A. Belhadj-Mostefa Médecine Interne

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1 A. Belhadj-Mostefa Médecine Interne
ECG A. Belhadj-Mostefa Médecine Interne

2 ECG normal : l’activation cardiaque normale
Cœur=organe automatique Automatisme lié à des cellules spécialisées Propagation d’une activité électrique  activité contractile L’ensemble de ces cellules = tissu nodal Tissu nodal composé de ≠ structures anatomiques permettant la propagation de l’activité électrique des oreillettes vers les ventricules

3 Activité électrique du coeur
BRANCHE DROITE BRANCHE GAUCHE NŒUD AURICULO VENTRICULAIRE FAISCEAU DE HIS NŒUD SINUSAL Deux types de tissus Le tissu nodal : naissance et conduction de l’influx Le tissu myocardique : contraction 27/01/04 Activité électrique du coeur 3

4 Activité électrique du coeur
6 dérivations précordiales dans un plan  horizontal V1 : 4e espace intercostal droit au bord du sternum V2 : 4e espace intercostal gauche au bord du sternum V3 : à mi-distance de V2 et V4 V4 : 5e espace intercostal gauche sur la verticale médio-claviculaire V5 : 5e espace intercostal gauche sur la ligne axillaire antérieure V6 : 5e espace intercostal gauche sur la ligne axillaire moyenne 27/01/04 Activité électrique du coeur 4

5 ECG normal : Technique d’enregistrement 4
Conditions d’enregistrement: Électrodes placées en contact avec la peau avec un gel conducteur ou de l’eau Patient couché sur le dos Détendu  éviter les contractions musculaires (parasites)

6 ECG normal : Lecture l’enregistrement de l’activité électrique du cœur à partir des différentes dérivations (enregistre chacune une « partie » du cœur). Enregistre successivement : dépolarisation auriculaire (L’onde P) La repolarisation auriculaire (non vue) Le ralentissement du NAV (l’espace PR) La dépolarisation ventriculaire (Polyphasique = Complexe QRS) La repolarisation ventriculaire (Le segment ST et l’onde T) Le tout est suivi par un « repos » électrique = La ligne de base isoélectrique.

7 Activité électrique du coeur
P T P Ligne isoélectrique q s Repolarisation ventriculaire Dépolarisation auriculaire Dépolarisation ventriculaire + repolarisation auriculaire 7

8 L’ECG NORMAL

9 Calcul de la fréquence La fréquence cardiaque est déterminée par la fréquence des complexes QRS, qu’ils soient ou non précédés d’une onde P. Elle se calcule grossièrement selon le nombre de carreaux qui séparent deux complexes QRS successifs, selon la règle 300/150/100/75/60/50. 5 carreaux = 1 seconde = fréquence à 60 cycles/min

10 Nomenclature du complexe QRS
QS Qr Rs rS qs rSr’ rSR’ 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.

11 AXE ELECTRIQUE DU COEUR

12 AXE ELECTRIQUE DU COEUR

13 AXE ELECTRIQUE DU COEUR

14 ECG normal : Technique d’enregistrement 4
Conditions d’enregistrement: Électrodes placées en contact avec la peau avec un gel conducteur ou de l’eau Patient couché sur le dos Détendu  éviter les contractions musculaires (parasites)

15 Enregistre successivement :
ECG normal : Lecture l’enregistrement de l’activité électrique du cœur à partir des différentes dérivations (enregistre chacune une « partie » du cœur). Enregistre successivement : dépolarisation auriculaire (L’onde P) La repolarisation auriculaire (non vue) Le ralentissement du NAV (l’espace PR) La dépolarisation ventriculaire (Polyphasique = Complexe QRS) La repolarisation ventriculaire (Le segment ST et l’onde T) Le tout est suivi par un « repos » électrique = La ligne de base isoélectrique.

16 Hypertrophie auriculaire

17 Hypertrophie ventriculaire

18 Evolution et progression normale de l’onde R de V1 à V6, en fonction de l’épaisseur du muscle traversé En situation normale, l’augmentation progressive de l’épaisseur du myocarde sous-jacent provoque une augmentation progressive de la déflexion positive : R augmente, S diminue parallèlement, et V6 est grossièrement le miroir de V1

19 Infarctus non transmural en regard de V3 à V5
Le muscle cicatriciel est électriquement inerte, il n’y a pas de progression harmonieuse de l’onde R, une onde Q de petite taille peut apparaître. Le tracé enregistre : - en V3, un aspect rS suite au rabotage de R ; - en V4, un aspect qr ou qR ; - en V5, un aspect qR ; - en V6, un aspect normal du complexe.

20 Les 10 commandements d’un ECG normal
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 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. .2 Chamberlain DAC. Personal communications.

21 1er commandements 1.0 R PR interval L’intervalle PR doit être compris entre 120 et 200 millisecondes ou 3 to 5 petits carreaux 0.5 T P Millivolts Q 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. S -0.5 200 400 600 Millisecondes

22 2ème commandement 1.0 P R T Q S La largeur du complexe QRS ne doit pas excéder 110 ms, soit moins de 3 petits carreaux 0.5 Millivolts 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. -0.5 QRS 200 400 600 Milliseconds

23 3ème commandement I II III aVR aVL aVF Le complexe QRS doit être dominant dans les dérivations D I et II Rule 3 The QRS complex should be dominantly upright in leads I and II. Slight disparities are likely to be acceptable.

24 4ème commandement I II III aVR aVL aVF Les ondes QRS et T tendent à avoir la même direction dans les dérivations standards Rule 4 The QRS and T waves tend to have the same direction in the standard leads.

25 Toutes les ondes sont négatives
5ème commandement Toutes les ondes sont négatives en avR P Q T S 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.

26 6ème commandement V6 V5 V4 V3 V2 V1 Rule 6 The normality of QRS complexes recorded from the precordial leads is dependent on both morphological and dimensional criteria. Les ondes R dans les dérivations précordiales doivent croître de V1 jusqu’à au moins V4

27 7ème commandement I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 Rule 7 The ST segment should start isoelectric except in V1 and V2 where it may be elevated. Le segment ST doit débuter de manière isoélectrique excepter en V1 et V2 où il peut être surélever

28 Les ondes P doivent être positive en DI, DII, et V2 à V6
8ème commandement I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 Rule 8 In leads I, II, and V2 to V6 the P waves should be upright. Les ondes P doivent être positive en DI, DII, et V2 à V6

29 9ème commandement I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 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. Il ne doit pas y avoir d’onde Q ou alors une petite onde q inférieure à 0.04 seconds en DI, DII, V2 à V6

30 Les ondes T doivent être positive en DI, DII, V2 à V6
10ème commandement I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 Rule 10 In leads I, II, and V2 to V6 the T wave must be upright. Les ondes T doivent être positive en DI, DII, V2 à V6

31 Changements caractéristiques d’un IDM
Élévation du segment ST Sous élévation du segment ST dans les dérivations opposées à l’IDM Ondes Q pathologiques Ondes R diminuées d’amplitude Ondes T inversées 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.

32 Élévation du segment ST
Survient précocemment Survient dans les dérivations en face de l’infarctus Une surélévation discrète de ST peut être normal en V1 ou V2 R P Q ST 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.

33 Ondes Q pathologiques De durée minimale de 0.04 secondes
La profondeur doit excéder de 25% de l’onde R correspondante R P Q T ST 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.

34 Modifications de l’onde T
R P Q T ST Survient après le retour à la normale de ST 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.

35 BLOC DE BRANCHE IDM antérieur BBG belmosah@live.fr I II III
aVR aVL aVF V1 V2 V3 V4 V5 V6 I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 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.

36 Sequence des modifications dans l’IDM
R R R ST T ST P P P T Q S Q Q 1 minute 1 heure Qq heures R ST P P ST T P 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. T T Q Q Q J1 Qq semaines 1 mois

37 IDM antérieur I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
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. Artère coronaire gauche

38 IDM inférieur I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
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. Artère coronaire droite

39 IDM latéral I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
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. artère circonflexe gauche

40 I aVR V1 V4 ANT POST LATERAL ANT SEPTAL II aVL V2 V5 ANT LAT V3 V6 III
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. ANT LAT V3 V6 III aVF INFERIEUR

41 Critères dg d’un IDM Durée Q > 0.04 seconds
Profondeur Q > 25% de l’onde R Sus décalage ST dans les dérivations faisant face à l’IDM Sous décalage ST dans les dérivations opposées à l’IDM) T inversées et profondes dérivations adjacentes à l’IDM Arythmies cardiaques 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.