JORNADA DE PREPARACIÓN DE RESPUESTA EN COSTA

Richard J. Harper and Christopher F. Richards

ELECTROCARDIOGRAPHIC HIGHLIGHTS

Reversed electrodes: clues to detection L arm–R arm

• Inverted P wave and QRS complex in lead I

• Unexpected right or extreme QRS axis deviation

• Inverted P wave in lead I, together with normal precordial R wave progression (i.e., not dextrocardia)

L arm–L leg

• Lead III is upside down (may not appear abnormal)

• Leads I and II switched; aVL and aVF switched; aVR no change

• P wave is unexpectedly larger in lead I than in lead II R arm–L leg

• P-QRS-T upside down in all leads except lead aVL

• Upright P-QRS-T in lead aVR R leg–L leg

• Looks like normal electrode placement

• Immaterial because of similarity of potentials in lower extremities

R leg–L arm

• Lead III is practically a flat line R leg–R arm

• Lead II is practically a flat line L arm–L leg and R arm–R leg

• Lead I is practically a flat line

• Leads aVL and aVR are same polarity and amplitude

• Lead II is upside-down image of lead III 16

CHAPTER4: Electrode Misplacement and Artifact 17

Limb Electrode Misplacement

Although algorithms have been developed for identifying all non–R leg electrode reversals, they are often too complicated for daily use.²They do, however, offer two useful points to consider when there is concern about possible limb electrode reversal. The normal P wave axis in the frontal plane should lie between 0 and 75 degrees. Deviation suggests ectopic atrial rhythm, dextrocardia, or electrode reversal. Lead aVR should normally consist of inverted P, QRS, and T waves.

If this is not the case, particularly if that pattern exists in another lead, electrode reversal should be suspected.

R Arm–L Arm Reversal. Arm electrode reversal is the most common error of electrode reversal and is perhaps the easiest to detect (Fig. 4-1).³It causes an absolute inversion of lead I wave forms; most noticeably, the P wave and QRS complex will be inverted, resulting in a right or extreme QRS axis deviation. Lead II inscribes the wave form of lead III and lead III that of lead II. Because the partial common lead is also changed, lead aVR becomes lead aVL, and vice versa. The common lead for aVF remains the combined arm electrodes

A

B

FIGURE 4-1• A, ECG obtained from a normal volunteer. This ECG will serve as a comparison for all those in subsequent figures, except those in Figures 4-3A, 4-3B, and 4-8. B, Arm electrode reversal. ECG from same individual as in A, with left and right arm electrodes reversed. In lead I, note the P, QRS, and T wave changes, which are unexpected in a patient without dextrocardia. Note also the unusually “normal” appearance of aVR.

When limb electrode reversal is suspected:

• Always attempt to obtain a prior ECG for comparison.

• Repeat the ECG, checking the leads for proper placement.

• Reversal of limb electrodes produces P, QRS, and T axis shifts.

You should suspect limb electrode reversal:

• When the QRS axis is unexpectedly abnormal.

• When P waves are inverted in the limb leads—particularly lead II and lead I.

• When aVR is upright and another lead looks like aVR.

• When leads I, II, or III are a virtual flat line.

You should suspect precordial electrode reversal:

• When normal P, QRS, and T progression across the precordium is interrupted.

ELECTROCARDIOGRAPHIC PEARLS

18 SECTIONI: THE NORMAL ELECTROCARDIOGRAM

FIGURE 4-2 • L arm–L leg reversal.

ECG from same individual as in Figure 4-1A, with the left arm and left leg elec-trodes reversed. Note that leads I and II are reversed, as are aVL and aVF. Lead aVR is unchanged, and lead III is inverted. At first glance, this tracing does not appear abnormal—without an old tracing for comparison. Note, however, that the P wave is larger in lead I than in lead II, a tip-off that L arm–L leg reversal has occurred.

A

B

FIGURE 4-3• A, L arm–L leg reversal in the setting of acute myocardial infarction. ECG showing ST elevation in leads I and aVL. This would suggest a high lateral acute myocardial infarction, with ischemic changes inferiorly (i.e., ST depression and T wave inversion)—although there is no ST elevation in V5

or V6. Note, however, that the P wave is larger in lead I than in lead II, a clue that on this tracing, there is L arm–L leg electrode reversal. B, ECG from same patient with corrected limb electrode placement. This is from the same individual as in A, approximately 30 minutes later. The L arm and L leg electrodes are now properly placed. As a result, ST elevation is seen in leads II, III, and aVF, and reciprocal ST depression is seen in leads I and aVL. Note also that the precordial electrodes have been repositioned across the right chest, and show evidence of concomitant right ventricular infarction (i.e., ST segment elevation in V3Rto V6R) with posterior involvement (i.e., ST segment-T wave changes in leads V1to V2).

and therefore is unchanged. The common lead for the unipo-lar chest leads is the combined input of the three limb elec-trodes, and as a result the precordial chest leads are unaffected by limb electrode reversal (see Fig. 4-1).

L Arm–L Leg Reversal. Reversal of the L arm and L leg electrodes is more difficult to detect owing to the lack of reli-able P wave inversion. Lead III is inverted by this connection.

Lead I becomes lead II and lead II is lead I. Lead aVR is unchanged, whereas leads aVF and aVL are exchanged.

In short, the lateral limb leads (I and aVL) are now inferior, and two of the three inferior limb leads (II and aVF) are now lateral—while the third (III) is upside down (Fig. 4-2).

A helpful marker for detection is the P wave—a taller P wave in lead I compared with lead II, or a biphasic P wave in lead III with positive terminal component, suggests L arm–L leg reversal⁴(Fig. 4-3).

R Arm–L Leg Reversal. Switching the R arm and L leg elec-trode inverts lead II. Lead I and III are exchanged and inverted. Although leads aVF and aVR are reversed, lead aVL is unchanged. This electrode reversal is fairly easy to detect by the upright P, QRS, and T waves in lead aVR, as well as the very abnormal QRS axis (and inverted P wave) in lead I caused by the electrode reversals (Fig. 4-4).

R Leg Reversals. Electrode reversals involving the R leg create different patterns. Reversal of the R leg and L leg electrodes will likely go undetected, and is unimportant because there is almost no difference between the electrical potential of the legs. Reversal of the R leg electrode with either of the arm electrodes produces a characteristic and easily detectable change in the ECG. The lack of potential difference between the legs produces an asystolic, “flat line” appearance in the one limb lead that uses the L leg electrode and the CHAPTER4: Electrode Misplacement and Artifact 19

FIGURE 4-4 • R arm–L leg reversal.

On this ECG, note that only lead aVL is unchanged from that in Figure 4-1A. All other nonprecordial leads appear bizarre, including the “normal” appearance of aVR.

FIGURE 4-5 • R leg–R arm reversal.

The characteristic “flat line” appearance in lead II signals misconnection of the R leg electrode. The point of misconnection can be deduced by remembering that the R leg electrode serves as a ground. Lead II wave forms are the result of electrical forces from the R arm position toward the L leg.

Because the R arm electrode has been mistakenly replaced by the R leg electrode, there is essentially no potential difference between those two points—thus a flat line appears in lead II.

misconnected R leg electrode. Misconnection of the R leg electrode to the L arm makes lead III a flat line. Likewise, misconnection of the R leg electrode to the R arm causes lead II to have a flat line appearance (Fig. 4-5). Finally, placing both leg electrodes on the arms and the arm electrodes on the legs (but preserving sidedness) results in a flat line in lead I.³ Precordial Electrode Misplacement

Misconnection of two of the precordial electrodes interrupts the smooth transition of the R waves across the precordium and is easily detected by the careful observer. Incorrect place-ment of the first two precordial electrodes an interspace too high or too low may also lead to spurious recordings on the ECG. Low placement may mask incomplete right bundle branch block or right ventricular hypertrophy, and high place-ment may falsely suggest them (Fig. 4-6).

Artifact

ECG artifact is attributed to external (environmental) causes versus internal (patient) etiologies. Most external artifact is

due to 60-Hz electrical interference; this comes from other alternating current–requiring devices in the vicinity of the patient while the tracing is recorded. Artifact can also result from a technical problem anywhere between the ECG and the patient, including the cables and their connections. Patient movement, whether involuntary (e.g., cough, hiccups, tremor, breathing) or voluntary (e.g., limb movement) is responsible for many of the internal sources of artifact.^5,6

Electrode contact to the patient’s skin can be considered an internal source of artifact. Skin impedance is minimized if the electrode is placed over an area that is not a bony promi-nence or pulsating artery; if hairy, the area should be clipped rather than shaven. Furthermore, drying the skin is as impor-tant as cleaning is to minimize associated artifact.^6,7Lead arti-facts may be isolated to an offending electrode by considering the leads involved (Fig. 4-7).

When movement artifact is substantial or physical consid-erations prevent conventional limb lead placement, the limb leads may be moved to a more proximal location. This does cause predictable changes in the ECG. Limb lead voltages may increase to a minor extent and the axis is often shifted to the right, inferiorly and posteriorly. Changes associated with acute 20 SECTIONI: THE NORMAL ELECTROCARDIOGRAM

FIGURE 4-6• Misplacement of leads V1and V2. The appearance of a new incomplete right bundle branch block in this tracing is actually due to the fact that V1and V2were placed an interspace too high. Compare this tracing with the normal one featured in Figure 4-1A.

FIGURE 4-7 • Artifact due to patient movement. Here, the individual featured in Figure 4-1A is moving his R arm while the tracing is being recorded.

The leads principally affected are, logically, I, II, and aVR because all involve the R arm electrode directly. V1, as the most rightward precordial lead, is also displaying significant artifact.

myocardial infarction (MI), particularly posterior MI, may be lost or falsely suggested. Torso positioning produces the greatest impact in the left arm because of its proximity to the myocardium.⁸

Differentiation of artifact from real abnormality is obvi-ously important, but not always easy. The following character-istics are suggestive of artifact-induced pseudodysrhythmia as opposed to true dysrhythmia: (1) lack of symptoms or hemo-dynamic changes during the event; (2) appearance of “normal”

ventricular complexes among dysrhythmic beats; (3) associa-tion with body movement (Figs. 4-8 and 4-9); (4) tracing base-line instability during and immediately after the apparent dysrhythmia; and (5) visible “notching” in the complexes of the pseudodysrhythmia that are synchronous with the ventric-ular complexes that precede and follow the apparent rhythm disturbance.^9,10

References

1. Kors J, van Herpen G: Accurate automatic detection of electrode interchange in the electrocardiogram. Am J Cardiol 2001;88:396.

CHAPTER4: Electrode Misplacement and Artifact 21

FIGURE 4-8• Artifact due to patient shivering. The shivering in this mildly hypothermic patient makes P wave differentiation difficult.

FIGURE 4-9 • Artifact due to drug use. This ECG rhythm strip is from a 47-year-old man with agitation from methamphetamine use. The patient’s move-ment creates artifact mimicking the polymorphic ventricular tachycardia rhythm, torsades de pointes.

2. Ho KK, Ho SK: Use of the sinus P wave in diagnosing electrocardio-graphic limb lead misplacement not involving the right leg (ground) lead.

J Electrocardiol 2001;34:161.

3. Surawicz B, Knilans TK: Chou’s Electrocardiography, 5th ed.

Philadelphia, WB Saunders, 2001.

4. Abdollah H, Milliken JA: Recognition of electrocardiographic left arm/

left leg reversal. Am J Cardiol 1997;80:1247.

5. Chase C, Brady WJ: Artifactual electrocardiographic change mimicking clinical abnormality on the ECG. Am J Emerg Med 2000;18:312.

6. Surawicz B: Assessing abnormal ECG patterns in the absence of heart disease. Cardiovasc Med 1977;2:629.

7. Oster CD: Improving ECG trace quality. Biomed Instrum Technol 2000;34:219.

8. Pahlm O, Haisty WKJ, et al: Evaluation of changes in standard electro-cardiographic QRS waveforms recorded from activity-compatible proxi-mal limb lead positions. Am J Cardiol 1992;68:253.

9. Lin SL, Wang SP, Kong CW, et al: Artifact simulating ventricular and atrial arrhythmia. Jpn Heart J 1991;32:847.

10. Littman L, Monroe MH: Electrocardiographic artifact [letter]. N Engl J Med 2000;342:590.

Clinical Features

The electrocardiographic (ECG) changes during the first year of life reflect the switch from fetal to infant circulation, the maturation of the autonomic nervous system, and the increas-ing muscle mass of the left ventricle. The size of the right and left ventricles changes predictably as the neonate becomes an infant, then a child, then an adolescent. Because of the physi-ologic stresses on the right ventricle during fetal development, the right ventricle is larger and thicker at birth than the left ventricle. Normally, by approximately 1 month of age, the left ventricle is slightly larger. By 6 months of age, the left ven-tricle is twice the thickness of the right. By adolescence, the left ventricle is at least 2.5 times as thick as the right.¹

Frequently, additional precordial leads are included on a pediatric ECG (V3R, V4R, and V7). These give additional insight into the activity of the right ventricle and posterior left ventricle, which are immediately beneath these leads. This information is particularly useful for ongoing evaluation of cardiac physiology in patients with complex congenital abnormalities. In most pediatric patients, however, these leads can be ignored or covered without affecting the remainder of the ECG interpretation.

22

Table 5-1 summarizes the significant yet normal changes that occur in cardiac physiology during the transitions from fetus to newborn, infant, child, and adolescent. The table includes age-based normal ranges for heart rate, QRS axis, PR and QRS intervals, and R and S wave amplitudes. Because such vast changes occur in the first year of life, 7 of the 12 age groupings involve the newborn and infant phases. After infancy, these changes are more subtle and more gradual as the child’s ECG becomes more and more like that of the adult.

Electrocardiographic Manifestations

P Wave. The most useful leads for review of P waves are leads II and V1. P-pulmonale or right atrial abnormality can be diagnosed in the presence of a peaked, tall P wave in lead II. In the first 6 months of life, the P wave must measure at least 3 mm to be pathologic. Thereafter, an elevation of 2 mm is adequate to establish this diagnosis.¹P-mitrale or left atrial abnormality (LAA) can be diagnosed with a biphasic P wave in V1that has a terminal inferior component of one box wide and one box deep. Although LAA can also be diagnosed in the presence of a notched P wave in lead II in adults, this find-ing is a normal variant in approximately 25% of pediatric patients.²

QRS Complex. QRS complex duration is somewhat shorter than in adults, presumably because of decreased muscle mass.²Diagnoses of conduction disturbances must take this into account. The QRS complex is pathologically prolonged when it is longer than 0.08 sec in a patient 8 years of age or younger. In an older child or adolescent, a QRS duration of greater than 0.09 sec is also pathologic¹(Table 5-1 and Fig. 5-1).

T Wave. The T waves in the pediatric ECG are quite variable. The change from right to left ventricular dominance in the first few days of life is reflected in the T waves.¹The T wave is frequently upright in the first week of life through-out the precordium²(Fig. 5-1). Thereafter, almost all of the T waves are upright except for aVR and V1to V3, where the T waves remain inverted (Figs. 5-2 and 5-3). The T waves in leads V1to V3are usually inverted from the newborn period ELECTROCARDIOGRAPHIC HIGHLIGHTS

• Because of right ventricular dominance in infants, the QRS axis demonstrates a marked rightward shift with a high R/S ratio in leads V₁and V₂, and low ratio in V₅and V₆.

• Normal PR segment and QRS complex intervals are shorter early in infancy because of lesser cardiac muscle mass.

• With the exception of the first week of life, T wave inversion is common in children, particularly in V₁to V₃, and is known as a juvenile pattern.

• Heart rates are generally higher in infants and young children, and decrease with age to adulthood.

• ^{A QT}Cinterval as long as 0.49 sec is considered normal in the first 6 months of life.

Chapter 5