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ECG diagnosis errors are frequently observed in clinical practice. Misdiagnosis due to ECG errors can lead to incorrect clinical diagnoses, affecting the choice of appropriate treatment plans. Therefore, improving the accuracy of ECG diagnoses is extremely important.

This article will analyze some common causes of ECG diagnosis errors based on years of experience in reading ECGs, combined with relevant literature, and propose corresponding countermeasures to prevent diagnostic errors, for reference in work and study.

1. Poor performance of ECG instruments causing ECG errors

In recent years, with the rapid development of computer technology, biomedical technology, and ECG analysis technology, the development and production of ECG instruments have also progressed rapidly. However, there are still certain differences in the ECG instruments provided by various manufacturers, and some lower-quality ECG instruments can cause distortion in the ECG, creating misleading diagnostic impressions. When errors occur due to poor instrument performance, manufacturers should be contacted immediately for repairs, improvements in machine performance, or replacement with higher-quality ECG instruments.

2. Human operational errors and artificial artifacts leading to ECG diagnosis errors

Many misdiagnoses occur due to failure to recognize and eliminate certain human errors during ECG analysis. A study on ECG diagnosis errors found that human operational errors and artificial artifacts account for about 1%. In China, it is estimated that ECGs are recorded for hundreds of millions of people each year, making the number of misdiagnoses due to human operational errors and artifacts staggering. Therefore, mastering correct operational techniques and preventing human positional errors is very important.

2.1 Common operational errors

2.1.1 Reversed lead connections for left and right arms

This is a common operational error, where the left and right upper limb leads are mistakenly connected, resulting in the six limb lead ECG resembling that of right heart positioning, i.e., I is inverted (P and T waves of lead I are inverted, QRS main wave is downward), lead II is swapped with lead III, and lead aVR is swapped with lead aVL, while lead aVF remains normal. Observing the chest lead patterns, there are no characteristic changes of right heart ECG, which can help in differentiation. In addition to the errors mentioned above, care should also be taken to avoid incorrect connections of upper and lower limb leads.

The simplest method to identify reversed lead connections is to observe the ECG pattern of lead aVR. Normally, the P wave and T wave of lead aVR are both downward, and the main QRS wave is also downward. If the aforementioned errors occur, it generally causes the P wave and T wave of lead aVR to be upright. Whenever such abnormal changes are observed, one should consider the possibility of incorrect lead connections, and immediately check and correct the erroneous connections before recording again to avoid misdiagnosis.

2.1.2 Improper placement of chest electrodes

This error can affect the amplitude of the QRS complex. When the electrode position is raised by 2 cm, the R wave amplitude significantly decreases, and an rS type wave may become a QS type, potentially being misdiagnosed as myocardial infarction. The method to prevent this error is strict adherence to operational standards; the technicians or nurses recording the ECG should have undergone standardized ECG training and possess a training certificate. When hospitalized patients undergo repeated ECG recordings, the positions of the chest electrodes should be marked to avoid positional changes during subsequent recordings, which could lead to diagnostic errors.

2.1.3 Impact of using interference keys

Most ECG machines are equipped with interference keys. Using the interference key can reduce the total amplitude of the P, Q, R, S, and T waves.

Reports indicate that using the anti-AC interference key alone can reduce the amplitude by an average of 13.16%;

Using the anti-myogenic interference key alone can reduce it by 8.43%;

Using both keys together can average a reduction of 17.54%, with significant differences (P<0.001).

It is recommended to avoid using interference keys whenever possible, especially to avoid using both keys together. In special circumstances where interference keys are used, it should be noted in the ECG images and other relevant data to ensure the authenticity and comparability of the images.

2.2 Common artificial artifacts

These include external AC current interference, patient muscle tremors, unstable ECG baseline, loose or disconnected lead wires, poor ground contact, poor electrode contact, phone ringing or mobile phone interference, improper timing of pressing the voltage calibration key, and patient constitution or pathological factors, all of which can alter the ECG waveform.

2.2.1 External AC current interference

This is characterized by a very regular fine waveform visible in all leads at a frequency of 50-60 times per second. The source of interference should be identified, such as checking for AC electrical devices in the surrounding environment, whether the patient’s limbs are in contact with a metal bed, whether the electrode plates are clean or rusted, whether the skin preparation under the electrode plates is adequate, whether the electrode plates are too tightly or loosely bound, and whether there are loose or broken lead wires or poor performance of the ECG machine, and take immediate action.

2.2.2 Muscle tremor interference

Muscle tremor interference typically presents as rapid irregular fine spikes at a frequency of 10-300 times, which can easily be misdiagnosed as atrial fibrillation. The cause of this should be investigated, such as excessive mental tension of the subject, low room temperature, tight contact between the electrode plates and the skin, narrow examination beds preventing muscle relaxation, pathological convulsions and tremors, such as hyperthyroidism and tremor paralysis.

2.2.3 Unstable ECG baseline, fluctuating up and down or suddenly rising and falling

This severely impacts the correct judgment of ST-T. The cause should be immediately identified and corrected. Common causes include patient movement of the body or limbs during ECG recording, unstable breathing causing fluctuations in the chest lead ECG baseline, rust on electrode plates, excessive or insufficient conductive paste, overly taut lead wires, poor contact between the electrode plates and the skin, or depletion of the internal dry battery of the ECG machine or unstable AC power supply voltage.

2.2.4 Loose or disconnected lead wires

This can lead to a sudden absence of waveform in the ECG for a period, easily misinterpreted as sinus arrest or sinoatrial block, but careful reading will reveal no electrical activity in that segment. Immediate checks should be made to ensure that the electrode plate connections are secure, there are no disconnections, and whether the lead wire ends have any copper wire falling off or breaking, and appropriate measures should be taken. Poor installation or incorrect connection of the ground wire can cause poor ground contact.

The ECG shows characteristics of continuous medium-frequency low-amplitude uniform sawtooth waveforms. When this type of interference occurs, adjusting the ground wire contact can immediately eliminate the artifact. Another important role of the ground wire is to prevent leakage current from the ECG machine from posing a danger to the patient’s life. Please pay attention!

3. Failure to develop a systematic analysis habit for ECGs or insufficient detail in reading ECGs leading to misdiagnosis

Developing a scientific method and habit for ECG analysis, and reading ECGs step by step, is crucial for ensuring the accuracy of ECG diagnoses and preventing errors. Careful and detailed reading of the ECG, and if necessary, analyzing and comparing each lead and wave is key to avoiding diagnostic errors. Many highly skilled physicians make diagnostic errors mainly due to carelessness.

3.1 Several common situations

3.1.1 Failure to notice the voltage calibration mark

Inexperienced physicians often overlook the voltage calibration mark, misdiagnosing a normal ECG as high voltage or low voltage. During the examination, if the automatic recording device is not used, a voltage mark should be made at both ends of all leads that have not changed; if some leads have changed the voltage calibration, the changed voltage mark should be made at both ends of all leads that have altered the voltage calibration, and their height and damping should be regularly checked.

3.1.2 Ignoring the P-R segment

The P-R segment reflects changes in the P-Ta segment and can provide valuable diagnostic information, such as acute pericarditis, atrial infarction, and atrial injury. Ignoring the P-R segment offset may lead to missing early ECG changes of acute pericarditis or atrial infarction. The ECG manifestations of pericarditis traditionally include widespread ST-T changes, flat T waves, isoelectric, bidirectional or inverted, and may also present low voltage QRS complexes and sinus tachycardia as three major characteristics.

Recent studies have found that cardiac electrical alternans, the ST segment elevation in lead V6, and the ratio of T wave to P wave are new major features of pericarditis ECG changes, especially the elevation of the PR segment in lead aVR, which is characteristic and has high diagnostic value.

The ECG characteristics of acute pericarditis with PR segment offset are: (1) The PR segment offset vector points to the upper right (or right back), thus the PR segment in lead aVR (occasionally seen in lead V1) is always elevated, while most leads such as I, II, III, aVF, and V4~V6 have a lowered PR segment; (2) The offset amplitude is 0.05~0.15mV; (3) Regardless of whether it is elevated or lowered, the offset shape is mostly horizontal; (4) The direction of the PR segment offset is opposite to the ST segment vector, thus the leads with elevated ST segments have lowered PR segments, and conversely, the leads with lowered ST segments have elevated PR segments, especially prominent in lead aVR.

The PR segment offset is also one of the characteristic ECG manifestations of acute pericarditis, generally appearing in the early first or second stages of acute pericarditis, that is, before the elevated ST segment returns to the isoelectric line and before the T wave inversion, and the duration is relatively short (as shown in Table 1). It may be the earliest ECG abnormality in acute pericarditis, or even the only visible ECG change, and has early diagnostic value, which should be emphasized.

3.1.3 Not noticing the shortened P-R interval

This can lead to misdiagnosing pre-excitation syndrome as bundle branch block, ventricular hypertrophy, or myocardial infarction. Some may only notice the normal P-R interval without noticing the pre-excitation wave at the start of the QRS, QRS widening, and accompanying secondary ST-T changes, leading to missing Mahaim bundle pre-excitation waves.

The ECG manifestations of pre-excitation waves or pre-excitation syndromes formed by the Mahaim bundle are as follows:

1. The ECG shows pre-excitation syndrome similar to left bundle branch block patterns, where the pre-excitation wave increases at higher heart rates and decreases or disappears at lower heart rates. This is frequency-dependent, intermittent pre-excitation syndrome, which differs from left bundle branch block in that patients are generally younger and without organic heart disease, and experience tachycardia.

2. The change in QRS morphology from negative to positive in the chest leads occurs after lead V4, with r waves in leads V2–V4 greater than 40 ms, and q waves in leads V5–V6 decreasing or disappearing.

3. After atrial fibrillation occurs, the size of the pre-excitation wave varies significantly.

4. The QRS electrical axis is between 0° and 75°.

5. In cases of reentrant tachycardia, the QRS complex is wide and deformed, resembling a left bundle branch block pattern. The electrical axis is significantly leftward, sometimes resembling the QRS-T morphology of right ventricular apex pacing. The main QRS wave in leads V1–V4 is downward, while lead I remains R-type.

6. Mahaim bundle pre-excitation waves and Mahaim bundle pre-excitation syndrome are rare and should be distinguished from anterior wall myocardial infarction and left bundle branch block.

3.1.4 Ignoring J waves

The J point is the junction between the end of the QRS complex and the ST segment; if its amplitude increases and persists for a certain time, it is called a J wave. Ignoring J waves may lead to missing ECG changes associated with hypothermia, hypercalcemia, and ischemic J waves.

3.1.5 Failing to recognize hidden P waves (P′ waves) within the ST-T segment

This can lead to missing certain arrhythmias such as atrial premature beats, atrial tachycardia with atrioventricular block, second-degree and complete atrioventricular block, etc. If a protrusion is found in the ST segment, or if the T wave has notches or deformations, attention should be paid to whether there are hidden P waves or P′ waves within.

3.1.6 Not conducting a comprehensive observation and measurement of QRS duration

This can lead to misinterpreting certain components of the QRS complex (the initial Q wave or terminal S wave) as retrograde P waves. Finding the lead with the widest QRS complex for measurement can reveal that the so-called retrograde P wave is actually part of the QRS complex.

3.1.7 Ignoring U waves

Small U waves are a normal component of the ECG; an increase in U wave amplitude suggests hypokalemia or the effect of certain medications (such as quinidine). Large U waves are often associated with Torsades de Pointes ventricular tachycardia. Upright T waves in chest leads with inverted U waves (after resting or exercise tests) are an important indicator for diagnosing myocardial ischemia.

3.1.8 Not recognizing λ (Lambda) waves leading to misdiagnosis

Lambda waves are characterized by notches at the terminal part of the ascending and descending branches of the QRS complex, combined with a downward-sloping ST segment and inverted T wave, resembling the Greek letter λ (Lambda). In the past, some cases were considered atypical Brugada syndrome, but both the ECG manifestations and clinical characteristics, as well as molecular biological examination results, indicate clear differences from Brugada syndrome. Therefore, λ waves have been recognized as an independent ECG marker for identifying patients at high risk of sudden cardiac death.

Lambda (λ) waves manifest as downward-sloping ST segments in the inferior leads; resembling non-ischemic “single-cell action potential-like” changes or composite waves of QRS-ST, created by the slow decline of the ST segment and the subsequent T wave inversion.

3.1.9 Ignoring lead aVR

In the six-axis system, lead aVR is located in the right upper quadrant of the frontal plane, with its negative pole at the left lower 300 degrees, positioned between leads I and II. Due to the emergence of chest leads and the emphasis on leads I and II, lead aVR is often overlooked. In recent years, scholars have pointed out that lead aVR has significant application value in diagnosing ischemic heart disease, myocardial infarction, arrhythmias (differentiating left anterior fascicular block, wide QRS tachycardia, and narrow QRS tachycardia), acute pericarditis, predicting malignant arrhythmias, and acute pulmonary embolism. For instance, Vereckei proposed a simplified new process for differentiating wide QRS tachycardia using lead aVR in 2008 (Figure 15), which is simple, quick, and relatively accurate, suitable for clinical emergencies, with accuracy, sensitivity, and specificity being 91.5%, 96.5%, and 75%, respectively.

Figure 15: Vereckei’s simplified new process for differentiating wide QRS tachycardia using lead aVR

4. Lack of differential diagnostic ability for similar ECG changes leading to misdiagnosis

Insufficient systematic knowledge of ECG and failure to recognize some ECG changes with diagnostic value can lead to incorrect diagnoses.

4.1 Not conducting a comprehensive observation, making diagnoses based solely on individual lead waveforms

For instance, if the P wave amplitudes in leads II and III are similar, the P wave in lead I may be flat and difficult to detect. If one does not understand Einthoven’s equation, it is easy to misdiagnose based solely on the waveform of lead I as junctional rhythm.

4.2 Misdiagnosing TUP phenomena or multifocal atrial tachycardia as atrial fibrillation.

4.3 Confusing normal variants or positional Q waves with pathological Q waves

Abnormal Q waves appearing in leads aVL, III, and aVF, and QS types appearing in leads V1 or even V2 may be normal variants or positional Q waves. Noticing that related leads such as I, II, and V3 show no abnormal changes and no significant ST-T changes, lowering one intercostal space to record chest leads and recording the ECG vector map can help in differential diagnosis.

It is important to emphasize that the ECG vector map can provide a more accurate basis for differential diagnosis, so please pay attention!

4.4 Misdiagnosing left bundle branch block or left ventricular hypertrophy-induced changes in right chest leads as anterior wall myocardial infarction

Left bundle branch block and left ventricular hypertrophy can both present as QS types in leads V1–V2, and combined with corresponding ST segment elevation, can easily be misdiagnosed as anterior wall myocardial infarction. Noticing the morphology, degree, and stability of the QRS voltage elevation in chest leads and the elevation of ST segments in right chest leads can make differentiation straightforward. If necessary, the ECG vector map should be used for differentiation.

4.5 Misdiagnosing sinus tachycardia with “giant R wave” ST segment elevation as ventricular tachycardia

Multi-lead observation can easily reveal that the QRS waves in leads without ST segment elevation are not widened; although TP fusion occurs, careful observation will show that there is a related P wave before each QRS complex.

4.6 Missing severe hyperkalemia

In cases with widened QRS duration and flattened or absent P waves, one should consider the possibility of hyperkalemia. If there are clinical causes for hyperkalemia, immediate treatment should be initiated without waiting for laboratory reports, as the patient may experience cardiac arrest during the waiting period.

4.7 Misdiagnosing atrial flutter with 2:1 atrioventricular conduction as sinus tachycardia or atrial tachycardia

This occurs because one of the F waves overlaps with the ST-T segment. When encountering narrow QRS tachycardia at around 150/min, one should consider atrial flutter with 2:1 atrioventricular conduction, carefully observing leads II, III, aVF, and V1, and if necessary, using carotid sinus massage to assist in diagnosis.

4.8 Misdiagnosing multifocal atrial tachycardia as atrial fibrillation

Because both have fast and irregular ventricular rates. Careful observation will reveal that in the former, there is a related P wave before each QRS complex, with variable P wave morphology and an unstable P-R interval.

4.9 Ignoring the Wenckebach phenomenon

Grouped heartbeats often contain the Wenckebach phenomenon, measuring the P-P or R-R intervals, noting whether there is a “gradually shortening and then lengthening” characteristic. Based on the number of P-P (R-R) intervals within the Wenckebach phenomenon and the missing heartbeats, one can calculate the atrial or ventricular rates to make an accurate diagnosis.

4.10 Misdiagnosing branch-type ventricular tachycardia as supraventricular tachycardia with intraventricular conduction delay

When tachycardia presents with right bundle branch block and left axis deviation, one should be alert to the possibility of branch-type ventricular tachycardia. Careful observation of each lead is necessary, noting any atrioventricular dissociation, and if necessary, using esophageal leads to reveal the true atrial activity.

5. Aging or deficiency of ECG knowledge leading to misdiagnosis

5.1 Misdiagnosing interference-related atrioventricular dissociation as high-degree atrioventricular block. First-degree atrioventricular block with relative acceleration of atrial rate can exhibit ECG changes similar to high-degree atrioventricular block. Based on the R-P interval of ventricular capture + P-R interval, one can infer the atrial rate that receives conduction, thus excluding high-degree atrioventricular block. Complete atrioventricular dissociation is only one of the conditions for diagnosing complete atrioventricular block; another condition is that the ventricular rate is significantly slow (<45/min). Atrioventricular dissociation where the ventricular rate is close to the atrial rate is often interference-related. If the atrial rate exceeds the ventricular rate, it is block-related atrioventricular dissociation, i.e., complete atrioventricular block.

5.2 A P-R interval ≥0.12s does not necessarily reflect a conduction relationship between the P wave and the QRS wave; it may also indicate a coupling relationship.

When a sinus rhythm and junctional rhythm form atrioventricular dissociation, the diagnostic criteria for ventricular capture are: (1) it appears early; (2) the P-R interval reaches a conductive level, both must be present. In cases where the baseline rhythm has a significantly prolonged P-R interval, early appearing beats with a P-R interval ≥0.12s do not indicate a conduction relationship between the P wave and the QRS wave.

5.3 Misdiagnosing complete atrioventricular block as 2:1 atrioventricular block

This occurs because the atrial rate is exactly double the ventricular rate, with two P waves visible before each QRS complex. Careful measurement will show that the P-R interval is not constant, whereas in 2:1 atrioventricular block, the P-R interval is constant.

5.4 Misdiagnosing rapid atrial fibrillation as supraventricular tachycardia

In rapid atrial fibrillation, due to the indistinct f waves and the fast ventricular rate, the R-R interval seems regular, easily leading to misdiagnosis as supraventricular tachycardia. Careful measurement will reveal that the R-R intervals are still irregular, often >0.03s.

5.5 Misdiagnosing pre-excitation with atrial fibrillation as ventricular tachycardia

WPW syndrome with Af occurs in 11-39% (significantly higher than the general population of 0.5-2%). Manifestations are more prominent in the manifest than the concealed; multiple pathways are more common than single pathways; QRS complexes in WPW syndrome with atrial fibrillation are wide and deformed, requiring careful differentiation from atrial fibrillation with ventricular tachycardia. The differences are shown in Table 1. In ventricular tachycardia, the R-R intervals may also be irregular, but the difference between R-R intervals is <0.03s, whereas in pre-excitation with atrial fibrillation, the difference is often >0.03s.

Table 1: Key differentiation points between WPW syndrome with Af and Af with ventricular tachycardia

WPW Syndrome with Af	Af with Ventricular Tachycardia
RR interval difference	≥130ms	<130ms
Wide QRS morphology	Variable (depending on pre-excitation degree) initial vector same as δ vector, often showing blunt	Same source morphology (occasional ventricular fusion wave)
Narrow QRS regularity	Delayed appearance (increased conduction through normal pathways)	Early appearance (ventricular capture)
Clinical situation	History of recurrent SVT, showing WPW syndrome ECG manifestations before and after episodes	Often has organic heart disease, especially during exacerbation of heart failure, myocardial ischemia, electrolyte disturbances, medication effects, etc.

5.6 Diagnosing occasional long R-R intervals in atrial fibrillation as combined second-degree atrioventricular block

Atrial fibrillation with hidden conduction in the atrioventricular junction can lead to long R-R intervals. If one of the following two criteria is met, it can be diagnosed as second-degree atrioventricular block:

(1) R-R intervals lasting 1.5s or more, with a ventricular rate below 40 beats per minute. In a long interval of 1.5s, the ectopic impulses of atrial fibrillation have not conducted downwards. Although some cases may relate to hidden conduction, it is unreasonable to explain it solely by hidden conduction. Clinically, long R-R intervals often appear in cases of digitalis overdose or late atrial fibrillation, whereas early atrial fibrillation and patients not using digitalis never exhibit long R-R intervals. Therefore, in most cases, R-R intervals longer than 1.5s are caused by second-degree atrioventricular block. If it occurs more than three times, it can avoid coincidental occurrences, making the diagnosis more reliable.

(2) Occurrence of junctional or ventricular escape beats, occurring three times or more. The appearance of escape beats indicates that the ventricular rate has slowed to a level that endangers circulatory function, with the ECG revealing long and constant R-R intervals in irregular ventricular rates. In junctional escape, the escape cycle lasts 1-1.5s, equivalent to 40-60 beats per minute, with the escape QRS complexes appearing supraventricular in morphology, the same as other QRS complexes, or slightly different due to accompanying non-timing-related intraventricular conduction differences. In ventricular escape, the QRS complexes are wide and deformed (≥0.12s), with the escape cycle lasting 1.5-2.4s. In junctional escape, since the QRS complexes are the same as normal, the diagnosis relies on delayed appearance, fixed escape cycles, and constant R-R intervals.

5.7 Not understanding the diagnostic methods and steps for wide QRS tachycardia

Common causes of wide QRS tachycardia (WRT) include ventricular tachycardia (VT), supraventricular tachycardia (SVT) with intraventricular conduction delay, bundle branch block, and WPW syndrome with SVT. Their ECG (ECG) manifestations are similar, but their clinical significance differs, making differential diagnosis extremely important. Many ECG technicians cannot proficiently master the diagnostic methods and steps for wide QRS tachycardia, such as the Brugada four-step method, the WRT differentiation criteria proposed by Griffith, the four-step method using lead aVR to differentiate wide QRS tachycardia, and the Vi/Vt value diagnosis for wide QRS tachycardia, which leads to incorrect differentiation between ventricular tachycardia and supraventricular tachycardia with intraventricular conduction delay, and between ventricular tachycardia and supraventricular tachycardia with bypass conduction.

Figure 26: Brugada four-step method

6. Ignoring clinical data leading to ECG misdiagnosis

Many ECG changes are non-specific, and only by combining the ECG changes with clinical data can reliable judgments be made. For instance:

6.1 Not understanding the patient’s age, gender, and clinical situation, leading to normal variants being diagnosed as pathological conditions.

6.2 For suspected idiopathic long QT syndrome or Brugada syndrome patients, it is crucial to inquire about the history of syncope and cases of sudden death in family members. Figure 27 shows a patient with recurrent syncope, where the ECG shows a prolonged QT interval and exhibits U wave electrical alternans. Understanding their family history and past syncope history can confirm the diagnosis of hereditary long QT syndrome.

6.3 In distinguishing wide QRS tachycardia, the medical history is very important; a history of no heart disease and recurrent wide QRS tachycardia, especially in younger patients, often suggests supraventricular tachycardia or pre-excitation syndrome; a history of organic heart disease, especially following myocardial infarction, should first consider ventricular tachycardia, with predictive accuracy reaching 85% in patients with old myocardial infarction; right ventricular dysplasia and long QT syndrome often have family histories; drug toxicity and electrolyte disturbances leading to wide QRS tachycardia often have corresponding medical histories for reference.

6.4 The ECG can be a double-edged sword in diagnosing pulmonary embolism. To correctly utilize the ECG for diagnosing pulmonary embolism, it must be combined with the patient’s history and various auxiliary examination results. The symptoms and signs of pulmonary embolism are non-specific, and one must be adept at identifying issues from the clinical syndrome, needing timely auxiliary examinations for confirmation. The ECG manifestations of pulmonary embolism resemble myocardial ischemia in coronary heart disease and can easily be confused with old myocardial infarction.

6.5 Elevated T waves should raise suspicion for hyperkalemia. If a patient presents with oliguria or anuria, disappearing or indistinct P waves, widened QRS waves, and elevated T waves, it may suggest a diagnosis of hyperkalemia. If this patient also presents with sinus tachycardia or other supraventricular tachycardias, without attention to the medical history, it could be misdiagnosed as ventricular tachycardia.

6.6 In some acute pericarditis cases, ST segment elevation may only be significant in a few leads and may resemble AMI. It is essential to combine the medical history (nature of chest pain), myocardial enzymes, and echocardiographic examination results for judgment.

Note

This article is sourced from: Zhu Xiaoxiao ECG News

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