Ecg part introduction

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ECG basic
Introduction to ECG
Important Examples of ECG
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  • QRS waveform nomenclature
    The ECG consists of a small deflection called the P wave, arising from the atria, a more complicated deflection called the QRS complex due to ventricular depolarisation and a final T wave resulting from repolarisation of the ventricles.
    The QRS complex of waves is the largest deflection of the ECG and is always spiky in shape. All sharp deflections resulting from electrical activation of the ventricles are called QRS complexes. However, these waves can vary immensely in size, and arrangement.
    The QRS complex is very important when diagnosing myocardial infarction. In order to be able to describe these complexes, a nomenclature for the waves is needed. This can be done using combinations of the letters q, r, s, Q, R, S, lower case letters denoting small waves and upper case larger waves.
    The first positive wave is labelled with r or R
    Any second positive wave is labelled r´ or R´
    A negative wave which follows an R wave or r wave is labelled S or s
    A negative wave that precedes an R or r wave, is labelled a q or Q wave
    Any wave that is entirely negative is labelled qs or QS.
    Using these rules and nomenclature all QRS complexes can be described, enabling more accurate diagnosis.
  • The 10 rules for a normal ECG
    For an ECG to be determined as normal, Chamberlain has described 10 rules which must be met.1 The next ten slides will outline these rules.
  • Rule 1
    As described in Module 3, the PR interval is the time from initiation of depolarisation of the atria to initiation of the depolarisation of the ventricles. The PR interval should be 120 to 200 milliseconds, or 3 to 5 little squares. A longer PR may imply a block in conduction and a shorter interval indicates a vulnerability to arrhythmias.
  • Rule 2
    The QRS complex is due to depolarisation of the ventricles. The width of the QRS complex should not exceed 110 ms (less than 3 little squares). A wider QRS is sometimes seen in healthy people, but may represent an abnormality of intraventricular conduction.
  • Rule 3
    The QRS complex should be dominantly upright in leads I and II. Slight disparities are likely to be acceptable.
  • Rule 4
    The QRS and T waves tend to have the same direction in the standard leads.
  • Rule 5
    All waves are negative in lead aVR. This has to be so: aVR represents electrical activity as “seen” from the right shoulder. The sinus node is placed top right in the heart nearest the right shoulder, and the electrical activity is moving downwards and leftwards towards the left ventricle.
  • Rule 6
    The normality of QRS complexes recorded from the precordial leads is dependent on both morphological and dimensional criteria.
  • Rule 7
    The ST segment should start isoelectric except in V1 and V2 where it may be elevated.
  • Rule 8
    In leads I, II, and V2 to V6 the P waves should be upright.
  • Rule 9
    There should be no Q wave or only a small q less than 0.04 seconds in width in I, II, V2 to V6.
  • Rule 10
    In leads I, II, and V2 to V6 the T wave must be upright.
  • Characteristic changes in AMI
    The 12-lead ECG is the most useful investigation for confirming the diagnosis of acute myocardial infarction, locating the site of the infarct and monitoring the progress. It is therefore very important to know the changes that occur in this situation.
    The only diagnostic evidence of a completed myocardial infarction seen on the ECG are those in the QRS complexes. In the early stages changes are also seen in the ST segment and the T wave, and these can be used to assist diagnosis of myocardial infarctions.
    Shortly after infarction there is an elevation of the ST segment seen over the area of damage, and opposite changes are seen in the opposite leads. Several hours later pathological Q waves begin to form, and tend to persist. Later the R wave becomes reduced in size, or completely lost. Later still, the ST segment returns to normal, and at this point the T wave also decreases, eventually becoming deeply and symmetrically inverted.
    Although these changes occur sequentially, it is very unlikely they will all be clearly observed by the paramedic or GP. A patient can present at any stage and a progression through the ECG changes will not be seen. It is important to recognise these features as they occur rather than in association with each other. All these changes imply myocardial infarction, and will be discussed in more detail over the next few slides.
  • ST elevation
    ST segment elevation usually occurs in the early stages of infarction, and may exhibit quite a dramatic change.
    ST elevation is often upward and concave, although it can appear convex or horizontal. These changes occur in leads facing the infarction.
    ST elevation is not unique to MIs and therefore is not confirming evidence. Basic requirements of ST changes for diagnosis are: elevation of at least 1 mm in two or more adjoining leads for inferior infarctions (II, III, and aVF), and at least 2 mm in two or more precordial leads for anterior infarction. You should be aware that ST elevation can be seen in leads V1 and V2 normally. However, if there is also elevation in V3 the cause is unlikely to be physiological.
  • Deep Q wave
    The only diagnostic changes of acute myocardial infarction are changes in the QRS complexes and the development of abnormal Q waves. However, this may be a late change and so is not useful for the diagnosis of AMI in the pre-hospital situation.
    Remember that Q waves of more than 0.04 seconds , or 1 little square, are not generally seen in leads I, II or the precordial leads.
  • T wave inversion
    The T wave is the most unstable feature of the ECG tracing and changes occur very frequently under normal circumstances, limiting their diagnostic value.
    Subtle changes in T waves are often the earliest signs of myocardial infarction. However, their value is limited for the reason above, but for approximately 20 to 30% of patients presenting with MI, a T wave abnormality is the only ECG sign.
    The T wave can be lengthened or heightened by coronary insufficiency.
    T wave inversion is a late change in the ECG and tends to appear as the ST elevation is returning to normal. As the ST segment returns towards the isoelectric line, the T wave also decreases in amplitude and eventually inverts.
  • Bundle branch block
    Bundle branch block is the pattern produced when either the right bundle or the entire left bundle fails to conduct an impulse normally. The ventricle on the side of the failed bundle branch must be depolarised by the spread of a wave of depolarisation through ventricular muscle from the unaffected side. This is obviously a much slower process and usually the QRS duration is prolonged to at least 0.12 seconds (for right bundle branch block) and 0.14 seconds (for left bundle branch block).
    The ECG pattern of left bundle branch block (LBBB) resembles that of anterior infarction, but the distinction can readily be made in nearly all cases. Most importantly, in LBBB the QRS is widened to 140 ms or more. With rare exceptions there is a small narrow r wave (less than 0.04 seconds) in V1 to V3 which is not usually seen in anteroseptal infarction. There is also notching of the QRS best seen in the anterolateral leads, and the T wave goes in the opposite direction to the QRS in all the precordial leads. This combination of features is diagnostic. In the rare cases where there may be doubt assume the correct interpretation is LBBB. This will make up no difference to the administration of a thrombolytic on medical direction but for the present will be accepted as a contraindication for paramedics acting autonomously (see later slide).
    Right bundle branch block is characterised by QRS of 0.12 seconds or wider, an s wave in lead I, and a secondary R wave (R’) in V1. As abnormal Q waves do not occur with right bundle branch block, this remains a useful sign of infarction.
  • Sequence of changes in evolving AMI
    The ECG changes that occur due to myocardial infarction do not all occur at the same time. There is a progression of changes correlating to the progression of infarction.
    Within minutes of the clinical onset of infarction, there are no changes in the QRS complexes and therefore no definitive evidence of infarction. However, there is ST elevation providing evidence of myocardial damage.
    The next stage is the development of a new pathological Q wave and loss of the r wave. These changes occur at variable times and so can occur within minutes or can be delayed. Development of a pathological Q wave is the only proof of infarction.
    As the Q wave forms the ST elevation is reduced and after 1 week the ST changes tend to revert to normal, but the reduction in R wave voltage and the abnormal Q waves usually persist.
    The late change is the inversion of the T wave and in a non-Q wave myocardial infarct, when there is no pathological Q wave, this T wave change may be the only sign of infarction.
    Months after an MI the T waves may gradually revert to normal, but the abnormal Q waves and reduced voltage R waves persist.
    In terms of diagnosing AMI in time to make thrombolysis a life-saving possibility, the main change to look for on the ECG is ST segment elevation.
  • Location of infarction and its relation to the ECG: anterior infarction
    As was discussed in the previous module, the different leads look at different aspects of the heart, and so infarctions can be located by noting the changes that occur in different leads. The precordial leads (V1–6) each lie over part of the ventricular myocardium and can therefore give detailed information about this local area. aVL, I, V5 and V6 all reflect the anterolateral part of the heart and will therefore often show similar appearances to each other. II, aVF and III record the inferior part of the heart, and so will also show similar appearances to each other. Using these we can define where the changes will be seen for infarctions in different locations.
    Anterior infarctions usually occur due to occlusion of the left anterior descending coronary artery resulting in infarction of the anterior wall of the left ventricle and the intraventricular septum. It may result in pump failure due to loss of myocardium, ventricular septal defect, aneurysm or rupture and arrhythmias. ST elevation in I, aVL, and V2–6, with ST depression in II, III and aVF are indicative of an anterior (front) infarction. Extensive anterior infarctions show changes in V1–6 , I, and aVL.
  • Location of infarction and its relation to the ECG: inferior infarction
    ST elevation in leads II, III and aVF, and often ST depression in I, aVL, and precordial leads are signs of an inferior (lower) infarction. Inferior infarctions may occur due to occlusion of the right circumflex coronary arteries resulting in infarction of the inferior surface of the left ventricle, although damage can be made to the right ventricle and interventricular septum. This type of infarction often results in bradycardia due to damage to the atrioventricular node.
  • Location of infarction and its relation to the ECG: lateral infarction
    Occlusion of the left circumflex artery may cause lateral infarctions.
    Lateral infarctions are diagnosed by ST elevation in leads I and aVL.
  • Location of infarction: combinations
    The previous slides discussed the changes that occur in typical anterior, inferior and lateral infarctions. However, the area infarcted is not always limited to these areas and infarctions can extend across two regions. For example, an anterior infarction which is also on the lateral side of the heart is known as an anterolateral infarction.
    ST segment elevation in leads I and aVL represent a lateral infarction
    Anteroseptal infarctions show ST segment elevation in leads V1 to V4.
    ST elevation in V4 to V6 is typical of an anterolateral infarction
    ST elevation in II, III and aVF is typical of inferior infarction.
  • Diagnostic criteria for AMI
    Myocardial infarction is the loss of viable, electrically active myocardium. Diagnosis can therefore be made from the ECG. However, only changes in QRS complexes can provide a definite diagnosis. Changes in each of the leads must be noted, along with symptoms, as both are important in making a diagnosis.
    Excluding leads aVR and III, Q wave duration of more than 0.04 seconds or depth of more than 25% of the ensuing r wave are proof of infarction. Other criteria are the development of QS waves and local area low voltage r waves.
    Although these are useful diagnostic features, there are additional features that are associated with myocardial infarction as have been described in the previous slides. These include ST elevation in the leads facing the infarct, ST depression (reciprocal) in the opposite leads to the infarct, deep T wave inversion overlying and adjacent to the infarct, abnormally tall T waves facing the infarct, and cardiac arrhythmias. These extra features may aid in the diagnosis of myocardial infarction from an ECG.
  • Ecg part introduction

    1. 1. ECG diagnosis
    2. 2. The Normal Conduction System
    3. 3. Lead Position • A typical ECG report shows the cardiac cycle from 12 different vantage points (I, II, III, aVR, aVL, aVF, V1-V6), like viewing the event electrically from 12 different locations (like a 3D perspective).BUT only 10 electrodes are used. • Lead I represents activity that is going from the right arm to the left arm Lead II represents activity that is going from the right arm to the left leg Lead III represents activity that is going from the left arm to the left leg • • • • • • • • • • • aVL is placed on the left arm (or shoulder) aVF is placed on the left leg (or hip) aVR is placed on the right arm (or shoulder) V1- 4th intercostal space to the right of sternum V2- 4th intercostal space to the left of sternum V3- halfway between V2 and V4 V4- 5th intercostal space in the left mid-clavicular line V5- 5th intercostal space in the left anterior axillary line V6- 5th intercostal space in the left mid axillary line
    4. 4. NSR
    5. 5. • NORMAL
    6. 6. • NORMAL
    7. 7. • NSR , Juvenile T-wave inversion.
    8. 8. • NORMAL
    9. 9. WPW Syndrome
    10. 10. AF, Inferior Q waves
    11. 11. RBBB
    12. 12. 28 years with palpitations
    13. 13. • SVT
    14. 14. 4 years later
    15. 15. • DEVELOPPED AF
    16. 16. 50 years old syrian with mild CAD
    17. 17. • VT,THIS PT HAD SEVERE DCM,waiting for AICD
    18. 18. • Paced Rhythm
    19. 19. Waveforms and Intervals
    20. 20. Aims • • • • • 10 ECG rules Heart Rate ECG signs of M.I. Evolution of changes in M.I. Classical Appearences
    21. 21. QRS waveform nomenclature R r qR qRs Qrs QS Qr Rs rS qs rSr’ rSR’
    22. 22. The 10 rules for a normal ECG I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 .2
    23. 23. Rule 1 1.0 Millivolts 0.5 R PR interval PR interval should be 120 to 200 milliseconds or 3 to 5 little squares T P Q 0 S -0.5 0 200 400 Milliseconds 600
    24. 24. Rule 2 1.0 R The width of the QRS complex should not exceed 110 ms, less than 3 little squares Millivolts 0.5 T P Q 0 S -0.5 QRS 0 200 400 Milliseconds 600
    25. 25. Rule 3 I II III aVR aVL aVF The QRS complex should be dominantly upright in leads I and II
    26. 26. Rule 4 I II III aVR aVL aVF QRS and T waves tend to have the same general direction in the limb leads
    27. 27. Rule 5 All waves are negative in lead aVR P T Q S
    28. 28. Rule 6 V1 V2 V3 V4 V5 V6 The R wave in the precordial leads must grow from V1 to at least V4
    29. 29. Rule 7 I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 The ST segment should start isoelectric except in V1 and V2 where it may be elevated
    30. 30. Rule 8 I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 The P waves should be upright in I, II, and V2 to V6
    31. 31. Rule 9 I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 There should be no Q wave or only a small q less than 0.04 seconds in width in I, II, V2 to V6
    32. 32. Rule 10 I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 The T wave must be upright in I, II, V2 to V6
    33. 33. What is the heart rate? •www.uptodate.com •(300 / 6) = 50 bpm
    34. 34. What is the heart rate? •www.uptodate.com •(300 / ~ 4) = ~ 75 bpm
    35. 35. What is the heart rate? •(300 / 1.5) = 200 bpm
    36. 36. 10 Second Rule As most EKGs record 10 seconds of rhythm per page, one can simply count the number of beats present on the EKG and multiply by 6 to get the number of beats per 60 seconds. This method works well for irregular rhythms.
    37. 37. What is the heart rate? •The Alan E. Lindsay ECG Learning Center ; http://medstat.med.utah.edu/kw/ecg/ •33 x 6 = 198 bpm
    38. 38. Characteristic changes in AMI • • • • • ST segment elevation over area of damage ST depression in leads opposite infarction Pathological Q waves Reduced R waves Inverted T waves
    39. 39. ST elevation • Occurs in the early stages R ST P Q • Occurs in the leads facing the infarction • Slight ST elevation may be normal in V1 or V2
    40. 40. Deep Q wave • Only diagnostic change of myocardial infarction R ST • At least 0.04 seconds in duration P T Q • Depth of more than 25% of ensuing R wave
    41. 41. T wave changes • Late change R • Occurs as ST elevation is returning to normal ST P • Apparent in many leads T Q
    42. 42. Bundle branch block Anterior wall MI I II III aVR aVL aVF Left bundle branch block V1 V2 V3 V4 V5 V6 I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
    43. 43. Sequence of changes in evolving AMI R R T R ST ST P P Q S P T Q 1 minute after onset Q 1 hour or so after onset A few hours after onset R ST P ST P T Q A day or so after onset T P T Q Later changes Q A few months after AMI
    44. 44. Anterior infarction Anterior infarction I II III Left anterior descending artery (LAD) aVR aVL aVF V1 V2 V3 V4 V5 V6
    45. 45. Inferior infarction Inferior infarction I II III Right coronary Artery( RCA) OR Circumflex (LCX) aVR aVL aVF V1 V2 V3 V4 V5 V6
    46. 46. Lateral infarction Lateral infarction I II III Left circumflex coronary Artery OR DAIAGONAL branch of LAD aVR aVL aVF V1 V2 V3 V4 V5 V6
    47. 47. Location of infarct combinations I aVR LATERAL OR HIGH II aVL LATERAL V1 V4 SEPTAL ANT V2 V5 ANT V3 III INFERIOR aVF V6 LAT
    48. 48. Diagnostic criteria for AMI • • • • • Q wave duration of more than 0.04 seconds Q wave depth of more than 25% of ensuing r wave ST elevation in leads facing infarct (or depression in opposite leads) Deep T wave inversion overlying and adjacent to infarct Cardiac arrhythmias
    49. 49. Quick & Easy AXIS DETERMINATION  Left axis deviation - negative QRS in lead AVF I I AVF AVF  Right axis deviation - negative QRS in lead I I I AVF AVF  Severe Right axis deviation negative QRS in BOTH lead I and AVF I I AVF AVF
    50. 50. The QRS Axis By near-consensus, the normal QRS axis is defined as ranging from -30° to +90°. -30° to -90° is referred to as a left axis deviation (LAD) +90° to +180° is referred to as a right axis deviation (RAD)
    51. 51. Determining the Axis Predominantly Positive Predominantly Negative Equiphasic
    52. 52. The Quadrant Approach 1. Examine the QRS complex in leads I and aVF to determine if they are predominantly positive or predominantly negative. The combination should place the axis into one of the 4 quadrants below.
    53. 53. Quadrant Approach: Example 1 The Alan E. Lindsay ECG Learning Center http://medstat.med.utah.ed u/kw/ecg/ Negative in I, positive in aVF  RAD
    54. 54. Quadrant Approach: Example 2 The Alan E. Lindsay ECG Learning Center http://medstat.med.utah.ed u/kw/ecg/ Positive in I, negative in aVF  Predominantly positive in II Normal Axis (non-pathologic LAD) 
    55. 55. Thank U Very Much

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