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"ECG" redirects here. For other uses, see ECG (disambiguation).
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Image showing a patient connected to the 10 electrodes necessary for a 12-lead ECG

Electrocardiography (ECG or EKG[1] from Greek: kardia, meaning heart[2]) is the recording of the electrical activity of the heart. Traditionally this is in the form of a transthoracic (across the thorax or chest) interpretation of the electrical activity of the heart over a period of time, as detected by electrodes attached to the surface of the skin and recorded or displayed by a device external to the body.[3] The recording produced by this noninvasive procedure is termed an electrocardiogram (also ECG or EKG). It is possible to record ECGs invasively using an implantable loop recorder.

An ECG is used to measure the heart’s electrical conduction system.[4] It picks up electrical impulses generated by the polarization and depolarization of cardiac tissue and translates into a waveform. The waveform is then used to measure the rate and regularity of heartbeats, as well as the size and position of the chambers, the presence of any damage to the heart, and the effects of drugs or devices used to regulate the heart, such as a pacemaker.

Most ECGs are performed for diagnostic or research purposes on human hearts, but may also be performed on animals, usually for diagnosis of heart abnormalities or research.

Medical uses[edit]

Twelve-lead ECG of a 26-year-old male with an incomplete RBBB

General symptoms indicating use of electrocardiography include:

It is also used to assess patients with systemic disease, as well as monitoring during anesthesia and critically ill patients.[5]

Screening for coronary heart disease[edit]

Preventative Services Task Force do not recommend either the ECG or any other cardiac imaging procedure as a routine screening procedure in patients without symptoms and those at low risk for coronary heart disease.[6][7] This is because overuse of the procedure is more likely to supply incorrect supporting evidence for a nonexistent problem than to detect a true problem.[7] Tests that falsely indicate the existence of a problem are likely to lead to misdiagnosis, the recommendation of invasive procedures, or overtreatment, and the risks associated with managing false information are usually more troublesome than not using ECG results to make a health recommendation in low-risk individuals.[7]

Persons employed in certain critical occupations, such as aircraft pilots,[8] or in certain environments, such as high altitudes,[9] may be required to have an ECG as part of a regulatory regime.

Myocardial infarction[edit]

Characteristic changes seen on electrocardiography in myocardial infarction is included in the WHO criteria as revised in 2000.[10] According to these, a cardiac troponin rise accompanied by either typical symptoms, pathological Q waves, ST elevation or depression or coronary intervention are diagnostic of myocardial infarction.

Pulmonary embolism[edit]

Electrocardiogram of a patient with pulmonary embolism showing sinus tachycardia of approximately 150 beats per minute and right bundle branch block.

In pulmonary embolism, an ECG may show signs of right heart strain or acute cor pulmonale in cases of large PEs—the classic signs are a large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III (S1Q3T3).[11] This is occasionally (up to 20%) present, but may also occur in other acute lung conditions and has, therefore, limited diagnostic value. This S1Q3T3 pattern from acute right heart strain is termed the "McGinn-White sign" after the initial describers. The most commonly seen signs in the ECG is sinus tachycardia, right axis deviation, and right bundle branch block.[12] Sinus tachycardia was however still only found in 8–69% of people with PE.[13]

Other patterns of disease[edit]

The following table mentions some pathological patterns that can be seen on electrocardiography, followed by possible causes.

Shortened QT intervalHypercalcemia, some drugs, certain genetic abnormalities, hyperkalemia
Prolonged QT intervalHypocalcemia, some drugs, certain genetic abnormalities
Flattened or inverted T wavesCoronary ischemia, hypokalemia, left ventricular hypertrophy, digoxin effect, some drugs
Hyperacute T wavesPossibly the first manifestation of acute myocardial infarction, where T waves become more prominent, symmetrical, and pointed
Peaked T wave, QRS wide, prolonged PR, QT shortHyperkalemia, treat with calcium chloride, glucose and insulin or dialysis
Prominent U wavesHypokalemia


An ECG produces a pattern reflecting the electrical activity of the heart and usually requires a trained clinician to interpret it in the context of the signs and symptoms the patient presents with. It can give information regarding the rhythm of the heart[14] (whether or not the electrical impulse consistently arises from the part of the heart where it should and at what rate), whether that impulse is conducted normally throughout the heart, or whether any part of the heart is contributing more or less than expected to the electrical activity of the heart. It can also give information regarding the balance of salts (electrolytes) in the blood (e.g. hyperkalaemia) or even reveal problems with sodium channels within the heart muscle cells (Brugada syndrome).[15] Modern ECG machines often include analysis software that attempts to interpret the pattern but the diagnoses this produces may not always be accurate.[16]

It is one of the key tests performed when a heart attack (myocardial infarction or MI) is suspected; the ECG can identify whether the heart muscle has been damaged in specific areas, though not all areas of the heart are covered.[17] The ECG cannot reliably measure the pumping ability of the heart, for which ultrasound-based (echocardiography) or nuclear medicine tests are used. It is possible for a human or other animal to be in cardiac arrest, but still have a normal ECG signal (a condition known as pulseless electrical activity).


Tab electrode using silver/silver chloride sensing to detect a trace of voltage.[18]

The ECG device detects and amplifies the tiny electrical changes on the skin that are caused when the heart muscle depolarizes during each heartbeat. At rest, each heart muscle cell has a negative charge, called the membrane potential, across its cell membrane. Decreasing this negative charge toward zero, via the influx of the positive cations, Na+ and Ca++, is called depolarization, which activates the mechanisms in the cell that cause it to contract. During each heartbeat, a healthy heart will have an orderly progression of a wave of depolarisation that is triggered by the cells in the sinoatrial node, spreads out through the atrium, passes through the atrioventricular node and then spreads all over the ventricles. This is detected as tiny rises and falls in the voltage between two electrodes placed either side of the heart, which is displayed as a wavy line either on a screen or on paper. This display indicates the overall rhythm of the heart and weaknesses in different parts of the heart muscle.

Usually, more than two electrodes are used, and they can be combined into a number of pairs (For example: left arm (LA), right arm (RA), and left leg (LL) electrodes form the three pairs LA+RA, LA+LL, and RA+LL). The output from each pair is known as a lead. Each lead looks at the heart from a different angle. Different types of ECGs can be referred to by the number of leads that are recorded, for example 3-lead, 5-lead, or 12-lead ECGs (sometimes simply "a 12-lead"). A 12-lead ECG is one in which 12 different electrical signals are recorded at approximately the same time and will often be used as a one-off recording of an ECG, traditionally printed out as a paper copy. Three- and 5-lead ECGs tend to be monitored continuously and viewed only on the screen of an appropriate monitoring device, for example during an operation or whilst being transported in an ambulance. There may or may not be any permanent record of a 3- or 5-lead ECG, depending on the equipment used.

ECG graph paper[edit]

One second of ECG graph paper

The output of an ECG recorder is a graph (or sometimes several graphs, representing each of the leads) with time represented on the x-axis and voltage represented on the y-axis. A dedicated ECG machine would usually print onto graph paper that has a background pattern of 1-millimeter squares (often in red or green), with bold divisions every 5 mm in both vertical and horizontal directions.

It is possible to change the output of most ECG devices but it is standard to represent each mV on the y axis as 1 cm and each second as 25 mm on the x-axis (that is a paper speed of 25 mm/s). Faster paper speeds can be used, for example, to resolve finer detail in the ECG. At a paper speed of 25 mm/s, one small block of ECG paper translates into 40 ms. Five small blocks make up one large block, which translates into 200 ms. Hence, there are five large blocks per second. A calibration signal may be included with a record. A standard signal of 1 mV must move the stylus vertically 1 cm, that is, two large squares on ECG paper.


By definition, a 12-lead ECG will show a short segment of the recording of each of the twelve leads. This is often arranged in a grid of four columns by three rows, the first column being the limb leads (I,II, and III), the second column the augmented limb leads (aVR, aVL, and aVF), and the last two columns being the chest leads (V1-V6). It is usually possible to change this layout, so it is vital to check the labels to see which lead is represented. Each column will usually record the same moment in time for the three leads and then the recording will switch to the next column, which will record the heart beats after that point. It is possible for the heart rhythm to change between the columns of leads.

Each of these segments is short, perhaps one to three heart beats only, depending on the heart rate, and it can be difficult to analyse any heart rhythm that shows changes between heart beats. To help with the analysis, some ECG machines will print one or two "rhythm strips" as well along the bottom of the ECG paper. This will usually be lead II (which shows the electrical signal from the atrium, the P-wave, well) and shows the rhythm for the whole time the ECG was recorded (usually 5–6 sec). It is usually possible to set the machine to print a number of leads continuously if further information regarding the rhythm is required.

The term "rhythm strip" may also refer to the whole printout from a continuous monitoring system, which may show only one lead and is either initiated by a clinician or in response to an alarm or event.


The electrocardiogram, an important and basic diagnostic proof can even confuse a diagnosis due to a wrong interpretation. It has been previously reviewed the mechanisms behind equipment-related ECG artifacts. A good knowledge about the basic principles of ECG can be very valuable to solve these cases. For example due to Parkinson disease.[19]


Illustration depicting lead placement during electrocardiography

The term "lead" in electrocardiography causes much confusion because it is used to refer to two different things. In accordance with common parlance, the word lead may be used to refer to the electrical cable attaching the electrodes to the ECG recorder. As such, it may be acceptable to refer to the "left arm lead" as the electrode (and its cable) that should be attached at or near the left arm. Usually, 10 of these electrodes are standard in a "12-lead" ECG.

Alternatively (and some would say properly, in the context of electrocardiography), the word lead may refer to the tracing of the voltage difference between two of the electrodes and is what is actually produced by the ECG recorder. Each will have a specific name. For example "lead I" is the voltage between the right arm electrode and the left arm electrode, whereas "Lead II" is the voltage between the right arm and the left leg. (This rapidly becomes more complex as one of the "electrodes" may in fact be a composite of the electrical signal from a combination of the other electrodes). Twelve of this type of lead form a "12-lead" ECG.

To cause additional confusion, the term "limb leads" usually refers to the tracings from leads I, II, and III rather than the electrodes attached to the limbs.

Placement of electrodes[edit]

Ten electrodes are used for a 12-lead ECG. The electrodes usually consist of a conducting gel, embedded in the middle of a self-adhesive pad onto which cables clip. Sometimes the gel also forms the adhesive.[20] They are labeled and placed on the patient's body as follows:[21][22]

Proper placement of the limb electrodes, color-coded as recommended by the American Heart Association (a different colour scheme is used in Europe): The limb electrodes can be far down on the limbs or close to the hips/shoulders, but they must be even (left vs right).[23]
* When exercise stress tests are performed, limb leads may be placed on the trunk to avoid artifacts while ambulatory (arm leads moved subclavicularly and leg leads medial to and above the iliac crest).
Placement of the precordial leads
12 leads
Electrode label (in the USA)Electrode placement
RAOn the right arm, avoiding thick muscle.
LAIn the same location where RA was placed, but on the left arm.
RLOn the right leg, lateral calf muscle.
LLIn the same location where RL was placed, but on the left leg.
V1In the fourth intercostal space (between ribs 4 and 5) just to the right of the sternum (breastbone).
V2In the fourth intercostal space (between ribs 4 and 5) just to the left of the sternum.
V3Between leads V2 and V4.
V4In the fifth intercostal space (between ribs 5 and 6) in the mid-clavicular line.
V5Horizontally even with V4, in the left anterior axillary line.
V6Horizontally even with V4 and V5 in the midaxillary line.

Additional electrodes[edit]

The classical 12-lead ECG can be extended in a number of ways in an attempt to improve its sensitivity in detecting myocardial infarction involving territories not normally "seen" well. This includes an rV4 lead, which uses the equivalent landmarks to the V4 but on the right side of the chest wall (used in paediatric patients under 5 years of age due to the dominance of the right ventricle in this age group[24]) and extending the chest leads onto the back with a V7, V8 and V9.

The Lewis lead or S5 has the LA electrode placed in the second intercostal space to the right of the sternum with the RA at the fourth intercostal space. It is read as lead I and is supposed to demonstrate atrial activity much better to aid in identification of atrial flutter or broad-complex tachycardia.

A posterior ECG can aid in the diagnosis of a posterior myocardial infarction. This is performed by the addition of leads V7, V8 and V9 extending around the left chest wall toward the back.

Limb leads[edit]

In both the 5- and 12-lead configurations, leads I, II and III are called limb leads. The electrodes that form these signals are located on the limbs—one on each arm and one on the left leg.[25][26][27] The limb leads form the points of what is known as Einthoven's triangle.[28]

 I = LA - RA
 II = LL - RA
 III = LL - LA

Simplified electrocardiograph sensors designed for teaching purposes, e.g. at high-school level, are in general limited to three arm electrodes serving similar purposes.[29]

Unipolar vs. bipolar leads[edit]

The two types of leads are unipolar and bipolar. Bipolar leads have one positive and one negative pole.[30] In a 12-lead ECG, the limb leads (I, II and III) are bipolar leads. Unipolar leads also have two poles, as a voltage is measured; however, the negative pole is a composite pole (Wilson's central terminal, or WCT) made up of signals from multiple other electrodes.[31] In a 12-lead ECG, all leads except the limb leads are unipolar (aVR, aVL, aVF, V1, V2, V3, V4, V5, and V6).

Wilson's central terminal VW is produced by connecting the electrodes RA, LA, and LL together, via a simple resistive network, to give an average potential across the body, which approximates the potential at infinity (i.e. zero):

 V_W = \frac{1}{3}(RA+LA+LL)

Augmented limb leads[edit]

Leads aVR, aVL, and aVF are augmented limb leads (after their inventor Dr. Emanuel Goldberger known collectively as the Goldberger's leads). They are derived from the same three electrodes as leads I, II, and III. However, they view the heart from different angles (or vectors) because the negative electrode for these leads is a modification of Wilson's central terminal. This zeroes out the negative electrode and allows the positive electrode to become the "exploring electrode". This is possible because Einthoven's Law states that I + (-II) + III = 0. The equation can also be written I + III = II. It is written this way (instead of I − II + III = 0) because Einthoven reversed the polarity of lead II in Einthoven's triangle, possibly because he liked to view upright QRS complexes. Wilson's central terminal paved the way for the development of the augmented limb leads aVR, aVL, aVF and the precordial leads V1, V2, V3, V4, V5 and V6.

 aVR = RA - \frac{1}{2} (LA + LL) = \frac 32 (RA - V_W)
 aVL = LA - \frac{1}{2} (RA + LL) = \frac 32 (LA - V_W)
 aVF = LL - \frac{1}{2} (RA + LA) = \frac 32 (LL - V_W)

The augmented limb leads aVR, aVL, and aVF are amplified in this way because the signal is too small to be useful when the negative electrode is Wilson's central terminal. Together with leads I, II, and III, augmented limb leads aVR, aVL, and aVF form the basis of the hexaxial reference system, which is used to calculate the heart's electrical axis in the frontal plane. The aVR, aVL, and aVF leads can also be represented using the I and II limb leads:

\begin{align} aVR &= -\frac{I + II}{2}\\ aVL &= I - \frac{II}{2}\\ aVF &= II - \frac{I}{2} \end{align}

Precordial leads[edit]

The electrodes for the precordial leads (V1, V2, V3, V4, V5 and V6) are placed directly on the chest. Because of their close proximity to the heart, they do not require augmentation. Wilson's central terminal is used for the negative electrode, and these leads are considered to be unipolar (recall that Wilson's central terminal is the average of the three limb leads. This approximates common, or average, potential over the body). The precordial leads view the heart's electrical activity in the so-called horizontal plane. The heart's electrical axis in the horizontal plane is referred to as the Z axis.

Esophageal lead[edit]

lead story: Filtered esophageal left heart electrogram.

The filtered esophageal left heart electrogram is a semi-invasive method. This technique is able to provide additional marker from the left atrium and the left ventricle.

The filtered bipolar esophageal left atrial electrogram (LAE) recording, in combination with the surface ECG can be of advantage in all situations requiring doubtless recognition of the atrial activities. With this additional “left atrial marker channel” the atrial activities can easily be recognized even if they are superimposed by the QRS complex. Thus, LAE recording can be utilized, for example, to quickly differentiate tachycardias and extrasystolies and to diagnose DDD pacemaker malfunctions. As a special advantage in atrio-biventricular and conventional AV block pacing, the esophageal left atrial electrogram recoding enables measurement of interatrial conduction intervals, which are the major determinants of the optimal AV delays in VDD and DDD pacing.

Compared to the surface ECG, the filtered bipolar esophageal left ventricular electrogram allows a more direct determination of the extent of cardiac desynchronization in heart failure patients. Thus, the esophageal left ventricular conduction delay (LVCDE) could be used as an additional marker of interventricular dyssynchrony to justify implantation of biventricular pacing systems and to guide the positioning of the left ventricular electrode.

The recording of the esophageal left heart electrograms requires a bipolar esophageal electrode. For example, the TOslim (Osypka AG, Rheinfelden, Germany) can be used. It has to be applied perorally or transnasally either with or without any mild sedation. To eliminate artifacts in the esophageal left atrial electrogram and to improve the differentiation between the left atrial deflection and the ventricular complex, high-pass filtering is recommended. Best results can be obtained using Butterworth high-pass filter technique (for example: through the DC input of a standard ECG recorder in combination with the Rostockfilter (Osypka AG, Rheinfelden, Germany) or by using the esophageal electrogram option of the Biotronik ICS 3000 programmer. In this case, no further equipment is needed. [32]

Waves and intervals[edit]

Schematic representation of normal ECG
Animation of a normal ECG wave
Detail of the QRS complex, showing ventricular activation time (VAT) and amplitude
Upper limit of normal QT interval, corrected for heart rate according to Bazett's formula,[33] Fridericia's formula[34] and subtracting 0.02 s from QT for every 10 bpm increase in heart rate.[35] Up to 0.42 s (≤ 420 ms) is chosen as normal QTc of QTB and QTF in this diagram.

A typical ECG tracing of the cardiac cycle (heartbeat) consists of a P wave, a QRS complex, a T wave, and a U wave, which is normally invisible in 50 to 75% of ECGs because it is hidden by the T wave and upcoming new P wave.[36] The baseline of the electrocardiogram (the flat horizontal segments) is measured as the portion of the tracing following the T wave and preceding the next P wave and the segment between the P wave and the following QRS complex (PR segment). In a normal healthy heart, the baseline is equivalent to the isoelectric line (0 mV) and represents the periods in the cardiac cycle when there are no currents towards either the positive or negative ends of the ECG leads. However, in a diseased heart, the baseline may be depressed (e.g., cardiac ischaemia) or elevated (e.g., myocardial infarction) relative to the isoelectric line due to injury currents during the TP and PR intervals when the ventricles are at rest. The ST segment typically remains close to the isoelectric line as this is the period when the ventricles are fully depolarised and thus no currents can be in the ECG leads. Since most ECG recordings do not indicate where the 0 mV line is, baseline depression often gives the appearance of an elevation of the ST segment and conversely baseline elevation gives the appearance of depression of the ST segment.[37]

RR intervalThe interval between an R wave and the next R wave; normal resting heart rate is between 60 and 100 bpm.0.6 to 1.2 s
P waveDuring normal atrial depolarization, the main electrical vector is directed from the SA node towards the AV node and spreads from the right atrium to the left atrium. This turns into the P wave on the ECG.80ms
PR intervalThe PR interval is measured from the beginning of the P wave to the beginning of the QRS complex. The PR interval reflects the time the electrical impulse takes to travel from the sinus node through the AV node and entering the ventricles. The PR interval is, therefore, a good estimate of AV node function.120 to 200 ms
PR segmentThe PR segment connects the P wave and the QRS complex. The impulse vector is from the AV node to the Bundle of His to the bundle branches and then to the Purkinje fibers. This electrical activity does not produce a contraction directly and is merely traveling down towards the ventricles, and this shows up flat on the ECG. The PR interval is more clinically relevant.50 to 120 ms
QRS complexThe QRS complex reflects the rapid depolarization of the right and left ventricles. The ventricles have a large muscle mass compared to the atria, so the QRS complex usually has a much larger amplitude than the P-wave.80 to 100 ms
J-pointThe point at which the QRS complex finishes and the ST segment begins. It is used to measure the degree of ST elevation or depression present.N/A
ST segmentThe ST segment connects the QRS complex and the T wave. The ST segment represents the period when the ventricles are depolarized. It is isoelectric.80 to 120 ms
T waveThe T wave represents the repolarization (or recovery) of the ventricles. The interval from the beginning of the QRS complex to the apex of the T wave is referred to as the absolute refractory period. The last half of the T wave is referred to as the relative refractory period (or vulnerable period).160 ms
ST intervalThe ST interval is measured from the J point to the end of the T wave.320 ms
QT intervalThe QT interval is measured from the beginning of the QRS complex to the end of the T wave. A prolonged QT interval is a risk factor for ventricular tachyarrhythmias and sudden death. It varies with heart rate and, for clinical relevance, requires a correction for this, giving the QTc.Up to 420 ms in heart rate of 60 bpm
U waveThe U wave is hypothesized to be caused by the repolarization of the interventricular septum. It normally has a low amplitude, and even more often is completely absent. It always follows the T wave, and also follows the same direction in amplitude. If it is too prominent, suspect hypokalemia, hypercalcemia or hyperthyroidism.[38]
J waveThe J wave, elevated J-point or Osborn wave appears as a late delta wave following the QRS or as a small secondary R wave. It is considered pathognomonic of hypothermia or hypercalcemia.[39]

Originally, four deflections were noted, but after the mathematical correction for artifacts introduced by early amplifiers, a fifth deflection was discovered. Einthoven chose the letters P, Q, R, S, and T to identify the tracing that was superimposed over the uncorrected labeled A, B, C, and D.[40]

In intracardiac electrocardiograms, such as can be acquired from pacemaker sensors, an additional wave can be seen, the H deflection, which reflects the depolarization of the bundle of His.[41] The H-V interval, in turn, is the duration from the beginning of the H deflection to the earliest onset of ventricular depolarization recorded in any lead.[42]

Vectors and views[edit]

Graphic showing the relationship between positive electrodes, depolarization wavefronts (or mean electrical vectors), and complexes displayed on the ECG

Interpretation of the ECG relies on the idea that different leads (meaning the ECG leads I, II, III, aVR, aVL, aVF and the chest leads) "view" the heart from different angles. This has two benefits. First, leads that are showing problems (for example ST segment elevation) can be used to infer which region of the heart is affected. Second, the overall direction of travel of the wave of depolarisation can also be inferred, which can reveal other problems. This is termed the cardiac axis . Determination of the cardiac axis relies on the concept of a vector, which describes the motion of the depolarisation wave. This vector can then be described in terms of its components in relation to the direction of the lead considered. One component will be in the direction of the lead and this will be revealed in the behaviour of the QRS complex and one component will be at 90° to this (which will not). Any net positive deflection of the QRS complex (i.e., height of the R-wave minus depth of the S-wave) suggests the wave of depolarisation is spreading through the heart in a direction that has some component (of the vector) in the same direction as the lead in question.


Diagram showing how the polarity of the QRS complex in leads I, II, and III can be used to estimate the heart's electrical axis in the frontal plane

The heart's electrical axis refers to the general direction of the heart's depolarization wavefront (or mean electrical vector) in the frontal plane. With a healthy conducting system, the cardiac axis is related to where the major muscle bulk of the heart lies. Under normal circumstances, this is the left ventricle, with some contribution from the right ventricle. It is usually oriented in a right shoulder to left leg direction, which corresponds to the left inferior quadrant of the hexaxial reference system, although −30° to +90° is considered to be normal. If the left ventricle increases its activity or bulk, then there is said to be "left axis deviation" as the axis swings around to the left beyond −30°; however, in conditions wherein the right ventricle is strained or hypertrophied, then the axis swings around beyond +90° and "right axis deviation" is said to exist. Disorders of the conduction system of the heart can disturb the electrical axis without necessarily reflecting changes in muscle bulk.

Normal−30° to 90°NormalNormal
Left axis deviation−30° to −90°May indicate left anterior fascicular block or Q waves from inferior MI.Left axis deviation is considered normal in pregnant women and those with emphysema.
Right axis deviation+90° to +180°May indicate left posterior fascicular block, Q waves from high lateral MI, or a right ventricular strain patternRight deviation is considered normal in children and is a standard effect of dextrocardia.
Extreme right axis deviation+180° to −90°Is rare, and considered an 'electrical no-man's land'
The hexaxial reference system showing the orientation of each lead: For example, if the bulk of heart muscle is oriented at +60 degrees with respect to the SA node, lead II will show the greatest deflection and aVL the least.

In the setting of right bundle branch block, right or left axis deviation may indicate bifascicular block.

Lead groups[edit]

Of the 12 leads in total, each records the electrical activity of the heart from a different perspective, which also correlates to different anatomical areas of the heart for the purpose of identifying acute coronary ischemia or injury. Two leads that look at neighbouring anatomical areas of the heart are said to be contiguous. The relevance of this is in determining whether an abnormality on the ECG is likely to represent true disease or a spurious finding.

Diagram showing the contiguous leads in the same color
CategoryColor on chartLeadsActivity
Inferior leads'YellowLeads II, III and aVFLook at electrical activity from the vantage point of the inferior surface (diaphragmatic surface of heart)
Lateral leadsGreenI, aVL, V5 and V6Look at the electrical activity from the vantage point of the lateral wall of left ventricle
  • The positive electrode for leads I and aVL should be located distally on the left arm and, because of which, leads I and aVL are sometimes referred to as the high lateral leads.
  • Because the positive electrodes for leads V5 and V6 are on the patient's chest, they are sometimes referred to as the low lateral leads.
Septal leadsOrangeV1 and V2Look at electrical activity from the vantage point of the septal surface of the heart (interventricular septum)
Anterior leadsBlueV3 and V4Look at electrical activity from the vantage point of the anterior wall of the right and left ventricles (Sternocostal surface of heart)

In addition, any two precordial leads next to one another are considered to be contiguous. For example, though V4 is an anterior lead and V5 is a lateral lead, they are contiguous because they are next to one another. A common saying to remember the contiguous leads is "I see all leads" (inferior, septal, anterior and lateral).

Wiggers diagram, showing a normal ECG curve synchronized with other major events during the cardiac cycle

Lead aVR offers no specific view of the left ventricle. Rather, it views the inside of the endocardial wall to the surface of the right atrium, from its perspective on the right shoulder.

Filter selection[edit]

Modern ECG monitors offer multiple filters for signal processing. The most common settings are monitor mode and diagnostic mode. In monitor mode, the low-frequency filter (also called the high-pass filter because signals above the threshold are allowed to pass) is set at either 0.5 Hz or 1 Hz and the high-frequency filter (also called the low-pass filter because signals below the threshold are allowed to pass) is set at 40 Hz. This limits artifacts for routine cardiac rhythm monitoring. The high-pass filter helps reduce wandering baseline and the low-pass filter helps reduce 50- or 60-Hz power line noise (the power line network frequency differs between 50 and 60 Hz in different countries). In diagnostic mode, the high-pass filter is set at 0.05 Hz, which allows accurate ST segments to be recorded. The low-pass filter is set to 40, 100, or 150 Hz. As a consequence, the monitor mode ECG display is more filtered than diagnostic mode, because its passband is narrower.[43]

Electrocardiogram heterogeneity[edit]

ECG heterogeneity is a measurement of the amount of variance between one ECG waveform and the next. This heterogeneity can be measured by placing multiple ECG electrodes on the chest and then computing the variance in waveform morphology across the signals obtained from these electrodes. Recent research suggests ECG heterogeneity often precedes dangerous cardiac arrhythmias.

In the future, implantable devices may be programmed to measure and track heterogeneity. These devices have potential to help ward off arrhythmias by stimulating nerves such as the vagus nerve, delivering drugs such as beta-blockers and, if necessary, defibrillating the heart.[44]

Rhythm strip[edit]

Although multiple leads, and thus multiple electrical vectors, are commonly used in unison to gain diagnostic and therapeutic insight into cardiac status, monitoring one lead, referred to as a rhythm strip, can be useful to trend cardiac function in terms of heart rate, regularity, pauses, and basic rhythm.


The etymology of the word is derived from the Greek electro, because it is related to electrical activity, kardio, Greek for heart, and graph, a Greek root meaning "to write".

Alexander Muirhead is reported to have attached wires to a feverish patient's wrist to obtain a record of the patient's heartbeat while studying for his Doctor of Science (in electricity) in 1872 at St Bartholomew's Hospital.[45] This activity was directly recorded and visualized using a Lippmann capillary electrometer by the British physiologist John Burdon Sanderson.[46] The first to systematically approach the heart from an electrical point of view was Augustus Waller, working in St Mary's Hospital in Paddington, London.[47] His electrocardiograph machine consisted of a Lippmann capillary electrometer fixed to a projector. The trace from the heartbeat was projected onto a photographic plate that was itself fixed to a toy train. This allowed a heartbeat to be recorded in real time. In 1911 he still saw little clinical application for his work.

An early commercial ECG device (1911)

An initial breakthrough came when Willem Einthoven, working in Leiden, the Netherlands, used the string galvanometer he invented in 1901.[48] This device was much more sensitive than both the capillary electrometer Waller used and the string galvanometer that had been invented separately in 1897 by the French engineer Clément Ader.[49] Rather than using today's self-adhesive electrodes Einthoven's subjects would immerse each of their limbs into containers of salt solutions from which the ECG was recorded.

Einthoven assigned the letters P, Q, R, S, and T to the various deflections,[40] and described the electrocardiographic features of a number of cardiovascular disorders. In 1924, he was awarded the Nobel Prize in Medicine for his discovery.[50]

Though the basic principles of that era are still in use today, many advances in electrocardiography have been made over the years. The instrumentation, for example, has evolved from a cumbersome laboratory apparatus to compact electronic systems that often include computerized interpretation of the electrocardiogram.[51]

Fetal electrocardiography[edit]

Fetal electrocardiography records the electrical activity of a fetus, and when performed as a part of monitoring in childbirth, involves a single electrode being passed through the woman's cervix and attached to the baby's scalp.[52] According to a Cochrane review, monitoring the fetus using ECG plus cardiotocography (CTG) resulted in fewer instances of fetal scalp blood testing and less surgical assistance with the birth, compared to CTG alone.[52] There was no difference in the number of Caesarean deliveries and little to suggest the babies were in better condition at birth.[52]

See also[edit]


  1. ^ Abbreviated from the German word Elektro-kardiographie
  2. ^ Harper, Douglas. "cardio-". Online Etymology Dictionary. 
  3. ^ "ECG- simplified. Aswini Kumar M.D.". LifeHugger. Retrieved 11 February 2010. 
  4. ^ Walraven, G. (2011). Basic arrhythmias (7th ed.), pp. 1–11
  5. ^ a b c d e Masters, Jo; Bowden, Carole; Martin, Carole (2003). Textbook of veterinary medical nursing. Oxford: Butterworth-Heinemann. p. 244. ISBN 0-7506-5171-7. 
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  7. ^ a b c Consumer Reports; American Academy of Family Physicians (April 2012), "EKGs and exercise stress tests: When you need them for heart disease — and when you don't", Choosing Wisely: an initiative of the ABIM Foundation (Consumer Reports), retrieved 14 August 2012 
  8. ^ "Summary of Medical Standards". U.S. Federal Aviation Administration. 2006. Retrieved 27 December 2013. 
  9. ^ Nyman, L.-A. (20 August 2004) APEX Medical Examination for Work at High Altitude. apex-telescope.org
  10. ^ Alpert JS, Thygesen K, Antman E, Bassand JP (2000). "Myocardial infarction redefined—a consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction". J Am Coll Cardiol 36 (3): 959–69. doi:10.1016/S0735-1097(00)00804-4. PMID 10987628. 
  11. ^ McGinn S, White PD (1935). "Acute cor pulmonale resulting from pulmonary embolism". J Am Med Assoc 104 (17): 1473–80. doi:10.1001/jama.1935.02760170011004. 
  12. ^ Rodger M, Makropoulos D, Turek M, Quevillon J, Raymond F, Rasuli P, Wells PS (October 2000). "Diagnostic value of the electrocardiogram in suspected pulmonary embolism". Am. J. Cardiol. 86 (7): 807–9, A10. doi:10.1016/S0002-9149(00)01090-0. PMID 11018210. 
  13. ^ Amal Mattu; Deepi Goyal; Barrett, Jeffrey W.; Joshua Broder; DeAngelis, Michael; Peter Deblieux; Gus M. Garmel; Richard Harrigan; David Karras; Anita L'Italien; David Manthey (2007). Emergency medicine: avoiding the pitfalls and improving the outcomes. Malden, Mass: Blackwell Pub./BMJ Books. p. 10. ISBN 1-4051-4166-2. 
  14. ^ Braunwald E. (Editor), Heart Disease: A Textbook of Cardiovascular Medicine, Fifth Edition, p. 108, Philadelphia, W.B. Saunders Co., 1997. ISBN 0-7216-5666-8.
  15. ^ Van Mieghem C, Sabbe M, Knockaert D (2004). "The clinical value of the ECG in noncardiac conditions". Chest 125 (4): 1561–76. doi:10.1378/chest.125.4.1561. PMID 15078775. 
  16. ^ "Amal Mattu's Emergency ECG Video of the Week". Ekgumem.tumblr.com. 5 November 2012. Retrieved 28 February 2014. 
  17. ^ "2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care – Part 8: Stabilization of the Patient With Acute Coronary Syndromes". Circulation 112: IV–89–IV–110. 2005. doi:10.1161/CIRCULATIONAHA.105.166561. PMID 16314375. 
  18. ^ "CARDEX Electrodes". CARDEX. Retrieved 21 August 2014. 
  19. ^ Segura-Sampedro Juan Jose, Parra-Lopez Loreto, Sampedro-Abascal Consuelo, Muñoz-Rodrıguez Juan Carlos, Atrial Flutter EKG can be useless without the proper electrophysiological basis, International Journal of Cardiology (2014), doi: 10.1016/j.ijcard.2014.10.076
  20. ^ See images of ECG electrodes [1] [2]
  21. ^ "Einthoven's Triangle". Library.med.utah.edu. Retrieved 15 August 2009. [dead link]
  22. ^ AHA Diagnostic ECG Electrode Placement. WelchAllyn
  24. ^ "Paediatric ECG Interpretation – Life in the Fast Lane Medical Blog". Lifeinthefastlane.com. 20 August 2012. Retrieved 28 February 2014. 
  25. ^ "Lead Placement". Univ. of Maryland School of Medicine Emergency Medicine Interest Group. Archived from the original on 20 July 2011. Retrieved 15 August 2009. 
  26. ^ "Limb Leads – ECG Lead Placement – Normal Function of the Heart – Cardiology Teaching Package – Practice Learning – Division of Nursing – The University of Nottingham". Nottingham.ac.uk. Retrieved 15 August 2009. 
  27. ^ "Lesson 1: The Standard 12 Lead ECG". Library.med.utah.edu. Retrieved 15 August 2009. [dead link]
  28. ^ "Electrocardiogram explanation image". Retrieved 28 February 2014. 
  29. ^ Pasco Pasport EKG Sensor PS-2111, Sciencescope ECG Sensor, etc.
  30. ^ Fay Johnson ECG presentation. Cuesta College Home Page
  31. ^ "Electrocardiogram Leads". CV Physiology. 26 March 2007. Retrieved 15 August 2009. 
  32. ^ Ismer B: Utilization of the Esophageal Left Heart Electrogram in Cardiac Resynchronization and AV Block Patients. Hochschule Offenburg, Offenburg 2013, ISBN 978-3-943301-08-3
  33. ^ Bazett HC. (1920). "An analysis of the time-relations of electrocardiograms". Heart (7): 353–370. 
  34. ^ Fridericia LS (1920). "The duration of systole in the electrocardiogram of normal subjects and of patients with heart disease". Acta Medica Scandinavica (53): 469–486. 
  35. ^ Lesson III. Characteristics of the Normal ECG Frank G. Yanowitz, MD. Professor of Medicine. University of Utah School of Medicine. Retrieved on Mars 23, 2010
  36. ^ A movie by the National Heart Lung and Blood Institute explaining the connection between an ECG and the electricity in heart: What Is the Heart?
  37. ^ "Electrophysiological Changes During Cardiac Ischemia". Cvphysiology.com. 26 March 2007. Retrieved 28 February 2014. 
  38. ^ Andrew R Houghton; David Gray (27 January 2012). Making Sense of the ECG, Third Edition. Hodder Education. p. 214. ISBN 978-1-4441-6654-5. Retrieved 20 May 2012. 
  39. ^ The "Normothermic" Osborn Wave Induced by Severe Hypercalcemia
  40. ^ a b Hurst JW (3 November 1998). "Naming of the Waves in the ECG, With a Brief Account of Their Genesis". Circulation 98 (18): 1937–42. doi:10.1161/01.CIR.98.18.1937. PMID 9799216. 
  41. ^ H deflection. thefreedictionary.com citing: Mosby's Medical Dictionary, 8th edition. 2009
  42. ^ H-V interval. thefreedictionary.com citing: McGraw-Hill Concise Dictionary of Modern Medicine. 2002
  43. ^ Mark JB "Atlas of Cardiovascular Monitoring." p. 130. New York: Churchill Livingstone, 1998. ISBN 0-443-08891-8.
  44. ^ Verrier, Richard L.Dynamic Tracking of ECG Heterogeneity to Estimate Risk of Life-threatening Arrhythmias. CIMIT Forum. 25 September 2007.
  45. ^ Ronald M. Birse,rev. Patricia E. Knowlden Oxford Dictionary of National Biography 2004 (Subscription required) – (original source is his biography written by his wife – Elizabeth Muirhead. Alexandernn Muirhead 1848–1920. Oxford, Blackwell: privately printed 1926.)
  46. ^ Burdon Sanderson J; Page, F. J. M. (1878). "Experimental results relating to the rhythmical and excitatory motions of the ventricle of the frog heart". Proceedings of the Royal Society 27 (185–189): 410–14. doi:10.1098/rspl.1878.0068. 
  47. ^ Waller AD (1887). "A demonstration on man of electromotive changes accompanying the heart's beat". J Physiol (Lond) 8 (5): 229–34. PMC 1485094. PMID 16991463. 
  48. ^ Rivera-Ruiz M, Cajavilca C, Varon J (29 September 1927). "Einthoven's String Galvanometer: The First Electrocardiograph". Texas Heart Institute journal / from the Texas Heart Institute of St. Luke's Episcopal Hospital, Texas Children's Hospital 35 (2): 174–8. PMC 2435435. PMID 18612490. 
  49. ^ Interwoven W (1901). "Un nouveau galvanometre". Arch Neerl Sc Ex Nat 6: 625. 
  50. ^ Cooper JK (1986). "Electrocardiography 100 years ago. Origins, pioneers, and contributors". N Engl J Med 315 (7): 461–4. doi:10.1056/NEJM198608143150721. PMID 3526152. 
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  52. ^ a b c Neilson JP (2012). "Fetal electrocardiogram (ECG) for fetal monitoring during labour". Cochrane Database Syst Rev 4: CD000116. doi:10.1002/14651858.CD000116.pub3. PMID 22513897. 

External links[edit]