The lead wires are wrapped too closely together, and this artifact appears on the tracing.

Electrocardiographic artifacts are defined as electrocardiographic alterations, not related to cardiac electrical activity. As a result of artifacts, the components of the electrocardiogram (ECG) such as the baseline and waves can be distorted. Motion artifacts are due to shaking with rhythmic movement. Examples of motion artifacts include tremors with no evident cause, Parkinson’s disease, cerebellar or intention tremor, anxiety, hyperthyroidism, multiple sclerosis, and drugs such as amphetamines, xanthines, lithium, benzodiazepines, or shivering (due to hypothermia, fever (rigor due to shaking), cardiopulmonary resuscitation by chest compression (oscillations of great amplitude) and patients who move their limbs during the test, causing sudden irregularities in the ECG baseline that may resemble premature contractions or interfere with ECG wave shapes, or other supraventricular and ventricular arrhythmias. When the skeletal muscles experience shaking, the ECG is “bombarded” by apparently random electrical activity.

Keywords: artifacts, electrode misplacement, incorrect electrode interchange, tremor artifacts

An irregular electrocardiogram (ECG) baseline may resemble atrial fibrillation (AF) (Finsterer, Stöllberger, & Gatterer, 2003) or atrial flutter (Baranchuk & Kang, 2009; Barrett, Kelly, Halley, & Sugrue, 2007; Hwang, Chen, Sung, & Lee, 2014; Nam, Best, Greaves, & Dayananda, 2016; Prabhavathi, Ravindranath, Moorthy, & Manjunath, 2009), and a slow regular rhythm may suggest the possibility of AF with complete AV block or junctional escape rhythm. However, on a more thorough inspection, P waves are visible.

The presence of other electrical devices in the room where the ECG is being conducted may cause recordings with electrical interference. In such cases, any device that may interfere with the ECG signal should be turned off: these include cell phones within 25 cm of the ECG sensor module, electrical beds, surgical and fluorescent lamps.

The artifacts produced by alternating current cause a “darkened reinforcement” in the ECG baseline, often making an analysis of rhythm difficult. This is due to lack of filters for alternating current systems or a poor operation of the device.

To assess the cause of this artifact, the ECG should be charged to see the ECG is connected to a properly grounded outlet, the ECG should be recorded using the battery as the power source (Figure 1). It is important to identify this artifact, since artifacts may lead to performing unnecessary tests with additional costs and therapeutic interventions. For this reason, continuous education of technicians who record ECGs is essential.

In Parkinson's disease and parkinsonian syndromes, continuous muscle twitching can be mistaken for atrial flutter (pseudo‐atrial flutter) due to gross and constant irregularities with a 300 bpm rate. In such cases, electrodes should be placed at the upper part of the arms and legs (Figures 2 and ​3).

To eliminate limb tremors due to Parkinson’s disease, the electrodes should be placed at the roots of the limbs, which attenuates or abolishes the tremors and the myopotentials. Parkinsonian tremor may cause very wide complexes resembling VT. In a patient with a wide tachycardia complex and tremors, an artifact related to tremors should be considered (Sawhney & Campbell, 2014). A careful analysis of the ECG may exclude artifacts related to pseudo‐ventricular tachycardia (Llinas & Henderson, 1999; Riaz, Gardezi, & O'Reilly, 2010). The proper interpretation of ECGs and a correlation with clinical history are keys.

Some ECGs may resemble specific arrhythmias, such as VT (Ortega‐Carnicer, 2005) and atrial flutter (Handwerker & Raptopoulos, 2007) or atrial fibrillation. It is important to make a correct diagnosis because a mistaken diagnosis may lead to an unnecessary use of medications and procedures in a patient. The characteristics that help to differentiate VT from an artifact include:

1. Absence of hemodynamic impairment during the event;

2. Presence of normal beats in any lead;

3. An unstable baseline in the ECG before or after the event or both.

4. Association with body movement.

Huang et al. (2006) describe three signs that may help to differentiate VT from pseudo‐VT. The presence of any of these elements suggest pseudo‐VT:

• Sinus sign: one of the frontal leads (I, II, and III) may present normal sinus rhythm with P, QRS, and T waves.

• Spike sign: presence of small regular or irregular peaks between wide QRS complexes.

• Notch sign: overlapping notches in the artifact, appearing to be a wide QRS complex, coinciding with the duration of the cycle in which the sinus rhythm was recorded.

It has been estimated that errors in the placement of electrodes occur in 0.4% to 4% of ECGs performed (Kors & van Herpen, 2001). Incorrect connections of electrodes during ECG recordings may resemble rhythm or conduction alterations, myocardial ischemia or infarction. They also cause shifts in P waves and the QRS axis, and they may mimic ectopic atrial rhythms, fascicular block or dextrocardia; the latter occurring with left arm‐right arm reversal. When only precordial electrodes are reversed, or just those of the limbs, excluding the neutral lead, the shapes of waves are inverted or do not change, and the interval duration is not modified. The mistake can be recognized by the presence of unusual P‐QRS patterns, for example, negative P‐QRS in I or II, positive in aVR, P‐QRS complexes in an opposite direction to leads I and V6, etc. Computerized algorithms have been developed to detect recurrent placement of electrodes, such as those based on artificial neuronal networks, or correlation between original and rebuilt leads (Batchvarov, Malik, & Camm, 2007).

2.3.1. Accidental left arm‐right arm reversal (LA/RA)

In this case, negative P, QRS and T waves are recorded in lead I, compatible with dextrocardia but the precordial leads maintain the normal progression of QRS complexes, thus eliminating the possibility of dextrocardia (Figure 4).

Typical ECG of LA/RA reversal. Note negative P, QRS and T waves in I, QS pattern in II, III, and aVF followed by inverted T wave that can simulate inferior myocardial infarction. The clues for the correct diagnosis are the normal progression of QRS complexes in the precordial leads and all negative waves in lead I

Other elements that allow a diagnosis of LA/RA reversal are:

1. The presence of positive P and R waves in aVR.

2. The electrical axis of QRS with possible extreme shift to the right, i.e., located in the right upper quadrant between −90° and ±180°, north‐east quadrant, or “no man's land.”

2.3.2. Differential diagnosis with dextrocardia

In dextrocardia, lead I has inverted P, QRS, and T waves. Lead II: represents the usual III lead and vice versa. aVR and aVL are reversed and prominent negative deflections are observed in aVL instead of in aVR. aVF is not affected. The P axis (SÂP) is to the right and inferior at approximately +140°. The P wave is negative in aVL and I, positive in III and aVR.

Unlike the accidental mistaken RA/LA reversal, the precordial leads: from V1 through V6, unlike the accidental mistaken RA/LA reversal, have QRS complexes with R/r wave of progressively decreasing width: there is reverse progression of the r wave in the precordial leads from V1 through V6 (decreasing). V1 is the equivalent to the usual normal V2 and vice versa (Figures 5, ​6, ​7).

Typical example of dextrocardia. We observe SÂP at the right and below, pointing at approximately +120° (III); negative P wave in aVL and I, positive in III; inverse progression of R wave in precordial leads V2 through V5. This is the important key to differentiate it from LA/RA reversal

ECG‐VCG correlation in the horizontal plane in a case of dextrocardia. Negative P wave in V5–V6, the initial 10 ms vector is heading forward and to the left; QRS loop of clockwise rotation and predominantly located in the right posterior quadrant; reverse progression of R wave in precordial leads V1 through V6 (decreasing) and negative T wave in V5–V6

In reversal of the LA/LL electrodes, Einthoven's triangle rotates 180° vertically around an axis formed by aVR with the following effects on ECG: Lead III becomes inverted, leads I and II switch places, leads aVL and aVF switch places and aVR remains unchanged.

The P wave has a larger voltage in I than II (exchanged amplitude of P waves: this should raise the suspicion of accidental LA/LL lead reversal, and has a 90% accuracy if the patient is in sinus rhythm (Abdollah & Milliken, 1997; Velagapudi, Turagam, Ritter, & Dohrmann, 2017). However, Heden (2001) found a 90% sensitivity and 38% specificity for this abnormality.

LA/LL reversal has the tential to create a pseudo‐inferior wall infarct pattern on the ECG. LA/LL reversal also causes inverted P waves in III. This is an important clue to determine the presence of a lead reversal. Frequently this error will lead to a near isoelectric line in leads I, II, or III; which might be the only sign of LA/LL lead reversal in routine clinical practice.

The usual cause for this accidental LA/LL leads reversal is due to the leads not being inserted in the proper place in the cable junction box after cleaning (Figure 8).

• aVL and aVF are reversed.

The changes in precordial leads are null or minimal. There would be changes in amplitude or voltage if the “exchanged” electrode was the indifferent one, the one in the right leg).

A surprising historical fact is that the initial description of P voltage sign in I > II (PI > PII) and P with a positive final portion (minus‐plus P‐wave in III) was made by Goldberger in 1942 (Goldberger, 1942a,b), who was the creator of limb leads aVR, aVL, and aVF. Originally there were only three leads: I, II, and III.

2.3.3. Right arm/left leg (RA/LL) electrode reversal

The RA/LL electrode reversal may cause pseudo‐inferior myocardial infarction. However, unlike inferior infarction in sinus rhythm, P waves in leads aVF and II are also inverted. Lead II, I, and III become inverted, leads I and III switch places, leads aVR and aVF switch places, and lead aVL is unchanged (Figure 9a).

Schematic example of RA/LL reversal (a), LA/RL reversal (b) and bilateral arm‐leg reversal (c). (a) Einthoven's triangle rotates 180° around the axis formed by aVL. (b) Einthoven's triangle collapses to very thin “slice” with the RA electrode at its apex. (c) Einthoven's triangle collapses to a very thin slice with the LL electrode at its apex

2.3.4. Truncal or nonstandard limb leads placement

This may cause pseudo‐inferior or inferolateral myocardial infarction pattern, or disappearance of inferior or inferolateral infarction pattern (Sevilla et al., 1989) or QRS electrical axis deviation to the right (Bond et al., 2016).

2.3.5. Accidental reversal of right leg and right arm electrodes (RL/RA)

Diagnosis of RL/RA reversal should be suspected when a very small voltage is recorded (<0.1 mV) in limb lead II. RL/RA lead reversal has the following ECG features: lead I becomes an inverted lead III, lead II records a flat line, lead III is unchanged, lead aVL approximates an inverted lead III, and leads aVR and aVF become identical.

2.3.6. Accidental reversal Left Arm/Right Leg (LA/RL)

With LA/RL(N(neutral)) electrodes reversal, the LA/LL electrodes record almost identical voltages, with difference between them (i.e., lead III = zero). By Einthoven's law, perpendicular to aVR is ≈lead III. In this exchange of electrodes, the perpendicular to aVR becomes ≈lead II. The displacement of the neutral electrode renders leads aVL and aVF mathematically identical, such that they appear exactly alike (but different to the baseline ECG). LA/RL(N) lead reversal has the following ECG characteristics: Lead I becomes identical to lead II, lead II is unchanged, III has a flat line (zero potential), aVR approximately to an inverted II, aVL and aVF become identical and the precordial voltages may also be distorted, because the neutral electrode has been moved (Figure 9b).

2.3.7. Arms and legs reversal or bilateral arm‐leg reversal (LA/L and RA/L)

If the electrodes on each arm are switched with their corresponding leg electrode (LA with LL, RA with RL), the RA and LA electrodes (now sitting on adjacent feet) record almost identical voltages, which makes the difference between them negligible (lead I = zero). Leads II, III, and aVF become identical (equivalent to inverted lead III), as they are all now measuring the voltage difference between the left arm and the legs. The displacement of the neutral electrode renders leads aVL and aVR mathematically identical, such that they appear exactly alike (but different to the baseline ECG) (Figure 9c, Table 1).

Summary for recognition of electrocardiographic lead misplacements: Limb lead reversal, major and minors footprints and relative frequency

2.3.8. Normal and incorrect placement of precordial leads

A correct placement of precordial leads is basic for a proper performance of a tracing. (Kligfield et al., 2007; Rautaharju, Park, Rautaharju, & Crow, 1998).

Clues to recognize this type of misplacement of electrodes:

1. The bipolar inferior leads II or III and the bipolar lateral lead I show (almost) a straight line because they measure the potential difference between the two inferior limbs. This difference is minimal.

2. The other two bipolar leads of the limbs look identical, or one of them is an inverted image of the other.

3. Two of the leads of the unipolar limbs also look identical, while the third one looks like one of the bipolar limbs or their inverted image (Batchvarov et al., 2007).

The six precordial leads are called “V” leads, and numbered V1 through V6. A standardized procedure for locating and documenting ECG chest electrode positions is paramount for a correct tracing (Figure 10). A frequent mistake when performing an ECG is a positioning of the right precordial leads (V1, V2, V3); too high or too low, i.e., above the 4th intercostal space observed in 50% of tracings or inferior and left shift in 30%–50% of the cases in leads V4 through V6, which indicates that these lateral precordial leads are commonly placed outside their respective anatomical sites (Wenger & Kligfield, 1996).

Correct positioning of the precordial electrodes in the frontal projection (a) and supine position (b). The left arm should be a little apart from the chest to place electrodes V5 and V6. V1: in the 4th intercostal space, in the right sternal border; V2: in the 4th intercostal space, in the left sternal border; V3: halfway between electrodes V4 and V2; V4: in the 5th left intercostal space, in the midclavicular line (downward from the half of the clavicle point); V5: in the same level as electrode V4, the anterior axillary line (downward from the anterior axillary fold); and V6: in the same level as electrodes V4 and V5, in the midaxillary line (downward from the middle point of the armpit)

A mistaken placement of the right precordial leads may cause a greater negative component of P or totally negative P (García‐Niebla, Rodríguez‐Morales, Valle‐Racero, & de Luna, 2012) and triphasic pattern of the rSrʹ type, with narrow rʹ in V1 of pseudo‐incomplete right bundle branch block, poor progression of R or increased voltage of R from V1 to V3. Consequently, we should suspect an inappropriately high placement of right precordial leads in a patient with no heart disease, by the presence of negative P wave only in V1, mainly if accompanied by rSrʹ morphology. Also, the recording in V2 of a final negative component of the P wave often accompanied by a biphasic P wave in V1 with usual predominance of the negative component is also a strong indication of high placement of these leads, and may cause inappropriate progression of the R wave.

The low placement of the right electrodes in the 5th intercostal space usually is unnoticed, but at increased voltage of R, approximately 0.1 mV in V1–V2 for each inferior intercostal space will be observed (García‐Niebla et al., 2012).

Exchanging the V1 electrode with V3, red and green, respectively, may lead to R wave in V1 > V2–V3 (Figure ​12).

Excessive use of conductive gel on the precordial leads. The use of excessive conductive gel continuously throughout the precordium results in an ECG tracing with equal QRS complexes across the precordial leads, which corresponds to the mean of the electrical potentials in these leads

Eventually, the precordial electrode reversal may be confused with right ventricular hypertrophy (RVH). The following main criteria can be applied to confirm the diagnosis of RVH: R wave of V1 and V2 > 7 mm; S wave of V1 < 2 mm (0.2 mV); ventricular activation time greater than 40 ms in V1; positive T wave in V1 from 3 days of life up to 6 years of age, when the R/S ratio in this lead is greater than 1; negative “primary” (symmetrical) T waves in V1 and V2 in severe cases; R wave of V1 + S wave of V5 and/or V6 ≥ 10.5 mm (Sokolow‐Lyon index for the RV); and V5 and V6 ratio: R/S ratio in V5 and V6 ≥ 1 (Figure 11).

Using conductive gel in excessive amounts leads to the so‐called “large precordial lead,” resulting in “monotonous” QRSs in precordial leads (Figure 12).

Electrocardiography artifacts are frequent and may be readily identified in most cases. They include external and internal interference such as poor grounding of the device, interference by devices within the room such as cell phones within 25 cm of the ECG sensor module, electrical beds, surgical and fluorescent lamps, chest compression and decompression movements during CPR, artifacts produced by alternating current affecting the ECG baseline and mistaken placement in the cable junction box. With regard to patient related, muscle twitching is most prominent—causes of which include: shivering due to hypothermia, inappropriate cleansing of the skin, excess of precordial conductive gel, and mistaken placement of both limb and precordial leads. It is essential to perform periodic evaluations of the technicians in charge of performing the tracings with the aim of decreasing the all types of artifacts.

The authors do not have any conflict of interest regarding this work.

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