Clinical Electrocardiography: A Simplified Approach, 7th Edition (2006)


Chapter 2. Basic ECG Waves


In Chapter 1 , the general term electrical stimulation was applied to the spread of electrical stimuli through the atria and ventricles. The technical term for this cardiac electrical stimulation or activation isdepolarization. The return of heart muscle cells to their resting state after stimulation (depolarization) is called repolarization. These terms are derived from the fact that normal “resting” myocardial cells (atrial and ventricular cells) are polarized; that is, they carry electrical charges on their surface. Figure 2-1 A shows the resting polarized state of a normal atrial or ventricular heart muscle cell. Notice that the outside of the resting cell is positive and the inside is negative (about -90 mV [millivolts]).[*]

FIGURE 2-1  Depolarization and repolarization. A, The resting heart muscle cell is polarized; that is, it carries an electrical charge, with the outside of the cell positively charged and the inside negatively charged. B, When the cell is stimulated (S), it begins to depolarize (stippled area). C, The fully depolarized cell is positively charged on the inside and negatively charged on the outside. D, Repolarization occurs when the stimulated cell returns to the resting state. The direction of depolarization and repolarization is represented by arrows.Depolarization (stimulation) of the atria produces the P wave on the ECG, whereas depolarization of the ventricles produces the QRS complex. Repolarization of the ventricles produces the ST-T complex.

When a heart muscle cell is stimulated, it depolarizes. As a result, the outside of the cell, in the area where the stimulation has occurred, becomes negative and the inside of the cell becomes positive. This produces a difference in electrical voltage on the outside surface of the cell between the stimulated depolarized area and the unstimulated polarized area ( Fig. 2-1 B). Consequently, a small electrical current forms and spreads along the length of the cell as stimulation and depolarization occur, until the entire cell is depolarized ( Fig. 2-1 C). The path of depolarization can be represented by an arrow, as shown in Figure 2-1 B. For individual myocardial cells (fibers), depolarization and repolarization proceed in the same direction. For the entire myocardium, however, depolarization proceeds from the innermost layer (endocardium) to the outermost layer (epicardium), whereas repolarization proceeds in the opposite direction. The mechanism of this difference is not fully understood.

The depolarizing electrical current is recorded by the ECG as a P wave (when the atria are stimulated and depolarize) and as a QRS complex (when the ventricles are stimulated and depolarize).

After a time, the fully stimulated and depolarized cell begins to return to the resting state. This is known as repolarization. A small area on the outside of the cell becomes positive again ( Fig. 2-1 D), and the repolarization spreads along the length of the cell until the entire cell is once again fully repolarized. Ventricular repolarization is recorded by the ECG as the ST segment, T wave, and U wave. (Atrial repolarization is usually obscured by ventricular potentials.)

The ECG records the electrical activity of a large mass of atrial and ventricular cells, not that of just a single cell. Because cardiac depolarization and repolarization normally occur in a synchronized fashion, the ECG is able to record these electrical currents as specific waves (P wave, QRS complex, ST segment, T wave, and U wave).

In summary, regardless of whether the ECG is normal or abnormal, it records just two basic events: (1) depolarization, the spread of a stimulus through the heart muscle; and (2) repolarization, the return of the stimulated heart muscle to the resting state.

*  Membrane polarization is due to differences in the concentration of ions inside and outside the cell. See the Bibliography for references that present the basic electrophysiology of the resting membrane potential and cellular depolarization and repolarization (the action potential) that underlie the ECG waves recorded on the body surface.



The spread of stimuli through the atria and ventricles followed by the return of stimulated atrial and ventricular muscle to the resting state produces the electrical currents recorded on the ECG. Furthermore, each phase of cardiac electrical activity produces a specific wave or complex ( Fig. 2-2 ). The basic ECG waves are labeled alphabetically and begin with the P wave:



P wave—atrial depolarization (stimulation)



QRS complex—ventricular depolarization (stimulation)



ST segment, T wave, and U wave—ventricular repolarization (recovery)

FIGURE 2-2  The P wave represents atrial depolarization. The PR interval is the time from initial stimulation of the atria to initial stimulation of the ventricles. The QRS represents ventricular depolarization. The ST segment, T wave, and U wave are produced by ventricular repolarization.

The P wave represents the spread of a stimulus through the atria (atrial depolarization). The QRS complex represents stimulus spread through the ventricles (ventricular depolarization). The ST segment and T wave represent the return of stimulated ventricular muscle to the resting state (ventricular repolarization). The U wave is a small deflection sometimes seen just after the T wave. It represents the final phase of ventricular repolarization, although its exact mechanism is not known.

You are probably wondering why no wave or complex represents the return of stimulated atria to their resting state. The answer is that the atrial ST segment (STa) and atrial T wave (Ta) are generally not observed on the normal ECG because of their low amplitudes. (An important exception is described in Chapter 11 in the discussion of acute pericarditis, which often causes PR segment deviation.) Similarly, the routine ECG is not sensitive enough to record any electrical activity during the spread of stimuli through the atrioventricular (AV) junction (AV node and bundle of His). The spread of electrical stimuli through the AV junction occurs between the beginning of the P wave and the beginning of the QRS complex. This interval, known as the PR interval, is a measure of the time it takes for a stimulus to spread through the atria and pass through the AV junction.

In summary, the P-QRS-T sequence represents the repetitive cycle of the electrical activity in the heart, beginning with the spread of a stimulus through the atria (P wave) and ending with the return of stimulated ventricular muscle to its resting state (ST-T sequence). As shown in Figure 2-3 , this cardiac cycle repeats itself again and again.

FIGURE 2-3  The basic cardiac cycle (P-QRS-T) repeats itself again and again.



The P-QRS-T sequence is recorded on special ECG graph paper that is divided into gridlike boxes (Figs. 2-3 and 2-4 [3] [4]). Each of the small boxes is 1 millimeter square (1 mm2). The paper usually moves at a speed of 25 mm/sec. Therefore, horizontally, each unit represents 0.04 second (25 mm/sec × 0.04 sec = 1 mm). Notice that the lines between every five boxes are heavier, so that each 5-mm unit horizontally corresponds to 0.2 second (5 × 0.04 = 0.2). The ECG can therefore be regarded as a moving graph that horizontally corresponds to time, with 0.04- and 0.2-second divisions.

FIGURE 2-4  The ECG is usually recorded on a graph divided into millimeter squares, with darker lines marking 5-mm squares. Time is measured on the horizontal axis. With a paper speed of 25 mm/sec, each small (1-mm) box side equals 0.04 second and each larger (5-mm) box side equals 0.2 second. The amplitude of any wave is measured in millimeters on the vertical axis.

Vertically, the ECG graph measures the voltages, or amplitudes, of the ECG waves or deflections. The exact voltages can be measured because the electrocardiograph is standardized (calibrated) so that a 1-mV signal produces a deflection of 10-mm amplitude (1 mV = 10 mm). In most electrocardiographs, the standardization can also be set at one-half or two-times normal sensitivity.




The electrocardiograph must be properly calibrated so that a 1-mV signal produces a 10-mm deflection. The unit may have a special standardization button that produces a 1-mV wave. As shown inFigure 2-5 , the standardization mark (St) produced when the machine is correctly calibrated is a square wave 10 mm tall. If the machine is not standardized correctly, the 1-mV signal produces a deflection either more or less than 10 mm and the amplitudes of the P, QRS, and T deflections are larger or smaller than they should be. The standardization deflection is also important because standardization can be varied in most electrocardiographs (see Fig. 2-5 ). When very large deflections are present (as occurs, for example, in some patients who have an electronic pacemaker that produces very large spikes or who have high QRS voltage caused by hypertrophy), it may be advisable to take the ECG at one-half standardization to get the entire tracing on the paper. If the ECG complexes are very small, it may be advisable to double the standardization (e.g., to study a small Q wave more thoroughly). Some electronic electrocardiographs do not display the calibration pulse. Instead, they print the paper speed and standardization at the bottom of the ECG paper (25 mm/sec, 10 mm/mV).

FIGURE 2-5  Before taking an ECG, the operator must check to see that the machine is properly calibrated, so that the 1-mV standardization mark is 10 mm tall. A, Electrocardiograph set at normal standardization. B, One half standardization. C, Two times normal standardization.

Because the ECG is calibrated, any part of the P, QRS, and T deflections can be described in two ways; that is, both the amplitude (voltage) and the width (duration) of deflection can be measured. Thus it is possible to measure the amplitude and width of the P wave, the amplitude and width of the QRS complex, the amplitude of the ST segment deviation (if present), and the amplitude of the T wave. For clinical purposes, if the standardization is set at 1 mV = 10 mm, the height of a wave is usually recorded in millimeters, not millivolts. In Figure 2-3 , for example, the P wave is 1 mm in amplitude, the QRS complex is 8 mm, and the T wave is about 3.5 mm.

A wave or deflection is also described as positive or negative. By convention, an upward deflection or wave is called positive. A downward deflection or wave is called negative. A deflection or wave that rests on the baseline is said to be isoelectric. A deflection that is partly positive and partly negative is call biphasic. For example, in Figure 2-6 , the P wave is positive, the QRS complex is biphasic (initially positive, then negative), the ST segment is isoelectric (flat on the baseline), and the T wave is negative.

FIGURE 2-6  The P wave is positive (upward), and the T wave is negative (downward). The QRS complex is biphasic (partly positive, partly negative), and the ST segment is isoelectric (neither positive nor negative).

This chapter examines P, QRS, ST, T, and U waves in a general way. The measurements of heart rate, PR interval, QRS width, and QT interval are considered in detail, along with their normal values.


The P wave, which represents atrial depolarization, is a small positive (or negative) deflection before the QRS complex. (The normal values for P wave amplitude and width are described in Chapter 6 .)


The PR interval is measured from the beginning of the P wave to the beginning of the QRS complex ( Fig. 2-7 ). The PR interval may vary slightly in different leads, and the shortest PR interval should be noted. The PR interval represents the time it takes for the stimulus to spread through the atria and pass through the AV junction. (This physiologic delay allows the ventricles to fill fully with blood before ventricular depolarization occurs.) In adults the normal PR interval is between 0.12 and 0.2 second (three to five small box sides). When conduction through the AV junction is impaired, the PR interval may become prolonged. Prolongation of the PR interval above 0.2 second is called first-degree heart block (see Chapter 17 ).

FIGURE 2-7  Measurement of the PR interval (see text).


One of the most confusing aspects of electrocardiography for the beginning student is the nomenclature of the QRS complex. As noted previously, the QRS complex represents the spread of a stimulus through the ventricles. However, not every QRS complex contains a Q wave, an R wave, and an S wave—hence the confusion. The bothersome but unavoidable nomenclature becomes understandable if you remember several basic features of the QRS complex (see Fig. 2-8 ): When the initial deflection of the QRS complex is negative (below the baseline), it is called a Q wave; the first positive deflection in the QRS complex is called an R wave; a negative deflection following the R wave is called an S wave. Thus the following QRS complex contains a Q wave, an R wave, and an S wave:

FIGURE 2-8  QRS nomenclature (see text).


In contrast, the following complex does not contain three waves:


If, as shown, the entire QRS complex is positive, it is simply called an R wave. If the entire complex is negative, however, it is termed a QS wave (not just a Q wave, as might be expected).

Occasionally, the QRS complex contains more than two or three deflections. In such cases, the extra waves are called R′ (R prime) waves if they are positive and S′ (S prime) waves if they are negative.

Figure 2-8 shows the various possible QRS complexes and the nomenclature of the respective waves. Notice that capital letters (QRS) are used to designate waves of relatively large amplitude and small letters (qrs) label relatively small waves.

The QRS nomenclature is confusing at first, but it allows you to describe any QRS complex over the phone and to evoke in the mind of the trained listener an exact mental picture of the complex named. For example, in describing an ECG you might say that lead V1 showed an rS complex (“small r, capital S”):


You might also describe a QS (“capital Q, capital S”) in lead aVF:



The QRS width, or interval, represents the time required for a stimulus to spread through the ventricles (ventricular depolarization) and is normally 0.1 second or less ( Fig. 2-9 ). If the spread of a stimulus through the ventricles is slowed, for example, by a block in one of the bundle branches, the QRS width is prolonged. (The full differential diagnosis of a wide QRS complex is discussed inChapters 12 and 24 .)

FIGURE 2-9  Measurement of the QRS width (interval) (see text).


The ST segment is that portion of the ECG cycle from the end of the QRS complex to the beginning of the T wave ( Fig. 2-10 ). It represents the beginning of ventricular repolarization. The normal ST segment is usually isoelectric (i.e., flat on the baseline, neither positive nor negative), but it may be slightly elevated or depressed normally (usually by less than 1 mm). Some pathologic conditions such as myocardial infarction (MI) produce characteristic abnormal deviations of the ST segment. The very beginning of the ST segment (actually the junction between the end of the QRS complex and the beginning of the ST segment) is sometimes called the J point. Figure 2-10 shows the J point and the normal shapes of the ST segment. Figure 2-11 compares a normal isoelectric ST segment with abnormal ST segment elevation and depression.

FIGURE 2-10  Characteristics of the normal ST segment and T wave. The junction (J) is the beginning of the ST segment.

FIGURE 2-11  ST segments. A, Normal. B, Abnormal elevation. C, Abnormal depression.


The T wave represents part of ventricular repolarization. A normal T wave has an asymmetric shape; that is, its peak is closer to the end of the wave than to the beginning (see Fig. 2-10 ). When the T wave is positive, it normally rises slowly and then abruptly returns to the baseline.[*] When it is negative, it descends slowly and abruptly rises to the baseline. The asymmetry of the normal T wave contrasts with the symmetry of T waves in certain abnormal conditions such as myocardial infarction (see Chapters 8 and 9 ) and a high serum potassium level (see Chapter 10 ).

*  The exact point at which the ST segment ends and the T wave begins is arbitrary and sometimes impossible to define precisely.

The QT interval is measured from the beginning of the QRS complex to the end of the T wave ( Fig. 2-12 ). It primarily represents the return of stimulated ventricles to their resting state (ventricular repolarization). The normal values for the QT interval depend on the heart rate. As the heart rate increases (the RR interval shortens),[†] the QT normally shortens; as the heart rate decreases (the RR interval lengthens), the QT interval lengthens.

FIGURE 2-12  Measurement of the QT interval. The RR interval is the interval between two consecutive QRS complexes (see text).

The QT should be measured in the ECG lead (see Chapter 3 ) that shows the longest intervals. You can measure several intervals in that lead and use the average value. When the QT interval is long, it is often difficult to measure because the end of the T wave may merge imperceptibly with the U wave. As a result, you may be measuring the QU interval rather than the QT interval.

Table 2-1 shows approximate upper normal limits for the QT interval with different heart rates. Unfortunately, there is no simple rule for determining the normal limits of the QT interval. As a result of this problem, another index of the QT was devised. It is the rate-corrected QT or QTc. The rate-corrected QT can be obtained by dividing the actual QT by the square root of the RR interval (both measured in seconds):

TABLE 2-1   -- QT Interval

Upper Limits of Normal (Estimated)

Measured RR interval (sec)

Heart rate (per min)

QT interval upper normal limits (sec)
































Normally, the QTc is less than or equal to about 0.44 second.[*]

As a general rule: At heart rates of 80/min or less, a measured QT interval of more than half the RR interval is always prolonged. It is also important to note, however, that at heart rates below 80/min, the QT may be less than half the RR and still be significantly prolonged, and at heart rates above 80/min, a QT more than half the RR is not necessarily prolonged (see Table 2-1 ).

A number of factors can abnormally prolong the QT interval ( Fig. 2-13 ). For example, this interval can be prolonged by certain drugs used to treat cardiac arrhythmias (e.g., amiodarone, disopyramide, dofetilide, ibutilide, procainamide, quinidine, and sotalol), as well as a large number of other types of agents (tricyclic antidepressants, phenothiazines, pentamidine, and so forth). Specific electrolyte disturbances (low potassium, magnesium, or calcium levels) are important causes of QT prolongation. Hypothermia also prolongs the QT interval by slowing the repolarization of myocardial cells. The QT interval may be prolonged with myocardial ischemia and infarction (especially during the evolving phase) and with subarachnoid hemorrhage. QT prolongation may predispose patients to potentially lethal ventricular arrhythmias. (See the discussion of torsades de pointes in Chapter 16 .) The differential diagnosis of a long QT is summarized in Chapter 24 .

FIGURE 2-13  Abnormal QT interval prolongation in a patient taking quinidine. The QT interval (0.6 sec) is markedly prolonged for the heart rate (65 beats/min) (see Table 2-1 ). The rate-corrected QT interval (normally 0.44 sec or less) is also prolonged (0.63 sec).[*]Prolonged ventricular repolarization may predispose patients to develop torsades de pointes, a life-threatening ventricular arrhythmia (see Chapter 16 ).

*  In Fig. 2-13 , find the QTC. 

The QT interval may be shortened by digitalis in therapeutic doses or by hypercalcemia, for example. Because the lower limits of normal for the QT interval have not been well defined, only the upper limits are given in Table 2-1 .

†  The interval between successive QRS complexes is termed the RR interval.
*  A number of other formulas have been proposed for calculating a rate-corrected QT interval. None is ideal or universally accepted. Some authors give the upper limits of the QTc as 0.43 sec in men and 0.45 sec in women.

The U wave is a small, rounded deflection sometimes seen after the T wave (see Fig. 2-2 ). As noted previously, its exact significance is not known. Functionally, U waves represent the last phase of ventricular repolarization. Prominent U waves are characteristic of hypokalemia (see Chapter 10 ). Very prominent U waves may also be seen in other settings, for example, in patients taking drugs such as sotalol or one of the phenothiazines or sometimes after patients have had a cerebrovascular accident. The appearance of very prominent U waves in such settings, with or without actual QT prolongation, may also predispose patients to ventricular arrhythmias (see Chapter 16 ).

Normally, the direction of the U wave is the same as that of the T wave. Negative U waves sometimes appear with positive T waves. This abnormal finding has been noted in left ventricular hypertrophy and myocardial ischemia.



Two simple methods can be used to measure the heart rate (number of heartbeats per minute) from the ECG: box counting method and QRS counting method.


The easier way, when the heart rate is regular, is to count the number of large (0.2-sec) boxes between two successive QRS complexes and divide a constant (300) by this. (The number of large time boxes is divided into 300 because 300 × 0.2 = 60 and the heart rate is calculated in beats per minute or 60 seconds.)

For example, in Figure 2-14 , the heart rate is 75 beats/min, since four large time boxes are counted between successive R waves (300 ÷ 4 = 75). Similarly, if two large time boxes are counted between successive R waves, the heart rate is 150 beats/min. With five intervening large time boxes, the heart rate is 60 beats/min.

FIGURE 2-14  Heart rate (beats per minute) can be measured by counting the number of large (0.2-sec) time boxes between two successive QRS complexes and dividing 300 by this number. In this example, the heart rate is calculated as 300 ÷ 4 = 75 beats/min.

When the heart rate is fast or must be measured very accurately from the ECG, you can modify the approach as follows: Count the number of small (0.04-sec) boxes between successive R waves and divide a constant (1500) by this number. In Figure 2-14 , 20 small time boxes are counted between QRS complexes. Therefore the heart rate is 1500 ÷ 20 = 75 beats/min. (The constant 1500 is used because 1500 × 0.04 = 60 and the heart rate is being calculated in beats per 60 seconds.)


If the heart rate is irregular, the first method will not be accurate because the intervals between QRS complexes vary from beat to beat. In such cases you can determine an average rate simply by counting the number of QRS complexes in some convenient time interval (e.g., every 6 seconds or every 10 seconds) and multiplying this number by the appropriate factor to obtain the rate in beats per 60 seconds.



Counting the number of QRS complexes in 6-second intervals (and then multiplying this number by 10; Fig. 2-15 ) can be easily done in most acute settings because the top of the ECG paper used in bedside cardiac monitors and telemetry units is generally scored with vertical marks every 3 seconds[*] (see Fig. 2-14 ).



For conventional, full 12-lead ECG recordings, the rhythm strip at the bottom of the chart generally displays 10 consecutive seconds of data, so the number of QRS complexes in this entire interval can be multiplied by 10 to obtain the heart rate.

FIGURE 2-15  Measurement of heart rate (beats per minute) by counting the number of QRS complexes in a 6-second interval and multiplying this number by 10. In this example, 10 QRS complexes occur in 6 seconds. Therefore the heart rate is 10 × 10 = 100 beats/min. The arrows point to 3-second markers.

By definition, a heart rate exceeding 100 beats/min is termed tachycardia, and a heart rate slower than 60 beats/min is called bradycardia. (In Greek, tachys means “swift,” whereas bradys means “slow.”) Thus during exercise you probably develop a sinus tachycardia, but during sleep or relaxation your pulse rate may drop into the 50s or even lower, indicating a sinus bradycardia.

*  If 3-second marks are not present, you can simply count the number of QRS cycles in any 15-cm interval and multiply this number by 10. On the ECG graph, 1 sec = 25 mm = 2.5 cm; therefore, 15 cm = 6 seconds of data.



The ECG actually consists of two separate but normally related parts: an atrial ECG, represented by the P wave; and a ventricular ECG, represented by the QRS-T sequence. With completely normal rhythm, when the sinus node is pacing the heart, the P wave (atrial stimulation or depolarization) always precedes the QRS complex (ventricular stimulation or depolarization) because the atria are electrically stimulated first. Therefore the P-QRS-T cycle is usually considered as a unit. In some abnormal conditions, however, the atria and the ventricles can be stimulated by separate pacemakers. For example, suppose that the AV junction is diseased and stimuli cannot pass from the atria to the ventricles. In this situation, a new (subsidiary) pacemaker located below the level of the block in the AV junction may take over the task of pacing the ventricles while the sinus node continues to pace the atria. In this case, stimulation of the atria is independent of stimulation of the ventricles, and the P waves and QRS complexes have no relation to each other. This type of arrhythmia is called complete heart block and is described in detail in Chapter 17 . ( Figure 17-5 shows an example of this abnormal condition in which the atrial and ventricular ECGs are independent of each other.)



Up to this point, this chapter has considered only the basic components of the ECG. Several general items need to be emphasized before actual ECG patterns are discussed.



The ECG is a recording of cardiac electrical activity. It does not directly measure the mechanical function of the heart (i.e., how well the heart is contracting and performing as a pump). Thus a patient with acute pulmonary edema may have a normal ECG. Conversely, a patient with a grossly abnormal ECG may have normal cardiac function.



The ECG does not directly depict abnormalities in cardiac structure such as ventricular septal defects and abnormalities of the heart valves. It only records the electrical changes produced by structural defects. In some patients, however, the clinician can infer a specific structural diagnosis such as mitral stenosis, pulmonary embolism, or myocardial infarction from the ECG because typical electrical abnormalities may develop in such patients.



The ECG does not record all the heart's electrical activity. The electrodes placed on the surface of the body record only the currents that are transmitted to the area of electrode placement. Therefore there are actually “silent” electrical areas of the heart. For example, the ECG is not sensitive enough to record depolarization of pacemaker cells in the sinus node occurring just before the P wave. As noted earlier, the conventional electrocardiograph does not generally record repolarization of the atria. (For an important exception, see the discussion of pericarditis in Chapter 11 .) In addition, the conventional ECG does not detect the spread of stimuli through the AV junction. The electrical activity of the AV junction can be recorded using a special apparatus and a special electrode placed in the heart (His bundle electrogram). Further, the ECG records the summation of electrical potentials produced by innumerable cardiac muscle cells. Therefore the presence of a normal ECG does not necessarily mean that all these heart muscle cells are being depolarized and repolarized in a normal way.

For these reasons, the ECG must be regarded as any other laboratory test, with proper consideration for both its uses and its limitations (see Chapter 23 ).

The 12 ECG leads are described in Chapter 3 . Normal and abnormal ECG patterns are discussed in subsequent chapters.



The ECG, whether normal or abnormal, records two basic physiologic processes: depolarization and repolarization:



Depolarization (the spread of stimulus through the heart muscle) produces the P wave from the atria and the QRS complex from the ventricles.



Repolarization (the return of stimulated muscle to the resting state) produces the atrial ST segment and T wave (which are ordinarily not seen on the ECG) and the ventricular ST segment, T wave, and U wave.

ECGs are recorded on special paper that is divided into gridlike boxes. Each small box is 1 mm2. Each millimeter horizontally represents 0.04 second. Each 0.2 second is denoted by a heavier vertical line. ECG deflections are usually standardized so that a 1-mV signal produces a 10-mm deflection. Therefore each millimeter vertically represents 0.1 mV. Each 5-mm interval is denoted by a heavier horizontal line.

Four basic intervals are measured on the ECG:



The heart rate, measured in beats/min can be quickly calculated in two ways: Method 1 (box counting): Count the number of large (0.2-sec) time boxes between two successive R waves, and divide the constant 300 by this number (see Fig. 2-14 ). If you want a more accurate measurement of the rate, divide the constant 1500 by the number of small (0.04-sec) time boxes between two successive R waves. 
Method 2 (QRS counting): Count the number of QRS complexes that occur every 6 or 10 seconds, and multiply this number by 10 or 6, respectively.



The PR interval is measured from the beginning of the P wave to the beginning of the QRS complex. The normal PR interval is from 0.12 to 0.2 second.



The QRS interval is normally 0.1 second or less in width.



The QT interval is measured from the beginning of the QRS complex to the end of the T wave. It varies with the heart rate, becoming shorter as the heart rate increases.

These four intervals can be considered the “vital signs” of the ECG because they give essential information about the electrical stability (or instability) of the heart.





Calculate the heart rate in each of the following examples.




Name the major abnormality in each example. 




Slowing of conduction in the atrioventricular (AV) node is most likely to do which of the following?



Prolong the PR interval



Prolong the QRS interval



Prolong the QT interval



All of the above



A block in the left bundle branch is most likely to do which of the following?



Prolong the PR interval



Prolong the QRS interval



Prolong the QT interval



All of the above



Name the component waves of the QRS complexes shown below. 




Name four factors that may prolong the QT interval.



Which of the following events is never observed on a clinical 12-lead ECG?



Atrial depolarization



Atrial repolarization



His bundle depolarization



Ventricular depolarization



Ventricular repolarization

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