# Electrocardiography

(Redirected from Electrocardiogram)
"ECG" redirects here. For other uses, see ECG (disambiguation).
"EKG" redirects here. For the musical album, see E·K·G.
Electrocardiography
Intervention
Image showing a patient connected to the 10 electrodes necessary for a 12-lead ECG
ICD-9-CM 89.52
MeSH D004562
MedlinePlus 003868

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

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

The U.S. 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

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

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

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

Shortened QT interval Hypercalcemia, some drugs, certain genetic abnormalities, hyperkalemia Hypocalcemia, some drugs, certain genetic abnormalities Coronary ischemia, hypokalemia, left ventricular hypertrophy, digoxin effect, some drugs Possibly the first manifestation of acute myocardial infarction, where T waves become more prominent, symmetrical, and pointed Hyperkalemia, treat with calcium chloride, glucose and insulin or dialysis Hypokalemia

## Function

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).

## Principles

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.

## ECG graph paper

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.

### Layout

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.

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

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.[18] They are labeled and placed on the patient's body as follows:[19][20]

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).[21]
* 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).
Electrode label (in the USA) Electrode placement
RA On the right arm, avoiding thick muscle.
LA In the same location where RA was placed, but on the left arm.
RL On the right leg, lateral calf muscle.
LL In the same location where RL was placed, but on the left leg.
V1 In the fourth intercostal space (between ribs 4 and 5) just to the right of the sternum (breastbone).
V2 In the fourth intercostal space (between ribs 4 and 5) just to the left of the sternum.
V3 Between leads V2 and V4.
V4 In the fifth intercostal space (between ribs 5 and 6) in the mid-clavicular line.
V5 Horizontally even with V4, in the left anterior axillary line.
V6 Horizontally even with V4 and V5 in the midaxillary line.

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[22]) 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.

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.[23][24][25] The limb leads form the points of what is known as Einthoven's triangle.[26]

• Lead I is the voltage between the (positive) left arm (LA) electrode and right arm (RA) electrode:
$I = LA - RA$
• Lead II is the voltage between the (positive) left leg (LL) electrode and the right arm (RA) electrode:
$II = LL - RA$
• Lead III is the voltage between the (positive) left leg (LL) electrode and the left arm (LA) electrode:
$III = LL - LA$

Simplified electrocardiograph sensors designed for teaching purposes, e.g. at high-school level, are in general limited to three arm electrodes serving similar purposes.[27]

The two types of leads are unipolar and bipolar. Bipolar leads have one positive and one negative pole.[28] 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.[29] 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):

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

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.

• Lead augmented vector right (aVR)' has the positive electrode (white) on the right arm. The negative electrode is a combination of the left arm (black) electrode and the left leg (red) electrode, which "augments" the signal strength of the positive electrode on the right arm:
$aVR = RA - \frac{1}{2} (LA + LL) = \frac 32 (RA - V_W)$
• Lead augmented vector left (aVL) has the positive (black) electrode on the left arm. The negative electrode is a combination of the right arm (white) electrode and the left leg (red) electrode, which "augments" the signal strength of the positive electrode on the left arm:
$aVL = LA - \frac{1}{2} (RA + LL) = \frac 32 (LA - V_W)$
• Lead augmented vector foot (aVF) has the positive (red) electrode on the left leg. The negative electrode is a combination of the right arm (white) electrode and the left arm (black) electrode, which "augments" the signal of the positive electrode on the left leg:
$aVF = LL - \frac{1}{2} (RA + LA) = \frac 32 (LL - V_W)$

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}

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.

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. [30]

## Waves and intervals

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,[31] Fridericia's formula[32] and subtracting 0.02 s from QT for every 10 bpm increase in heart rate.[33] 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.[34] 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.[35]

Feature Description Duration
RR interval The 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 wave During 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 interval The 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 segment The 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 complex The 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 120 ms
J-point The 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 segment The 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 wave The 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 interval The ST interval is measured from the J point to the end of the T wave. 320 ms
QT interval The 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 wave The 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.[36]
J wave The 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.[37]

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.[38]

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.[39] 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.[40]

## Vectors and views

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.

### Axis

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° Normal Normal 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 pattern Right 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.

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
Category Color on chart Leads Activity
Inferior leads' Yellow Leads II, III and aVF Look at electrical activity from the vantage point of the inferior surface (diaphragmatic surface of heart)
Lateral leads Green I, aVL, V5 and V6 Look 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 leads Orange V1 and V2 Look at electrical activity from the vantage point of the septal surface of the heart (interventricular septum)
Anterior leads Blue V3 and V4 Look 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

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.[41]

## Electrocardiogram heterogeneity

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.[42]

## Rhythm strip

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.

## History

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.[43] This activity was directly recorded and visualized using a Lippmann capillary electrometer by the British physiologist John Burdon Sanderson.[44] 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.[45] 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.[46] 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.[47] 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,[38] and described the electrocardiographic features of a number of cardiovascular disorders. In 1924, he was awarded the Nobel Prize in Medicine for his discovery.[48]

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.[49]

## Fetal electrocardiography

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.[50] 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.[50] There was no difference in the number of Caesarean deliveries and little to suggest the babies were in better condition at birth.[50]

## References

1. ^ Abbreviated from the German word Elektro-Kardiographie
2. ^ Harper, Douglas. "cardio-". Online Etymology Dictionary.
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37. ^ The "Normothermic" Osborn Wave Induced by Severe Hypercalcemia
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