The term atrial abnormalities encompasses atrial enlargement, atrial blocks, and abnormalities of atrial repolarization. The following general principles should be emphasized 2:
Atria become dilated rather than hypertrophied.
P-wave voltage is influenced by extracardiac factors that increase it (eg, hypoxia, increased sympathetic tone) or decrease it (eg, emphysema, atrial fibrosis).
The atrial repolarization wave is usually hidden within the QRS complex (see Fig. 12–1).
Right atrial enlargement (RAE) is mainly present in patients with congenital and valvular heart diseases affecting the right side of the heart and in patients with cor pulmonale (see Fig. 12–23B and C) (Figs. 12–22 and 12–23). Typically, the P wave is increased in voltage but not in length.
Top: Scheme of atrial depolarization in (A) normal P wave, (B) right atrial enlargement (RAE), and (C) left atrial enlargement (LAE). Bottom: three examples of these P waves.
Morphology of P wave: (A) normal (NL); (B) right atrial enlargement—P pulmonale (Pulm.): P axis [ÂP] to the right; (C) right atrial enlargement—P congenitale (Cong.): ÂP slightly to the left); (D) left atrial enlargement (LAE; P mitrale); and (E) biatrial enlargement (BAE). FP, frontal plane; HP, horizontal plane.
The diagnostic criteria of RAE are based on P-wave abnormalities (positive voltage of P ≥ 2.5 mm in II and/or positive voltage > 1.5 mm in V1). These criteria have low sensitivity and somewhat higher specificity.2
Left atrial enlargement (LAE) is seen in patients with mitral and aortic valvular disease, IHD, hypertension and some cardiomyopathies (see Figs. 12–22C and 12–23D). Typically, the P wave is bimodal in some leads and +/– in V1 with evident final negative deflection.
The diagnostic criteria of LAE are as follows2: (1) P wave with a duration 0.12 second or longer, especially seen in leads I or II, generally bimodal, but with normal height, and (2) diphasic P wave in V1 with evident final negative deflection of at least 0.04 second of duration because the second part of the loop is directed backward due to LAE (see Fig. 12–23D, horizontal plane). These two criteria have good specificity (close to 90%; few false-positive cases) but discrete sensitivity (< 60%; more false-negative cases). The +/– P-wave morphology in II, III, and VF with a P of at least 0.12 second is a very specific criterion and has a high positive predictive value (100% in valvular heart disease and cardiomyopathies). However, it has a low sensitivity and low negative predictive value for LAE.
The most important diagnostic criteria of biatrial enlargement are the following (see Fig. 12–23E)2: (1) P wave in lead II that is taller (≥ 2.5 mm) and wider (≥ 0.12 s) than normal, (2) first part of P wave that is positive and peaked in V1-V2 (positive mode > 1.5 mm) with a slow negative deflection (width ≥ 4 mm), (3) signs of LAE with right ÂP; the opposite case is not valid because the ÂP can be on the left side in isolated RAE of patients with congenital heart diseases, and (4) presence of atrial fibrillation (AF) along with QRS changes suggestive of RAE. Frequently, more than one criterion is found (P ≥ 120 ms in FP + P± in V1 with first part peaked and a slow negative mode).
The concept of a block means that in a certain part of the heart (sinoatrial junction, atria, AV junction, or ventricles), the electrical stimulus encounters overall significant difficulties for its conduction. A first-degree or partial block (P-IAB) occurs when conduction is slow but the stimulus passes through the area but with slow conduction. A third-degree or advanced block (A-IAB) is when the stimulus does not pass completely through the zone but perhaps could pass at a very slower heart rate; therefore, we call it advanced, not complete. A second-degree block is when the stimulus sometimes passes and sometimes does not2.
The conduction delay in interatrial block occurs between the right and left atria (Fig. 12–24). Although usually associated with LAE, it may also exist as an isolated finding in cases of pericarditis, IHD, old age, and other conditions.22
Top: Example of atrial activation and characteristics of the P loop in the frontal plane (FP) and the morphology of P wave in VF in normal conditions (A) and in a case of partial (B) and advanced (C) interatrial block with left atrial retrograde activation. Bottom left: Leads I, II, and III in advanced interatrial block with left atrial retrograde activation, with direction of the activation vectors of the first and second part of the P wave and three consecutive P waves with +/ morphology in VF. Bottom right: Esophageal and intracavitary recordings demonstrating the sequence of activation in this type of interatrial block (high right atrium [HRA], low right atrium [LRA], and high esophageal [HE] lead with –/+ morphology).
In P-IAB, the stimulus reaches the left atrium via the normal pathway, but with certain delay. The diagnostic criterion of P-IAB is a P wave with a duration at least 0.12 second in the frontal plane.26,27,28 The P-wave length and, consequently, the bimodal morphology of the P wave seen in lead II (which is the most typical lead to detect an isolated P-IAB) are similar to the P wave occurring in LAE. In fact, the delay in interatrial conduction, rather than the left atrium dilation, generally explains the morphology observed with an LAE. However, the morphology of the P wave in the horizontal plane, especially in V1, is usually different. In case of isolated interatrial block (eg, pericarditis), the second part of the loop is not directed so much backward because there is no LAE, and consequently, the P-wave morphology in V1 is positive or only presents a small negative part.
In A-IAB (see Fig. 12–24),27,28 the stimulus does not reach the left atrium via the normal path but by retrograde left atrial activation.28 The diagnostic criteria of A-IAB are as follows27: (1) P wave with a duration of at least 0.12 second and +/– in II, III, and VF, and (2) often, P wave +/– in V1 to V3 or V4. The prevalence of A-IAB increases with age, being very low before 50 years of age and approaching 25% in centenarians in whom an increase of dementia and stroke associated with A-IAB has been detected.22 This type of block is frequently accompanied, especially when it is present in patients with advanced heart disease, by supraventricular arrhythmias, particularly AF and/or atrial flutter (Bayes syndrome).29,30,31
Abnormalities of Atrial Repolarization
The atrial repolarization wave (ST-Ta) usually has a polarity opposed to the P wave and is not visible because it is hidden within the QRS complex. In cases of great sympathetic overdrive in normal individuals, an ST-Ta depression may be seen (see Fig. 12–17C). Moreover, in some cases of remarkable atrial enlargement, pericarditis, or atrial infarction, especially in the presence of a long PR interval, shifts of ST-Ta may be observed (Fig. 12–25).
A. PR-segment elevation morphology in a case of pericarditis. B. PR depression in atrial extension of anterior myocardial infarction.
Morphologies of ventricular enlargement are secondary to a hypertrophy rather than to dilatation, unlike what occurs in the atria. Slight or even moderate degrees of enlargement of either of the ventricles, mainly the right, or of both at the same time, may not produce abnormalities in the ECG.
The superiority of echocardiography over the ECG for the diagnosis of ventricular enlargement, mainly of the left ventricle, is evident (the sensitivity is much higher, and the specificity is similar). However, when a ventricular enlargement is diagnosed with an ECG, the accuracy of the ECG is greater than that of the echocardiogram in predicting heart disease evolution and prognosis.
For details on the diagnosis of RVE and/or left ventricular enlargement (LVE) combined with ventricular block (QRS complex duration > 120 milliseconds), the reader is referred to Bayés de Luna2 and McFarlane and Lawrie.14
Right Ventricular Enlargement
RVE is found especially in congenital heart diseases, valvular heart diseases, and cor pulmonale. The changes produced by RVE move the loop rightward and either frontward or backward. This is more a result of a delay of activation of the right ventricle, rather than an increase of the right ventricle mass (which generally never overcomes the mass of the left ventricle). Figure 12–26 shows the changes that RVE may produce in ventricular activation expressed as ventricular loops and how these changes may explain the different ECG patterns. Basically, a large part of the QRS loop is going to the right (presence of S in V6) but sometimes with an anterior loop (R or RS in V1) and occasionally with a posterior loop (rS or QS in V1).
In right ventricular enlargement (RVE) with electrocardiographic repercussion, the horizontal loop of the QRS is always directed to the right, either forward or backward. When it is directed forward, different morphologies may be recorded (from A to D cases with more advanced degree of RVE). A patient may have a morphology changing from one to another during the course of the disease. However, in general, heart diseases with mild to moderate RVE present with type A or type B morphologies, and those with severe RVE present with type D. If the loop is directed posteriorly, then the morphologies are of types E or F. The QS morphology is seen in the V1 lead in type E, whereas rS or rSr′ is seen in type F; both cases are accompanied by a significant S in V6. The lower part of the figure shows that the morphology of QRS in V1 depends more on the severity and grade of RVE than on the etiology of the disease. Left: Mild mitral stenosis (1) and advanced mitral stenosis with severe pulmonary hypertension (2). Middle: Long-standing chronic cor pulmonale without severe pulmonary hypertension (3) and subacute cor pulmonale with severe pulmonary hypertension (4). Right: Congenital moderate pulmonary stenosis (5) and severe valvular pulmonary stenosis (6). Cong. H.D, congenital heart disease; COPD, chronic obstructive pulmonary disease; Mitral V.D., mitral valve disease.
The lower part of Fig. 12–26 shows three cases of RVE of different etiologies (see legend) in which the ECG pattern in V1 (with more or less R wave) is related more to RVE degree than to RVE etiology.
The ECG criteria (low sensitivity, high specificity) most frequently used for the diagnosis of RVE are shown in Table 12–1.
Morphology of V1: (1) Morphologies with dominant or exclusive R wave in V1 are very specific but not very sensitive (< 10%) for the diagnosis of RVE because the loop that gives rise to them (anterior and to the right; see Fig. 12–26B–D) is observed in a small number of cases with RVE (especially in some congenital heart diseases such as pulmonary stenosis). In these cases, the prominent R in V1 is also seen in V2 and V3. Moreover, the repolarization presents an ST-segment depression and a negative and asymmetric T wave (strain pattern; Fig. 12–26, Fig. 12–27A), except in newborns because they may present with an exclusive R wave with a positive T wave. On the contrary, in cases of pulmonary stenosis from tetralogy of Fallot, the morphology in V1 is similar to that in isolated pulmonary stenosis, but in V2, there is an rS morphology. Other causes that may present a dominant R pattern in V1 must be ruled out (Table 12–2). (2) The presence of rsR′ is especially typical of atrial septal defect and sometimes may also be seen in moderate pulmonary stenosis. (3) The rS or even the QS morphology in V1, with RS in V6, may often be observed in the early phases of RVE, or with rS in V6 in advanced cases of chronic cor pulmonale (see Fig. 12–26B).
Morphology of V6. The presence of evident forces directed to the right, which are expressed as an evident S wave in V5 to V6, is one of the most important ECG diagnostic criteria (see Figs. 12–26 and 12–27; see Table 12–1).
SI, SII, SIII. This morphology is frequently seen in chronic cor pulmonale with QS pattern in V1 and RS pattern in V6. Note that this pattern may be secondary to positional changes or it may simply be a normal variant.2 Nonetheless, an abnormal P wave favors the diagnosis of RVE (see Fig. 12–27B).
Electrical axis: ÂQRS of at least +110°. Inferoposterior hemiblock, vertical heart, and lateral infarction must be ruled out. This criterion is quite specific (> 95%) but relays low sensitivity.
A. An 8-year-old patient with important pulmonary valve stenosis, with a gradient of more than 100 mm Hg. The patient presents a typical morphology of right ventricular enlargement (RVE) with R wave–type systolic overload (strain) from V1 to V3. B. Patient with RVE caused by advanced chronic obstructive pulmonary disease with posterior and right QRS loop types SI, SII, SIII.
TABLE 12–1.Electrocardiographic Criteria of Right Ventricular Enlargement ||Download (.pdf) TABLE 12–1. Electrocardiographic Criteria of Right Ventricular Enlargement
| ||Criterion ||Sensitivity (%) ||Specificity (%) |
|V1 ||R/S V1 ≥ 1 || 6 ||98 |
| ||R V1 ≥ 7 mm || 2 ||99 |
| ||qR in V1 || 5 ||99 |
| ||S in V1 < 2 mm || 6 ||98 |
| ||IDT in V1 ≥ 0.35 s || 8 ||98 |
|V5–V6 ||R/S V5–V6 ≤ 1 ||16 ||93 |
| ||R V5–V6 < 5 mm ||13 ||87 |
| ||S V5-V6 ≥ 7 mm ||26 ||90 |
|V1 + V6 ||HV1+ SV5–V6 > 10.5 mm ||18 ||94 |
| ||ÂQRS ≥ 110° || || |
|ÂQRS ||SI, SII, SIII ||15 ||96 |
| || ||24 ||87 |
The combination of more than one of these criteria increases the diagnostic possibilities. The differential diagnosis of exclusive or predominant R wave in V1(R, Rs, or RSR′ pattern) is shown in Table 12–2.
TABLE 12–2.Morphologies with Dominant R or (r’) R’ in V1: Clinical Setting, Typical Morphologies in V1, QRS Width, and Morphology of P in V1 ||Download (.pdf) TABLE 12–2. Morphologies with Dominant R or (r’) R’ in V1: Clinical Setting, Typical Morphologies in V1, QRS Width, and Morphology of P in V1
The ECG signs indicative of right ventricle acute overload (decompensation of cor pulmonale or pulmonary embolism) are as follows32:
Change in the ÂQRS (> 30° to the right of its usual position)
Transient negative T waves, sometimes very evident in the right precordial leads
SI, QIII with negative TIII pattern (McGinn-White pattern) in the frontal plane and an RS or rS pattern in V6 (Fig. 12–28)
Appearance of a complete right bundle branch block morphology, often with ST-segment elevation
A. A 59-year-old patient presenting a typical McGinn-White pattern (SI, QIII with negative T wave in lead III and rSr′ in V1) in the course of pulmonary embolism. B. The electrocardiogram findings after the recovery of the patient still show negative T waves in the precordial leads, but the McGinn-White pattern and the r′ in V1 have disappeared.
The latter two criteria are highly specific but have low sensitivity for important pulmonary embolism (see Cor Pulmonale). Nevertheless, the clinical setting and comparison with previous ECGs are important to make a differential diagnosis of both processes.
Left Ventricular Enlargement
LVE is found in hypertension, IHD, valvular heart disease, cardiomyopathies, and some congenital heart diseases. In general, in patients with LVE, the maximum QRS vector of the loop increases its voltage and is directed more posteriorly than normal (Fig. 12–29). This explains why the QRS complex negativity predominates in the right precordial leads (see Fig. 12–29A–C). Occasionally, the maximum vector is not directed posteriorly (it is located close to 0°). This implies a tall R wave that is seen even in V2, especially in cases of apical hypertrophic cardiomyopathy (see Fig. 12–29E).
The most characteristic loops of left ventricular enlargement (LVE): (A) with the initial forces to the right and a positive T wave; (B) observed in cases of LVE that are not long-standing and with mild septal fibrosis; (C) QRS loops initially to the left and with counterclockwise rotation or figure-of-eight rotation on horizontal plane (HP); corresponds to significant LVE seen in advanced heart diseases with significant septal fibrosis; (D) QRS loop with q wave of pseudonecrosis that occurs in cases of hypertrophic cardiomyopathy due to the presence of important septal vector; (E) QRS loop pointed approximately 0° on the HP with a very peaked T loop pointed upward, backward, and rightward characteristic for the apical type of hypertrophic cardiomyopathy. Bottom: Two examples of aortic valve disease, one (left) with mild septal fibrosis and normal ECG and VCG (presence of q wave in V6 as expression of first vector) and the other (right) with important septal fibrosis and abnormal electrocardiography (ST-T with strain pattern) and VCG (absence of q wave in V6). See in the HP (H) with amplification of the loop (SE = 16) now in the left the qR in V6 coincides with initial vector forces of the loop in the negative hemifield of V6, and in the right with R in V6 the initial forces go directly to the left. FP, frontal plane.
The ECG pattern changes during disease evolution. The pattern of “strain” appears more in relation with the duration of the disease than with the presence of different types of hemodynamic overload. However, in aortic valve disease, a q wave in V5 to V6 is found more frequently in long-standing aortic regurgitation than in aortic stenosis (Fig. 12–30). The disappearance of the q wave in V6 is probably more related to interstitial septal fibrosis, a substrate of partial left bundle branch block, than to hemodynamic overload31 (see Figs. 12–29 and 12–30).
Examples of different electrocardiogram morphologies seen in the evolutionary course of aortic stenosis (note the appearance of strain pattern) (A) and aortic regurgitation (note the decrease of q wave and the appearance of strain pattern) (B).
The presence of noticeable signs that are suggestive of LVE (high voltage of the QRS together with inverted ST-T wave—strain pattern) in an asymptomatic patient without heart murmur or hypertension suggests hypertrophic cardiomyopathy. The ECG does not correlate with the gene mutation,33 but there are two at least ECG changes suggestive of hypertrophic cardiomyopathy: (1) the striking negative T waves (see Fig. 12–29E) and (2) the presence of a deep and narrow q waves (see Fig. 12–29D).
Sometimes the LVE pattern, at least partially, and especially the changes in ST-T may be resolved in a few months with pharmacologic treatment, as occurs in hypertension or after surgery (valvular heart disease).
Various diagnostic criteria exist for LVE,34,35,36,37 with varying sensitivity and specificity, as shown in Table 12–3. It is usually possible to diagnose an LVE through an ECG in patients with severe hypertension, whereas this diagnosis is difficult in asymptomatic normotensive adults. However, the value of the ECG diagnostic criteria shown in Table 12–3 is lower in hypertensive patients. For these patients, the following criterion is useful: sum of the QRS voltage of 12 ECG leads greater than 120 mm.37
TABLE 12–3.Electrocardiographic Criteria of Left Ventricular Enlargement ||Download (.pdf) TABLE 12–3. Electrocardiographic Criteria of Left Ventricular Enlargement
|Voltage Criteria ||Sensitivity (%) ||Specificity (%) |
| 1. RI + SII > 25 mm ||10.6 ||100 |
| 2. RVL > 11 mm ||11 ||100 |
| 3. RVL > 7.5 mm ||22 ||96 |
| 4. SV1 + RV5-V6 ≥ 35 mm (Sokolow-Lyon) ||22 ||100 |
| 5. RV6-V6> 26 mm ||25 ||98 |
| 6. RVL + SV3 > 28 mm (men) or > 20 mm (women) (Cornell voltage criterion) ||42 ||96 |
| 7. Cornell voltage duration measurement QRS duration × Cornell voltage > 2436 mm/seg ||51 ||95 |
| 8. In V1-V6, the deepest S + the tallest R > 45 mm ||45 ||93 |
| 9. Romhilt-Estes score > 4 points ||55 ||85 |
| 10. Romhilt-Estes score > 5 points ||35 ||95 |
The ECG diagnosis of biventricular enlargement is even more difficult than that of the enlargement of just one ventricle. This is true because the increased opposing forces of both ventricles often counterbalance each other or the notable predominance of the enlargement of one ventricle completely masks the enlargement of the other. Therefore, even those criteria that have fair specificity only have a moderate sensitivity.38
The following ECG patterns are used for the diagnosis of biventricular enlargement:
Tall R wave with s in V5 and V6, rSR′ pattern in V1, and P wave of biatrial enlargement
Tall R wave in V5 and V6, with an ÂQRS shifted to the right (≥ 90°). The presence of an inferoposterior hemiblock associated with LVE and an asthenic body build must be ruled out.
Small S wave in V1, deep S wave in V2, predominant R wave in V5 and V6, and an ÂQRS shifted to the right in the frontal plane or an SI–, SII–, SIII–type morphology
The presence, especially in the elderly, of QRS complexes within normal limits but with significant repolarization abnormalities (negative T wave and depression of the ST segment), mainly when the patient presents with AF. This type of ECG can be found in the elderly with advanced heart diseases and biventricular enlargement.
Blocks at the ventricular level can occur on the right side (Table 12–4) or on the left side (Table 12–5). They can affect the entire ventricle (global block) or only part of it (zonal or divisional block). The blockage of electrical impulses, in the ventricles or in the whole heart (see interatrial blocks) is called a first-degree (partial) block when the impulses pass through the area but with a delay; second-degree block when the stimulus sometimes passes and sometimes does not; and third-degree (advanced) block when the passage of stimulus is blocked.2 The term advanced is preferred over complete, because one can not know whether the stimulus would pass at a very lower heart rate. Second-degree block is known as aberrancy of conduction and is explained in Section 6).
TABLE 12–4.Right Ventricular Block ||Download (.pdf) TABLE 12–4. Right Ventricular Block
|Global (right bundle branch block) |
Third-degree (advanced): Morphologies corresponding to type III of the Mexican school13: slurred rSR′ in V1 and qRS with slurred S in V6 with QRS ≥ 0.12 s
First-degree (partial): Morphologies corresponding to type I: rSR′ in V1 of the Mexican school with QRS < 0.12 s13
Second-degree: Intermittent block morphology; corresponds to a special type of ventricular aberrancy
|Zonal or divisional |
|Experimentally, it originates electrocardiogram morphologies of the SI, SII, SIII or RI, SII, SIII type.23 In clinical practice, these morphologies are difficult to differentiate from normal variants or right ventricular enlargement (the changes in P and T waves may help). The SI, RII, RIII morphology must also be explained by inferoposterior hemiblock. |
TABLE 12–5.Left Ventricular Block ||Download (.pdf) TABLE 12–5. Left Ventricular Block
|Global (left bundle branch block) |
Third-degree (advanced): Corresponds to type III of the Mexican school13: slurred R in V6 and QS of rS in V1 with QRS ≥ 0.12 s
First-degree (partial): Corresponds to types I and II of the Mexican school13: isolated R in V6 with more or less slurring but QRS < 0.12 s
Second-degree: Intermittent block morphology; corresponds to a special type of ventricular aberrancy
|Zonal or divisional |
Hemiblocks47,48: The block is located in the superoanterior or inferoposterior divisions of the left bundle branch. Superoanterior hemiblock originates a qR pattern in leads I and VL and an rS pattern in leads II, III, and VF, whereas inferoposterior hemiblock originates an RS pattern in lead I and VL and a qR pattern in leads II, III, and VF.
Block of the middle fibers probably produces RS morphologies in V1, although the prominent R in V1 may also be explained by some degree of right bundle branch block.
In global ventricular block, the conduction delay usually occurs in the proximal part of the right or left branches. For this reason, the global ventricular block is known as bundle branch block.
Advanced or third-degree bundle branch blocks, both right and left, have the following characteristics2,13:
Depolarization of the ventricle corresponding to the blocked branch that occurs transseptally, beginning at the contralateral ventricle. This phenomenon explains the QRS complex widening (≥ 0.12 second) caused by a small number of Purkinje fibers in the septum and the peculiar QRS complex morphology, both in right and left bundle branch blocks, caused by the loop-hemifield correlation (Figs. 12–31, 12–32, and 12–33).
Diagnosis is mainly based on data provided by the horizontal plane leads V1 and V6 and the frontal plane lead VR.
Slurring at the end of the small of the QRS is usually opposed to the T wave.
Septal repolarization dominates over that of the left ventricular free wall and is responsible for the ST-T changes.
In general, the anatomic changes are more diffuse than the ECG expression.
A. Example of how activation occurs in complete right bundle branch block and how the different lead morphologies are explained with the loop-hemifield correlation. B. A typical electrocardiogram of complete right bundle branch block (see text).
Different degrees of bundle branch block from normal electrocardiogram to partial and complete right bundle branch block (RBBB; Top) and left bundle branch block (LBBB; Bottom).
A. Example of how activation occurs in complete left bundle branch block and how different lead morphologies are explained by the loop-hemifield correlation. B. A typical electrocardiogram in complete left bundle branch block.
Partial or first-degree bundle branch block presents a QRS complex with a duration less than 120 milliseconds, which gives rise to morphologies that are sometimes indistinguishable from some patterns seen in homolateral ventricular enlargement (see Fig. 12–32).
Zonal or divisional left blocks (hemiblocks) have been studied more in depth, both from the anatomic and electrophysiologic viewpoints, compared with right zonal blocks.
There are four intraventricular fascicles: right bundle branch, trunk of the left bundle branch, and the superoanterior and inferoposterior divisions of the left bundle. A block of the middle fibers (septal fascicle) of the left bundle can probably also occur (see later). Therefore, in addition to the block of one fascicle, blocks of two fascicles (bifascicular block) or three fascicles (trifascicular) may occur.
Advanced or Third-Degree Right Bundle Branch Block
In third-degree right bundle branch block (RBBB), the depolarization of the right ventricle occurs entirely through the septum from the left side, originating the formation of vectors 3 and 4 and causing the global change in QRS loop. The classic ECG morphologies, which result from the loop-hemifield correlation in the frontal and horizontal planes, are shown in Fig. 12–31. The repolarization is from right to left at septal level in case of proximal RBBB or at peripheral level in case of peripheral block. Consequently, the T wave is negative in V1 and positive in V6.
The blockade location, both in advanced and partial block, is usually proximal. Nevertheless, a block located in the distal part of the branch or in the right ventricle Purkinje network is often seen in some congenital heart diseases (eg, Ebstein anomaly, atrial septal defect, following surgery for tetralogy of Fallot) and in some cardiomyopathies (eg, arrhythmogenic right ventricular cardiomyopathy), giving rise to morphologies similar to those of classic complete or partial bundle branch block but with some specific patterns. See Table 12–2 concerning the differential diagnosis of tall R wave in V1.
The presence of advanced RBBB does not usually represent a poor prognosis in the absence of overt heart disease. However, it predicts an adverse outcome if it appears after acute MI, concomitantly with acute dyspnea (resulting from probable pulmonary embolism) or during an ACS caused by occlusion of the left anterior descending coronary artery (LAD) proximal to the first septal branch, which is the branch perfusing the right bundle.2
The ECG diagnostic criteria are as follows (see Fig. 12–31 and Table 12–4):
QRS of at least 0.12 second with midfinal slurring
V1: rSR′ with slurred R wave and a negative T wave
V6: qRS with evident S wave slurring and positive T wave
VR: QR with evident R wave slurring and negative T wave
T wave with its polarity opposed to QRS slurring
Partial or First-Degree Right Bundle Branch Block
In first-degree RBBB, the delay of the activation in the entire ventricle is less important. This explains why the QRS is narrower and the morphology shows less prominent forces to the right (see Fig. 12–32).
The ECG diagnostic criteria are as follows:
QRS complex duration less than 0.12 second
Morphology with rsR′ or rsr′ pattern or even rs (RS) in V1, final r in VR, and s wave in VL and V6, but with fewer notches and slurring2
A similar pattern may be seen in some cases of RVE, as in atrial septal defect, because of a delay of activation of some parts of the right ventricle as a result of the enlargement (see Fig. 12–26C).
Experimentally,23,39 the injury of the fibers of the superoanterior zone of the right ventricle often causes ECG morphologies of the SI, SII, SIII types.23 Less frequently, the injury of the inferoposterior zone may originate SI RII RIII pattern. In clinical practice, these morphologies are difficult to differentiate from normal variants or RVE.2 The changes in P and T waves may help in the differential diagnosis. The SI, RII, RIII morphology must also be found in the inferoposterior hemiblock.
Advanced or Third-Degree Left Bundle Branch Block
In third-degree left bundle branch block (LBBB), the left ventricle activation is through the septum from the right side and differs completely from normal activation. This transseptal activation causes the formation of four vectors, which are characteristic of this type of block and explain the global change in the QRS loop. The classic ECG morphologies, caused by the loop-hemifield correlation in the frontal and horizontal planes, are shown in Fig. 12–33. The repolarization in case of more advanced LBBB is directed from left to right with the T loop opposite in direction to QRS (discordant LBBB).40 This explains the negativity of T wave in leads I, V5, and V6. The T wave is normally located opposite slurring and dominant deflection of the QRS complex. In cases of less advanced LBBB, the T wave is often concordant with the QRS (T-wave positive in leads I, V5, and V6). Also, the concordant repolarization may be explained, in a few cases, by associated IHD.
The morphology of the distal blocks is similar to that of the classic proximal complete left ventricular block but with more significant final slurrings of the QRS complex. Wherever the global block is located (proximal or distal), when the delay is significant, an R-wave morphology in V6 and a QS complex in V1, with a QRS of at least 0.12 second, are generated.
The presence of LBBB by itself necessitates the exclusion of heart disease and periodic surveillance. In the acute and chronic phase of IHD, as happens with RBBB,2 LBBB is a marker of poor outcomes. The polarity of T wave concordant with QRS is associated with better prognosis and less comorbidity.40 The presence of LBBB pattern after acute infarction41 or that appears with exercise has worse prognosis.42 Also associated with a worse prognosis is the LBBB that appears after transaortic valve implantation,43 and in heart failure, especially, if associated with AF.44,45 Finally, the morphology of QRS in V3 may help to diagnose the etiology of LBBB.46
The diagnostic criteria of third-degree LBBB are as follows (see Fig. 12–33 and Table 12–5):
QRS of at least 0.12 second, sometimes greater than 0.16 second, especially with midportion slurring
V1: QS or rS with a tiny r wave and positive T wave
I and V6: single R with its peak after the initial 0.06 second
VR: QS with positive T wave
T-wave polarity is opposed to the QRS complex slurrings in more than two-thirds of cases (discordant LBBB)
Partial or First-Degree Left Bundle Branch Block
In first-degree LBBB, the activation delay in the entire ventricle is less significant (see Fig. 12–32) but is sufficient to conceal the first vector responsible for formation of r in V1 and q in V6. Because of this delay, this first vector is counteracted by the initial activation vector of RV and is not formed. The presence of septal fibrosis, demonstrated by biopsy in patients with aortic valve replacement also explains the lack of first vector (q wave) in left ventricular leads (I, VL, V6).2
The ECG diagnostic criteria are as follows:
QRS complex duration less than 0.12 second
A QS complex or a tiny r wave in V1 and a single R wave in I and V6
A similar morphology with disappearance of q in V6, which may be seen because of the presence of septal fibrosis31
Often present in LVE
Zonal (Divisional) Left Ventricular Block: Hemiblocks
These zonal blocks are much more known and well studied than the zonal blocks of the right ventricle, especially after the studies of Rosenbaum school.47,48 In zonal (divisional) left ventricular block, the stimulus is blocked in either the superoanterior or inferoposterior division of the left branch (hemiblocks) (Figs. 12–34 and 12–35; see also Fig. 12–13C). Only the ECG criteria of well-established (advanced) superoanterior and inferoposterior division of the left branch (superoanterior or inferoposterior hemiblocks according to Rosenbaum) will be discussed.
A. Location of the block and an example of how activation occurs in superoanterior hemiblock (SAH) and how different lead morphologies are explained by the loop-hemifield correlation. B. A typical example of SAH. Note the difference with the SI, SII, SIII pattern, in which case SII > SIII and SI is present. This results from the fact that in SAH, the final vector of depolarization is directed upward and to the left, and in SI, SII, SIII, the morphology is upward and to the right.
A. Location of the block and an example of how activation occurs in case of inferoposterior hemiblock (IPH) and how different lead morphologies are explained by the loop-hemifield correlation. B. Patient with QRS axis (ÂQRS) of approximately +50° (above) who presented suddenly during an acute coronary syndrome, an electrocardiogram showing ÂQRS of approximately +90° (below). This is a typical example of IPH (see text).
A change in left intraventricular activation occurs in both hemiblocks. As a consequence, the blocked area is depolarized with certain delay, which explains the typical ECG changes that can be seen.
Figure 12–34A shows the activation of the left ventricle in superoanterior hemiblock (SAH) or superoanterior divisional block, and the loop-hemifield correlation in the frontal and horizontal planes. In Fig. 12–34B, a typical example of an SAH is depicted, as well as differences with the SI, SII, SIII pattern (see legend for Fig. 12–34). The diagnosis of SAH may be made only using the ECG criteria.
The diagnostic criteria are as follows:
RS complex duration less than 0.12 second
ÂQRS deviated to the left (mainly between –45° and –75°). For the differential diagnosis, it is necessary to rule out other diseases with leftward ÂQRS, such as inferior necrosis, type II Wolff-Parkinson-White (WPW) syndrome, pacemaker implant, and SI, SII, SIII pattern (see Fig. 12–34B)
I and VL: qR; in advanced cases with slurring, especially in the descending part of the R wave
II, III and VF: rS with SIII > SII and RII > RII.
An S wave seen up to V6, with intrinsic deflection in V6 less than VL
In inferoposterior hemiblock (IPH) or divisional block, typical ECG morphology and clinical conditions, mainly the absence of RVE and asthenic habit, have to be present. It is also usually considered that evidence of left ventricular abnormalities must exist. Figure 12–35A shows the location of the block and the activation of the left ventricle in the case of an IPH or inferoposterior divisional block. In this figure, the typical ECG morphology, in frontal and horizontal planes, explained by the loop-hemifield correlation, can also be observed. In this case, the diagnosis is assured if the ECG pattern appeared abruptly, in the absence of another possible explanation (see Fig. 12–35B and legend).
The diagnostic criteria are as follows:
QRS complex duration less than 0.12 second
ÂQRS shifted to the right (between +90° and 110° or more for some authors and +140° for others)
I and VL: RS or rS
II, III, and VF: qR; in advanced cases with slurring, especially in the descending part of the R wave
Precordial leads: S wave up to V6, with an intrinsic deflection time in V6 less than VF
Block of the middle fibers, called septal block by the Brazilian school, probably produces RS morphology often with slurrings in S in V2 and a prominent R wave in V1. To confirm this diagnosis, the ECG pattern has to be transient. However, this intermittent RS pattern may be also recorded in the evolutive pattern of progressive RBBB.2
In this section, the ECG criteria of the three most characteristic bifascicular blocks—complete (or advanced) RBBB plus SAH, complete RBBB plus IPH, and bilateral bundle branch block—are discussed.
The diagnostic criteria of advanced RBBB plus SAH are as follows (Fig. 12–36A and B):
QRS complex duration greater than 0.12 second
QRS complex morphology: The first portion is directed as in SAH, upward and toward the left, whereas the second portion is directed as in complete global RBBB, anteriorly and toward the right (see Fig. 12–45A). If there is a significant left delay, it can counteract the right forces, giving rise to anterior but left final forces. Therefore, a tall R wave can be seen in V1, but without an S wave in I and, occasionally, also in V6. In this case, a complete LBBB appears to exist in the frontal plane and a complete RBBB in the horizontal plane (“masked” block)49 (see Fig. 12–36B). Sometimes this pattern may be transient.50 A masked bifascicular block usually indicates a worse outcome, even if a pacemaker is implanted.2
Types of bifascicular block. A. Advanced right bundle branch block and typical superoanterior hemiblock. B. “Masked” bifascicular block. C. Advanced right bundle branch block and inferoposterior hemiblock in a 56-year-old man with chronic ischemic heart disease but without asthenic body type and right ventricle enlargement (see text).
The diagnostic criteria of advanced RBBB plus IPH (Fig. 12–36C) are as follows:
QRS complex duration greater than 0.12 second
QRS complex morphology: The first portion of the QRS complex is directed downward, as in IPH, whereas the second portion is directed anteriorly and toward the right, as in complete RBBB. This diagnosis requires the presence of some clinical conditions, as occurs in isolated IPH (see Inferoposterior Hemiblock section).
In bilateral bundle branch block, there is an alternation of complete RBBB and LBBB morphologies in the ECG. This diagnosis requires a pacemaker to be implanted.
There are several types of trifascicular blocks, but their coverage is beyond the scope of this chapter (see Bayés de Luna2). The most frequent features are as follows:
RBBB alternating with the block of one of two left bundle branch divisions (Rosenbaum-Elizari syndrome)2,47 (Fig. 12–37)
Once the block of three fascicles has been confirmed by an ECG (RBBB alternating with superoanterior and inferoposterior fascicle blocks) (see Fig. 12–37), a pacemaker should be implanted as soon as possible because the patient may suddenly develop a paroxysmal AV block.2
Bifascicular blocks with a long PR segment. Note that a long PR segment may also be caused by a block at a proximal location (bundle of His); thus, electrophysiologic studies are required to confirm their occurrence.
Alternating bifascicular block (Rosenbaum-Elizari syndrome). A. Advanced right bundle branch block plus superoanterior hemiblock is shown. B. The following day, the frontal QRS axis (ÂQRS) changed from –60° to +130°, indicating the appearance of an inferoposterior hemiblock instead of superoanterior hemiblock.
Ventricular preexcitation is considered to exist when the electric stimulus reaches the ventricles earlier (early excitation) than via the normal conduction system.2 Early excitation can be explained by the presence of Kent bundles, which are accessory pathways with accelerated conduction that connect the atria with the ventricles (WPW-type preexcitation).51 The conduction through the Kent bundles may be anterograde, retrograde, or in both directions. In rare cases, there are also other anomalous bundles (atypical preexcitation). In more than 80% of these cases, they consist of long slowly conducting atriofascicular or AV bypass tracts. Other rare anomalous bundles are the fasciculoventricular and nodofascicular tracts, which include the formerly named Mahaim fiber.52 In addition, the presence of an accelerated AV conduction or the rare occurrence of an atrio-His bundle may cause a short PR-type preexcitation.53
The clinical importance of preexcitation lies in its association with supraventricular tachycardias; its potential to trigger malignant ventricular arrhythmia; and the risk of being confounded with other processes, especially in case of a WPW preexcitation (see the following section).
WPW-type preexcitation is diagnosed by an ECG that shows a short PR interval plus QRS-T abnormalities, primarily caused by a slurred upstroke at the beginning of the QRS complex known as the delta wave (Fig. 12–38).
Short PR interval: The PR interval generally lasts between 0.08 and 0.11 second. However, a WPW-type preexcitation may also occur with a normal PR interval in the following instances: (1) conduction block in the anomalous pathway; (2) preexcitation far from the sinus node (left side), frequently with a long anomalous pathway; and (3) atypical preexcitation presenting normal PR intervals. The only way to corroborate that the PR interval is shorter, in order to confirm the diagnosis, is by making a comparison with the baseline ECG tracing without preexcitation.
QRS-T abnormalities (Figs. 12–39 and 12–40): The QRS complexes show an abnormal morphology with a width greater than the baseline QRS complex (often > 0.11 second) and a characteristic initial slurring (delta wave). These features are secondary to the initial activation through the contractile myocardium where there are few Purkinje fibers. Different degrees of preexcitation (or delta wave) may be observed (see Fig. 12–38A–C).
Left: Wolff-Parkinson-White (WPW)-type preexcitation and short PR-type preexcitation. Right: Top: Delta waves of different magnitude: (A) minor preexcitation and (B, C) significant preexcitation; middle: three consecutive QRS complexes with evident preexcitation; below: short PR-type preexcitation.
Morphologies in Wolff-Parkinson-White-type preexcitation according to the ventricular location of the accessory atrioventricular pathway in the following zones: (A) right anteroseptal (AS); (B) right ventricular free wall (RVFW); (C) posteroseptal (PS); and (D) left ventricular free wall (LVFW). EEP, early preexcitation.
Electrocardiogram examples in the Wolff-Parkinson-White-type preexcitation with accessory atrioventricular pathway located in the right anteroseptal zone (A), right ventricular free wall (B), posteroseptal zone (C), and left ventricular free wall (D).
The QRS complex morphology in the different surface ECG leads depends on the location of the epicardial zone of earlier excitation. The vector of the first 20 milliseconds on the ECG (first vector of the delta wave, which can be measured in the ECG) is located at different sites on the frontal plane according to where the earlier ventricular epicardial excitation occurred first (see Fig. 12–39). As a result, the WPW-type preexcitation may be divided into four types (see Fig. 12–39A–D).2 Examples of these four types are displayed in Fig. 12–40.
Different algorithms have been proposed to predict the location of the anomalous pathway.54 One of the most popular was published by Milstein et al.55
Repolarization is altered except in cases with minor preexcitation. Repolarization abnormalities are secondary to the alteration in depolarization, and the pathology is more severe when the T-wave polarity opposes that of the preexcited R wave, as when the preexcitation is greater (see Fig. 12–38A–C).
Changes in the degree of preexcitation are frequent, and they may be abrupt or progressive (Fig. 12–41). Preexcitation can increase if the conduction of the stimulus through the AV node is depressed (eg, vagal maneuvers, drugs), or in contrast, preexcitation can decrease if the AV node conduction is enhanced (eg, physical exercise).
Different situations that manifest the variability of the Wolff-Parkinson-White-type preexcitation. A. Accordion effect. The first five complexes are equal and present a short PR interval, whereas preexcitation decreases in the following four complexes, and the PR is somewhat less short (0.12 second). Finally, preexcitation disappears in the last three complexes, and the PR is 0.16 second. B. Conduction over the accessory pathway alternates with normal conduction. The PR interval, when the conduction is over the accessory pathway, is observed at the limit of normal (in this lead, 0.12 second), but it is shorter than with normal conduction (0.15 second). C. Intermittent preexcitation. In the first three complexes, there is a short PR interval (0.08 second) and a delta wave, whereas in the rest of the strip, the delta wave disappears, but the short PR persists (0.10 second). This allows us, from the surface electrocardiogram, to suggest the existence of two pathways, one that bypasses the atrioventricular node (short PR type) and the other with an abnormal atrioventricular bundle and a very short PR interval. D. Intermittent preexcitation that simulates lateral infarction.
Regarding the differential diagnosis of WPW-type preexcitation, type-A and type-B preexcitations (see Fig. 12–39) should be differentiated with LBBB (see Fig. 12–40A and B); type-C preexcitation (see Fig. 12–39) with inferolateral infarction, RBBB, or RVE (see Fig. 12–40C); and type-D preexcitation (see Fig. 12–39) with lateral infarction or RVE (see Fig. 12–40D). In all of these cases, the short PR interval and the presence of a delta wave are decisive data for the diagnosis of WPW-type preexcitation.
Paroxysmal arrhythmias in patients with a WPW ECG pattern constitute the WPW syndrome. Patients with WPW preexcitation frequently present macro-reentrant paroxysmal tachycardia. They show a narrow QRS because the stimulus is activating the ventricles via normal AV conduction and a QRS-P′ less than P′-QRS (orthodromic tachycardia) (Fig. 12–42D). In cases of paroxysmal reentrant tachycardia exclusively resulting from the intranodal (junctional) circuit, the P′ mimics the end of QRS or is hidden within it (see Chap. 84). Indeed, approximately 40% to 50% of paroxysmal tachycardias are attributed to a reentry, including an accessory pathway. In a few cases, the anterograde arm of the circuit is via the anomalous Kent bundle, and the QRS complex is wide during the tachycardia (antidromic tachycardia) (see Chap. 84).
A 50-year-old patient with type IV Wolff-Parkinson-White (WPW) syndrome is shown, who presents with a crisis of atrial fibrillation (A) and atrial flutter (B) that mimics ventricular tachycardia. The diagnosis of atrial fibrillation is supported by the history (knowing that the patient has WPW syndrome) and the following characteristics of the electrocardiogram: (1) the wide complexes have a very irregular rhythm and are more or less wider (present more or less preexcitation); and (2) the narrow complexes (the sixth and the last one on the top) are sometimes close (the last complex) and sometimes far (sixth complex) to the previous QRS. In sustained ventricular tachycardia, the QRS complexes are regular, and in the presence of narrow complexes, the QRS complexes are always close to the previous one (capture beats). B. In WPW syndrome with flutter, the differential diagnosis with sustained ventricular tachycardia based only on electrocardiogram is more difficult because the RR are regular. C. Patient with crisis of atrial fibrillation with a very fast response of the ventricles (> 300 ×′) and, sometimes, very narrow R-R intervals (< 200 ms). After a very short R-R interval, a crisis of ventricular fibrillation was triggered (arrow), which had to be resolved by electric cardioversion. D. Patient with reciprocating tachycardia. The conduction in this circuit is retrograde over the accessory AV pathway and anterograde via the normal AV conduction. The RP′ ratio is smaller than P′R ratio, which is typical for reciprocating tachycardia that involves an accessory atrioventricular pathway.
AF and flutter episodes are also more frequent than in the general population. This is attributed to the rapid retrograde conduction, via the abnormal pathway, of a ventricular premature complex that may reach the atria during a vulnerable atrial period. Another possibility is that paroxysmal tachycardia triggers other arrhythmias, such as AF/flutter. The risk of these arrhythmias is two-fold. First, AF/flutter in patients with an ECG pattern of WPW can be mistaken for sustained ventricular tachycardia, with the associated consequences (Fig. 12–42A and B). Indeed, the differential diagnosis by surface ECG between atrial flutter in WPW syndrome and ventricular tachycardia is especially difficult (see Fig. 12–42B) The second potential risk, in the presence of AF/flutter, is that the accessory pathway may transmit to the ventricle more stimuli than normal, facilitating the possibility of reaching the ventricle in its vulnerable period. Consequently, this can result in ventricular fibrillation and sudden death (Fig. 12–42C).56,57
In general, the atypical preexcitation that presents reentrant arrhythmias occurs through a long atriofascicular or AV pathway. The other bundles, which include the classic Mahaim fiber, are general bystanders and do not participate in the circuit in reentrant tachycardia.
The ECG in normal sinus rhythm is normal in the majority of cases or presents minimal preexcitation (absence of q wave in leads I and V6 and rS morphology in lead III).58
The arrhythmias are less frequent and usually of reentrant junctional type. During preexcited tachycardia, the anterograde conduction is through an atypical bundle (antidromic tachycardia) with retrograde conduction by right bundle branch. Therefore, the morphology is usually of LBBB with left ÂQRS. Generally, there is a late R/S precordial transition zone (at V4 to V6), and in the cases of antidromic tachycardia through Kent bundle and LBBB pattern, the transition zone occurs earlier (R/S in V2 to V3) (see Chap. 84).
Short PR-Type Preexcitation
Short PR-type preexcitation, described by Lown et al,53 is evidenced by a short PR interval without changes in QRS morphology (see Fig. 12–38).
By a surface ECG, it is impossible to differentiate between a hyperconductive AV node, the most frequent, and preexcitation occurring via an atrio-His bundle, which bypasses the AV node slow conduction area and, therefore, does not modify the QRS complex morphology. However, it is easy to differentiate them by intracavitary ECG because this will show a short AV interval in case of a hyperconductive AV node and a short HV interval or even an absent H deflection in the presence of an atrio-hisian tract.
The association with arrhythmias and sudden death is less frequent in short PR-type preexcitation than in the WPW-type preexcitation. Nevertheless, in case of AF, the ventricular response may be very fast because of the presence of a short PR-type preexcitation, and this can be a problematic situation.
From the electrophysiologic point of view, according to the importance and duration of ischemia, the TAPs of myocardial cells present the following changes: (1) delay of the repolarization that corresponds to primary T-wave changes, (2) formation of “low-quality” TAP (change in shape) that corresponds to changes of ST, and (3) lack of formation of TAP that explains the presence of the Q wave.
From the surface ECG point of view, the most typical ECG changes resulting from ischemia are as follows2,59,60,61,62,63,64,65,66: (1) primary T-wave changes that include T waves that are wider, peaked, and/or taller and T-wave flat or negative; (2) primary ST deviations, including ST segment shifts (up and down) from baseline; and (3) changes of QRS (Q wave of necrosis and reciprocal patterns) and changes in the mid-late part of QRS (fractionated QRS).
However, ischemia may induce many other changes, including the following:
Prolongation of QT interval that may be considered a part of the changes in the T wave. It is present in the first moments of acute transmural ischemia when there is an increase in duration of TAP of the endocardium, making the T wave wider and taller and lengthening the QT interval.67
Changes in P wave, especially in atrial infarction60
Distortion of QRS complex, especially in very severe ischemia59,60,61,68,69
Appearance of different types of bradyarrhythmias (sinus bradycardia and AV block); tachyarrhythmias (especially AF and premature ventricular contractions, which may lead to ventricular tachycardia and unfortunately to ventricular fibrillation); and intraventricular block (eg, RBBB when the LAD occlusion is proximal to the first septal branch that perfuses the right bundle)60
First, we will explain how the different models of experimental occlusion of the coronary artery produce different ECG changes. Then, discussion will focus on the changes in T wave, ST segment, and QRS complex that are induced by experimental and clinical ischemia and their electrophysiologic mechanisms. Finally, the ECG changes that appear during the evolution of different clinical settings of IHD, their diagnostic criteria, and the most important clinical and prognostic implications of these ECG changes will be discussed.
Changes in Electrocardiography under Different Models of Experimental Ischemia Caused by Coronary Occlusion
After experimental coronary occlusion of the LAD in dogs, performed with an open chest and with the electrodes located in the pericardial sac, Bailey and La Due70 found (Fig. 12–43, 1) that the first ECG change induced by ischemia was negativity of the T wave, which was called ECG pattern of ischemia. This was followed by an ST-segment elevation that he called ECG pattern of injury, and finally, a Q wave appeared, which was called ECG pattern of necrosis (see Fig. 12–43, 1). This terminology was accepted by several groups.13 Thus, it was considered that in patients with IHD, the presence of a negative T wave represented a grade of acute ischemia that was less severe than an ST-segment elevation.
1. Electrocardiographic patterns that are shown sequentially after the experimental acute occlusion of a coronary artery in a dog with open chest with the subsequent transmural infarction. The pattern that was seen was as follows: ischemia (negative T wave), injury (ST-segment elevation), and necrosis (pathologic q wave). 2. Electrocardiographic recording after the occlusion of a coronary artery in an experimental animal with its thorax closed. It changes from a subendocardial ischemia pattern (tall and peaked T wave) (B) to a pattern of a subepicardial injury, transmural in clinical practice (ST-segment elevation) (C), when the acute clinical ischemia is more severe. Finally, the q wave of necrosis develops (D), accompanied as time passes by an increasingly evident pattern of subepicardial ischemia (it is transmural after the occlusion of a coronary artery, although it is expressed as experimental subepicardial in the electrocardiogram). In the chronic phase, the pattern of negative T wave is related more to changes that necrosis has induced in the repolarization than to a presence of clinical ischemia.
However, when the experiment to occlude the artery was performed in awake dogs with an unopened chest,71 the changes in the ECG were similar to the ECG changes that occurred in coronary spasm or transmural MI in humans (Fig. 12–43, 2). The negative T wave only appeared as a late manifestation, when the acute ischemia was already vanishing or had already disappeared. Therefore, a flat or negative T wave represents postischemic changes rather than the first phase of acute ischemia. Thus, it is a frequent mistake to consider the presence of a negative T wave as an indicator of active ischemia.
Morphology of T-Wave Changes and Electrophysiologic Experimental Mechanisms
It has been demonstrated by different experimental open chest methods that when ischemia or similar effect is induced (eg, by cooling the tissue)7,8,72 in the epicardium or in a part of tissue close to the recording electrode, the TAP of this zone presents a delay of repolarization without changing its shape, and a flat or negative T wave appears (Fig. 12–44B). When the same procedure is performed in the endocardium or in a part of tissue far from the electrode, a delay of repolarization is induced in this zone, and a peaked and usually taller T wave appears (Fig. 12–44A).
A. Experimental subendocardial ischemia. Subepicardial repolarization is complete, but the transmembrane action potential (TAP) in the subendocardium is longer than normal (TAP prolongation further beyond the normal at D- point) because the subendocardium is not completely repolarized. Thus, the vector that is generated between the already polarized area in the subepicardium with positive charges and the subendocardial area still with incomplete repolarization with negative charges caused by the ischemia in that area, named ischemic vector, is directed from the subendocardium to the subepicardium, with the head facing the subepicardium, even though the direction of the repolarization phenomenon goes away from it because the direction of the phenomenon (
) goes from the less ischemic area (subepicardium) to the more ischemic area (subendocardium). Therefore, the subepicardium faces the ischemic vector head (positive charge of the dipole), which explains why the T wave is more positive than normal. In experimental subepicardial ischemia, a similar but inverse phenomenon (B
) occurs, which explains the development of flattened or negative T waves.
The electrophysiologic explanation of these changes in T wave (more positive T wave and flat or negative T wave) caused by experimental subendocardial and subepicardial ischemia, that are found in these areas that present delay of repolarization (prolonged TAP), may be explained (see Fig. 12–44) by two concepts: the summation of TAPs of subendocardium and subepicardium (the longer is located in the ischemic zone), and the concept of ischemic vector. According to these concepts, the area with delayed TAP (named ischemic area), either in the subendocardium or in the subepicardium, was not fully repolarized at the time when the other area was already repolarized. Therefore, it still presents negative charges. As repolarization starts in the zone that is more perfused, the sense of repolarization (see Fig. 12–44) will face the ischemic zone. However, as this zone presents more negative changes, a flow of current having a vectorial expression is generated, going from more ischemic to less ischemic zones. Then, the vector of ischemia with the positive change in the head is directed away from the ischemic area and originates a more positive T wave in experimental subendocardial ischemia and a flat or negative T wave in experimental subepicardial ischemia. Note that the vector of necrosis is also directed away from the necrosis area (see Fig. 12–46), but on the contrary, the vector of the area with greater ischemia (injury area) is directed toward this area (see Figs. 12-49 and 12–50).
T-Wave Changes in Patients with Ischemic Heart Disease
In clinical settings, the explanation of T-wave changes caused by ischemia is in some aspects different (see Electrocardiography in Ischemic Heart Disease).72,73
Peaked, symmetrical, wider, and/or taller T wave. This morphology, accompanied by a lengthening of the QT interval, appears in the beginning of acute transmural ischemia resulting from total coronary occlusion, sometimes accompanied by slight ST depression. As a consequence of the occlusion, there is first subendocardial involvement. Different factors explain the susceptibility of the subendocardium to the development of ischemia. These include the greater dependence of this region on diastole perfusion and the greater degree of energy expenditure of this area during systole.60
This initial subendocardial ischemia, also demonstrated by contrast-enhanced cardiovascular magnetic resonance (CE-CMR),74 produces a delay of repolarization in this area and, as a result, a lengthening of the TAP of the subendocardium, explaining the increase of the QT interval and usually also the presence of wider, peaked, symmetric, and/or taller T waves (see Fig. 12–44A; Fig. 12–45).
Crisis of coronary spasm (Prinzmetal angina) recorded by Holter electrocardiography. A. Control. B. Initial pattern of a very tall T wave (subendocardial ischemia). C. Huge pattern of ST-segment elevation. D to F. Resolution toward normal values. Total duration of the crisis was 2 minutes.
As mentioned earlier, the results of animal experiments performed with unopened chest71 coincide with the ECG changes that often appear in different clinical settings of transmural or near-transmural ischemia that are the consequence of total or near-total coronary occlusion, such as coronary spasm (see Fig. 12–45),75,76 hyperacute phase of ST-segment elevation ACS (STE-ACS; see Fig. 12–60A), and percutaneous coronary intervention (PCI).63 In the majority of cases, after a short period of peaked T wave with QT prolongation, an evident ST-segment elevation appears (see Fig. 12–60A). Later on, if ischemia persists, the ECG pattern may evolve to Q-wave MI.
In addition, a tall, positive, and symmetrical T wave is frequently seen in a chronic phase of Q-wave MI. This is the expression of the mirror image of a negative T wave. The most frequent leads where this is seen are I, VL, and V1 to V3 as mirror images of inferolateral involvement (Fig. 12–46, 2).
1-A. Observe the comparison between the normal activation and the activation in an extensive anterior infarction. The vector of infarction (VI) is directed backward, and the loop-hemifield correlation explains the appearance of the Q wave in anterior leads. 1-B. Example of myocardial infarction (MI) of anteroseptal zone. 2-A. Note the comparison between normal activation and activation in inferior infarction with lateral extension (RS in V1). The vector of infarction is directed upward in the frontal plane, and a loop-hemifield correlation explains the appearance of a Q wave in inferior leads. 2-B. Example of MI of inferolateral zone.
CHANGES IN T WAVE
Peaked, wider, and/or taller T waves, accompanied by increased QT interval length:
These are usually the initial changes in case of total occlusion of a coronary artery.
The electrocardiographic (ECG) pattern is explained by the brusque presence of ischemia in the subendocardium that produces a delay of repolarization (transmembrane action potential [TAP]) in this area (long QT interval).
These may also be seen in chronic phase of ischemic heart disease as a mirror pattern.
Flat or negative T wave: The deepness of the negative T wave is variable, and the QT interval is usually prolonged.
Negative T waves do not usually represent acute active ischemia but rather are the expression of postischemic changes.
In Q-wave myocardial infarction, there is probably the consequence of the changes of depolarization resulting from necrosis.
In the other circumstances, the ECG pattern is explained, in the presence of transmural involvement, by the fact that the electrode is closer to epicardium than to endocardium and records the ECG changes that are present in the subepicardium (caused by delayed repolarization—delayed TAP), as occurs in experimental subepicardial involvement.
None of these clinical situations represents acute active ischemia. Rather, they indicate postischemic changes.
The involvement of the left ventricle wall is usually transmural in the presence of a flat/negative T wave. No clinical situation caused by ischemia presents exclusively with subepicardial involvement. Therefore, the theories that explain the presence of flat/negative T waves in experimental clinical ischemia (see Fig. 12–44B) are not useful in the clinical setting. Probably, the negative T wave seen in these clinical cases, associated with acute transmural ischemia (ST↑) that has subsided, may be explained by the mechanisms shown in Fig. 12–47.
Origin of negative and deep T wave that appear after acute ST-segment elevation in clinical setting. The ST-segment elevation is hyperacute ischemia (the tsunami), and the negative T wave is the panoramic view that appear after the ischemia (the tsunami) is over. A. Because of the increased transmembrane action potential (TAP) duration of the transmural area affected, the sum of the TAP of this area with the shorter TAP of neighboring areas explains the negative T wave. B. The explanation based on ischemic vector theory .
A long list of conditions, apart from IHD, may present with changes in the T wave (symmetric-wide and/or taller than normal, flat, or negative).2,60 Tables 12–6 and 12–7 summarize the most important conditions, and Fig. 12–48 presents some of the most striking examples.
TABLE 12–6.Causes of a More Positive Than Normal T Wavea ||Download (.pdf) TABLE 12–6. Causes of a More Positive Than Normal T Wavea
Normal variant: vagotonia, athletes, the elderly, and so on
Moderate left ventricular hypertrophy in heart diseases with diastolic overload (eg, aortic regurgitation)
Advanced atrioventricular block (tall and peaked T wave in the narrow QRS complex escape rhythm)
V1-V2 as a mirror image of inferolateral subepicardial ischemia or secondary to left ventricular hypertrophy
TABLE 12–7.Causes of Negative or Flattened T Wavesa ||Download (.pdf) TABLE 12–7. Causes of Negative or Flattened T Wavesa
Normal variants: children, black people, hyperventilation, and women (eg, right precordial leads); may sometimes be diffuse (global T-wave inversion of an unknown origin); frequently occurs in women
Pericarditis. In this condition, the image is usually extensive but generally not with significant negativity.
Cor pulmonale and pulmonary embolism
Myocarditis and cardiomyopathies
Mitral valve prolapse: not always. If it appears, it does so particularly in II, III, and VF and/or V5 and V6.
Strokes; relatively infrequent
Myxedema: usually flat T wave or only slightly negative
Athlete, with or without ST-segment elevation. Hypertrophic cardiomyopathy, especially apical type, must be ruled out.
After the administration of certain drugs (eg, prenylamine, amiodarone) (flattened T wave)
In hypokalemia, the T wave can flatten.
Abnormalities secondary to left ventricular hypertrophy or to left bundle branch block
Intermittent left bundle branch block and other situations of intermittent abnormal activation (eg, pacemakers, Wolff-Parkinson-White syndrome) “electrical memory”
T wave morphologies in conditions other than ischemic heart disease. 1. Some morphologies of flattened or negative T wave: (A, B) V1 and V2 of a healthy 1-year-old girl; (C, D) alcoholic cardiomyopathy; (E) myxedema; (F) negative T wave after paroxysmal tachycardia in a patient with initial phase of cardiomyopathy; (G) bimodal T with long QT frequently seen after long-term amiodarone administration; (H) negative T wave with very wide base, sometimes observed in stroke; (I) negative T wave preceded by ST-segment elevation in an apparently healthy tennis player; (J) very negative T wave in a case of apical cardiomyopathy; and (K) negative T wave in a case of intermittent left bundle branch block in a patient with no apparent heart disease (cardiac memory according to Rosenbaum school). 2. Tall peaked T wave in case of (A) variant of normality (vagotonia with early repolarization); (B) alcoholism; (C) left ventricular enlargement; (D) stroke; and (E) hyperkalemia.
Notably, taller T waves of ischemic origin are very transient (see Figs. 12–45 and 12–60A). The persistent high-voltage T wave, seen in V1 to V2 in cases of chronic lateral infarction (see Fig. 12–46B), is an indirect (mirror) pattern, rather than a direct pattern, of tall T wave caused by ischemia.
In cases with a negative T wave, chronic pericarditis is the most important condition for a clinical differential diagnosis because this disease also presents with pain in the acute phase. The negative T wave of pericarditis (see Fig. 12–77) is usually more extensive, does not present mirror pattern in the frontal plane, and is less intensive (negative) than in cases of IHD, especially in post–Q-wave MI (see Fig. 12–46).
Morphologies of ST Deviations and Electrophysiologic Experimental Mechanism
The area of the myocardium with significant and persistent ischemia (called the area of injury) presents an evident diastolic depolarization. From an experimental point of view, two injury currents are generated as a consequence of an important ischemia—one occurring during systole and the other during diastole. However, the injury current generated during systole is the only one considered because the ECG equipment is adjusted by alternating current amplifiers to maintain a stable isoelectric baseline during diastole, despite the existence of diastolic depolarization that would change the QT interval. The area with systolic injury current presents a “low-quality” TAP (eg, slower upstroke, lower voltage, smaller area).
ST-segment depression is recorded in some patients with abrupt decreased blood flow without total occlusion, such as in non–ST-segment elevation acute coronary syndrome (non–STE-ACS), and in patients who present with ischemia due to increased demand, such as an angina of effort. The electrocardiographic (ECG) pattern is explained by important and predominant ischemia in the subendocardium that induces a more important change of the shape of the transmembrane action potential in this area (ST-segment depression).
ST-segment elevation is mainly recorded in patients with abrupt decreased blood flow that usually presents as a total coronary occlusion, such as in STE-ACS. The ECG pattern is explained in the presence of transmural clinical ischemia, because the electrode closer to the epicardium than the endocardium records the ECG changes that are present in the epicardium, as occurs in experimental subepicardial injury. The same pattern may be recorded in cases of transient acute ischemia with or without atherothrombosis (eg, coronary spasm).
The evaluation of direct and mirror images of ST deviations is important for diagnostic and prognostic purposes.
The ECG pattern of the ST segment during an important diastolic depolarization caused by an experimental injury induced in open chest animals varies depending on the location of the injury. Thus, an ST-segment depression is observed if the injury affects the subendocardium, whereas an ST-segment elevation is recorded if the experimental injury is transmural. These two situations may be explained considering the concepts of TAP summation and the vector of severe ischemia.2,14,72,73
Figure 12–49 shows how the sum of the TAPs of the subendocardium and the subepicardium with a TAP of subendocardium with slower upstroke and smaller size may explain the presence of ST-segment depression following a subendocardial injury (ECG pattern of subendocardial injury; see Fig. 12–49A) or of ST-segment elevation after transmural injury (ECG pattern of transmural ischemia that is known as ECG pattern of injury).
On the other hand, according to the concept of severe ischemia (injury vector) when the zone with low-quality TAP (injured zone) is on the subendocardium (Fig. 12–50A), at the end of depolarization (end of systole), this zone presents fewer negative charges. Consequently, a flow of current exists from the zone with more negative charges to the low-quality TAP zone with fewer negative charges. This originates an injury vector with fewer negative charges (relatively positive) in the head, which points to the zone with low-quality TAP, or the injured zone. If this zone is limited to subendocardium, therefore, the injury vector points toward the subendocardium (injured zone) and is expressed as an ST-segment depression in the surface leads (see Fig. 12–50A). Likewise, when the injured zone is more important and becomes transmural, this zone is relatively less negative (relatively positive), and the injury vector that starts in the subendocardium points toward this zone and is recorded in the surface lead as an ST-segment elevation (Fig. 12–50B).
A. The sum of the transmembrane action potential (TAP) in the subendocardium (TAP with smaller area) and the TAP of the rest of V1 (normal) explains the ST-segment depression. B. The area with severe subendocardial ischemia presents fewer negative charges than the rest of V1 and is thus relatively positive. For this reason, the ischemic vector of this severe ischemic area (named injury vector) points to the subendocardium and is recorded as negative from the end of QRS in the surface electrocardiogram.
A. The transmembrane action potential (TAP) in the transmural zone affected by severe transmural ischemia presents an inverted polarity with a slower descent. The sum of this TAP with the normal TAPs of neighboring areas explains the electrocardiography morphology with ST-segment elevation. B. The vector of severe transmural ischemia (historically called the subepicardial injury vector) is directed from the subendocardium to the subepicardium and is recorded as ST-segment elevation. This results from the fewer negative charges in the affected transmural zone compared to the rest of the myocardium and explains why this zone is relatively positive.
ST-Segment Deviations in Patients with Ischemic Heart Disease
See also Electrocardiography in Ischemic Heart Disease. ST-segment depression appears in the following circumstances:
In patients usually with preexistent IHD who present with NSTE-ACS without total occlusion of the artery. In these cases, there is important involvement of subendocardial flow, as a consequence of sudden but not total cessation of blood flow. The ST-segment depression tends to normalize from the acute to the subacute phases (Fig. 12–51A; see legend).
In patients with IHD who, as a consequence of exercise or stress, have an increased demand for flow, but where it cannot be supplied because there is a fixed stenosis and a decrease in subendocardial flow. In these cases, different types of ST-segment depression may appear (Fig. 12–51B). As the stenosis is fixed, there is no total occlusion and thus no transmural ischemia.
A. A 65-year-old patient with non–Q-wave infarction due to left main trunk subocclusion. Note the evolutionary patterns from 1 to 4 during the first week until the normalization of the ST segment. B. Different types of subendocardial injury patterns that appeared in the course of an exercise test: (1) horizontal displacement of the ST segment; (2) descendent displacement; (3) concave displacement; and (4) ST-segment depression from J point with ascendant morphology and with rapid up-sloping. This is usually seen in normal cases. The coronary angiography was abnormal in 1, 2, and 3, and normal in 4. These changes are especially visible in leads with dominant r wave, especially V3, V4, V5, V6, I, and VL, and/or inferior leads with dominant r wave.
ST-segment depression in clinical practice usually appears because the subendocardium is more vulnerable to ischemic damage than the rest of the ventricular wall, and thus, it may be affected without transmural involvement if the occlusion is subtotal. When the subendocardial/subepicardial ratio is reduced to approximately 40%, the flow ratio decreases dramatically. This occurs during exercise and mental stress and also when there is an increased left ventricle end-diastolic pressure.63 In these cases, the TAP of the subendocardium resulting from extensive and already existent ischemia shows a change in its shape but not a prolongation of the TAP duration, as happens in the first minutes of total occlusion in patients usually without previous ischemia. This explains why, in one case, a taller T wave appears (see Fig. 12–44B), whereas in the other case, an ST-segment depression occurs (see Fig. 12–49B).
ST-segment elevation appears in transmural ischemia, often after a period of taller and wider T wave (STE-ACS). Usually, these patients do not present with a previous important ischemia. The ST-segment elevation tends to normalize from the acute to the chronic phases (Figs. 12–52 and 12–53) (see Acute Coronary Syndrome with Narrow QRS: Evolutionary Changes).
This figure shows the different evolution of ST-segment elevation acute coronary syndrome (STE-ACS) before the reperfusion era in 1970 (especially primary percutaneous coronary intervention [PCI]) (1) and in current treatment 2010 (2). 1. In 1970 a 72-year-old patient with an extensive anterior infarction caused by left anterior descending proximal occlusion. Note the evolutionary patterns without current treatment (1970s): (A) 30 minutes after the onset of pain, (B) 3 hours later, (C) 3 days later, and (D) 3 weeks later. 2. In 2010, (A) a 63-year-old man with significant STE-ACS; (B) after PCI, a negative T wave appears; (C) the patient presents with angina, the ST segment pseudonormalizes, and again, a new PCI was performed that demonstrated intrastent thrombosis; and (D) after the procedure, the electrocardiogram again shows a negative T wave.
A. In ST-segment elevation in precordial leads, as a consequence of left anterior descending coronary artery (LAD) occlusion, the ST segment changes in reciprocal leads (II, III, and aVF), allowing us to identify whether the occlusion is in the proximal (above) or distal LAD (below). B. In case of ST-segment elevation in inferior leads (II, III, and aVF), the ST changes in other leads, in this case lead I, providing information on whether the inferior infarction is caused by right coronary artery (RCA; above) or left circumflex artery (LCX; below) occlusion (see text).
To explain the appearance of this pattern, we have to consider that even the injured zone is transmural and the surface electrodes located closer to the epicardium are recording the ECG pattern as in the case of the experimental subepicardial injury that presented a change of the TAP shape in the subepicardial layers and a less negative charge (relatively positive) (see Fig. 12–50B, right).
Because the injury patterns develop at the end of the depolarization, which corresponds to the end of generation of QRS at the beginning of repolarization, the ECG expression of injury starts during the first part of the ST segment. Therefore, in cases of relevant injury, there is an elevation of the S wave, which persists along the whole ST segment and usually encompasses a T wave that becomes negative (see Electrocardiogram in Acute Coronary Syndrome with ST-Segment Elevation).
An ST-segment elevation may also be recorded in other clinical settings that are not related to atherothrombosis, such as isolated coronary spasm75,76 and Takotsubo syndrome (TTS)60,78,79 (see Electrocardiographic Changes in Ischemia Not Related to Atherothrombosis).
The leads that face the head of the vector of injury in transmural acute ischemia record an ST-segment elevation, whereas the leads facing the tail of the injury vector record an ST-segment depression. The global study of direct and mirror images of the ST deviations in different leads is crucial to correctly diagnosis the location of the injury and to understand the corresponding prognostic implications (see Fig. 12–53 and Electrocardiogram in Acute Coronary Syndrome with ST-Segment Elevation).
Q wave of necrosis may appear when there is, as a result of a myocardial infarction, a myocardial zone with important diastolic depolarization and lack of formation of transmembrane action potential. This zone usually surpasses the endocardium layer and encompasses part of the left ventricle that depolarizes within the first 40 to 50 ms.
The changes in the mid to late part of QRS (fractioned QRS) have the same cause but take place in the areas of late left ventricle activation.
The list of conditions that, apart from IHD, may present an ST-segment elevation or depression is large.2,60
Tables 12–8 and 12–9 summarize the most important conditions of ST-segment depression and elevation not caused by IHD. On the other hand, Fig. 12–54 shows the most typical variants that present with ST-segment elevation or depression. In the first phase of pericarditis, a disease that also presents with chest pain, the most striking change is an elevation of the ST segment. Many conditions can also present with ST-segment depression, although usually small. The most important factor to take into account is the correlation of the clinical symptoms with the deviations of the ST segment. The diagnostic criteria for considering the deviations (ups and downs) of ST suggestive of ACS and all their prognostic implications will be discussed later (see Acute Coronary Syndrome with Narrow QRS: Evolutionary Changes).
TABLE 12–8.Most Frequent Causes of ST-Segment Elevationa ||Download (.pdf) TABLE 12–8. Most Frequent Causes of ST-Segment Elevationa
Normal variants: chest abnormalities, early repolarization, vagal overdrive. In vagal overdrive, ST-segment elevation is mild and generally accompanies the early repolarization image. T wave is tall and asymmetric.
Athletes. Sometimes an ST-segment elevation exists that even mimics an acute infarction with or without negative T wave, at times prominent. No coronary involvement has been found, but this image has been observed in athletes who die suddenly; thus, its presence implies the need to rule out hypertrophic cardiomyopathy.
Acute pericarditis in its early stage and myopericarditis
Hyperkalemia. The presence of a tall peaked T wave is more evident than the accompanying ST-segment elevation, but sometimes it may be evident
Arrhythmogenic right ventricular dysplasia
Dissecting aortic aneurysm
Toxicity secondary to cocaine abuse, drug abuse, etc.
TABLE 12–9.Most Frequent Causes of ST-Segment Depressiona ||Download (.pdf) TABLE 12–9. Most Frequent Causes of ST-Segment Depressiona
Normal variants (generally slight ST-segment depression): sympathetic overdrive; neurocirculatory asthenia, hyperventilation, etc.
Drugs: diuretics, digitalis, etc.
Mitral valve prolapse
Secondary to bundle branch block or ventricular hypertrophy. Mixed images are frequently generated.
A. The most frequent cases of ST-segment elevation apart from ischemic heart disease: (1) pericarditis; (2) hyperkalemia; (3) athletes; and (4) typical Brugada pattern with coved ST-segment elevation. The saddle-type variant of Brugada syndrome has to be differentiated from normal variant. B. ST-segment depression resulting from causes other than ischemia: (1) digitalis effect (note the typical morphology with ST-segment depression and short QT in patients with slow atrial fibrillation); (2) hypokalemia in a patient with congestive heart failure taking high doses of furosemide; and (3) mitral valve prolapse.
Q Wave of Necrosis: Electrophysiologic Mechanisms
The activation of the subendocardial area is very fast because the density of Purkinje fibers is so great that the electrodes located in this area do not record any positive deflection (1 and 2 in Fig. 12–55A). Later on, the subsequent activation of the other part of the left ventricle wall records progressively greater R waves until a unique R wave is recorded from the epicardium (5 in Fig. 12–55A).
A. Normal ventricular depolarization, being very rapid in the subendocardium, does not generate detectable potentials because this zone is very rich in Purkinje fibers (QS in 1 and 2). Starting from the border zone with subepicardium (3), morphologies with an increasing R wave (rS, RS, and RS) are registered (3 to 5) up to exclusive R wave in the most external part of epicardium (6). As a consequence, in cases of experimental necrosis, the Q wave will be recorded only when it reaches subepicardium and then will originate Q waves of higher or lower voltage according to the extension of necrosis. A qR morphology will be recorded in 3 and QR in 4 and 5, up to QS if the necrosis is transmural. B. This figure shows, according to the theory of the electrical window of Wilson, how clinical transmural infarction originates QS morphology. C. An infarction affecting subendocardium and a part of subepicardium may give rise to QR morphology without necessarily being transmural. D. Finally, an infarction affecting basal areas or a part of myocardial wall, but in a form of patches, with necrosis-free zones, allows early formation of depolarization vectors that will be recorded as R waves but with slurrings or small voltage (fractioned QRS).
In the presence of MI, the diastolic depolarization in the infarcted area is so important that it cannot be excited and does not originate a TAP. Therefore, a Q wave is generated when the infarcted area surpasses the subendocardium and affects part of the myocardium that is depolarized within the first 40 to 50 milliseconds64 (Fig. 12–55B and C).
The Q wave of necrosis may be explained by two theories. The first theory is the theory of the electrical window of Wilson. According to this theory, the transmural infarcted area acts as an electrical window and, consequently, the electrode that faces that area records the negativity of the intracavitary QRS (Q wave of necrosis) (see Fig. 12–55B).
The second theory is the theory of the infarction vector. This theory proposes that the infarcted area generates a vector (infarction vector) that has the same magnitude, but opposite direction, to the one that would have been generated at the same zone in the absence of infarction. Therefore, the infarction vector moves away from the infarcted area (see Fig. 12–46). As we have stated, the ventricular depolarization changes that originate the Q wave occur when the infarction area is depolarized within the first 40 milliseconds of ventricular activation.
Anomalies in the mid-to-late part of QRS, such as slurring, rsr′, and low voltage in the left precordial leads (Fig. 12–55D), are called fractioned QRS.65,66 Fractioned QRS may occur as a consequence of alterations of ventricular activation after 40 to 50 milliseconds (basal segments according to standardized myocardial segmentation nomenclature by Cerqueira et al80). The fractioned QRS may appear either isolated or with a Q wave. It may be caused by a necrotic area that does not involve the whole wall (see Fig. 12–55D).
The MI with fractioned QRS forms part of the non–Q-wave MI, which will be discussed later (see Myocardial Infarction Without Q Wave or Equivalent).
Changes in QRS in Patients with Ischemic Heart Disease
The appearance of the Q wave of necrosis in the evolutionary changes of STE-ACS is evidence that the patient has evolved to MI, involving an area that surpasses the subendocardium (see Fig. 12–55B). However, this is not an irreversible pattern. In fact, in a few cases, such as aborted MI and Prinzmetal angina, the presence of Q waves may be transient (see Electrocardiography in Ischemic Heart Disease).
The criteria to diagnose a Q wave as abnormal and the location of MI, according to the presence of the Q wave in different leads, are discussed later in Q-Wave Myocardial Infarction (see Table 12–11).
As with changes in the T-wave and ST-segment deviations, the presence of a mirror image of the Q wave of necrosis is also very important for diagnostic purposes. It is especially evident that, in patients with IHD, the presence of a prominent R wave in V1 may be the only manifestation of abnormality. It is currently known that this R wave result from a lateral, not a posterior, MI (see Q-Wave Myocardial Infarction).81,82
Recently, it has been reported that the presence of fractioned QRS provides a more accurate criterion for the diagnosis of necrosis than the existence of a Q wave.65 However, it is necessary to match these morphologies with the clinical setting because they may also be seen in normal subjects.
The fractioned QRS also arises in other diseases or circumstances, such as ventricular aneurysm83 and Brugada syndrome.84
The specificity of the pathologic Q wave (Table 12–10) for diagnosing myocardial necrosis is relatively high. However, it must be noted that similar “Q” waves are seen in other processes. The diagnosis of acute MI is based not only on ECG findings, but also on the clinical setting, as well as on enzymatic changes. The presence of ST-T alterations accompanying a pathologic Q wave gives support to an IHD as the cause for this ECG pattern. However, as indicated later, in 5% to 25% of infarctions (higher incidence in inferior infarction), the Q wave disappears with time; thus, the sensitivity of the ECG for detecting old infarction is not very high (Fig. 12–56).
TABLE 12–10.More Common Pitfalls in the Electrocardiogram Interpretation of Acute Coronary Syndromea ||Download (.pdf) TABLE 12–10. More Common Pitfalls in the Electrocardiogram Interpretation of Acute Coronary Syndromea
|ECG Patterns(•) and Pitfalls (*) ||Type of ACS and Involved Artery ||Zone and Characteristics of Involvement |
A. • ST-segment depression in V1-V4:
(1) In the hyperacute phase, prominent ST-segment depression in V1, horizontal/downsloping, without significant terminal positive T wave in V1-V2
(2) In more advanced stages, ST horizontal descent with + T wave
* Consider it to be a non–STE-ACS and mirror image more evident than direct image
Probably, it is true STE-ACS (STE-ACS equivalent) mirror pattern due to LCX occlusion (rarely distal RCA)
Patients have ongoing active symptoms
|Transmural lateral involvement |
B. • Leads V1-V4: Isoelectric ST segment with tall, wide, positive T wave; often a transient pattern
* Consider that the ECG is normal because of few changes in the ECG; few mirror images
Hyperacute phase of STE-ACS; patient with angina
Repeat ECG in a few minutes
Evolving to LAD total occlusion
|Subendocardial involvement evolving to transmural involvement |
C. • Leads V3-V5: ST ↓plus tall positive T wave, without tachycardia, that evolves to Q-wave MI; change occurs in hours
* Consider that the PCI is not emergent
Non–STE-ACS evolving to STE-ACS, usually in hours
Usually LAD subocclusion evolving to total occlusion
Patients have ongoing symptoms
|Nontransmural involved wall evolving to transmural involvement |
D. • Leads V1-V3: Non–STE-ACS with isoelectric ST segment with mild negative T wave in V1-V3
* Consider the problem is over
Resolution phase (spontaneous, drugs, PCI) of non–STE-ACS; LAD subocclusion that may be important
Patients usually have resolution of symptoms
|No transmural involvement |
E. • Leads V1 to V4-V5: Isoelectric ST segment with deep symmetrical negative T wave; not angina at this moment
* Consider to be non-STE-ACS
Resolution phase (spontaneous, drugs, PCI) of non–STE-ACS caused by LAD subocclusion (or occlusion with collaterals)
Patients usually have resolution of symptoms
|At least in some cases, transmural edema that disappears if pattern normalizes |
F. • ST-segment elevation in I and aVL without evident ST-segment depression in V1-V2
* Consider LCX occlusion; often mirror image more evident than direct image
STE-ACS usually caused by first diagonal occlusion
Patients usually have ongoing active symptoms
|Transmural involvement mid/low anterolateral wall |
G. • ST-segment depression in ≥ 7 leads + ST-segment elevation in aVR-V1 and without evident final positive T wave in V1-V2; in the absence of LVH, LBBB, IVCD
* Do not consider it to be left main subocclusion
Non–STE-ACS of high risk
Left main trunk or three-vessel disease subocclusion
|No transmural involvement |
H. • ST-segment elevation in I, aVL, V2 to V3-6; no ST-segment elevation in aVR and V1; frequent RBBB + superoanterior hemiblock; severe clinical/hemodynamic state
* Do not recognize that it corresponds to a complete left main trunk occlusion
|STE-ACS caused by left main trunk occlusion with severe hemodynamic state ||Transmural involvement |
I. • ST-segment elevation < 1 mm in inferior leads or < 2 mm in precordial leads
* Consider that it is a non–STE-ACS; often mirror image is more evident than direct image
Hyperacute phase of STEMI
LAD, RCA, or LCX occlusion
|Transmural ischemia |
J. • LBBB pattern
* Consider that alterations in repolarization are caused by the LBBB. Sgarbossa’s criteria not identified
Hyperacute phase of STEMI
LAD, RCA, or LCX occlusion
|Transmural ischemia |
Spontaneous evolutionary pattern in V1-V2 seen in myocardial infarction (MI) caused by occlusion of the left anterior descending coronary artery. Now, after current effective treatment, the changes may be very different (see Fig. 12–52). This is a typical case of ST-segment elevation MI that presents Q-wave MI without residual ischemia. See on the right the scheme of the left ventricle (LV) wall: (1) normal, (2) with predominant subendocardial ischemia, (3) with transmural ischemia, (4) with necrosis and often surrounded by zone of ischemic tissue, (5) chronic necrosis without ischemic tissue.
The principal causes of the pathologic Q wave, other than myocardial necrosis, are listed in Table 12–10.
As already stated, there are many other changes in the ECG parameters that are induced by ischemia. Some of them, such as lengthening of the QT interval, have already been discussed. For more information on other ECG changes, such as for instance those of the P wave in case of atrial infarction consult Bayés de Luna,2 Surawicz,12 and Bayés de Luna and Fiol-Sala.60