Basic and Bedside Electrocardiography, 1st Edition (2009)

Chapter 2. Basic Electrocardiography

The Normal Sinus Impulse

·         The sinus node is the origin of the normal electrical impulse. Although there are other cells in the heart that can also discharge spontaneously, the sinus node has the fastest rate of discharge and is the pacemaker of the heart.

·         Normal Sinus Rhythm: Any impulse originating from the sinus node is called normal sinus rhythm. The sinus node discharges at a rate of 60 to 100 beats per minute (bpm), although the rate could vary depending on the metabolic needs of the body.

o    Sinus bradycardia: When the rate of the sinus node is <60 bpm, the rhythm is called sinus bradycardia.

o    Sinus tachycardia: When the rate is >100 bpm, the rhythm is called sinus tachycardia.

o    Sinus arrhythmia: When the sinus impulse is irregular, the rhythm is called sinus arrhythmia.

·         The electrical impulse that is generated from the sinus node spreads from the atria to the ventricles in an orderly sequence. In this manner, contraction of the atria and ventricles is closely synchronized to maximize the efficiency of the heart as a pump (Fig. 2.1).

Figure 2.1: Diagrammatic Representation of the Sinus Node and Conduction System. The sinus node is the origin of the normal electrical impulse and is the pacemaker of the heart. The sinus impulse spreads to the atria before it is propagated to the ventricles through the atrioventricular node and special conduction system.

Activation of the Atria—The P Wave

·         The Sinus Impulse: When the sinus node discharges, no deflection is recorded because the impulse from the sinus node is not strong enough to generate an electrical signal. The first deflection that is recorded after the sinus node discharges is the P wave.

·         P Wave: The P wave is the first deflection in the electrocardiogram (ECG) and is due to activation of the atria.

o    Configuration: The configuration of the normal sinus P wave is smooth and well rounded. Because the sinus node is located at the upper border of the right atrium, the sinus impulse has to travel from the right atrium to the left atrium on its way to the ventricles. The first half of the P wave therefore is due to activation of the right atrium (Fig. 2.2A). The second half is due to activation of the left atrium (Fig. 2.2B).

o    Duration: The width or duration of the normal sinus P wave measures ≤2.5 small blocks (≤0.10 seconds). This is the length of time it takes to activate both atria.

o    Amplitude: The height or amplitude of the normal sinus P wave also measures ≤2.5 small blocks (≤0.25 mV).

Figure 2.2: Atrial Activation—the P Wave. When the sinus node discharges, no electrical activity is recorded in the electrocardiogram. The first deflection is the P wave, which represents activation of the atria. The initial half of the P wave represents activation of the right atrium and the terminal half represents activation of the left atrium.

Activation of the Atrioventricular Node

·         After depolarization of the atria, the only pathway by which the sinus impulse can reach the ventricles is through the atrioventricular (AV) node and intraventricular conduction system.

·         The AV node: The AV node consists of a network of special cells that normally delay conduction of the atrial impulse to the ventricles. As the impulse traverses the AV node on its way to the ventricles, it does not generate any electrical activity in the ECG. Therefore, an isoelectric or flat line is recorded immediately after the P wave (Fig. 2.3).

Intraventricular Conduction System

After the impulse emerges from the AV node, it is conducted rapidly through the His bundle, bundle branches, and fascicles, which constitute the intraventricular conduction system, before terminating in a branching network of Purkinje fibers. The spread of the electrical impulse in the His-Purkinje system also does not cause any deflection in the ECG, similar to that of the AV node. This is represented as a continuation of the isoelectric or flat line after the P wave.

Figure 2.3: Activation of the Atrioventricular Node and His-Purkinje System. Propagation of the impulse at the atrioventricular node and His-Purkinje system will not cause any deflection in the electrocardiogram and is represented as an isoelectric or flat line after the P wave.

Activation of the Ventricles—The QRS Complex

·         QRS Complex: The QRS complex represents activation of the ventricles. The QRS complex generates the largest deflection in the ECG because the ventricles contain the largest mass of muscle cells in the heart, collectively referred to as the myocardium (Fig. 2.4).

o    The spread of the sinus impulse through the His-Purkinje system is very rapid and efficient, but is electrically silent with no impulse recorded in the ECG. The QRS complex is recorded only when the impulse has spread from the Purkinje fibers to the myocardium.

o    The myocardium can be arbitrarily divided into three layers: the endocardium, which is the inner layer, the mid-myocardium, and the epicardium, which is the outer layer of the myocardium.

o    The Purkinje fibers are located in the endocardium of both ventricles. Because the electrical impulse arrives first at the Purkinje fibers, the ventricles are activated from endocardium to epicardium in an outward direction.

o    The QRS complex corresponds to phase 0 of the action potential of all individual myocardial cells of both ventricles. Because the ventricles consist of a thick layer of myocardial cells, not all cells are depolarized at the same time. Depolarization of the whole myocardium can vary from 0.06 to 0.10 seconds or longer. This duration corresponds to the width of the QRS complex in the ECG.

Figure 2.4: Activation of the Ventricles—the QRS Complex. Activation of the ventricles is represented as a QRS complex in the electrocardiogram. Because the Purkinje fibers are located in the endocardium, the endocardium is the first to be activated. The impulse spreads from endocardium to epicardium in an outward direction. Arrows point to the direction of activation.

The QRS Complex

·         QRS Complex: The QRS complex has various waves that go up and down from baseline. These waves are identified as follows: Q, R, S, R′, and S′. If additional waves are present, R″ or S″ designations may be added. Regardless of the size of the deflections, capital and small letters are used empirically mainly for convenience, although, generally, capital letters designate large waves and small letters, small waves (Fig. 2.5).

·         Q wave: The Q wave is defined as the first wave of the QRS complex below the baseline. If only a deep Q wave is present (no R wave), the QRS complex is described as a QS complex.

·         R wave: The R wave is defined as the first positive (upward) deflection of the QRS complex. If only an R wave is present (no Q wave or S wave), the QRS complex is described as an R wave.

·         S wave: The S wave is the negative deflection after the R wave.

·         R′: The R′ (R prime) is the next positive wave after the S wave.

·         S′: The S′ (S prime) is the next negative deflection after the R′.

·         R″ or S″: These waves are rarely used, however if additional waves are needed to describe the QRS complex, the letter R″ (R double prime) is used for the next positive wave and S″ (S double prime) for the next negative wave.

·         QRS complex: The QRS complex is identified as a QRS complex regardless of the number of waves present. Thus, a tall R wave without a Q wave or S wave is still identified as a QRS complex.

Figure 2.5: QRS Nomenclature. Diagram shows how the waves are identified in the QRS complex.

The J Point, ST Segment, and T Wave

·         The QRS complex is followed by a flat line called the ST segment. The end of the QRS complex and beginning of the ST segment is called the J point. The flat ST segment is followed immediately by another positive deflection called the T wave.

o    J point: The J point, also called the J junction, marks the end of the QRS complex and beginning of the ST segment (Fig. 2.6).

o    ST segment: The ST segment starts from the J point to the beginning of the T wave. The ST segment is flat or isoelectric and corresponds to phase 2 (plateau phase) of the action potential of the ventricular myocardial cells. It represents the time when all cells have just been depolarized and the muscle cells are in a state of sustained contraction. The ventricular muscle cells are completely refractory during this period and cannot be excited by an outside stimulus.

o    T wave: The T wave represents rapid ventricular repolarization. This segment of ventricular repolarization corresponds to phase 3 of the transmembrane action potential. During phase 3, the action potential abruptly returns to its resting potential of -90 mV.

·         The J point, ST segment, and T wave represent the whole process of ventricular repolarization corresponding to phases 1, 2, and 3 of the transmembrane action potential. Repolarization returns the polarity of the myocardial cells to resting potential and prepares the ventricles for the next wave of depolarization.

Figure 2.6: Repolarization of the Ventricles. Ventricular repolarization begins immediately after depolarization and starts at the J point, which marks the end of the QRS complex, and extends to the end of the T wave. This corresponds to phases 1, 2, and 3 of the action potential. Ventricular repolarization allows the ventricles to recover completely and prepares the myocardial cells for the next wave of depolarization.

The PR Interval, QRS Complex, and QT Interval

·         The duration of the PR interval, QRS complex, and QT interval are routinely measured in the standard 12-lead ECG. These intervals are shown in Figure 2.7.

o    PR interval: The PR interval is measured from the beginning of the P wave to the beginning of the QRS complex. If the QRS complex starts with a Q wave, the PR interval is measured from the beginning of the P wave to the beginning of the Q wave (P-Q interval), but is nevertheless called PR interval. The normal PR interval measures 0.12 to 0.20 seconds in the adult. It includes the time it takes for the sinus impulse to travel from atria to ventricles. The PR interval is prolonged when there is delay in conduction of the sinus impulse to the ventricles and is shortened when there is an extra pathway connecting the atrium directly to the ventricle.

o    QRS complex: The QRS complex is measured from the beginning of the first deflection, whether it starts with a Q wave or an R wave, and extends to the end of the last deflection. The normal QRS duration varies from 0.06 to 0.10 seconds. The QRS duration is increased when there is ventricular hypertrophy, bundle branch block, or when there is premature excitation of the ventricles because of the presence of an accessory pathway.

Figure 2.7: The PR Interval, QRS Complex, and QT Interval. The PR interval is measured from the beginning of the P wave to the beginning of the QRS complex. The QRS complex is measured from the beginning of the first deflection to the end of the last deflection and the QT interval is measured from the beginning of the QRS complex to the end of the T wave.

The QT Interval

·         QT Interval: The QT interval includes the QRS complex, ST segment, and T wave corresponding to phases 0 to 3 of the action potential. It is measured from the beginning of the QRS complex to the end of the T wave. Note that the presence of a U wave is not included in the measurement. In assessing the duration of the QT interval, multiple leads should be selected and the QT interval is the longest QT that can be measured in the whole 12-lead ECG recording.

·         QTc: The QT interval is affected by heart rate. It becomes longer when the heart rate is slower and shorter when the heart rate is faster. The QT interval therefore should always be corrected for heart rate. The corrected QT interval is the QTc.

Figure 2.8: The QT Interval. The QT interval is measured from the beginning of the QRS complex to the end of the T wave. When the heart rate is >70 bpm, one can “eyeball” that the QTc is normal if the QT interval is equal to or less than half the R-R interval. When this occurs, no calculation is necessary. If the QT interval is more than half the R-R interval, the QTc may not be normal and should be calculated (see example in Fig. 2.9).

o    The simplest and most commonly used formula for correcting the QT interval for heart rate is the Bazett formula shown here.

o    The normal QTc should not exceed 0.42 seconds in men and 0.44 seconds in women. The QTc is prolonged when it measures >0.44 seconds in men and >0.46 seconds in women and children.

o    An easy rule to remember in calculating the QTc when the heart rate is >70 bpm is that the QTc is normal (<0.46 seconds) if the QT interval is equal to or less than half the R-R interval (Fig. 2.8).

Figure 2.9: Calculating the QTc. If a calculator is not available, the QTc can be calculated by using Table 2.1. The preceding R-R interval is measured because the QT interval is dependent on the previous R-R interval. In this figure, the QT interval (10 small blocks) is more than half the preceding R-R interval (14 small blocks), thus the QTc may not be normal and should be calculated as shown in the text. The right panel is a reminder that the QT interval is equivalent to the total duration of the action potential (phases 0 to 3).

·         Calculating the QTc: Table 2.1 is useful in calculating the QTc when a calculator is not available. In the example in Figure 2.9, the short technique of visually inspecting the QT interval can be used because the heart rate is >70 bpm. The QT interval (10 small blocks) is more than half the preceding R-R interval (14 small blocks). Thus, the QTc may not be normal and needs to be calculated.

o    First: Measure the QT interval: The QT interval measures 10 small blocks. This is equivalent to 0.40 seconds (Table 2.1, column 1, QT interval in small block).

o    Second: Measure the R-R interval: The R-R interval measures 14 small blocks, which is equivalent to 0.56 seconds. The square root of 0.56 seconds is 0.75 seconds (seeTable 2.1).

o    Finally: Calculate the QTc: Using the Bazett formula as shown below: QTc = 0.40 ÷ 4 0.75 = 0.53 seconds. The QTc is prolonged.

·         Rapid calculation of the QTc using the Bazett formula is shown below.

·         The Normal U Wave: The end of the T wave completes the normal cardiac cycle, which includes the P wave, the QRS complex, and the T wave. The T wave, however, may often be followed by a small positive deflection called the U wave. The U wave is not always present, but it may be the last complex in the ECG to be recorded (Fig. 2.10).

o    The size of the normal U wave is small, measuring approximately one-tenth of the size of the T wave.

o    U waves are best recorded in the anterior precordial leads V2 and V3 because these chest leads are closest to the ventricular myocardium.

o    U waves are usually visible when the heart rate is slow (<65 bpm) and rarely visible with faster heart rates (>95 bpm).

Table 2.1 Calculating the QTc

 QT Interval

       

QT (Small Blocks)

QT (sec)

R-R Interval (Small Blocks)

Heart Rate (Beats per Minute)

R-R Interval (sec)

Square Root of R-R Interval (sec)

45

1.80

45

33

1.80

1.34

44

1.76

44

34

1.76

1.33

43

1.72

43

35

1.72

1.31

42

1.68

42

36

1.68

1.30

41

1.64

41

37

1.64

1.28

40

1.60

40

38

1.60

1.26

39

1.56

39

39

1.56

1.25

38

1.52

38

39

1.52

1.23

37

1.48

37

41

1.48

1.22

36

1.44

36

42

1.44

1.20

35

1.40

35

43

1.40

1.18

34

1.36

34

44

1.36

1.17

33

1.32

33

45

1.32

1.15

32

1.28

32

47

1.28

1.13

31

1.24

31

48

1.24

1.11

30

1.20

30

50

1.20

1.10

29

1.16

29

52

1.16

1.08

28

1.12

28

54

1.12

1.06

27

1.08

27

56

1.08

1.04

26

1.04

26

58

1.04

1.02

25

1.00

25

60

1.00

1.00

24

0.96

24

63

0.96

0.98

23

0.92

23

65

0.92

0.96

22

0.88

22

68

0.88

0.94

21

0.84

21

71

0.84

0.92

20

0.80

20

75

0.80

0.89

19

0.76

19

79

0.76

0.87

18

0.75

18

83

0.75

0.87

17

0.68

17

88

0.68

0.82

16

0.64

16

94

0.64

0.80

15

0.60

15

100

0.60

0.77

14

0.56

14

107

0.56

0.75

13

0.52

13

115

0.52

0.72

12

0.48

12

125

0.48

0.69

11

0.44

11

136

0.44

0.66

10

0.40

10

150

0.40

0.63

9

0.36

9

167

0.36

0.60

8

0.32

8

188

0.32

0.57

7

0.28

7

214

0.28

0.53

 Column 2 converts the measured QT interval to seconds; the last column converts the measured R-R interval to its square  root.

o     

·   

·   

·  A normal U wave is upright in all leads except aVR because the axis of the U wave follows that of the T wave.

·  The origin of the normal U wave is uncertain, although it is believed to be due to repolarization of the His-Purkinje system.

·         Abnormal U Wave: U waves are often seen in normal individuals, but can be abnormal when they are inverted or when they equal or exceed the size of the T wave. This occurs in the setting of hypokalemia.

·         T-Q Segment: The T-Q segment is measured from the end of the T wave of the previous complex to the Q wave of the next QRS complex. It represents electrical diastole corresponding to phase 4 of the action potential.

Figure 2.10: The U Wave and T-Q Segment. The U wave is the last deflection in the electrocardiogram and is best recorded in leads V2and V3 because of the close proximity of these leads to the ventricular myocardium. The cause of the U wave is most likely the repolarization of the His-Purkinje system. U waves are abnormal when they are inverted or become unduly prominent, as may be seen in the setting of hypokalemia. The T-Q segment corresponds to phase 4 of the action potential. It marks the end of the previous action potential and the beginning of the next potential.

Summary of ECG Deflections

See Figure 2.11.

·         P wave: The P wave represents activation of the atria.

·         PR interval: The PR interval starts from the beginning of the P wave to the beginning of the QRS complex and represents the time required for the sinus impulse to travel from the atria to the ventricles.

·         PR segment: The PR segment starts at the end of the P wave to the beginning of the QRS complex and corresponds to the time it takes for the impulse to travel from AV node to ventricles.

·         QRS complex: This represents activation of all the muscle cells in the ventricles and corresponds to phase 0 of the action potential.

·         J point: The J point marks the end of the QRS complex and beginning of the ST segment. It corresponds to phase 1 of the action potential.

·         ST segment: The ST segment is the isoelectric portion between the J point and the beginning of the T wave. It corresponds to phase 2 (plateau) of the action potential.

·         T wave: The T wave represents rapid repolarization of the ventricles and corresponds to phase 3 of the action potential.

·         QT: The QT interval is measured from the beginning of the QRS complex to the end of the T wave and corresponds to electrical systole.

·         TQ: The TQ segment starts from the end of the T wave to the beginning of the next QRS complex. This represents phase 4 of the action potential and corresponds to electrical diastole.

·         U wave: The U wave, if present, is the last positive deflection in the ECG. It is likely due to repolarization of the His-Purkinje system.

Figure 2.11: Summary of the Electrocardiogram Waves, Intervals, and Segments.

Abnormal Waves in the ECG

·         There are other waves in the ECG that have been described. These waves are not normally present but should be recognized because they are pathologic and diagnostic of a clinical entity when present.

o    Delta wave: The delta wave is a slow and slurred upstroke of the initial portion of the QRS complex and is usually seen in conjunction with a short PR interval (Fig. 2.12A). Its presence is diagnostic of the Wolff-Parkinson-White syndrome. Delta waves are caused by an accessory pathway that connects the atrium directly to the ventricles across the atrioventricular groove resulting in pre-excitation of the ventricles (see Chapter 20, Wolff-Parkinson-White Syndrome).

o    Osborn wave: The Osborn wave, also called a J wave, is a markedly exaggerated elevation of the J point that results in an H shape configuration of the QRS complex. The presence of the Osborn wave is associated with hypothermia or hypercalcemia (Fig. 2.12B).

o    Epsilon wave: The epsilon wave is an extra notch at the end of the QRS or early portion of the ST segment most commonly seen in V1 to V3. This extra notch represents delayed activation of the outflow tract of the right ventricle and is diagnostic of arrhythmogenic right ventricular dysplasia, also called arrhythmogenic right ventricular cardiomyopathy (Fig. 2.12C). Arrhythmogenic right ventricular dysplasia is an inherited form of cardiomyopathy characterized by the presence of fibrofatty infiltrates within the myocardium of the right ventricle that can result in ventricular arrhythmias. It is a common cause of sudden cardiac death in young individuals.

Figure 2.12: Abnormal Waves in the electrocardiogram. (A) Delta waves characterized by slowly rising upstroke of the QRS complex from preexcitation (Wolff-Parkinson-White syndrome). (B) Osborn waves, which resemble an “h” because of hypothermia and hypercalcemia. (C) Epsilon waves seen as extra notch after the QRS in V1, V2, or V3 diagnostic of arrhythmogenic right ventricular dysplasia.

Figure 2.13: The Transmembrane Action Potential and the Surface Electrocardiogram. Transmembrane action potential of a ventricular myocardial cell (A) and the corresponding surface electrocardiogram (B). Phase 0 of the action potential is equivalent to the QRS complex, phase 1 the J point, phase 2 the ST segment, phase 3 the T wave, and phase 4 the TQ segment. Note that repolarization and depolarization of the myocardium occur during systole, which corresponds to the QT interval. Diastole, which is phase 4, the rest period, corresponds to the TQ interval.

Transmembrane Action Potential and the Surface ECG

·         The diagram (Fig. 2.13) shows the relationship between the action potential of a single ventricular myocardial cell and the surface ECG. A complete cardiac cycle can be divided into two phases: systole and diastole.

o    Systole: Systole corresponds to the QT interval and includes:

§  Depolarization: Depolarization is phase 0 of the action potential. This is equivalent to the QRS complex in the ECG.

§  Repolarization: Repolarization includes phases 1, 2, and 3, which correspond to the J point, ST segment, and T wave in the ECG.

o    Diastole: Diastole occurs during phase 4, or the resting period of the cell. This corresponds to the TQ segment in the ECG.

Figure 2.14: Electrical and Mechanical Systole and Diastole. The electrocardiogram (ECG), left ventricular, left atrial, and aortic root pressure tracings are shown. Electrical systole corresponds to the QT interval in the ECG. Mechanical systole starts from S1 (first heart sound) because of closure of the mitral (M1) and tricuspid (T1) valves, and extends to S2 (second heart sound) because of closure of the aortic (A2) and pulmonic (P2) valves. There is a slight electromechanical delay from the onset of the QRS complex to the onset of S1. Electrical diastole is equivalent to the TQ segment in the ECG. This is equivalent to mechanical diastole, which starts from S2 and extends to S1.

Timing of Systole and Diastole

Figure 2.15: Normal Electrocardiogram. The rhythm is normal sinus with a rate of 62 beats per minute.

·         It is important to recognize that the ECG represents electrical events and that a time lag occurs before mechanical contraction and relaxation.

o    Systole: In the ECG, electrical systole starts with the QRS complex and ends with the T wave corresponding to the QT interval. At bedside, mechanical systole begins with the first heart sound or S1 and ends with the second sound or S2 (Fig. 2.14).

o    Diastole: In the ECG, diastole starts at the end of the T wave to the next Q wave (TQ). At bedside, diastole extends from S2 to S1.

The 12-Lead ECG

Figure 2.16: Prominent U Waves. Twelve-lead electrocardiogram showing U waves in almost all leads. U waves are usually seen when the heart rate is slow and are most prominent in the anterior precordial leads because these leads are closest to the ventricles. The U waves are marked by the arrows.

Shown here are examples of complete 12-lead ECGs. A continuous lead II rhythm strip is recorded at the bottom of each tracing. The first ECG (Fig. 2.15) is a normal ECG. The second ECG (Fig. 2.16) shows prominent U waves in an otherwise normal ECG.

The Normal Electrocardiogram

The ECG Deflections

·         The P wave represents activation of the atria.

·         The QRS complex represents activation of the ventricles.

·         The T wave represents rapid repolarization of the ventricles.

·         U wave represents repolarization of the His-Purkinje system.

Segments and Intervals

·         PR interval represents the time it takes for the sinus impulse to travel from the atria to the ventricles.

·         QT interval represents electrical systole and extends from the onset of the QRS complex to end of the T wave.

·         The J point marks the end of the QRS complex and beginning of the ST segment.

·         JT interval is the QT interval without the QRS complex.

·         The ST segment begins immediately after the QRS complex and extends to the onset of the T wave.

·         TQ interval represents electrical diastole and extends from the end of the T wave to the beginning of the next QRS complex.

The ECG Deflections, Segments, and Intervals and their Clinical Implications

·         The P wave: The sinus node does not leave any imprint when it discharges. The P wave is the first deflection in the ECG and indicates that the sinus impulse has spread to the atria. The P wave therefore represents activation of the atria and is the only ECG evidence that the sinus node has discharged.

·         The sinus P wave

o    Because the sinus impulse is not represented in the ECG when the sinus node discharges, the configuration of the P wave is the main criterion in identifying that the impulse is sinus or non-sinus in origin. The sinus node is located at the right upper border of the right atrium close to the entrance of the superior vena cava. Because of its anatomic location, the sinus impulse has to travel from right atrium to left atrium in a leftward and downward (inferior) direction. This is represented in the ECG as an upright P wave in leads I, II, and aVF, as well as in V3 to V6. Lead II usually records the most upright P wave deflection and is the most important lead in recognizing that the rhythm is normal sinus. If the P wave is inverted in lead II, the impulse is unlikely to be of sinus node origin.

o    The sinus impulse follows the same pathway every time it activates the atria; thus, every sinus impulse has the same P wave configuration.

o    The P wave duration should not exceed 2.5 small blocks (≤0.10 seconds or 100 milliseconds). The height of the P wave also should not exceed 2.5 small blocks (≤2.5 mm) and is measured vertically from the top of the baseline to the top of the P wave. The duration of the P wave represents activation of the left and right atria. According to the American College of Cardiology/American Heart Association/Heart Rhythm Society, the P wave duration should be measured in at least three leads that are recorded simultaneously—preferably leads I, II, and V1—from the beginning of the P wave to the end of the P wave. The P wave is abnormal when there is increased amplitude or duration, when the shape of the wave is peaked, notched, or bifid, or when it is inverted or absent in lead II.

§  Increased duration of the P wave: A prolonged P wave suggests enlargement of the left atrium or intraatrial block.

§  Increased amplitude of the P wave: Increased P wave amplitude suggests enlargement of the right atrium.

o    Activation of the atria is immediately followed by atrial contraction. The mechanical contraction of the atria is not audible. However, when the ventricles are stiff or noncompliant, as occurs when there is left ventricular hypertrophy, a fourth heart sound (S4) may be audible because of vibrations caused by blood hitting the ventricular walls during atrial contraction. A fourth heart sound may not be present when there are no P waves; for instance, when the rhythm is junctional or when there is atrial fibrillation.

o    Ta wave: The P wave may be followed by a repolarization wave called the Ta wave. The Ta wave is the T wave of the P wave. The Ta wave is small and is usually not visible because it becomes obscured by the coinciding QRS complex. The direction of the Ta wave in the ECG is opposite that of the P wave. Thus, when the P wave is upright, the Ta wave is inverted.

·         The PR interval: The PR interval represents the time required for the sinus impulse to reach the ventricles. It includes the time it takes for the sinus impulse to travel through the atria, AV node, bundle of His, bundle branches, fascicles of the left bundle branch, and the Purkinje network of fibers until the ventricles are activated.

o    The normal PR interval measures 0.12 to 0.20 seconds in the adult. The PR interval is measured from the beginning of the P wave to the beginning of the QRS complex. The longest as well as the shortest PR interval in the 12-lead ECG tracing should be measured so that delay in the conduction of the sinus impulse to the ventricles and premature excitation of the ventricles are not overlooked.

§  Prolonged PR interval: The PR interval is prolonged when it measures >0.20 seconds (200 milliseconds). This delay in the conduction of the sinus impulse from atria to ventricles is usually at the level of the AV node. The whole 12-lead ECG is measured for the longest PR interval preferably leads I, II, and V1.

§  Short PR interval: The PR interval is short when conduction of the impulse from atria to ventricles is shorter than normal (<0.12 seconds or 120 milliseconds). This usually occurs when an accessory pathway or bypass tract is present connecting the atrium directly to the ventricle or when conduction of the impulse across the AV node is enhanced because of a small AV node or from pharmacologic agents that speed AV nodal conduction. This will also occur when there is an ectopic impulse, meaning that the P wave originates from the atria or AV junction and not from the sinus node.

·         PR segment: The PR segment is the isoelectric or flat line between the P wave and the QRS complex and is measured from the end of the P wave to the beginning of the QRS complex. It represents the spread of the impulse at the AV node and His-Purkinje system, with most of the delay occurring at the level of the AV node. This delay is important so that atrial and ventricular contraction is coordinated and does not occur simultaneously. Because the PR segment is isoelectric, it is used as baseline for measuring the various deflections in the ECG.

·         QRS complex: The QRS complex is the next deflection after the P wave. It represents activation of both ventricles. It is the largest complex in the ECG because the ventricles contain the largest mass of working myocardium in the heart. This is in contrast to the thinner muscles in the atria, which corresponds to a smaller P wave. The first portion of the ventricle to be activated is the middle third of the ventricular septum because the left bundle branch is shorter than the right bundle branch.

o    Waves of the QRS complex: The QRS complex consists of the following waves or deflections: Q, R, S, R′, S′, R″, and S″. The use of capital and small letters in identifying the waves of the QRS complex is arbitrary.

o    Duration of the QRS complex: The QRS complex is measured from the beginning of the first deflection, which may be a Q wave or R wave, to the end of the last deflection. The width or duration of the QRS complex normally varies from 0.06 to 0.10 seconds in the adult but may be less in infants and children. The QRS complex corresponds to phase 0 of the transmembrane action potential of a single muscle cell. Because there are millions of muscle cells in the ventricles that are activated, the total duration of the QRS complex will depend on how efficiently the whole ventricle is depolarized. Thus, when there is increased muscle mass due to hypertrophy of the left ventricle or when there is delay in the spread of the electrical impulse because of bundle branch block or the impulse originates directly from the ventricles or from a ventricular pacemaker, the duration of the QRS complex becomes prolonged.

o    Amplitude: The height of the QRS complex in the limb leads should measure ≥5 mm in at least one lead. This includes the total amplitude above and below the baseline. In the chest lead, it should measure ≥10 mm in at least one lead.

§  Low voltage: Low voltage is present when the tallest QRS complex in any limb lead is <5 mm or the tallest complex in any chest lead is <10 mm. Low voltage may be confined only to the limb leads or only to the chest leads or it may be generalized involving both limb and chest leads. Low voltage can occur when transmission of the cardiac impulse to the recording electrode is diminished because of peripheral edema, ascites, anasarca, chronic obstructive pulmonary disease (especially emphysema), obesity, pericardial, or pleural effusion. Low voltage can also occur if the recording electrode is distant from the origin of the impulse.

§  Increased voltage: The voltage of the QRS complex may be increased when there is hypertrophy of the ventricles. It may be a normal finding in young adults.

o    Electrical versus mechanical systole: The onset of the QRS complex marks the beginning of electrical systole, which is hemodynamically silent. After the ventricles are depolarized, there is a brief delay before the ventricles contract causing both mitral and tricuspid valves to close during systole. Closure of both mitral and tricuspid valves is audible as the first heart sound (S1), which marks the beginning of mechanical systole.

·         QT interval: The QT interval is measured from the beginning of the QRS complex to the end of the T wave. The American College of Cardiology/American Heart Association/Heart Rhythm Society recommend that the QT interval should be measured using at least three different leads and should be the longest QT interval that can be measured in the 12-lead ECG.

o    The QT interval is measured from the earliest onset of the QRS complex to the latest termination of the T wave.

o    The duration of the QT interval is affected by heart rate. Thus, the QT interval corrected for heart rate is the QTc. The QTc is calculated using the Bazett formula: QTc (in seconds) = QT interval (in seconds) ÷ square root of the preceding R-R interval (in seconds).

o    The normal QTc is longer in women than in men. The QTc interval should not exceed 0.44 seconds (440 milli seconds) in women and 0.42 seconds (420 milliseconds) in men. A prolonged QT interval is defined as a Tc >0.44 seconds (440 milliseconds) in men and >0.46 seconds (460 milliseconds) in women and children. If bundle branch block or intraventricular conduction defect of >0.12 seconds is present, the QTc is prolonged if it measures >0.50 seconds (500 milliseconds).

o    A prolonged QTc interval can be acquired or inherited. It predisposes to the occurrence of a ventricular arrhythmia called torsades de pointes. A prolonged QTc, either acquired or inherited, should always be identified because this subtle abnormality can be lethal.

o    The difference between the longest and shortest QT interval, when the QT intervals are measured in all leads in a 12-lead ECG, is called QT dispersion. Wide QT dispersion of >100 milliseconds predicts a patient who is prone to ventricular arrhythmias.

·         J Point: The end of the QRS complex and the beginning of the ST segment is called the J point. The J point marks the end of depolarization and the beginning of repolarization of the transmembrane action potential.

o    J point elevation: J point elevation is frequently seen in normal patients and can be attributed to the difference in repolarization between the endocardial and epicardial cells. The ventricular epicardium exhibits a spike and dome configuration during phases 1 and 2 of the action potential that is not present in the endocardium. This difference in potential during early repolarization causes current to flow between the endocardium and epicardium. This current is recorded as elevation of the J point in the surface ECG. The difference in repolarization becomes even more pronounced in the setting of hypothermia or hypercalcemia. When the J point becomes very prominent, it is often called a J wave or Osborn wave.

·         ST segment: The ST segment is the interval between the end of the QRS complex and the beginning of the T wave. This corresponds to the plateau (phase 2) of the transmembrane action potential. During phase 2, the transmembrane potential of the ventricular myocardial cells remains constant at 0 mV for a relatively long period. Thus, the ST segment remains isoelectric and at the same baseline level as the PR and TP segments. An ST segment is considered abnormal when it deviates above or below this baseline by 1 mm. The ST segment is also abnormal when there is a change in its morphology such as when it becomes concave or convex or has an upsloping or downsloping configuration. Contraction of the ventricular myocardium is sustained due to entry of calcium into the cell, which triggers the release of more calcium from intracellular storage sites, namely the sarcoplasmic reticulum. During this period, the ventricles are absolutely refractory to any stimuli.

o    ST elevation in normal individuals: Elevation of the ST segment is often seen in normal healthy individuals especially in men. In one study, 91% of 6014 normal healthy men in the US Air Force aged 16 to 58 had 1 to 3 mm of ST segment elevation. ST elevation therefore is an expected normal finding in men.

§  The ST elevation in normal healthy males is commonly seen in a younger age group especially among African American men. The prevalence declines gradually with age. In one study, ST elevation of at least 1 mm was present in 93% of men aged 17 to 24 years, but in only 30% by age 76 years. In contrast, women less commonly demonstrate ST elevation, and its presence is not age related. In the same study, approximately 20% of women had ST elevation of at least 1 mm and there was no age predilection.

§  ST segment elevation in normal healthy individuals was most often seen in precordial leads V1 to V4 and was most marked in V2. The morphology of the normal ST elevation is concave.

§  The ST segment elevation in men is much more pronounced than that noted in women with most of the men having ST elevation of ≥1 mm. Most women have ST elevation measuring <1 mm. Thus, ST elevation of <1 mm has been designated as a female pattern and ST elevation of at least 1 mm associated with a sharp take-off of the ST segment of at least 208 from baseline, has been designated as a male pattern. The pattern is indeterminate if ST elevation of at least 1 mm is present but the takeoff of the ST segment from baseline is <20°. The male and female patterns can be visually recognized without making any measurements in most normal ECGs.

§  Another pattern of ST segment elevation seen in normal healthy individuals is one associated with early repolarization. This type of ST elevation is often accompanied by a J wave at the terminal end of the QRS complex. The ST elevation is most frequently seen in V4 and is frequently accompanied by tall and peaked T waves (see Chapter 23, Acute Coronary Syndrome: ST Elevation Myocardial Infarction).

§  Another ST elevation considered normal variant is the presence of ST elevation accompanied by inversion of the T wave in precordial leads V3 to V5.

o    Abnormal ST elevation: Abnormal causes of ST elevation include acute myocardial infarction, coronary vasospasm, acute pericarditis, ventricular aneurysm, left ventricular hypertrophy, hyperkalemia, left bundle branch block, and the Brugada syndrome. This is further discussed in Chapter 23, Acute Coronary Syndrome: ST Elevation Myocardial Infarction.

·         T wave: The T wave corresponds to phase 3 of the transmembrane action potential and represents rapid repolarization. The different layers of the myocardium exhibit different repolarization characteristics.

o    Repolarization of the myocardium normally starts from epicardium to endocardium because the action potential duration of epicardial cells is shorter than the other cells in the myocardium. Thus, the onset of the T wave represents the beginning of repolarization of the epicardium and the top of the T wave corresponds to the complete repolarization of the epicardium.

o    Repolarization of the endocardium takes longer than repolarization of the epicardium. Therefore, the repolarization of the endocardium is completed slightly later at the downslope of the T wave.

o    In addition to the endocardial and epicardial cells, there is also a population of M cells constituting 30% to 40% of the mid-myocardium. The M cells have different electrophysiologic properties with repolarization taking even longer than that seen in epicardial and endocardial cells. M cell repolarization consequently corresponds to the end of the T wave.

o    The duration and amplitude of the T wave is variable, although, generally, the direction (axis) of the T wave in the 12-lead ECG follows the direction of the QRS complex. Thus, when the R wave is tall, the T wave is upright, and when the R wave is smaller than the size of the S wave, the T wave is inverted.

o    The shape of the normal T wave is rounded and smooth and slightly asymmetric with the upstroke inscribed slowly and the downslope more steeply. The T wave is considered abnormal if the shape becomes peaked, notched, or distorted or if the amplitude is increased to more than 5 mm in the limb leads and >10 mm in the precordial leads. It is also abnormal when the T wave becomes symmetrical or inverted. This is further discussed in Chapter 24 (Acute Coronary Syndrome: Non-ST Elevation Myocardial Infarction and Unstable Angina).

o    At bedside, the end of the T wave coincides with the closure of the aortic and pulmonic valves. This is audible as S2 during auscultation. The aortic second heart sound therefore can be used for timing purposes to identify the end of left ventricular systole and beginning of diastole. Any event before the onset of S2 is systolic and any event occurring after S2 (but before the next S1) is diastolic.

·         TQ interval: The TQ interval is measured from the end of the T wave to the onset of the next QRS complex. It corresponds to phase 4 of the transmembrane action potential. The T-P or TQ segment is used as the isoelectric baseline for measuring deviations of the J point or ST segment (elevation or depression) because the transmembrane action potential is at baseline and there is no ongoing electrical activity at this time. Thus, the TQ segment is not affected by other waves. However, if there is sinus tachycardia and the PR interval is markedly prolonged and the P wave is inscribed at the end of the T wave, then the long PR segment is used as an alternate baseline for measuring deviations of the J point or ST segment.

o    T-P segment: The T-P segment is a subportion of the TQ interval, which represents the interval between the end of ventricular repolarization (end of T wave) and the onset of the next sinus impulse (P wave). It marks the end of the previous cycle and the start of the next cardiac cycle beginning with the sinus impulse. This segment usually serves as baseline for measuring deviations of the J point or ST segment.

·         At bedside, diastole starts with the closure of the aortic and pulmonic valves (audible as the second heart sound S2) and continues until the closure of the mitral and tricuspid valves (audible as the first heart sound S1). This closely corresponds to the TQ interval in the ECG.

·         The U wave: Although a U wave may be seen as another deflection after the T wave, this is not consistently present. U waves are commonly visible when the heart rate is slow (usually <65 bpm) and are rarely recorded with heart rates above 95 bpm. U waves are best recorded in the anterior precordial leads due to the proximity of these leads to the ventricular myocardium. Repolarization of the His-Purkinje system coincides with the inscription of the U wave in the ECG and is more delayed than the repolarization of the M cells. The U wave therefore is most probably because of repolarization of the His-Purkinje system.

o    The U wave follows the direction of the T wave and QRS complex. Thus, the U wave is upright when the T wave is upright. When the U wave is inverted or prominent, it is considered pathologic.

o    An abnormal U wave indicates the presence of myocardial disease or electrolyte abnormality. Prominent U waves may be due to hypokalemia or drugs such as quinidine. Inversion of the U wave is always pathologic and is most commonly due to myocardial ischemia, hypertension, or valvular regurgitation. Its presence may be transient or it may be more persistent.

·         Abnormal waves: The delta wave, epsilon wave, and Osborn wave are other waves in the ECG that should be recognized because these waves are pathologic. J. Willis Hurst traced the historical origin of these waves as follows:

o    Delta wave: The slow, slurred upstroke of the QRS complex, associated with the Wolff-Parkinson-White syndrome, is due to premature excitation of the ventricle because of the presence of an accessory pathway connecting the atrium directly to the ventricle. This early deflection of the QRS complex is called the delta wave because it resembles the shape of a triangle (Δ) which is the symbol of the Greek capital letter delta. (Note that the slow slurred upslope of the initial QRS complex resembles the left side of the triangle.)

o    Epsilon wave: The epsilon wave is associated with right ventricular dysplasia and represents late activation of the right ventricular free wall. This is represented as a small deflection at the end of the QRS complex and is best recorded in leads V1 to V3. Epsilon comes next to the Greek letter delta. The delta wave occurs at the beginning of the QRS complex (because of early activation of the ventricle and is a preexcitation wave), whereas the epsilon wave occurs at the end of the QRS complex (because of late activation of the free wall of the right ventricle and is a postexcitation wave).

o    Osborn wave: When the J point is exaggerated, it is called J wave. The wave is named after Osborn, who described the association of this wave to hypothermia.

Suggested Readings

Antzelevitch C. The M Cell. J Cardiovasc Pharmacol Ther. 1997;2:73-76.

Ariyarajah V, Frisella ME, Spodick DH. Reevaluation of the criterion for interatrial block. Am J Cardiol. 2006;98:936-937.

Buxton AE, Calkins H, Callans DJ, et al. ACC/AHA/HRS 2006 key data elements and definitions for electrophysiology studies and procedures: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Data Standards (ACC/AHA/HRS Writing Committee to Develop Data Standards on Electrophysiology). J Am Coll Cardiol.2006;48:2360-2396.

Correale E, Battista R, Ricciardiello V, et al. The negative U wave: a pathogenetic enigma but a useful often overlooked bedside diagnostic and prognostic clue in ischemic heart disease.Clin Cardiol. 2004;27:674-677.

Dunn MI, Lipman BS. Basic physiologic principles. In: Lipman-Massie Clinical Electrocardiography. 8th ed. Chicago: Yearbook Medical Publishers, Inc; 1989:24-50.

Hurst JW. Naming of the waves in the ECG, with a brief account of their genesis. Circulation. 1998;98:1937-1942.

Marriott HJL. Complexes and intervals. In: Practical Electrocardiography. 5th ed. Baltimore: Williams and Wilkins; 1972: 16-33.

Moss AJ. Long QT syndrome. JAMA. 2003;289:2041-2044.

Phoon CKL. Mathematic validation of a shorthand rule for calculating QTc. Am J Cardiol. 1998;82:400-402.

Sgarbossa EB, Wagner GS. Electrocardiography. In: Textbook of Cardiovascular Medicine. 2nd ed. Editor is Topol EJ Philadelphia: Lippincott-Williams and Wilkins; 2002:1330-1383.

Surawicz B. U waves: facts, hypothesis, misconceptions and misnomers. J Cardiovasc Electrophysiol. 1998;9:1117-1128.

Surawicz B, Parikh SR. Prevalence of male and female patterns of early ventricular repolarization in the normal ECG of males and females from childhood to old age. J Am Coll Cardiol. 2002;40:1870-1876.

Yan GX, Antzelevitch C. Cellular basis for the normal T wave and the electrocardiographic manifestations of the long-QT syndrome. Circulation. 1998;98:1928-1936.

Yan GX, Lankipalli RS, Burke JF, et al. Ventricular repolarization components of the electrocardiogram, cellular basis and clinical significance. J Am Coll Cardiol. 2003;42:401-409.

Yan GX, Shimizu W, Antzelevitch C. Characteristics and distribution of M cells in arterially perfused canine left ventricular wedge preparations. Circulation. 1998;98:1921-1927.