Since its introduction in 1903 by Willem Einthoven, the 12-lead ECG has been the most important test for interpreting cardiac rhythms and conduction system abnormalities. The ECG has had a tremendous role in detecting myocardial ischemia; evaluating a diverse spectrum of cardiac abnormalities such as valvular heart disease, cardiomyopathy, pericarditis, and hypertensive disease; and monitoring drug treatment such as antiarrhythmic therapy; as well as detecting metabolic disturbances.
In the prehospital setting, ECGs have proven very effective in detecting life-threatening dysrhythmias and acute coronary conditions requiring immediate prehospital intervention or definitive care in a cardiac catheterization laboratory.1
Two groups of leads are used to record an ECG:
* Limb or extremity leads. The three bipolar leads (I, II and III) measure the difference in potential between electrodes at two extremities, and the three unipolar leads (aVR, aVL and aVF) measure the cardiac voltage at one site relative to the central terminal.
* Precordial or chest leads. Leads V1 through V6 measure the difference in voltage between electrodes placed in specific positions and the central terminal.
In order to get a correct 12-lead ECG recording, the electrodes should be positioned as follows:
* RA–on the right upper limb, avoiding thick muscles
* LA–on the left upper limb, avoiding thick muscles and symmetrical to RA
* RL–the neutral lead, on the right lower limb
* LL–on the left lower limb and symmetrical to RL.
The following electrodes obtain the electrical recordings for the limb leads:
* V1–fourth intercostal space, to the right of the sternum
* V2–fourth intercostal space, to the left of the sternum
* V3–midway between V2 and V4
* V4–fifth intercostal space, midclavicular line
* V5–anterior axillary line, same level as V4
* V6–midaxillary line, same level as V4 and V5.
* Patient movement is the most common reason for ECG artifact. Other causes include resting involuntary muscular activity such as in Parkinson disease, tremor caused by medications such as amphetamines and beta-agonists, chest compressions such as in cardiopulmonary resuscitation, shivering caused by hypothermia, an external electromagnetic field from other devices in the room, insufficient amount of electrode gel, loose connections, and misplaced leads.
What are the harmful effects of ECG lead misplacement on diagnosis and subsequent patient management steps? What ECG findings are associated with different lead misplacements? How can we differentiate lead misplacement from other causes with similar ECG findings?
Although no specific number is found in the literature, an estimated 0.4% to 4% of all recorded ECGs are recorded using misplaced leads.2
Lead misplacement can cause providers to miss ST-segment changes and R-wave progression or think they are present when they are not. Misplaced leads also can make a normal electrical axis appear as a pathologic left or rightward axis, and misrepresent the location of a bundle branch block or infarct. Misplacement can mimic a life-threatening dysrhythmia, confuse the diagnosis with dextrocardia or MI, delay proper treatment, or lead to inappropriate and potentially harmful treatment.
Reversed limb leads are the most common culprit in ECG lead misplacement, and reversing the RA and LA is the most frequent mistake. On the ECG, this appears as negative P waves and QRS complexes in lead I, which is uncommon even in patients with cardiac disease. At first glance, this can be confused with dextrocardia. In this context, normal R-wave progression can play a key role in differentiation (the R wave amplitude increases and S wave amplitude decreases from V1 through V6) in lead misplacement as opposed to being poor R-wave progression with a negative QRS complex in V6 in dextrocardia.
Reversing RA and LL can cause negative P waves, QRS complexes, and T waves in leads I, II, III, and aVF (known as complete inversion), which can mimic inferior-wall MI. However, inferior-wall MI is characterized by changes in leads II, III, and aVF, and reciprocal changes in leads I and aVL. However, the inclusion of lead I in the inversion, the unique complete inversion (including P waves and QRS complexes), and the absence of reciprocal ST-segment depression (especially in aVL) all point toward RA–LL lead reversal, rather than inferior-wall MI.
Reversal of RL and RA or LA causes one lead to record a zero potential difference between lower extremities: lead II in the case of RL–RA reversal, and lead III in the case of RL–LA reversal. On the ECG, the result is far-field signal, a ﬀat line with a tiny deflection representing the QRS complex. An RL–LL reversal is totally benign and causes no changes at all.
Reversing LA and LL causes inversion in lead III, left axis deviation, and a P wave in lead I that is larger in amplitude than the P wave in lead II. This type of reversal can be difficult to identify because it can be confused with left axis deviation, which is very common in hospitalized patients.
Electrodes for limb leads can be placed anywhere on the limb without affecting the resulting ECG. But torso-positioned limb electrodes can mislead the picture and even the diagnosis, especially if they are placed close to the heart or if the resulting ECG is compared with a standard ECG for the same patient. Placing the limb electrodes on the torso changes the voltage recorded, and can overestimate or underestimate atrial overload and left ventricular hypertrophy, or show pseudo ST–T changes (ST-segment depression or T-wave inversion) or pseudo Q waves that can be misinterpreted as acute myocardial ischemia.
Another common way of recording cardiac electrical activity is to use cardiac monitors, which use fewer leads and electrodes and provide a derived 12-lead ECG. Although these derived 12-lead ECGs are dependable for detecting new bundle branch blocks or ST-segment changes of acute myocardial ischemia (conditions that require urgent care), they should not be compared with standard ECGs when precise amplitude measurements are needed, for example when determining whether reperfusion therapy has succeeded in resolving ischemic ST-segment changes. In summary, avoid serial comparisons between standard ECGs and torso-positioned ECGs or derived ECGs.
The correct placement of V1 is key, because it is the first precordial lead and the reference for placing the other precordial leads. Misplacing V1 one intercostal space above the correct place will result in all other precordial leads being misplaced superiorly. The result is poor R-wave progression on ECG (which can also be caused by precordial lead reversal), and can mimic anterior-wall MI.
Identifying ECG misplacement can be challenging. Remember that in an ECG with correct lead placement, lead I will have a positive P wave and a positive R wave, aVR will have a negative P wave and a negative R wave, the largest P wave amplitude will appear in lead II, R-wave amplitude increases progressively from V1 to V4, and S-wave amplitude decreases progressively from V4 to V6.
If misplacement is suspected, look for these clues: Abnormal signs or amplitudes of specific waves in specific leads, extremely deviated cardiac axis, and very low voltage. The REVERSE mnemonic summarizes common lead reversals and their significance (Figure 3).3
Undetected lead misplacement can cause misdiagnoses and treatment errors. Practitioners should have a low threshold of suspicion for lead misplacement, be familiar with the normal variations of the ECG, be able to recognize the characteristics of various types of lead misplacement, and avoid serial comparisons between ECGs recorded in different ways.
Our case presentation is a good illustration of the importance of recognizing lead misplacement on the ECG, to avoid unnecessary or inappropriate management. The normal repeat ECG confirms that the patient did not have an MI, but rather angina or atypical chest pain, possibly related to gastroesophageal reflux.
1. Sejersten M, Sillesen M, Hansen PR, et al. Effect on treatment delay of prehospital teletransmission of 12-lead electrocardiogram to a cardiologist for immediate triage and direct referral of patients with ST-segment elevation acute myocardial infarction to primary percutaneous coronary intervention. Am J Cardiol
2. Bond RR, Finlay DD, Nugent CD, et al. A simulation tool for visualizing and studying the effects of electrode misplacement on the 12-lead electrocardiogram. J Electrocardiol
© 2013 American Academy of Physician Assistants.
3. Baranchuk A, Shaw C, Alanazi H, et al. Electrocardiography pitfalls and artifacts: the 10 commandments. Crit Care Nurse