Arrhythmia Recognition: The Art of Interpretation

The duration of the wave itself can vary between 0.08 and 0.11 seconds in normal adults. The axis of the P wave is usually directed downward and to the left, the direction the electrical impulse travels on its journey to the atrioventricular (AV) node and the atrial appendages.

The Tp wave, which represents repolarization of the atria, deflects in the opposite direction of the P wave (Figure 4-16). It is usually not seen because it occurs at the same time as the QRS wave and is obscured (buried) by that more powerful complex. However, you can sometimes see it when there is no QRS after the P wave. This occurs in AV dissociation or nonconducted beats. You may also see it in PR depression, or in the ST-segment depression present in very fast sinus tachycardias. It appears as ST depression because the QRS comes sooner in the cycle, and the Tp wave—if it is negative—draws the ST segment downward.

The PR interval represents the time period from the beginning of the P wave to the beginning of the QRS complex (Figure 4-18). It includes the P wave and the PR segment, both discussed previously. The PR interval covers all of the events from the initiation of the electrical impulse in the SA node up to the moment of ventricular depolarization. The normal duration is from 0.12 seconds to 0.20 seconds. If the PR interval is shorter than 0.11 seconds, it is considered shortened. A PR interval longer than 0.20 seconds is a first-degree AV block, which we will talk about in a later section. The PR interval can be quite long, sometimes 0.40 seconds or greater. The term PQ interval is sometimes used interchangeably if there is a Q wave as the initial component of the QRS complex.

The QRS complex represents ventricular depolarization. It is composed of two or more waves (Figure 4-19). Each wave has its own name or label. These can become quite complex. The main components are the Q, R, and S waves. By convention, the Q wave is the first negative deflection after the P wave. The Q wave can be present or absent. The R wave is the first positive deflection after the P. This will be the initial wave of the QRS complex if there is no Q present. The first negative deflection after the R wave is the S wave. If there are additional components in the QRS complex, they will be named as prime waves (see Figure 4-14).

The Q wave can be benign, or it can be a sign of dead myocardial tissue. A Q wave is considered significant if it is 0.03 seconds or wider, or its height is equal to or greater than one-third the height of the R wave (Figure 4-20). If it meets either of these criteria, it indicates a myocardial infarction (MI) over the region involved. If it doesn’t, it is not a significant Q wave (Figure 4-21). Insignificant Q waves are commonly found in I, aVL, and V₆, where they are due to septal innervation. These are therefore called septal Qs.

REMINDER

An illustration of two ECG complexes show that Q waves are significant if they are greater than or equal to 0.03 seconds or greater than or equal to one-third the height of the R wave. — Figure 4-20 Use your calipers! Measure the depth of the Q wave and then walk that distance up to see if you can fit it three times into the R wave.

© Jones & Bartlett Learning.

The R-wave peak time (formerly known as the intrinsicoid deflection) is measured from the beginning of the QRS complex to the beginning of the downslope of the R wave in leads that begin with an R wave and do not contain a Q wave (Figure 4-22). It represents the amount of time it takes the electrical impulse to travel from the Purkinje system in the endocardium to the surface of the epicardium immediately under an electrode. It is shorter (up to 0.035 seconds) in the right precordial leads, V₁ through V₂, because the right ventricle is thin in comparison with the left. It is longer (up to 0.045 seconds) in the left precordial leads, V₅ to V₆, because of the left ventricle’s greater thickness. Now, can you imagine what would cause the R-wave peak time to be prolonged? You will see a longer R-wave peak time if there is a thicker myocardium, as in ventricular hypertrophy, or when it takes longer for the electrical system to conduct that area, because of an intraventricular conduction delay such as, for instance, a left bundle branch block.

Now, having made the statements about ST elevation and normal variants above, we need to make a clarification that you will hear many more times. Any ST elevation in a symptomatic patient should be considered significant and representative of myocardial injury or infarction until proven otherwise. Don’t make the mistake of calling an acute MI a normal variant! Just because an ST segment is not elevated enough to meet the guidelines for the administration of thrombolytics (presently 1 mm in two contiguous leads) does not mean that it is benign. You must have a high index of suspicion in these cases and try to obtain an old ECG to compare.

The ST segment represents an electrically neutral time for the heart. The ventricles are between depolarization (QRS complex) and repolarization (T wave). Mechanically, this represents the time that the myocardium is maintaining contraction in order to push the blood out of the ventricles. As you can imagine, very little blood would be expelled if the ventricles only contracted for 0.12 seconds.

Why should the T wave be in the same direction as the QRS? If it represents repolarization, shouldn’t it be opposite the QRS? For the answer, we need to go back to the concept of ventricular excitation. The Purkinje system is near the endocardium; therefore, electrical depolarization should begin in the endocardium and move out toward the epicardium (Figure 4-25, top arrow).

You would expect repolarization to occur in the same direction because the cell that was first depolarized should be the first to repolarize, but this is not the case. Because of increased pressure on the endocardium during contraction, the repolarization wave travels in the opposite direction, from the epicardium back to the endocardium (Figure 4-25, bottom arrow). Remember, a negative wave—and repolarization is a negative wave—traveling away from the electrode is perceived the same as a positive wave moving toward it. Hence, the normal T wave should be in the same direction as the QRS. There are exceptions in some pathologic states.

The T wave should be asymmetrical, with the first part rising or dropping slowly and the latter part moving much faster (Figure 4-26). The way to check for symmetry of the T wave, if the ST segment is elevated, is to draw a perpendicular line from the peak of that wave to the baseline and then compare the symmetry of the two sides, ignoring the ST segment (Figure 4-27). Symmetric Ts can be normal, but are usually a sign of pathology.

The QT interval is the section of the ECG complex encompassing the QRS complex, the ST segment, and the T wave—from the beginning of the Q to the end of the T (Figure 4-28). It represents all of the events of ventricular systole, from the beginning of ventricular depolarization to the end of the repolarization cycle. The interval varies with heart rate, electrolyte abnormalities, age, and sex. A prolonged QT is a harbinger of possible arrhythmias, especially torsade de pointes. This is not a common occurrence, but it is life threatening. The QT interval should be shorter than one half of the preceding R-R interval (the interval between the peaks of the two preceding R waves). There are various formulas to evaluate the significance of a QT interval, but the most useful one is to evaluate the QTc (discussed next).

REMINDER

Normal duration: Approximately 410–420 ms

Prolonged QTc: 450 ms in men; 460 ms in women

Highly prolonged: Greater than 500 ms

Shortened QTc: ≤ 390 ms

Formulas (use a scientific calculator to make your life easier):

Bazett’s formula:

Fridericia’s formula:

Framingham formula: QTc = QT + 0.154 (1 − RR)

Hodges formula: QTc = QT + 1.75 (heart rate − 60)

The QTc interval stands for the QT corrected interval. What is it corrected for? Heart rate. As the heart rate decreases, the QT interval lengthens; conversely, as the heart rate increases, the QT interval shortens. This makes it hard to calculate the interval at which the QT is normal. By calculating the QTc interval, we can state that the upper limit of the normal QTc is less than 0.45 seconds or 450 ms in men and 0.46 seconds or 460 ms in women.¹ Anything above those levels is considered prolonged. In addition, any QTc that is greater than 0.50 seconds or 500 ms is considered very highly abnormal, and the patient should be considered at risk of lethal arrhythmias (see discussion of torsade de pointes in Chapter 33, Polymorphic Ventricular Tachycardia and Torsade de Pointes). The patient should be quickly assessed and the issue addressed without delay, especially if he or she is symptomatic.

We saw that the QTc could be prolonged. What happens if it is the opposite—short? Any number that is less than 0.39 seconds or 390 ms is considered a short QTc,¹ and the patient should be evaluated for the presence of short QT syndrome. The short QT syndrome refers to an autosomally transmitted genetic disorder that causes a channelopathy (defect in the channels that control movement of electrolytes through the cell membrane). Short QT syndrome is characterized by a short QT interval (≤ 390 ms) that does not significantly vary despite changes in heart rates, tall or peaked T waves, and no structural abnormalities of the heart. Symptoms include palpitations and syncope. The most important aspect of this syndrome is that it is associated with a higher incidence of sudden cardiac death. Patients should be evaluated by a cardiologist or electrophysiologist as soon as possible, and they should be admitted and monitored if symptomatic.

Common formulas for calculating the QTc appear in the Reminder box. Each formula has inherent strengths and weakness. Further discussion is beyond the scope of this book, but we encourage you to do some additional reading (a good place to start is the article by Rautaharju et al.,¹ which we reference at the end of this chapter). We are providing you with the four most commonly used formulas. Most ECG machines will automatically calculate the interval for you. However, you must manually verify this computerized interval to make sure it is correct. The stakes at both ends of the spectrum, shortened or prolonged, are too high to trust the machine.

The U wave is a small, flat wave sometimes seen after the T wave and before the next P wave (Figure 4-29). Various theories have arisen about what it represents, including ventricular depolarization and endocardial repolarization. Nobody knows for sure. It can be seen in normal patients, especially in the presence of bradycardia. It can also be seen in hypokalemia (low potassium). One valuable point is that there can be no possibility of hyperkalemia in the presence of a U wave (more about this later). The only other clinical significance of the U is that it can sometimes cause an inaccuracy in measuring the QT interval. This can lead to a longer-than-accurate value because some machines may include this interval in their measurements. ECG computers are notorious for this miscalculation.

Another is the P-P interval, the distance between two identical points on one P wave and the next (Figure 4-30). This interval will be very useful in evaluating the patient for rhythm abnormalities. Examples include Wenckebach second-degree heart block, atrial flutter, and third-degree heart block. We will discuss these rhythm abnormalities later in the book.

CLINICAL PEARL

The true baseline of the ECG is a line drawn from the TP of one complex to the TP of another. The PR segment should fall on this line, but many times it does not. Fluctuations from the baseline may signify pathology.