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Vector of infarction

Figure 1.11 Magnetic resonance imaging. (A) Thoracic horizontal axial plane at the level of the xy line of the drawing on the right side of the figure. The four walls can be adequately observed anterior (A), septal (S), lateral (L) and inferior (I), represented by the inferobasal portion of the wall (segment 4 of Cerqueira statement) that bends upwards in this case (B). The infarction vector generated principally in segments 4 and 10 in case of very lean individuals (Figure 1.13C) it faces lead V3 and not V1 (line CD). On the contrary, the vector of infarction that arises... Figure 1.11 Magnetic resonance imaging. (A) Thoracic horizontal axial plane at the level of the xy line of the drawing on the right side of the figure. The four walls can be adequately observed anterior (A), septal (S), lateral (L) and inferior (I), represented by the inferobasal portion of the wall (segment 4 of Cerqueira statement) that bends upwards in this case (B). The infarction vector generated principally in segments 4 and 10 in case of very lean individuals (Figure 1.13C) it faces lead V3 and not V1 (line CD). On the contrary, the vector of infarction that arises...
Since mid-1960s it was defended that infarction of the posterior wall presents a vector of infarction that faces V1-V2 and therefore explains RS (R) morphology in these leads (Perloff, 1964). [Pg.16]

In theory the presence of subendocardial or transmural injury in completely opposite areas of the heart may decrease or even conceal the two injury vectors (Madias, 2006). However, in practice, this does not occur usually, because the ischaemia is usually due to occlusion of only one vessel and this does not generate equal and opposed injured areas (Rautaharju, 2006). Furthermore, with the same amount of injury in two opposite areas, it is more visible in the surface ECG of the injury area that is more close to subepicardium. In the chronic phase it is more often seen that a new vector of infarction in opposed area may cancel the Q-wave pattern of a previous infarction (see Figure 5.38). [Pg.62]

In the chronic phase in case of dominant RCA occlusion, there is involvement of inferior wall and some part of the lateral wall. This explains the Q wave in inferior leads and sometimes V5— V6 but not in lead I and aVL. Also, it explains the RS morphology in VI because the vector of infarction of lateral wall points to VI (see Figure 1.9). In case of occlusion of very dominant LCX, as all the lateral wall maybe infarcted, we may find in chronic phase QR morphology in lead I and aVL, but usually not QS (see Figure 5.34), which is seen much more often in cases of occlusion of D1. [Pg.90]

Figure 5.3 (A) Under normal conditions, the overall QRS vector (R) is made up of the sum of the different ventricular vectors (1 + 2 + 3 + 4). (B) When a necrotic (infarcted) area exists, the vector of infarction has the same magnitude as the previous vector, but has an opposite direction (3 ). This change of direction of the initial depolarisation electrical forces of a portion of the heart, the necrotic (infarcted) area, also implies the change of the overall vector direction (R ). (C) The development of... Figure 5.3 (A) Under normal conditions, the overall QRS vector (R) is made up of the sum of the different ventricular vectors (1 + 2 + 3 + 4). (B) When a necrotic (infarcted) area exists, the vector of infarction has the same magnitude as the previous vector, but has an opposite direction (3 ). This change of direction of the initial depolarisation electrical forces of a portion of the heart, the necrotic (infarcted) area, also implies the change of the overall vector direction (R ). (C) The development of...
As we have previously affirmed, predominantly subendocardium infarctions can generate an infarction Q wave if they affect subepicardium areas of the ventricular wall that are in contact with the subendocardium, even though the wall is not homogeneously or necessarily transmurally affected. This occurs because in these situations a vector of infarction can arise (Q wave) (Figure 5.2C). Only when the stimulus reaches normal areas will an R wave be generated (QR complex). [Pg.131]

The explanation of the Q wave of necrosis can be made on the basis of the theory of the electrical window of Wilson or on the formation of a vector of infarction. According to the first theory, the... [Pg.131]

According to the vector of infarction theory, the infarction Q wave is of the same magnitude but in opposite direction to the one normally generated by the infarcted area (Figure 5.3B, C). The vector of infarction, thus, moves away from the infarcted area (see Figs. 5.3-5.5). For this reason, the beginning of ventricular depolarisation changes its... [Pg.131]

Figure 5.4 (A) Observe the comparison between the normal activation and the activation in case of an extensive anterior infarction. The vector of infarction is... Figure 5.4 (A) Observe the comparison between the normal activation and the activation in case of an extensive anterior infarction. The vector of infarction is...
In Figures 5.4 and 5.5 the changes that, as a consequence of the presence of the vector of infarction, are generated in the ventricular depolarisation loops in the presence of two prototype infarctions (anteroseptal and inferolateral areas, respectively) are represented. Said changes explain the presence of Q waves in the different leads by means of the loop-hemifield correlation. Some of the ECG morphologies and the QRS loops correlations in the seven types of infarctions, according to the classification... [Pg.132]

Figure 5.5 (A) See the comparison between normal activation and activation in case of inferolateral infarction. The vector of infarction is directed upwards and a... Figure 5.5 (A) See the comparison between normal activation and activation in case of inferolateral infarction. The vector of infarction is directed upwards and a...
The leads that face the vector of infarction tail record morphologies with the Q wave of necrosis (QS or QR complexes). Throughout this book we will use this concept - vector of infarction and changes that it generates in the morphology of the QRS loop and its projection in its respective... [Pg.133]

Since the high-septal area is depolarised after the first 40 milliseconds, the infarction of this area does not generate vector of infarction that can originate Q waves. In these cases, changes the final portions of the QRS complex may be present. For the typical pattern of this type of infarction to appear, it is required, then, that the infarction involves the middle-low portion of the septum. The other parts may or may not be involved. [Pg.142]

A QS pattern from V1-V2 to V3-V6 may be due in some rare cases to theproximal occlusion of a very long LAD and, as a result, the infarction is larger. It is explained by the cancelling out of the inferior and mid-anterior vector of infarctions, which precludes the recording of a Q wave in the inferior and VL leads (Figure 5.7B). [Pg.148]

The presence of two or more true Q-wave MI may be suggested by the criteria mentioned above. However, in clinical practice nowadays, after the consensus of ESC/ACC (Alpert et al., 2000), there are more patients that present two or more infarctions. Very often some of them are small non-Q-wave MI infarctions that correspond frequently to necrossete type . The CE-CMR can allow us to detect with great accuracy the presence of two or more infarctions (Figure 5.40), although, as we have already pointed, sometimes the vector of infarction oftwo Mis may cancel each other (Figure 5.38). Itis... [Pg.167]

In case of IPH associated with an extensive anterior infarction including mid-anterior wall, the vector of infarction (B) counteracts the initial depolarisation vector (1) (Figure 5.57) and generates a change in the QRS loop that is directed rightwards and downwards. Thus, it explains the QS morphology in I and VL (Figure 5.57). [Pg.177]


See other pages where Vector of infarction is mentioned: [Pg.11]    [Pg.14]    [Pg.16]    [Pg.26]    [Pg.130]    [Pg.133]    [Pg.137]    [Pg.140]    [Pg.148]    [Pg.177]    [Pg.177]    [Pg.177]    [Pg.177]    [Pg.178]    [Pg.283]    [Pg.305]   
See also in sourсe #XX -- [ Pg.145 , Pg.152 ]




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