The interpretation of an ECG should be systematically approached in a sequential way. In this chapter, the normal value of each parameter at different ages and other ECG variants to ensure a successful ECG interpretation is discussed consecutively (Bayés de Luna, 2012; Bayés de Luna and Baranchuk, 2017). In Chapter 19, we discuss the diagnostic value of all the abnormalities of the ECG parameters. Figure 7.1A shows the temporal relationship between the different ECG waves and intervals, and Figure 7.1B shows the most frequent QRS, P, and T morphologies. In Figure 7.2, may be seen the normal activation of the atria (A), and this sequential activation according to the Lewis diagram (B). In Figure 7.2C, may be seen the infrequent alterations of P and QRS, relationship in the rare cases of sinoventricular conduction. Heart rhythm can be sinusal or ectopic. Allectopic rhythms correspond to different types of arrhythmias (see Chapters 14–18). Sinus rhythm has the following characteristics: Under normal conditions, the discharge cadence at rest oscillates between 60 and 100 bpm and a slight variability exists between the RR intervals. Sometimes, particularly in children, this variability is more evident, most commonly related to respiration. In different pathological situations, the RR variability can be decreased, which has important clinical implications (see Chapter 25). Under very rare pathological conditions, usually in the presence of important ionic disturbances (severe hyperkalemia) (see Chapter 23), the conduction of the sinus stimulus to the ventricles is normal through especialized fibers, but atrial activation is delayed (which explains delay of inscription of P wave and the short PR interval) or that P wave may be hidden in QRS, which explains sinus rhythm without a visible P wave (sinoventricular conduction) (Figure 7.2C). Also in exceptional situations, sinus rhythm may be concealed due to extensive atrial fibrosis in the presence of large atria, particularly in valvular diseases that do not initiate measurable potentials on the surface ECG (see Figure 15.37). However, in some leads, often in V1, a small P wave may be seen. Sinus rhythm is the normal rhythm of the heart. At rest, the normal sinus rate oscillates between 60 and 100 bpm. The rate will normally decrease with rest and sleep and increase with variables such as emotion, exercise, and fever. All types of normal and pathological sinus bradycardia and tachycardia will be discussed later (see Chapters 15 and 17). The heart rate can be calculated, approximately, according to the number of 0.20 s spaces (which are the spaces separated by thick lines on the ECG paper when the recording paper speed is 25 mm/s) occurring in an RR cycle (Table 7.1). Another method is to count the RR cycles occurring in 6 s and multiply this number by 10. We will describe first the different parameters of the P wave, the wave of atrial depolarization. To use the ECG for the study of atrial P wave in normal conditions and in pathology, we have to study the different components of the P wave, P wave parameters, named P wave indices by Magnani (Magnani et al., 2010). These indices may be modified in the presence of right and left atrial enlargement and atrial blocks (see Chapter 9). The reference values are taken from studies performed in samples of healthy people (Magnani et al. 2010). These parameters of P are used for: (i) Diagnosis of interatrial block (IAB); (ii) Diagnosis of right and left atrial enlargement. The sensitivity for the diagnosis of right and left atrial enlargement is low; (iii) To know the risk of AF, stroke, and even dementia and death. Figure 7.1 (A) Temporal relationship between the different ECG waves and nomenclature of the various intervals and segments. (B) (A) The most frequent QRS complex morphologies. (B) P and T wave morphologies. Figure 7.2 (A and B) Normal activation of the heart, with Lewis diagram. (C) One example of sinoventricular conduction with short PR interval or hidden P wave due to delay of inscription of P wave. Table 7.1 Calculation of heart rate according to the RR interval We will briefly describe the indices more frequently used for all these purposes (Figure 7.3) (Tables 7.2 and 7.3) (Cooksey et al. 1977). Figure 7.3 From A to E we can see the more frequently P wave índices, with the principal characteristic that define all of them. Table 7.2 P wave height and duration in normal adults Adapted from Cooksey et al. (1977). a Twenty‐five per cent of the series had a small terminal negative deflection of the P wave in lead V1. Figure 7.4 P wave morphologies in the different leads, as determined by the projection of the P loop in the positive and negative lead hemifields (see text). In a vertical heart, we have a negative P wave in aVL and in a horizontal heart, we have a negative P wave in III. It depends on the P loop rotation as is well demonstrated in Figure 7.7. According to loop rotation (counterclockwise in the FP and HP in the case of sinus rhythm and clockwise in the case of ectopic rhythm), the P wave morphology in III and V1 varies. The wave of atrial repolarization (see Chapter 5, Figure 5.17) is very flat follows the P wave and usually is hidden in the QRS complex (Figure 5.17) although in the presence of sympathetic overload may be seen (Figure 7.6). May be also recorded in cases of pericarditis and atrial infarction (Chapter 9). The atrial rhythm may be sinusal or ectopic and depending on that the P loop rotation will be different and also the morphology of the P wave in III, V1, and aVL (Figure 7.7). Figure 7.5 Procedure for measuring height and width of the P wave. Figure 7.6 (A) A typical example of sympathetic overdrive. ECG of a 22‐year‐old male obtained with Holter continuous recording method during a parachute jump. (B) Drawing of the tracing that shows how the PR and ST segments form the arch of a circumference with its center located in the lower third of the R downstroke. Figure 7.7 According to loop rotation (counterclockwise in the FP and HP in the case of sinus rhythm and clockwise in the case of ectopic rhythm), the P wave morphology in III and V1 varies. Table 7.2 shows the mean and range of P wave height, duration, and PR interval in different leads. One recent study has demonstrated that the PR interval is longer in men and in older age (Magnani et al. 2010). It can be shortened due to sympathetic overdrive and prolonged in vagal predominance. The PR interval can be abnormal (shorter or longer) in different pathological situations: shorter, especially in pre‐excitation syndromes (see Figure 12.2), and in some active arrhythmias (Chapter 15), and longer in different types of AV block (see Figures 17.11 and 17.12). The PR segment is the distance between the end of P wave and QRS. It is normally isoelectric, but in sympathetic overdrive, it may be seen as downsloping (Figures 7.6 and 7.8). It may also have an abnormal configuration (upsloping, or more often, downsloping) in pericarditis or atrial infarction (Figure 7.5, see also Figures 9.33, 9.35 ,and 19.4). To measure the exact PR interval, it is best to utilize a device with at least three channels. The true PR interval is obtained by measuring from the onset of the P wave to the onset of the QRS complex in any of the three leads (see Figure 7.8). Figure 7.8 Measurement of heart rate, PR interval, and QT interval. Heart rate. The arrow is at the onset of a QRS complex. From the arrow, two cardiac cycles are measured. This distance correlates on the ruler with the heart rate, in this case 60 bpm. PR interval. The true PR interval is the distance between the first inscription of P wave and QRS complex in any lead. In this case (see solid lines), this happens in lead III but not in I and II. The QT interval represents the sum of depolarization (QRS complex) and repolarization (ST segment and T wave). Often, particularly in the presence of a flat T wave or a U wave, it is difficult to measure the QT interval properly. It is commonly accepted that this measurement should be performed using a consistent method to ensure that equivalent measurements are taken when the QT interval is studied sequentially. The most suitable method entails considering the end of repolarization at a point where the tangent line following the descendent slope of the T wave crosses the isoelectric line, as seen in Figure 7.9. This figure also shows how to measure the QT interval in special situations (see Figure 7.9). Table 7.3 shows the normal range of QT intervals for various ages and gender groups. Figure 7.9 Method for measuring QT interval. The normal QT is usually less than half the RR interval. See examples of normal QT (1), long QT (2), and short QT (3 and 4). JTp = Jpoint‐T peak. Tpe = T peak‐end. Table 7.3 QTc prolongation in different age groups, based on the Bazett formula: Values within the normal interval, borderline values, and altered values. It is necessary to correct the QT interval for heart rate (QTc). The QT is clearly long when it is greater than half the RR distance. Usually, the QTc is shorter than 440 ms (99th percentile is 470 ms for men and 480 ms for women). In clinical practice, QTc may be measured with a ruler (see Figure 7.8), and it is considered that its duration should not exceed approximately 10% of the corresponding value according to heart rate. The time of day can influence the measurement as QT is longer in the evening and at night (Bexton et al. 1986; Morganroth et al. 1991), in addition to being longer in women than in men (Molnar et al. 1996). A long QT interval may be related to an inherited heart disease (congenital long QT syndrome) (Moss and Kass 2005) (see Figure 21.10) and can be acquired in diseases such as heart failure and cardiac ischemia, in some electrolyte imbalances (especially hypokalemia), and after the intake of different drugs. It is considered that a drug should not increase the QTc by > 30 ms and that a change of 60 ms may result in torsades de pointes (TdP) and sudden cardiac death. Nevertheless, TdP rarely occurs unless the QTc exceeds 500 ms (Bayés de Luna and Baranchuk 2017). A short QT interval can be found in cases of early repolarization, digitalis effect, hypermagnesemia, acidosis, among other conditions, and, rarely, in some genetic disorders associated with sudden death (short QT syndrome). Usually, in the latter case, the QT is < 300 ms and the T wave is peaked and tall, especially in V2–V3. The study of a normal QRS complex encompasses: (i) its FP axis (ÂQRS); (ii) polarity, morphology, and voltage. This is commonly between 0° and 90°, more toward 0° in the horizontal heart and toward 90° in the vertical heart. Normal hearts do not present ÂQRS beyond −30° (at −30° the differential diagnosis with partial superoanterior hemiblock must be performed), or +110° (at > 90° the possibility of right ventricular enlargement or inferoposterior hemiblock must be excluded). The morphology of the QRS complex according to the loop–hemifield correlation (see Figures 1.5 and 1.6), and the projection of QRS on different hemifields in the FP and HP in a heart without rotations (intermediate heart) can be seen in Figures 7.10 and 7.11. Figure 7.10 Projection of the QRS loop on the FP and HP in an intermediate heart, and morphology of the 12 ECG leads, as determined by whether the loop lies in the positive or negative hemifield of the different leads. In the case of vertical or horizontal heart, we can do the same. Figure 7.11 Different QRS morphologies in the six frontal plane leads, as determined by whether the QRS loop lies in the positive or negative hemifield of each lead (see text). Figure 7.12 (A) Drawing showing the location of the J point. (B) The J point (arrow) in an ECG tracing. The ST segment is the distance between the end of the QRS (J point) and the onset of the T wave. Under normal conditions, this union is smooth and upsloping and usually short (Figure 7.12). Table 7.4 Q wave voltage in millimeters in different leads and at different ages (Adapted from Winsor 1956). Figure 7.13 Different morphologies of atypical ST segment and T wave in the absence of heart disease. (A) Vagal overdrive and early repolarization in a 25‐year‐old man. (B) Sympathetic overdrive during a crisis of paroxysmal tachycardia in a 29‐year‐old woman. (C) Straightening of ST in a healthy 45‐year‐old woman. (D) Flattened ST and symmetric T in a 75‐year‐old man without heart disease. (E) Another illustration of early repolarization. (F) A 20‐year‐old man with pectus excavatum. Normal variant of ST segment ascent (saddle morphology). (G) Straightening of ST with prolongation of QT at the expense of the ST segment in a 22‐year‐old male with hypocalcemia from renal insufficiency. (H) ST elevation even > 1 mm with mild convexity to isoelectric line that may be seen relatively often, especially in healthy young men. Table 7.5 R wave amplitudes in millimeters in different leads and at different ages* (Adapted from Winsor 1956). * Adapted from American Heart Association (1956). The reference points to measure ST segment elevation or depression are TP (or UP) intervals before and after the ST segment of interest (Figure 7.17A). If these intervals are not at the same level (isoelectric), the PR interval of the same cycle is used as a reference level—baseline line (Figure 7.17A). The level of the ECG tracing at the onset of the QRS complex is used if the PR interval has a downsloping morphology. ST segment elevation is measured from the upper part of the isoelectric reference line to the upper part of the ST segment and depression is measured from the lower part of the reference line to the lower part of the ST segment (Figure 7.17C). At times, with a normal resting ECG, an exercise ECG test is required to determine the possible existence of ischemic heart disease. The test response must be compared with the clinical data to reach a diagnosis of ischemic heart disease. An ST segment that departs from a descended J point but rapidly attains the isoelectric line (depressed, rapid‐ascent ST segment represents a physiologic response by the ST segment (QX/QT < 0.5) (Figure 7.17B). At other times with a normal basal ECG after the exercise ECG test, the depressed ST segment slowly crosses the isoelectric line or stays depressed and pulls the T wave down, both of which are abnormal responses (Figure 7.17C,D). Table 7.6 S wave amplitudes in millimeters in different leads and at different ages* (Adapted from Winsor 1956). * Adapted from American Heart Association (1956). The study of the normal T wave encompasses: (i) its frontal plane axis, (ii) polarity and morphology, and (iii) voltage. Normal values range from 0° to +70°, with the limits of normality at +80° and −40°. The ÂT situated more to the left appears in sympathetic overdrive and in obese subjects with left ÂQRS. However, even in very lean normal individuals with right ÂQRS, a negative but not deep T wave can be seen in III and aVF, and a flattened T can be seen in lead II. A widened spatial QRS/T angle measured by VCG is pathological and a marker of bad outcome (Kardys et al. 2003) (see Chapter 3). This can be synthesized from the ECG (Rautaharju et al. 2007). However, it is probable that the measurement of QRS/T angle in FP by surface ECG may have similar values (see Chapter 3). Normal T wave morphology depends on the relationship between the ventricular repolarization loop and the positive or negative hemifields of the different leads (Figure 7.18). Figure 7.18 shows the T loop and its projection on FP and HP and Table 7.7 gives the range and mean values of the normal T wave voltage in 12 leads and for different ages. Although typically the normal T wave has a slow ascent and more rapid descent (see Figure 7.12), this morphology is frequently absent in normal cases. Relatively often, especially in women and older persons with no evidence of heart disease, the T wave shows a symmetric inscription (see Figure 7.13C,D). However, this pattern may also be seen in the early phase of left ventricular hypertrophy and is consistent with suspected ischemia under some specific clinical conditions (see Chapters 13 and 20). Figure 7.14 Typical ECG of early repolarization of benign type. See the ascent of the J point and ST elevation, especially in mid/left precordial leads (see text). Figure 7.15 Drawing of ECG pattern of early repolarization seen especially in inferior leads with J point ≥ 2 mm. This corresponds to potentially malign pattern. In the frontal plane, the T wave usually follows, with some, usually small, differences, the direction of the QRS. In I, the T wave should be positive. In the vertical heart in aVL, the QRS is of low voltage and in this case, the T wave is usually negative. The T wave is also positive in II; sometimes is of low voltage or even flattened. In III, aVF, and aVL, it can be positive, flattened, or negative, according to the direction of the T loop. In aVR, it is always negative. A significant difference with ÂQRS direction is abnormal (see before). In the horizontal plane, it is usually located more forward than the QRS (compare Figures 7.10 and 7.18). Because of this, in V1, the T wave is flattened, slightly negative or slightly positive. However, a deep negative T wave in V1 is rarely seen in normal subjects and it is even rarer in V1–V2. It is more frequent in women and Black people. An absolutely positive and symmetric T wave in V1 is not common in normal individuals; if this appears, especially if it is peaked, and precordial pain is present, the possibility of acute ischemia must be ruled out (Figure 13.10). In V2, T is generally positive, but it can be flattened or even negative but usually asymmetrical, in some middle‐aged women and Black people with no apparent heart disease. In both cases, exceptionally, without any known cause, it can be negative in other precordial leads. From V3 to V6, T should be positive. The voltage of the T wave is lower and the duration is longer than that of the QRS complex because ventricular repolarization is slower than depolarization. The height of the T wave does not usually exceed 6 mm in the frontal leads or 10 mm in the left precordial leads. Occasionally, the T waves are very high (up to 16–18 mm in V2–V4, especially in vagal overdrive, while in sympathetic overdrive coinciding with tachycardia, the voltage of the T wave is usually lower. In any case, T is taller in the leads that face the ÂT. A very high T wave can be a variant of normality, but abnormalities such as hyperkalemia, subendocardial ischemia, some kinds of left ventricular enlargement, alcoholism, etc., should be excluded (Figures 13.10 and 13.15). Figure 7.16 See the diagnostic differential features of ECG patterns of (A) type II Brugada, (B) athletes, and (C) pectus excavatum (see Table 21.9). Figure 7.17 (A) Normal resting ECG. (B) A normal ECG response to exercise. Although the J point is depressed, the X point is rapidly reached so that QX/QT < 0.5. In (C) and (D) two types of abnormal response can be seen. The U wave coincides with the supernormal excitation phase in the cardiac cycle. The electrophysiological origin of the U wave is not clear, although there are some experimental studies that suggest it is caused by repolarization of the Purkinje fibers or afterpotentials (Surawicz 1998, 2008). Recently, it has been postulated (Postema et al. 2009) that an increase or decrease in U wave amplitude is modulated by either an increase or decrease of the inward rectifier repolarizing current Ik1 occurring in the terminal part of the action potential. The U wave is a small, low‐voltage wave that, when it is recorded, follows the T wave and normally has the same polarity. If not, it is always pathologic. It is best recorded in V3 and V4 and in elderly people (Figure 7.19). Hypokalemia and bradycardia cause it to be more evident. Its voltage can also increase with digitalis and quinidine administration, hypercalcemia, etc. Figure 7.18 T loop and its projection on FP and HP. Observe the corresponding morphologies determined by the projection of the T loop in the positive or negative lead hemifields. A negative U wave in the precordial leads facing the left ventricle is a highly specific sign of heart disease, appearing especially in left ventricular hypertrophy and/or related to ischemia (see Figures 10.20, 20.15, and 20.26). Characteristically, the presence of negative U waves in right precordial leads in the presence of chest pain is highly suggestive of left anterior descending coronary artery occlusion. The abnormalities of repolarization encompass not only the U wave alterations already mentioned, but especially the T wave disturbances and the abnormal deviations of the ST segment. These abnormalities may be of primary origin or secondary to changes of depolarization (Bayés de Luna 2012). These are changes of normal T wave such as T wave higher than normal or flat/negative often with prolonged QT interval. These changes are due to delayed transmembrane action potential (TAP) in some regions of the heart or some layers of the left ventricle, that appear sometimes transiently, as a result of acute subendocardial ischemia (tall and symmetric T waves) or more frequently due to transmural post‐ischemic changes (deep negative T waves in V1–V4). The symmetric and positive T wave in V1–V2 in the chronic phase of lateral MI may be a mirror pattern of post‐ischemic lateral involvement and not a sign of acute ischemia. Other causes, such as ischemic stroke, electrolyte imbalance, etc., may also explain changes in T wave polarity (Chapters 13 and 20). Primary ST deviations include the abnormal elevations and depressions of ST. They are due to changes of TAP in some regions of the heart or in some layers of the left ventricle as a consequence of acute ischemia or other causes (see changes in ST segment) (see Chapter 13). Table 7.7 T wave amplitudes in millimeters in different leads and at different ages* (Adapted from Winsor 1956). * Adapted from American Heart Association (1956). Figure 7.19 Healthy 70‐year‐old male (my father). Observe the prominent U wave in V3. Secondary changes encompass ST depression and/or asymmetric negative T wave and are due to changes in shape and duration of TAP of the ventricles secondary to conduction delays (bundle branch block) (see Chapter 11) and/or ventricular hypertrophy (strain pattern) (Bacharova et al. 2010) (see Chapters 10 and 22). Sometimes a mixed pattern (primary and secondary) may be seen (Figure 10.28C,D) (see Chapter 10).
Chapter 7
Characteristics of the Normal Electrocardiogram: Normal ECGWaves and Intervals
A systematic and sequential approach to ECG interpretation
Heart rhythm
Heart rate
P wave
Number of 0.20 s spaces
Heart rate
1
300
2
150
3
100
4
75
5
60
6
50
7
43
8
37
9
33
P wave indices (Figure 7.3)
Lead I
Lead II
Lead III
Lead V1a
P height (mV)
Mean
0.49
1.03
0.69
0.40
Range
0.2 to 1.0
0.3 to 2.0
0 to 2.0
0.05 to 0.80
P duration (s)
Mean
0.08
0.09
0.07
0.05
Range
0.05 to 0.12
0.05 to 0.12
0.02 to 0.13
0 to 0.08
PR interval (s)
Mean
0.16
0.16
0.16
Range
0.12 to 0.20
0.12 to 0.20
0.12 to 0.20
How to distinguish if an atrial wave is sinusal or ectopic (Figure 7.5)
Atrial repolarization (Figure 7.6)
PR interval and PR segment (Table 7.2; and Figures 7.1 and 7.8)
QT interval (Figure 7.8) (Malik and Camm 2004; Bayés de Luna 2019; Goldenberg et al. 2008; Anttonen et al. 2009) (see also Chapters 19, 21, and 24)
Value
1–15 years old
Adult men
Adult women
Normal
< 440 ms
< 430 ms
< 450 ms
Borderline
440–460 ms
430–450 ms
450–470 ms
Altered (prolonged)
> 460 ms
> 450 ms
> 470 ms
QRS complex
Axis of the QRS in the FP (ÂQRS)
Polarity, morphology, and voltage
ST segment and T and U waves
ST segment
Normal variants:
Limb leads
Precordial leads
Lead
Age
No. cases
Mean
Range
Lead
Age
No. cases
Mean
Range
I
24 hr
32
0.5
0.0–0.5
V1
24 hr
41
0.0
0.0–0.0
0–2 yr
72
0.7
0.0–2.0
0–2 yr
72
0.0
0.0–0.0
3–5
72
0.1
0.0–1.0
3–5
72
0.0
0.0–0.0
6–10
72
0.2
0.0–2.0
6–10
72
0.0
0.0–0.0
12–16
68
0.1
0.0–3.0
12–16
49
0.0
0.0–0.0
Adults
500
0.9
3.0–4.0
Adults
121
0.0
0.0–0.0
II
24 hr
32
1.5
0.0–5.0
V2
24 hr
41
0.0
0.0–0.0
0–2 yr
72
1.3
0.0–3.0
0–2 yr
72
0.0
0.0–0.0
3–5
72
0.3
0.0–2.0
3–5
72
0.0
0.0–0.0
6–10
72
0.5
0.0–3.0
6–10
72
0.0
0.0–0.0
12–16
68
1.2
0.0–2.5
12–16
49
0.0
0.0–0.0
Adults
500
1.1
0.0–4.0
Adults
121
0.0
0.0–0.0
III
24 hr
32
2.5
0.5–9.0
V3
24 hr
41
0.0
0.0–0.0
0–2 yr
72
1.6
0.0–4.0
0–2 yr
72
0.0
0.0–0.0
3–5
72
1.4
0.0–3.0
3–5
72
0.0
0.0–0.0
6–10
72
0.6
0.0–3.0
6–10
72
0.4
0.0–1.0
12–16
68
1.6
0.0–5.0
12–16
49
0.0
0.0–0.7
Adults
500
1.4
0.0–6.0
Adults
121
0.0
0.0–0.5
aVR
24 hr
32
2.4
0.0–4.0
V4
24 hr
41
1.3
0.0–1.5
0–2 yr
16
1.6
0.0–10.5
0–2 yr
72
0.1
0.0–1.0
2–4
16
2.9
0.0–10.0
3–5
72
0.3
0.0–2.5
5–10
53
1.4
0.0–10.0
6–10
72
0.2
0.0–1.5
11–14
15
1.0
0.0–8.0
10–15
49
0.1
0.0–2.4
Adults
151
2.0
0.0–8.0
Adults
121
0.1
0.8–1.6
aVL
24 hr
32
1.3
0.0–2.0
V5
24 hr
41
2.2
0.0–5.5
0–2 yr
16
0.1
0.0–0.5
0–2 yr
72
0.8
0.0–6.0
2–4
16
0.2
0.0–1.0
3–5
72
0.8
0.0–3.0
5–10
53
0.1
0.0–1.0
6–10
72
0.6
0.0–4.0
11–14
15
0.1
0.0–0.5
10–15
49
0.3
0.0–2.1
Adults
151
0.2
0.0–3.5
Adults
121
0.5
0.0–2.1
aVF
24 hr
32
1.8
0.0–6.0
V6
24 hr
41
1.3
0.0–2.0
0–2 yr
16
1.2
0.0–4.5
0–2 yr
72
1.1
0.0–3.0
2–4
16
1.3
0.0–4.0
3–5
72
0.7
0.0–2.5
5–10
53
0.5
0.0–3.0
6–10
72
0.4
0.0–3.0
11–14
15
0.4
0.0–2.0
10–15
49
0.5
0.0–1.7
Adults
151
0.5
0.0–3.0
Adults
121
0.4
0.8–2.7 
Limb leads
Precordial leads
Lead
Age
No. cases
Mean
Range
Lead
Age
No. cases
Mean
Range
I
24 hr
32
2.6
0.0–5.5
V1
24 hr
41
16.7
3.0–23.0
0–2 yr
72
4.2
0.0–10.0
0–2 yr
16
7.0
1.0–14.5
3–5
72
5.0
2.0–10.0
2–4
16
7.5
1.0–14.0
6–10
72
5.0
2.0–9.0
8–10
16
3.6
1.0–9.0
10–15
49
4.8
1.3–11.4
11–14
15
5.1
0.5–15.5
Adults
121
5.3
0.7–11.4
Adults
151
2.3
0.0–70
II
24 hr
32
5.5
1.0–2 1. 0
V2
24 hr
41
21.0
3.0–41.0
0–2 yr
72
5.7
0.0–14.0
0–2 yr
16
13.0
4.5–22.0
3–5
72
7.6
3.0–12.0
2–4
16
12.7
5.0–25.0
6–10
72
7.2
3.0–13.0
8–10
16
7.8
2.0–14.0
10–15
49
9.1
3.7–16.8
11–14
15
8.4
1.5–23.5
Adults
121
7.1
1.8–16.8
Adults
151
5.9
0.0–16.0
III
24 hr
32
8.8
2.0–21.0
V3
24 hr
41
20.0
14.0–26.0
0–2 yr
72
5.6
1.0–11.0
0–2 yr
16
14.0
3.0–24.0
3–5
72
5.6
2.0–10.0
2–4
16
13.4
6.0–25.0
6–10
72
4.2
0.5–13.0
6–10
16
8.4
5.0–12.5
10–15
49
6.0
0.7–15.8
11–14
15
9.2
3.0–22.0
Adults
121
3.8
0.3–13.1
Adults
151
8.9
0.5–26.0
aVR
24 hr
32
3.7
0.0–9.0
V4
24 hr
41
19.0
3.0–32.0
0–2 yr
16
1.0
0.5–4.0
0–2 yr
16
20.0
3.5–35.0
2–4
16
1.3
0.0–3.0
2–4
16
18.5
9.0–30.0
8–10
16
1.2
0.5–6.0
8–10
16
14.9
4.0–30.0
11–14
15
1.2
0.5–8.0
11–14
15
17.2
7.0–28.0
Adults
151
0.8
0.0–5.0
Adults
151
14.2
4.0–27.0
aVL
24 hr
32
2.1
1.0–6.0
V5
24 hr
41
12.0
4.5–21.0
0–2 yr
16
4.0
0.5–8.0
0–2 yr
16
16.0
2.5–25.0
2–4
16
3.1
0.5–7.0
2–4
16
18.4
10.0–26.0
8–10
16
1.2
0.5–8.8
8–10
16
17.4
6.0–28.0
11–14
15
1.6
0.5–6.0
11–14
15
16.4
6.0–29.0
Adults
151
2.1
0.0–10.0
Adults
151
12.1
4.0–26.0
aVF
24 hr
32
6.6
2.0–20.0
V6
24 hr
41
4.5
0.0–11.0
0–2 yr
16
8.8
0.5–16.0
0–2 yr
16
12.0
2.0–20.0
2–4
16
9.5
0.5–19.5
2–4
16
14.6
8.0–23.0
8–10
16
8.5
3.5–14.0
8–10
16
12.5
6.0–19.1
11–14
15
10.5
5.0–21.0
11–14
15
13.5
4.0–25.0
Adults
151
1.3
0.0–20.0
Adults
151
9.2
4.0–22.0
Measurement of the ST segment shifts
Limb leads
Precordial leads
Lead
Age
No. cases
Mean
Range
Lead
Age
No. cases
Mean
Range
I
24 hr
32
6.3
0.0–15.0
V1
24 hr
41
10.0
0.0–28.0
0–2 yr
72
3.9
0.0–7.0
0–2 yr
16
4.8
0.5–14.0
2–5
72
2.5
0.0–6.0
2–4
16
8.8
3.0–16.0
6–10
72
1.6
0.0–3.0
8–10
16
8.6
3.0–16.0
10–15
49
1.8
0.0–6.8
11–14
15
11.6
0.0–20.0
Adults
121
1.0
0.0–3.6
Adults
121
8.6
2.0–25.0
II
24 hr
32
3.2
0.0–7.0
V2
24 hr
41
22.0
1.0–42.0
0–2 yr
72
2.7
0.0–5.0
0–2 yr
16
9.3
0.5–21.0
2–5
72
1.6
0.0–4.0
2–4
16
16.0
8.5–30.0
6–10
72
1.4
0.0–3.5
8–10
16
16.8
8.0–30.0
10–15
49
1.6
0.0–4.9
11–14
15
20.8
7.0–36.0
Adults
121
1.2
0.0–4.9
Adults
151
12.7
0.0–29.0
III
24 hr
32
2.3
0.0–3.0
V3
24 hr
41
26.4
0.0–39.0
0–2 yr
72
1.1
0.0–3.5
0–2 yr
16
10.2
0.5–23.0
2–5
72
0.8
0.0–5.0
2–4
16
12.7
3.5–21.0
6–10
72
0.7
0.0–4.0
8–10
16
16.3
8.0–27.0
10–15
49
0.9
0.0–5.3
11–14
15
14.8
1.0–30.0
Adults
121
1.2
0.0–5.5
Adults
151
8.8
0.0–25.0
aVR
24 hr
32
3.9
0.0–9.5
V4
24 hr
41
23.0
0.0–42.0
0–2 yr
16
6.3
0.0–14.0
0–2 yr
16
10.2
2.0–22.0
2–4
16
5.9
0.0–14.0
2–4
16
9.0
0.0–20.0
8–10
16
4.9
0.0–10.0
8–10
16
11.2
4.0–17.0
11–14
15
8.3
0.0–17.0
11–14
15
8.0
1.0–16.0
Adults
151
4.3
0.0–13.0
Adults
151
5.2
0.0–20.0
aVL
24 hr
32
6.6
0.0–16.0
V5
24 hr
41
12.0
1.5–30.0
0–2 yr
16
3.4
0.0–7.0
0–2 yr
16
6.1
1.0–13.0
2–4
16
2.7
0.0–6.0
2–4
16
4.4
0.0–11.0
8–10
16
3.2
0.0–7.0
8–10
16
5.7
0.5–12.0
11–14
15
3.1
0.0–9.0
11–14
15
3.7
0.5–8.0
Adults
151
0.4
0.0–18.0
Adults
151
1.5
0.0–6.0
aVF
24 hr
32
3.0
0.0–7.5
V6
24 hr
41
4.5
0.0–13.0
0–2 yr
16
0.7
0.0–2.5
0–2 yr
16
2.5
0.0–7.5
2–4
16
2.1
0.0–14.0
2–4
16
1.6
0.5–5.0
8–10
16
0.7
0.0–2.0
8–10
16
1.1
0.0–4.0
11–14
15
0.8
0.0–2.5
11–14
15
0.9
0.0–2.0
Adults
151
0.2
0.0–8.0
Adults
151
0.6
0.0–7.0
T wave
Axis on the frontal plane (ÂT)
QRS/T spatial angle
Normal polarity: Morphology and voltage
U wave
Abnormalities of repolarization
Primary T wave disturbances
Primary ST deviations
Limb leads
Precordial leads
Lead
Age
No. cases
Mean
Range
Lead
Age
No. cases
Mean
Range
I
24 hr
41
0.3
2.0 to 3.0
V1
24 hr
32
1,3
−4.0 to 6.0
0–2 yr
72
2.6
0.5 to 5.0
0–2 yr
16
−2.3
−4.5 to −0.5
3–5
72
1.7
0.0 to 4.0
2–4
16
−2.2
−5.5 to −1.0
6–10
72
2.0
0.5 to 4.0
8–10
16
−1.7
−3.0 to 1.5
10–15
49
2.6
1.1 to 6.8
11–14
15
−1.3
−3.5 to 0.2
Adults
500
3.0
1.0–5.0
Adults
151
0.2
−4.0 to 4.0
II
24 hr
41
1.2
0.0 to 3.0
V2
24 hr
32
1.3
−7.5 to 9.0
0–2 yr
72
2.4
1.0 to 4.0
0–2 yr
16
−2.4
−6.0 to −0.4
3–5
72
1.8
0.5 to 4.0
2–4
16
−2.6
−7.0 to −3.0
6–10
72
2.1
0.5 to 5.0
8–10
16
0.0
−3.5 to 5.0
10–15
49
3.0
0.9 to 6.5
11–14
15
0.7
−1.5 to 3.5
Adults
500
3.8
1.0 to 6.5
Adults
151
5.5
3.0 to 18.0
III
24 hr
41
1.0
−1.0 to 3.0
V3
24 hr
32
−0.4
−7.0 to 4.0
0–2 yr
72
0.2
0.0 to 3.0
0–2 yr
16
−0.7
−5.0 to 4.5
3–5
72
0.2
0.0 to 1.5
2–4
16
−0.7
−5.0 to −5.0
6–10
72
0.1
0.0 to 1.0
8–10
16
1.8
−2.0 to 4.5
10–15
49
0.4
−1.9 to 3.1
11–14
115
1.7
0.0 to 5.0
Adults
500
0.8
−1.0 to 3.4
Adults
151
5.4
−2.0 to 16.0
aVR
24 hr
41
−0.4
−3.0 to 2.0
V4
24 hr
32
−0.6
−7.0 to 3.0
0–2 yr
16
−2.0
−3.0 to −0.5
0–2 yr
16
1.7
−2.5 to 5.0
2–4
16
−2.5
−5.0 to −1.5
2–4
16
2.4
0.0 to 11.0
8–10
16
−2.0
−3.5 to −0.2
8–10
16
3.2
0.0 to 9.0
11–14
15
−2.2
−4.0 to −1.5
11–14
15
3.3
0.0 –7.0
Adults
151
−2.3
−5.0 to 1.5
Adults
151
4.8
0.0 to 17.0
aVL
24 hr
41
0.1
−1.5 to 2.0
V5
24 hr
32
1.3
−4.0 to 5.0
0–2 yr
16
0.7
−0.5 to 2.0
0–2 yr
16
2.6
1.2 to 5.0
2–4
16
1.4
−0.5 to 3.0
2–4
16
3.4
0.0 to 7.0
8–10
16
0.7
−1.0 to 2.5
8–10
16
4.1
0.5 to 11.0
11–14
15
0.8
0.5 to 2.0
11–14
15
3.1
1.0 to 5.0
Adults
151
0.5
−4.0 to 6.0
Adults
151
3.4
0.0 to 9.0
aVF
24 hr
41
0.9
−1.0 to 3.0
V6
24 hr
32
1.2
−3.0 to 6.0
0–2 yr
16
0.6
0.8 to 3.5
0–2 yr
16
2.2
0.5 to 4.0
2–4
16
1.8
−0.2 to 4.0
2–4
16
3.2
1.5 to 5.0
8–10
16
1.4
−0.2 to 3.0
8–10
16
3.1
0.0 to 4.18
11–14
15
1.3
0.0 to 3.5
11–14
15
2.2
1.0 to 4.0
Adults
151
1.7
−0.5 to 5.0
Adults
151
2.4
−0.5 to 5.0
Secondary abnormalities of repolarization
Mixed pattern (primary and secondary)
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