CHAPTER 3 How to Make Basic ECG Measurements This chapter continues the discussion of ECG basics introduced in Chapters 1 and 2. Here we focus on recognizing components of the ECG in order to make clinically important measurements from these time–voltage graphical recordings. STANDARDIZATION (CALIBRATION) MARK The electrocardiograph is generally calibrated such that a 1-mV signal produces a 10-mm deflection. Modern units are electronically calibrated; older ones may have a manual calibration setting. ECG as a Dynamic Heart Graph The ECG is a real-time graph of the heartbeat. The small ticks on the horizontal axis correspond to intervals of 40 ms. The vertical axis corresponds to the magnitude (voltage) of the waves/deflections (10 mm = 1 mV) As shown in Fig. 3.1, the standardization mark produced when the machine is routinely calibrated is a square (or rectangular) wave 10 mm tall, usually displayed at the left side of each row of the electrocardiogram. If the machine is not standardized in the expected way, the 1-mV signal produces a deflection either more or less than 10 mm and the amplitudes of the P, QRS, and T deflections will be larger or smaller than they should be. The standardization deflection is also important because it can be varied in most electrocardiographs (see Fig. 3.1). When very large deflections are present (as occurs, for example, in some patients who have an electronic pacemaker that produces very large stimuli [“spikes”] or who have high QRS voltage Please go to expertconsult.inkling.com for additional online material for this chapter. caused by hypertrophy), there may be considerable overlap between the deflections on one lead with those one above or below it. When this occurs, it may be advisable to repeat 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, or augment a subtle pacing spike). 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”). Because the ECG is calibrated, any part of the P, QRS, and T deflections can be precisely described in two ways; that is, both the amplitude (voltage) and the width (duration) of a deflection can be measured. 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 Fig. 3.2, 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 called biphasic. For example, in Fig. 3.2 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. We now describe in more detail the ECG alphabet of P, QRS, ST, T, and U waves. The measurements of PR interval, QRS interval (width or duration), and QT/QTc intervals and RR/PP intervals are also described, with their physiologic (normative) values in adults.
Fig. 3.1 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.
COMPONENTS OF THE ECG P Wave and PR Interval The P wave, which represents atrial depolarization, is a small positive (or negative) deflection before the QRS complex. The normal values for P wave axis, amplitude, and width are described in Chapter 7. The PR interval is measured from the beginning of the P wave to the beginning of the QRS complex (Fig. 3.3). The PR interval may vary slightly in
different leads, and the shortest PR interval should be noted when measured by hand. 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, to optimize cardiac output.) In adults the normal PR interval is between 0.12 and 0.2 sec (three to f ive small box sides). When conduction through the AV junction is impaired, the PR interval may become prolonged. As noted, prolongation of the PR interval above 0.2 sec is called first-degree heart block (delay) (see Chapter 17). With sinus tachycardia, AV conduction may be facilitated by increased sympathetic and decreased vagal tone modulation. Accordingly, the PR may be relatively short, e.g., about 0.10–0.12 sec, as a physiologic finding, in the absence of Wolff–Parkinson–White (WPW) preexcitation (see Chapter 18). QRS Complex 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 possibility of confusion. The slightly awkward (and arbitrary) nomenclature becomes understandable if you remember three basic naming rules for the components of the QRS complex in any lead (Fig. 3.4): 1. When the initial deflection of the QRS complex is negative (below the baseline), it is called a Q wave. 2. The first positive deflection in the QRS complex is called an R wave. 3. A negative deflection following the R wave is called an S wave.
If, as shown earlier, the entire QRS complex is positive, it is simply called an R wave. However, if the entire complex is negative, it is termed a QS wave (not just a Q wave as you might expect).
of relatively large amplitude and small letters (qrs) label relatively small waves. (However, no exact thresholds have been developed to say when an s wave qualifies as an S wave, for example.)
The QRS naming system does seem confusing at first. But it allows you to describe any QRS complex and 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”): r S or a QS (“capital Q, capital S”): 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. Fig. 3.4 shows the major possible QRS complexes and the nomenclature of the respective waves. Notice that capital letters (QRS) are used to designate waves
QRS Interval (Width or Duration) The QRS interval represents the time required for a stimulus to spread through the ventricles (ventricular depolarization) and is normally about
≤0.10 sec (or ≤0.11 sec when measured by computer) (Fig. 3.5).a 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 will be prolonged. The differential diagnosis of a wide QRS complex is discussed in Chapters 18, 19 and 25.b ST Segment 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. 3.6). It represents the earliest phase 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 aYou may have already noted that the QRS amplitude (height or depth) often varies slightly from one beat to the next. This variation may be due to a number of factors. One is related to breathing mechanics: as you inspire, your heart rate speeds up due to decreased cardiac vagal tone (Chapter 13) and decreases with expiration (due to increased vagal tone). Breathing may also change the QRS axis slightly due to changes in heart position and in chest impedance, which change QRS amplitude slightly. If the rhythm strip is long enough, you may even be able to estimate the patient’s breathing rate. QRS changes may also occur to slight alterations in ventricular activation, as with atrial flutter and fibrillation with a rapid ventricular response (Chapter 15). Beat-to-beat QRS alternans with sinus tachycardia is a specific but not sensitive marker of pericardial effusion with tamponade pathophysiology, due to the swinging heart phenomenon (see Chapter 12). Beat-to-beat alternation of the QRS is also seen with certain types of paroxysmal supraventricular tachycardias (PSVTs; see Chapter 14). bA subinterval of the QRS, termed the intrinsicoid deflection, is defined as the time between the onset of the QRS (usually in a left lateral chest lead) to the peak of the R wave in that lead. A preferred term is R-peak time. This interval is intended to estimate the time for the impulse to go from the endocardium of the left ventricle to the epicardium. The upper limit of normal is usually given as 0.04 sec (40 msec); with increased values seen with left ventricular hypertrophy (>0.05 sec) and left bundle branch block (>0.06 sec). However, this microinterval is hard to measure accurately and reproducibly on conventional ECGs. Therefore, it has had very limited utility in clinical practice.
elevated or depressed normally (usually by less than 1 mm). Pathologic conditions, such as myocardial infarction (MI), that produce characteristic abnormal deviations of the ST segment (see Chapters 9 and 10), are a major focus of clinical ECG diagnosis. 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 called the J point. Fig. 3.6 shows the J point and the normal shapes of the ST segment. Fig. 3.7 compares a normal isoelectric ST segment with abnormal ST segment elevation and depression.
The terms J point elevation and J point depression often cause confusion among trainees, who mistakenly think that these terms denote a specific condition. However, these terms do not indicate defined abnormalities but are only descriptive. For example, isolated J point elevation may occur as a normal variant with the early repolarization pattern (see Chapter 10) or as a marker of systemic hypothermia (where they are called Osborn or J waves; see Chapter 11). J point elevation may also be part of ST elevations with acute pericarditis, acute myocardial ischemia, left bundle branch block or left ventricular hypertrophy (leads V1 to V3 usually), and so forth. Similarly, J point depression may occur in a variety of contexts, both physiologic and pathologic, as discussed in subsequent chapters and su
T Wave The T wave represents the mid-latter part of ventricular repolarization. A normal T wave has an asymmetrical shape; that is, its peak is closer to the end of the wave than to the beginning (see Fig. 3.6). 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 abnormal T waves in certain conditions, such as MI (see Chapters 9 and 10) and a high serum potassium level (see Chapter 11). The exact point at which the ST segment ends and the T wave begins is somewhat arbitrary and usually impossible to pinpoint precisely. However, for clinical purposes accuracy within 40 msec (0.04 sec) is usually acceptable
QT/QTc Intervals The QT interval is measured from the beginning of the QRS complex to the end of the T wave (Fig. 3.8). 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 (RR interval shortens), the QT interval normally shortens; as the heart rate decreases (RR interval lengthens), the QT interval lengthens. The RR interval, as described later, is the interval between consecutive QRS complexes. (The rate-related shortening of the QT, itself, is a complex process involving direct effects of heart rate on action potential duration and of neuroautonomic factors.)
The QT should generally be measured in the ECG lead (or leads) showing the longest intervals. A common mistake is to limit this measurement to lead II. You can measure several intervals 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. When reporting the QT (or related QTc) it might be helpful to cite the lead(s) use you used. Table 3.1 shows the approximate upper normal limits for the QT interval with different heart rates. Unfortunately, there is no simple, generally accepted rule for calculating the normal limits of the QT interval. The same holds for the lower limit of the QT. Because of these problems, a variety of indices of the QT interval have been devised, termed ratecorrected QT or QTc (the latter reads as “QT subscript c”) intervals. A number of correction methods have
been proposed, but none is ideal and no consensus has been reached on which to use. Furthermore, commonly invoked clinical “rules of thumb” (see below) are often mistakenly assumed on the wards. QT Cautions: Correcting Common Misunderstandings • A QT interval less than 1 2 the RR interval is NOT necessarily normal (especially at slower rates). • A QT interval more than 1 2 the RR interval is NOT necessarily long (especially at very fast rates). QT Correction (QTc) Methods 1. The Square Root Method The first, and still one of the most widely used QTc indices, is Bazett’s formula. This algorithm divides the actual QT interval (in seconds) by the square root of the immediately preceding RR interval (also measured in seconds). Thus, using the “square root method” one applies the simple equation: QTcQ = TRR Normally the QTc is between about 0.33–0.35 sec (330–350 msec) and about 0.44 sec or (440 msec). This classic formula has the advantage of being widely recognized and used. However, it requires taking a square root, making it a bit computationally cumbersome for hand calculations. More importantly, the formula reportedly over-corrects the QT at slow rates (i.e., makes it appear too short), while it under-corrects the QT at high heart rates (i.e., makes it appear too long).c 2. A Linear Method Not surprisingly, given the limitations of the square root method, a number of other formulas have been proposed for calculating a rate-corrected QT interval. cA technical point that often escapes attention is that implementing the square root method requires that both the QT and RR be measured in seconds. The square root of the RR (sec) yield sec½. However, the QTc, itself, is always reported by clinicians in units of seconds (not awkwardly as sec/sec½ = sec½). To make the units consistent, you should measure the RR interval in seconds but record it as a unitless number (i.e., QT in sec/√RR unitless), Then, the QTc, like the QT, will be expressed in units of sec.
We present one commonly used one, called Hodges method, which is computed as follows: QTcmsecQ = ()() .() Tmsec 175heart rate inbeatsmin 60 +− Or, equivalently, if you want to make the computation in units of seconds, not milliseconds: QTcsec QT sec 0 00175 heartrateinbeats min6 () () .() = +− 0beats min The advantage here is that the equation is linear. Note also that with both of the above methods (Bazett and Hodges), the QT and the QTc (0.40 sec or 400 msec) are identical at 60 beats/min. Multiple other formulas have been proposed for correcting or normalizing the QT to a QTc. None has received official endorsement. The reason is that no method is ideal for individual patient management. Furthermore, an inherent error/uncertainty is unavoidably present in trying to localize the beginning of the QRS complex and, especially, the end of the T wave. (You can informally test the hypothesis that substantial inter-observer and intra-observer variability of the QT exists by showing some deidentif ied ECGs to your colleagues and recording their QT measurements.)d Note also that some texts report the upper limits of normal for the QTc as 0.45 sec (450 msec) for women and 0.44 sec (440 msec) for men. Others use 450 msec for men and 460 for women. More subtly, a substantial change in the QTc interval within the normal range (e.g., from 0.34 to 0.43 sec) may be a very early warning of progressive QT prolongation due to one of the factors below. Many factors can abnormally prolong the QT interval (Fig. 3.9). For example, this interval can be prolonged by certain drugs used to treat cardiac arrhythmias (e.g., amiodarone, dronedarone, ibutilide, quinidine, procainamide, disopyramide, dofetilide, and sotalol), as well as a large number of other types of “non-cardiac” agents (fluoroquinolones, phenothiazines, pentamadine, macrolide dSome references advocate drawing a tangent to the downslope of the T wave and taking the end of the T wave as the point where this tangent line and the TQ baseline intersect. However, this method is arbitrary since the slope may not be linear and the end of the T wave may not be exactly along the isoelectric baseline. A U wave may also interrupt the T wave. With atrial fibrillation, an average of multiple QT values can be used. Clinicians should be aware of which method is being employed when electronic calculations are used and always double check the reported QT.
Fig. 3.9 Abnormal QT interval prolongation in a patient taking the drug quinidine. The QT interval (0.6 sec) is markedly prolonged for the heart rate (65 beats/min) (see Table 3.1). The rate-corrected QT interval (normally about 0.44–0.45 sec or less) is also prolonged.* Prolonged repolarization may predispose patients to develop torsades de pointes, a life-threatening ventricular arrhythmia (see Chapter 16). *Use the methods described in this chapter to calculate the QTc. Answers: 1. Using the “square root” (Bazett) method: QTc = QT/√RR = 0.60 sec/√0.92 = 0.63 sec. 2. Using Hodges method: QTc = QT + 1.75 (HR in beats/min − 60) = 0.60 + 1.75 (65 − 60) = 0.60 + 8.75 = 0.68 sec. With both methods, the QTc is markedly prolonged, indicating a high risk of sudden cardiac arrest due to torsades de pointes (see Chapters 16 and 21).
antibiotics, haloperidol, methadone, certain selective serotonin reuptake inhibitors, to name but a sample). Specific electrolyte disturbances (low potassium, magnesium, or calcium levels) are important causes of QT interval prolongation. Hypothermia 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 with T wave inversions) and with subarachnoid hemorrhage. QT prolongation is important in practice because it may indicate predisposition to potentially lethal ventricular arrhythmias. (See the discussion of torsades de pointes in Chapter 16.) The differential diagnosis of a long QT interval is summarized in Chapter 25. Table 3.1 gives (estimated) values of the upper range of the QT for healthy adults over a range of heart rates. The cut-off for the lower limits of the rate-corrected QT (QTc) in adults is variously cited as 330–350 msec. As noted, a short QT may be evidence of hypercalcemia, or of the fact that the
Fig. 3.10 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. Alternatively (and more accurately), the number of small (0.04-sec) time boxes between successive QRS complexes can be counted (about 20 small boxes here) and divided into 1500, also yielding a rate of 75 beats/min. patient is taking digoxin (in therapeutic or toxic doses). Finally, a very rare hereditary “channelopathy” has been reported associated with short QT intervals and increased risk of sudden cardiac arrest (see Chapter 21). U Wave 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 11). Very prominent U waves may also be seen in other settings, for example, in patients taking drugs such as sotalol, or quinidine, 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 in myocardial ischemia. RR Intervals and Calculation of Heart Rate We conclude this section on ECG intervals by discussing the RR interval and its inverse; namely the (ventricular) heart rate. Two simple classes of methods can be used to manually measure the ventricular or atrial heart rate (reported as number of heartbeats or cycles per minute) from the ECG (Figs. 3.10 and 3.11).
Fig. 3.11 Quick methods to measure heart rate. Shown is a standard 12-lead ECG with a continuous rhythm strip (lead II, in this case). Method 1A: Large box counting method (see Fig. 3.10) shows between four and five boxes between R waves, yielding rate between 75 and 60 beats/min, where rate is 300 divided by number of large (0.2-sec) boxes. Method 1B: Small box counting method more accurately shows about 23 boxes between R waves, where rate is 1500 divided by number of small (0.04 sec) boxes = 65 beats/min. Method 2: QRS counting method shows 11 QRS complexes in 10 sec = 66 beats/60 sec or 1 min. Note: the short vertical lines here indicate a lead change, and may cause an artifactual interruption of the waveform in the preceding beat (e.g., T waves in the third beat before switch to lead aVR, aVL, and aVF).
1. Box Counting Methods The easiest way, when the (ventricular) heart rate is regular, is to count the number (N) of large (0.2-sec) boxes between two successive QRS complexes and divide a constant (300) by N. (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, i.e., per 60 seconds.) For example, in Fig. 3.10 the heart rate is 75 beats/ min, because 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 f ive intervening large time boxes, the heart rate will be 60 beats/min. When the heart rate is fast or must be measured very accurately from the ECG, you can modify the box counting approach as follows: Count the number of small (0.04-sec) boxes between successive R (or S waves) waves and divide the constant (1500) by this number. In Fig. 3.10, 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 sec [beats/min].) Note: some trainees and attending physicians have adopted a “countdown” mnemonic by which they incant: 300, 150, 100, 75, 60 … based on ticking off the number of large (0.2-sec box sides) between QRS complexes. However, there is no need to memorize extra numbers: this countdown is simply based on dividing the number of large (0.2-sec) intervals between consecutive R (or S waves) into 300. If the rate is 30, you will be counting down for quite a while! But 300/10 = 30/min will allow you to calculate the rate and move on with the key decisions regarding patient care. 2. QRS Counting Methods If the heart rate is irregular, the first method will not be accurate because the intervals between QRS complexes vary from beat to beat. You can easily determine an average (mean) rate, whether the latter is regular or not, simply by counting the number of QRS complexes in some convenient time interval (e.g., every 10 sec, the recording length of most 12-lead clinical ECG records). Next, multiply this
number by the appropriate factor (6 if you use 10-sec recordings) to obtain the rate in beats per 60 sec (see Fig. 3.11). This method is most usefully applied in arrhythmias with grossly irregular heart rates (as in atrial fibrillation or multifocal atrial tachycardia). By definition, a heart rate exceeding 100 beats/ min is termed a tachycardia, and a heart rate slower than 60 beats/min is called a 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. (See Part III of this book for an extensive discussion of the major brady- and tachyarrhythmias.) HOW ARE HEART RATE AND RR INTERVALS RELATED? The heart rate is inversely related to another interval, described earlier: the so-called RR interval (or QRSto-QRS interval), which, as noted previously, is simply the temporal distance between consecutive, equivalent points on the preceding or following QRS. (Conveniently, the R wave peak is chosen, but this is arbitrary.) These measurements, when made using digital computer programs on large numbers of intervals, form the basis of heart rate variability (HRV) studies, an important topic that is outside our scope here but mentioned in the Bibliography and the online material.
Students should know that RR intervals can be converted to the instantaneous heart rate (IHR) by the following two simple, equivalent formulas, depending on whether you measure the RR interval in seconds (sec) or milliseconds (msec): InstantaneousHRinbeats min6 = InstantaneousHRinbeats min6 0RRinsec () = ,() 0 000 RR inmsec PP AND RR INTERVALS: ARE THEY EQUIVALENT? We stated in Chapter 2 that there were four basic sets of ECG intervals: PR, QRS, QT/QTc, and PP/ RR. Here we refine that description by adding mention of the interval between atrial depolarizations (PP interval). The atrial rate is calculated by the same formula given above for the ventricular, based on the RR interval; namely, the atrial rate (per min) = 60/PP interval (in sec). The PP interval and RR intervals are obviously the same when sinus
rhythm is present with 1 : 1 AV conduction (referred to as “normal sinus rhythm”). The ratio 1 : 1 in this context indicates that each P wave is successfully conducted through the AV nodal/His–Purkinje system into the ventricles. In other words: each atrial depolarization signals the ventricles to depolarize. However, as we will discuss in Parts II and III of this book, the atrial rate is not always equal to the ventricular rate. Sometimes the atrial rate is much faster (especially with second- or third-degree AV block) and sometimes it is slower (e.g., with ventricular tachycardia and AV dissociation).e ECG TERMS ARE CONFUSING! Students and practitioners are often understandably confused by the standard ECG terms, which are arbitrary and do not always seem logical. Since this terminology is indelibly engrained in clinical usage, we have to get used to it. But, it is worth a pause to acknowledge these semantic confusions (Box 3.1).
Beware: Confusing ECG Terminology! • The RR interval is really the QRS–QRS interval. • The PR interval is really P onset to QRS onset. (Rarely, the term PQ is used; but PR is favored even if the lead does not show an R wave.) • The QT interval is really QRS (onset) to T (end) inter
THE ECG: IMPORTANT CLINICAL PERSPECTIVES Up to this point only the basic components of the ECG have been considered. Several general items deserve emphasis before proceeding. 1. 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
The same rule can be used to calculate the atrial rate when non-sinus (e.g., an ectopic atrial) rhythm is present. Similarly, the atrial rate with atrial flutter can be calculated by using the flutter–flutter (FF) interval (see Chapter 15). Typically, in this arrhythmia the atrial rate is about 300 cycles/min. In atrial fibrillation (AF), the atrial depolarization rate is variable and too fast to count accurately from the surface ECG. The depolarization (electrical) rate of 350–600/ min rate in AF is estimated from the peak-to-peak fibrillatory oscillations.
a normal ECG. Conversely, a patient with an abnormal ECG may have normal cardiac function. 2. 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. However, in some conditions a specific structural diagnosis such as mitral stenosis, acute pulmonary embolism, or myocardial infarction/ischemia can be inferred from the ECG because a constellation of typical electrical abnormalities develops. 3. The ECG does not record all of the heart’s electrical activity. The SA node and the AV node are completely silent. Furthermore, the electrodes placed on the surface of the body record only the currents that are transmitted to the area of electrode placement. The clinical ECG records the summation of electrical potentials produced by innumerable cardiac muscle cells. Therefore, there are “silent” electrical areas of the heart that get “cancelled out” or do not show up because of low amplitude. For example, parts of the muscle
may become ischemic, and the 12-lead ECG may be entirely normal or show only nonspecific changes even while the patient is experiencing angina pectoris (chest discomfort due to myocardial ischemia). 4. The electrical activity of the AV junction can be recorded using a special apparatus and a special catheter placed in the heart (His bundle electrogram; see online material). Thus, 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. Furthermore, some abnormalities, including life-threatening conditions such as severe myocardial ischemia, complete AV heart block, and sustained ventricular tachycardia, may occur intermittently. 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 24). What’s next? The ECG leads, the normal ECG, and the concept of electrical axis are described in Chapters 4–6. Abnormal ECG patterns are then discussed, emphasizing clinically and physiologically important topics.