Inferior leads

Press-bemstein, m. amberoid, ambroid, -beu-tel, m. pressing bag, press bag, filter bag (for presses), -blei, n. (Mstal.) inferior lead obtained in the Carinthian process after the addition of charcoal, -druck, m. pressing pressure, press power. 

An ECG taken immediately on arrival reveals ST elevation of 3 mm in the inferior leads. 

Figures 3.18 and 3.19 show the evolution of two Mis from the acute phase with a huge ST-segment elevation until the appearance of Q wave of necrosis and negative T wave of subepicardial ischaemia. In Figure 3.20, a patient with chronic MI of inferior wall presents in the same ECG a different grade of ECG pattern of subepicardial ischaemia (negative and deep T wave in inferior leads, tall and positive T wave in right precordial leads as a mirror pattern and flat T wave in V6).

When the subepicardial injury occurs in the inferior and lateral wall (LCX or RCA occlusion), the direct pattern of the ST-segment elevation is seen in inferior leads and in the leads recorded in the back (posterior thoracic leads). In these cases, often an ST-segment depression is recorded in V1-V3 leads, as a mirror pattern of ST-segment elevation recorded in the back (Figure 4.15). 

In this case, the injury vector is directed anteriorly, upwards and somewhat to the left (Figure 4.20D). The projection of the injury vector in different positive and negative hemifields of different leads of FP and HP explains the ST-segment elevation from V2-V3 to V5-V6. However it does not usually explain the ST-segment elevation in V1 because the projection of this vector in the HP falls often a little to the left in the limit of negative hemifield of VI or close to it. Also, these correlations explain the ST-segment elevation in lead I, especially in VL, and the ST-segment depression in the inferior leads (III + VF > 2.5 mm)... 

Also, the ST-segment elevation is seen in the precordial and inferior leads in the presence of an STE-ACS due to the very proximal occlusion of the RCA before the RV marginal branches. In this case usually the ST-segment elevation in VI > V3-V4, while in an STE-ACS due to the distal occlusion of the LAD, the contrary occurs (i.e. the ST-segment elevation is VI < V3). Table 4.2 shows the ECG criteria that allow differentiating the culprit artery (proximal RCA or distal LAD) in the case of ST-segment elevation in precordial leads and inferior leads. 

Figure 4.24 (A) STE-ACS in subacute phase with evident ST-segment elevation in V2-V4 with isoelectric ST segment in inferior leads and ST-segment depression in VR with ST...

Table 4.2 The ST segment elevation in precordial leads (especially V1- V3-V4) and inferior leads (II, III and VF).

Inferior leads Usually ST t greater than in precordial leads, if not (Figure 10.4) there is ST fin V1 that is not seen in LAD distal occlusion ST t usually smaller than in precordial leads... 

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. 

Figure 4.36 (A) Typical ECG in case of STE-ACS due to occlusion of very dominant RCA distal to RV branches. Observe the ST-segment elevation in inferior leads (III > II) and ST-segment depression the ST-segment depression in V1-V3 (occlusion distal to the take-off of RV branches). Furthermore, the ST-segment elevation in V6 is greater than 2 mm (occlusion of very dominant RCA). In extreme right precordial leads the ST is isoelectric in V3R and...

Figure 4.39 Above STE-ACS due to occlusion of the obtuse marginal branch (OM). (A) Site of the occlusion. (B) Myocardial area at risk. (C) Polar map of the involved area. (D) Injury vector that is directed to the left (approximately 0° to +20° in the frontal plane) and somewhat backwards. Occasionally, if small, it hardly produces any ST-segment deviations. If they occur, the ST-segment elevation is observed in some lateral and inferior leads especially in I, II, VF and V6, with a usually...

In some cases of occlusion of dominant LCX, the ST-segment depression in V1-V3 is much evident than ST-segment elevation in inferior leads. In these cases usually the ST-segment depression in V3 is greater than that in VI. One... 

In the subacute or chronic phase due to involvement of the inferior and lateral walls, a Q wave in inferior leads sometimes with QII > QIII and lateral leads (V5-V6,1 and VL) and RS morphology in VI (even Rs) may be recorded (see Figure 5.34). 

From a clinical point of view, in the majority of cases, usually the most striking ECG abnormality found by the physician is ST-segment elevation located in the precordial leads (V1-V6) (anteroseptal zone) (Figure4.43) or in inferior leads (inferolateral zone) (Figure 4.45). We will see how we can identify not only the culprit artery, but also the occlusion site. 

It has been shown that in an STE-ACS due to distal to D1 and SI, occlusion of long LAD generates the ST-segment elevation in precordial leads and in II, III and VF. However, this morphology may also be explained by an occlusion in LAD in presence of a total RCA occlusion with collateral vessels from the LAD to the RCA, even in the absence of a considerably long LAD. There is not any ECG criterion that may help us to differentiate these two cases, because in both situations the ST-segment elevation in precordial leads is more important than in inferior leads. 

T wave and in the absence of abnormal Q wave in I and V6. Regarding Q wave in III, its significance depends on whether Q waves are also present in VF and II. Also is suggestive of MI the presence of R > I mm in VR in the presence of Q in inferior leads. The only presence of Q in lead III especially if is not wide (>40ms) is usually normal and frequently disappears with deep inspiration (Figure 5.42). These criteria present a high specificity (>90%) but low sensitivity (=50-60%). 

Proximal occlusion of a very long LAD whole anterior wall and a part of inferior and lateral wall are involved. In this situation, in some cases the ECG pattern may do not reflect the infarcted area due to the cancellation (more gray areas) of the vector of the middle segment of anterior wall (which explains the Q wave in VL) and the vector of inferior necrosis (which explains the Q wave in inferior leads). In this case only Q waves in some precordial leads may be recorded. The more basal part of anterior wall that is also usually infarcted does not generate Q wave of necrosis due to late depolarisation. 

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