas of the ventricles are activated at a rather late stage.  This generates the S-wave Late Ventricular Depolarisation

  13. Ventricular Repolarisation Finally, the ventricular muscle repolarises. This generates the T-wave Ventricular Repolarisation

  14. Cardiac Action Potentials Action potentials at the bottom edge of the ventricle are SHORTER than at the top. This helps to explain why the repolarisation of the ventricles (the T wave) gives a positive deflection on the ECG trace. You can see that the action potentials at the bottom of the ventricle repolarise before those at the top. Therefore the wave of repolarisation moves in the opposite direction to the wave of depolarisation. Not All Cardiac Actions Potentials Are The Same!!

  15. The ECG The ECG P Atrial Depolarisation QRS Ventricular Depolarisation T Ventricular Repolarisation U Though to be Septal Repolarisation

  16. The P Wave The P Wave Represents atrial depolarisation Small, rounded wave P Atrial Depolarisation

  17. The QRS Wave The QRS Wave Represents ventricular depolarisation Large, “pointed” wave Q Wave:The first negative deflection. R Wave:Any positive deflection. S Wave:Any negative deflection after an R wave. QRS Ventricular Depolarisation

  18. The T Wave The T Wave Large, rounded wave Represents ventricular repolarisation T Ventricular Repolarisation

  19. Measured from the beginning of the P wave to the beginning of the QRS complex Normal value: 0.12 – 0.2 secs 3 – 5 small squares PR Interval

  20. Measured from initial deflection of the QRS from the isoelectric line to the end of the QRS complex Normal value: < 0.12 secs less than 3 small squares QRS Duration

  21. Sinus Rhythm

  22. ATRIO-VENTRICULAR BLOCKS

  23. Atrio-Ventricular Heart Block 1st Degree Heart Block Measured from the beginning of the P wave to the beginning of the QRS complex Normal value: 0.12 – 0.2 secs 3 – 5 small squares PR Interval > 5 small squares

  24. Atrio-Ventricular Heart Block Prolonged PR interval: >0.2 secs Constant PR interval Regular ventricular rhythm 1st Degree Heart Block

  25. Atrio-Ventricular Heart Block 2nd Degree Heart Block Mobitz Type 1 Wenckebach Mobitz Type 2 Constant Periodic

  26. Atrio-Ventricular Heart Block Progressive Lengthening of PR interval, until a non-conducted P wave occurs. Usually occurs in a cyclic pattern 2nd Degree Heart Block – Mobitz Type 1 - Wenckebach

  27. Atrio-Ventricular Heart Block 2nd Degree Heart Block – Mobitz Type 1 - Wenckebach

  28. Atrio-Ventricular Heart Block P wave not followed by a QRS plus P wave normally conducted. (May be 2:1, 3:1, etc) PR interval of the conducted beat is constant. (May be normal or prolonged) Atrial rate is regular and normal. Ventricular rate may be regular (eg. 2:1) 2nd Degree Heart Block – Mobitz Type 2 – Constant Block

  29. Atrio-Ventricular Heart Block 2nd Degree Heart Block – Mobitz Type 2 – Constant Block

  30. Atrio-Ventricular Heart Block Normal 1 P:1 QRS conduction with occasional non-conducted P waves. PR interval of the conducted beat is regular. (May be normal or prolonged) 2nd Degree Heart Block – Mobitz Type 2 – Periodic Block

  31. Atrio-Ventricular Heart Block 2nd Degree Heart Block – Mobitz Type 2 – Periodic Block

  32. Atrio-Ventricular Heart Block Regular P waves at a normal rate Regular QRS complexes at a slow rate. (30 – 40 beats / min) No correlation between P waves and QRS complexes QRS may have abnormal shape 3rd Degree Heart Block – Complete Heart Block

  33. MYOCARDIAL ISCHAEMIA & INFARCTION

  34. Myocardial Ischaemia & Infarction What is an MI? …is when part of the HEART muscle dies because it has been starved of OXYGEN Heart Attack Myocardial Infarction Coronary Thrombosis

  35. Myocardial Ischaemia & Infarction There are 3 Coronary Arteries: LAD (Left main coronary artery) Circumflex artery (originates off the LAD) Right coronary artery All these sub-divide into smaller branches Coronary Arteries

  36. Myocardial Ischaemia & Infarction Myocardial Infarction Myocardial Infarction as a result of a blocked left anterior descending coronary artery

  37. Myocardial Ischaemia & Infarction Coronary Arteries Territory

  38. Myocardial Ischaemia & Infarction I, aVL, V5 & V6 V1 – V6 II, III & aVF

  39. Myocardial Ischaemia & Infarction ST Segments Note: “Upsloping” ST depression is not an ischaemic abnormality

  40. Myocardial Ischaemia & Infarction ST Segments

  41. Myocardial Ischaemia & Infarction Normal ECG prior to MI Hyperacute T wave change increased T wave amplitude and width may also see ST elevation Marked ST elevation with hyperacute T wave changes (transmural injury) Pathologic Q waves, less ST elevation, terminal T wave inversion (necrosis) Pathologic Q waves, T wave inversion (necrosis and fibrosis) Pathologic Q waves, upright T waves (fibrosis) Evolution of Acute MI

  42. Myocardial Ischaemia & Infarction Acute inferior myocardial infarction ST elevation in the inferior leads II, III and aVF Reciprocal ST depression in the anterior leads A 55 year old man with 4 hours of “crushing” chest pain

  43. Myocardial Ischaemia & Infarction Acute antero-lateral infarction ST elevation in I, aVL, V2 – V6 Reciprocal ST depression in inferior leads

  44. Myocardial Ischaemia & Infarction ECG Taken @ 11:01 am

  45. Myocardial Ischaemia & Infarction ECG Taken @ 11:12 am

  46. Myocardial Ischaemia & Infarction Narrowed Proximal LAD

  47. Myocardial Ischaemia & Infarction Interventional Procedure PTCA Percutaneous Transluminal Coronary Angioplasty PCI Percutaneous Coronary Intervention

  48. Myocardial Ischaemia & Infarction ST elevation Often within minutes of onset of MI, but may be delayed for several hours T Wave Inversion Slightly later than ST elevation ST elevation returns to iso-electric line Usually within 48-72 hours Q waves May take several hours to develop after onset of MI Evolution of Acute MI

  49. ELECTRODE POSITIONING

  50. Electrode Positioning RA – Right Wrist LA – Left Wrist LL – Left Ankle RL – Anywhere on Body (Records I, II, III, aVR, aVL, aVF) Limb Leads

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