Electrocardiography

Electrocardiography is the process of producing an

Electrocardiography
electrocardiogram (ECG or EKG[a]), a recording of the
heart's electrical activity.[4] It is an electrogram of the heart
which is a graph of voltage versus time of the electrical
activity of the heart[5] using electrodes placed on the skin.
These electrodes detect the small electrical changes that
are a consequence of cardiac muscle depolarization
followed by repolarization during each cardiac cycle
(heartbeat). Changes in the normal ECG pattern occur in
numerous cardiac abnormalities, including cardiac rhythm
disturbances (such as atrial fibrillation[6] and ventricular
tachycardia[7]), inadequate coronary artery blood flow
(such as myocardial ischemia[8] and myocardial
infarction[9]), and electrolyte disturbances (such as
hypokalemia[10] and hyperkalemia[11]).

Traditionally, "ECG" usually means a 12-lead ECG taken ECG of a heart in normal sinus rhythm
while lying down as discussed below. However, other
ICD-10-PCS R94.31
devices can record the electrical activity of the heart such
as a Holter monitor but also some models of smartwatch ICD-9-CM 89.52
are capable of recording an ECG. ECG signals can be MeSH D004562
recorded in other contexts with other devices.
MedlinePlus 003868
In a conventional 12-lead ECG, ten electrodes are placed
on the patient's limbs and on the surface of the chest. The overall magnitude of the heart's electrical
potential is then measured from twelve different angles ("leads") and is recorded over a period of time
(usually ten seconds). In this way, the overall magnitude and direction of the heart's electrical depolarization
is captured at each moment throughout the cardiac cycle.[12]

There are three main components to an ECG: the P wave, which represents depolarization of the atria; the
QRS complex, which represents depolarization of the ventricles; and the T wave, which represents
repolarization of the ventricles.[13]

During each heartbeat, a healthy heart has an orderly progression of depolarization that starts with
pacemaker cells in the sinoatrial node, spreads throughout the atrium, and passes through the
atrioventricular node down into the bundle of His and into the Purkinje fibers, spreading down and to the
left throughout the ventricles.[13] This orderly pattern of depolarization gives rise to the characteristic ECG
tracing. To the trained clinician, an ECG conveys a large amount of information about the structure of the
heart and the function of its electrical conduction system.[14] Among other things, an ECG can be used to
measure the rate and rhythm of heartbeats, the size and position of
the heart chambers, the presence of any damage to the heart's
muscle cells or conduction system, the effects of heart drugs, and
the function of implanted pacemakers.[15]

Contents
Medical uses
Screening
Electrocardiograph machines
Cardiac monitors
Electrodes and leads
Limb leads Use of real time monitoring of the
Augmented limb leads heart in an intensive care unit in a
Precordial leads German hospital (2015), the
Specialized leads monitoring screen above the patient
displaying an electrocardiogram and
Lead locations on an ECG report
various values of parameters of the
Contiguity of leads heart like heart rate and blood
Electrophysiology pressure

Interpretation
Theory
Background grid
Rate and rhythm
Axis
Amplitudes and intervals
Limb leads and electrical conduction through the heart
Ischemia and infarction
Artifacts
Diagnosis
History
Etymology
See also
Notes
References
External links

Medical uses
The overall goal of performing an ECG is to obtain information about the electrical functioning of the heart.
Medical uses for this information are varied and often need to be combined with knowledge of the structure
of the heart and physical examination signs to be interpreted. Some indications for performing an ECG
include the following:
 Chest pain or suspected myocardial infarction (heart
attack), such as ST elevated myocardial infarction
(STEMI)[16] or non-ST elevated myocardial infarction
(NSTEMI)[17]
Symptoms such as shortness of breath, murmurs,[18]
fainting, seizures, funny turns, or arrhythmias including
new onset palpitations or monitoring of known cardiac
arrhythmias
Medication monitoring (e.g., drug-induced QT
prolongation, Digoxin toxicity) and management of Normal 12-lead ECG
overdose (e.g., tricyclic overdose)
Electrolyte abnormalities, such as
hyperkalemia
Perioperative monitoring in which any
form of anesthesia is involved (e.g.,
monitored anesthesia care, general
anesthesia). This includes preoperative
assessment and intraoperative and
postoperative monitoring.
A 12-lead ECG of a 26-year-old male with an
Cardiac stress testing
incomplete right bundle branch block (RBBB)
Computed tomography angiography
(CTA) and magnetic resonance
angiography (MRA) of the heart (ECG is used to "gate" the scanning so that the anatomical
position of the heart is steady)
Clinical cardiac electrophysiology, in which a catheter is inserted through the femoral vein
and can have several electrodes along its length to record the direction of electrical activity
from within the heart.

ECGs can be recorded as short intermittent tracings or continuous ECG monitoring. Continuous monitoring
is used for critically ill patients, patients undergoing general anesthesia,[19][18] and patients who have an
infrequently occurring cardiac arrhythmia that would unlikely be seen on a conventional ten-second ECG.
Continuous monitoring can be conducted by using Holter monitors, internal and external defibrillators and
pacemakers, and/or biotelemetry.[20]

Screening

For adults, evidence does not support the use of ECGs among those without symptoms or at low risk of
cardiovascular disease as an effort for prevention.[21][22][23] This is because an ECG may falsely indicate
the existence of a problem, leading to misdiagnosis, the recommendation of invasive procedures, and
overtreatment. However, persons employed in certain critical occupations, such as aircraft pilots,[24] may be
required to have an ECG as part of their routine health evaluations. Hypertrophic cardiomyopathy
screening may also be considered in adolescents as part of a sports physical out of concern for sudden
cardiac death.[25]

Electrocardiograph machines
Electrocardiograms are recorded by machines that consist of a set of electrodes connected to a central
unit.[26] Early ECG machines were constructed with analog electronics, where the signal drove a motor to
print out the signal onto paper. Today, electrocardiographs use analog-to-digital converters to convert the
electrical activity of the heart to a digital signal. Many ECG machines are now portable and commonly
include a screen, keyboard, and printer on a small wheeled cart.
Recent advancements in electrocardiography include developing
even smaller devices for inclusion in fitness trackers and smart
watches.[27] These smaller devices often rely on only two
electrodes to deliver a single lead I.[28] Portable twelve-lead
devices powered by batteries are also available.

Recording an ECG is a safe and painless procedure.[29] The

machines are powered by mains power but they are designed with
several safety features including an earthed (ground) lead. Other
features include:

Defibrillation protection: any ECG used in healthcare

may be attached to a person who requires defibrillation
and the ECG needs to protect itself from this source of
energy.
Electrostatic discharge is similar to defibrillation A patient undergoing an ECG
discharge and requires voltage protection up to 18,000
volts.
Additionally, circuitry called the right leg driver can be
used to reduce common-mode interference (typically the
50 or 60 Hz mains power).
ECG voltages measured across the body are very small.
This low voltage necessitates a low noise circuit,
instrumentation amplifiers, and electromagnetic
shielding.
Simultaneous lead recordings: earlier designs recorded
each lead sequentially, but current models record An EKG electrode
multiple leads simultaneously.

Most modern ECG machines include automated interpretation algorithms. This analysis calculates features
such as the PR interval, QT interval, corrected QT (QTc) interval, PR axis, QRS axis, rhythm and more.
The results from these automated algorithms are considered "preliminary" until verified and/or modified by
expert interpretation. Despite recent advances, computer misinterpretation remains a significant problem
and can result in clinical mismanagement.[30]

Cardiac monitors

Besides the standard electrocardiograph machine, there are other devices capable of recording ECG signals.
Portable devices have existed since the Holter monitor was produced in 1962. Traditionally, these monitors
have used electrodes with patches on the skin to record the ECG, but new devices can stick to the chest as
a single patch without need for wires, developed by Zio (Zio XT), TZ Medical (Trident), Philips (BioTel)
and BardyDx (CAM) among many others. Implantable devices such as the artificial cardiac pacemaker and
implantable cardioverter-defibrillator are capable of measuring a "far field" signal between the leads in the
heart and the implanted battery/generator that resembles an ECG signal (technically, the signal recorded in
the heart is called an electrogram, which is interpreted differently). Advancement of the Holter monitor
became the implantable loop recorder that performs the same function but in an implantable device with
batteries that last on the order of years.
Additionally, there are available various Arduino kits with ECG sensor modules and smartwatch devices
that are capable of recording an ECG signal as well, such as with the 4th generation Apple Watch,
Samsung Galaxy Watch 4 and newer devices.

Electrodes and leads

Electrodes are the actual conductive pads attached to the body
surface.[32] Any pair of electrodes can measure the electrical
potential difference between the two corresponding locations of
attachment. Such a pair forms a lead. However, "leads" can also be
formed between a physical electrode and a virtual electrode, known
as Wilson's central terminal (WCT), whose potential is defined
as the average potential measured by three limb electrodes that are
attached to the right arm, the left arm, and the left foot,
Proper placement of the limb
respectively.[33]
electrodes. The limb electrodes can
Commonly, 10 electrodes attached to the body are used to form 12 be far down on the limbs or close to
ECG leads, with each lead measuring a specific electrical potential the hips/shoulders as long as they
difference (as listed in the table below).[34] are placed symmetrically.[31]

Leads are broken down into three types: limb; augmented limb; and
precordial or chest. The 12-lead ECG has a total of three limb leads
and three augmented limb leads arranged like spokes of a wheel in
the coronal plane (vertical), and six precordial leads or chest leads
that lie on the perpendicular transverse plane (horizontal).[35]

In medical settings, the term leads is also sometimes used to refer to

the electrodes themselves, although this is technically incorrect.[36]

The 10 electrodes in a 12-lead ECG are listed below.[37]

Placement of the precordial

electrodes
 Electrode
Electrode placement
name

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, lower end of inner aspect of calf muscle. (Avoid bony prominences)

LL In the same location where RL was placed, but on the left leg.
In the fourth intercostal space (between ribs 4 and 5) just to the right of the sternum
V1
(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 mid-axillary line.

Two types of electrodes in common use are a flat paper-thin sticker and a self-adhesive circular pad. The
former are typically used in a single ECG recording while the latter are for continuous recordings as they
stick longer. Each electrode consists of an electrically conductive electrolyte gel and a silver/silver chloride
conductor.[38] The gel typically contains potassium chloride – sometimes silver chloride as well – to permit
electron conduction from the skin to the wire and to the electrocardiogram.[39]

The common virtual electrode, known as Wilson's central terminal (VW), is produced by averaging the
measurements from the electrodes RA, LA, and LL to give an average potential of the body:

In a 12-lead ECG, all leads except the limb leads are assumed to be unipolar (aVR, aVL, aVF, V1 , V2 , V3 ,
V4 , V5 , and V6 ). The measurement of a voltage requires two contacts and so, electrically, the unipolar
leads are measured from the common lead (negative) and the unipolar lead (positive). This averaging for
the common lead and the abstract unipolar lead concept makes for a more challenging understanding and is
complicated by sloppy usage of "lead" and "electrode". In fact, instead of being a constant reference, VW
has a value that fluctuates throughout the heart cycle. It also does not truly represent the center-of-heart
potential due to the body parts the signals travel through.[40]

Limb leads

Leads I, II and III are called the limb leads. The electrodes that form these signals are located on the limbs –
one on each arm and one on the left leg.[41][42][43] The limb leads form the points of what is known as
Einthoven's triangle.[44]

Lead I is the voltage between the (positive) left arm (LA) electrode and right arm (RA)
electrode:
 The limb leads and augmented limb leads (Wilson's central terminal is used as the negative pole for
the latter in this representation)

Lead II is the voltage between the (positive)

left leg (LL) electrode and the right arm (RA)
electrode:

Lead III is the voltage between the (positive)

left leg (LL) electrode and the left arm (LA)
electrode:

Augmented limb leads

Leads aVR, aVL, and aVF are the augmented limb

leads. They are derived from the same three electrodes
as leads I, II, and III, but they use Goldberger's central terminal as their negative pole. Goldberger's central
terminal is a combination of inputs from two limb electrodes, with a different combination for each
augmented lead. It is referred to immediately below as "the negative pole".

Lead augmented vector right (aVR) has the positive electrode on the right arm. The negative
pole is a combination of the left arm electrode and the left leg electrode:
 Lead augmented vector left (aVL) has the positive electrode on the left arm. The negative
pole is a combination of the right arm electrode and the left leg electrode:

Lead augmented vector foot (aVF) has the positive electrode on the left leg. The negative
pole is a combination of the right arm electrode and the left arm electrode:

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.[45]

Older versions of the nodes (VR, VL, VF) use Wilson's central terminal as the negative pole, but the
amplitude is too small for the thick lines of old ECG machines. The Goldberger terminals scale up
(augments) the Wilson results by 50%, at the cost of sacrificing physical correctness by not having the same
negative pole for all three.[46]

Precordial leads

The precordial leads lie in the transverse (horizontal) plane, perpendicular to the other six leads. The six
precordial electrodes act as the positive poles for the six corresponding precordial leads: (V1 , V2 , V3 , V4 ,
V5 , and V6 ). Wilson's central terminal is used as the negative pole. Recently, unipolar precordial leads have
been used to create bipolar precordial leads that explore the right to left axis in the horizontal plane.[47]

Specialized leads

Additional electrodes may rarely be placed to generate other leads for specific diagnostic purposes. Right-
sided precordial leads may be used to better study pathology of the right ventricle or for dextrocardia (and
are denoted with an R (e.g., V5R). Posterior leads (V7 to V9 ) may be used to demonstrate the presence of a
posterior myocardial infarction. The Lewis lead or S5-lead (requiring an electrode at the right sternal border
in the second intercostal space) can be used to better detect atrial activity in relation to that of the
ventricles.[48]

An esophogeal lead can be inserted to a part of the esophagus where the distance to the posterior wall of
the left atrium is only approximately 5–6 mm (remaining constant in people of different age and
weight).[49] An esophageal lead avails for a more accurate differentiation between certain cardiac
arrhythmias, particularly atrial flutter, AV nodal reentrant tachycardia and orthodromic atrioventricular
reentrant tachycardia.[50] It can also evaluate the risk in people with Wolff-Parkinson-White syndrome, as
well as terminate supraventricular tachycardia caused by re-entry.[50]
An intracardiac electrogram (ICEG) is essentially an ECG with some added intracardiac leads (that is,
inside the heart). The standard ECG leads (external leads) are I, II, III, aVL, V1 , and V6 . Two to four
intracardiac leads are added via cardiac catheterization. The word "electrogram" (EGM) without further
specification usually means an intracardiac electrogram.[51]

Lead locations on an ECG report

A standard 12-lead ECG report (an electrocardiograph) shows a 2.5 second tracing of each of the twelve
leads. The tracings are most commonly arranged in a grid of four columns and three rows. The first column
is the limb leads (I, II, and III), the second column is the augmented limb leads (aVR, aVL, and aVF), and
the last two columns are the precordial leads (V1 to V6 ). Additionally, a rhythm strip may be included as a
fourth or fifth row.[45]

The timing across the page is continuous and not tracings of the 12 leads for the same time period. In other
words, if the output were traced by needles on paper, each row would switch which leads as the paper is
pulled under the needle. For example, the top row would first trace lead I, then switch to lead aVR, then
switch to V1 , and then switch to V4 , and so none of these four tracings of the leads are from the same time
period as they are traced in sequence through time.[52]

Contiguity of leads

Each of the 12 ECG leads records the electrical

activity of the heart from a different angle, and
therefore align with different anatomical areas of the
heart. Two leads that look at neighboring anatomical
areas are said to be contiguous.[45]

Category Leads Activity

Look at electrical activity from Diagram showing the contiguous leads in the same
Leads
Inferior the vantage point of the inferior
II, III color in the standard 12-lead layout
leads surface (diaphragmatic surface
and aVF
of heart)

I, aVL, Look at the electrical activity

Lateral V5 and from the vantage point of the
leads
V6 lateral wall of left ventricle

Look at electrical activity from

Septal V1 and the vantage point of the septal
leads V2 surface of the heart
(interventricular septum)

Look at electrical activity from

V3 and the vantage point of the anterior
Anterior
wall of the right and left
leads V4
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.

Electrophysiology
The study of the conduction system of the heart is called cardiac electrophysiology (EP). An EP study is
performed via a right-sided cardiac catheterization: a wire with an electrode at its tip is inserted into the right
heart chambers from a peripheral vein, and placed in various positions in close proximity to the conduction
system so that the electrical activity of that system can be recorded.[53] Standard catheter positions for an
EP study include "high right atrium" or hRA near the sinus node, a "His" across the septal wall of the
tricuspid valve to measure bundle of His, a "coronary sinus" into the coronary sinus, and a "right ventricle"
in the apex of the right ventricle.[54]

Interpretation
Interpretation of the ECG is fundamentally about understanding the electrical conduction system of the
heart. Normal conduction starts and propagates in a predictable pattern, and deviation from this pattern can
be a normal variation or be pathological. An ECG does not equate with mechanical pumping activity of the
heart, for example, pulseless electrical activity produces an ECG that should pump blood but no pulses are
felt (and constitutes a medical emergency and CPR should be performed). Ventricular fibrillation produces
an ECG but is too dysfunctional to produce a life-sustaining cardiac output. Certain rhythms are known to
have good cardiac output and some are known to have bad cardiac output. Ultimately, an echocardiogram
or other anatomical imaging modality is useful in assessing the mechanical function of the heart.[55]

Like all medical tests, what constitutes "normal" is based on population studies. The heartrate range of
between 60 and 100 beats per minute (bpm) is considered normal since data shows this to be the usual
resting heart rate.[56]

Theory

Interpretation of the ECG is ultimately that of pattern recognition.

In order to understand the patterns found, it is helpful to
understand the theory of what ECGs represent. The theory is
rooted in electromagnetics and boils down to the four following
points:[57]

depolarization of the heart toward the positive electrode

produces a positive deflection
depolarization of the heart away from the positive
electrode produces a negative deflection
repolarization of the heart toward the positive electrode
produces a negative deflection
QRS is upright in a lead when its axis
repolarization of the heart away from the positive
is aligned with that lead's vector
electrode produces a positive deflection

Thus, the overall direction of depolarization and repolarization

produces positive or negative deflection on each lead's trace. For example, depolarizing from right to left
would produce a positive deflection in lead I because the two vectors point in the same direction. In
contrast, that same depolarization would produce minimal
deflection in V1 and V2 because the vectors are
perpendicular, and this phenomenon is called isoelectric.

Normal rhythm produces four entities – a P wave, a QRS

complex, a T wave, and a U wave – that each have a
fairly unique pattern.

The P wave represents atrial depolarization.

The QRS complex represents ventricular
depolarization.
The T wave represents ventricular
repolarization. Schematic representation of a normal ECG
The U wave represents papillary muscle
repolarization.

Changes in the structure of the heart and its surroundings (including blood composition) change the patterns
of these four entities.

The U wave is not typically seen and its absence is generally ignored. Atrial repolarisation is typically
hidden in the much more prominent QRS complex and normally cannot be seen without additional,
specialised electrodes.

Background grid

ECGs are normally printed on a grid. The horizontal axis represents time and the vertical axis represents
voltage. The standard values on this grid are shown in the adjacent image at 25mm/sec:[58]

A small box is 1 mm × 1 mm and represents 0.1 mV × 0.04 seconds.

A large box is 5 mm × 5 mm and represents 0.5 mV × 0.20 seconds.

The "large" box is represented by a heavier line weight than the small boxes.
The standard printing speed in the United States is 25 mm per sec (5 big boxes per second), but in other
countries it can be 50 mm per sec. Faster speeds such as 100 and 200 mm per sec are used during
electrophysiology studies.

Not all aspects of an ECG rely on precise recordings or having a known scaling of amplitude or time. For
example, determining if the tracing is a sinus rhythm only requires feature recognition and matching, and
not measurement of amplitudes or times (i.e., the scale of the grids are irrelevant). An example to the
contrary, the voltage requirements of left ventricular hypertrophy require knowing the grid scale.

Rate and rhythm

In a normal heart, the heart rate is the rate at which the sinoatrial node depolarizes since it is the source of
depolarization of the heart. Heart rate, like other vital signs such as blood pressure and respiratory rate,
change with age. In adults, a normal heart rate is between 60 and 100 bpm (normocardic), whereas it is
higher in children.[59] A heart rate below normal is called "bradycardia" (<60 in adults) and above normal
is called "tachycardia" (>100 in adults). A complication of this is when the atria and ventricles are not in
synchrony and the "heart rate" must be specified as atrial or ventricular (e.g., the ventricular rate in
ventricular fibrillation is 300–600 bpm, whereas the atrial rate can be normal [60–100] or faster [100–
150]).[60]

In normal resting hearts, the physiologic rhythm of the heart is normal sinus rhythm (NSR). Normal sinus
rhythm produces the prototypical pattern of P wave, QRS complex, and T wave. Generally, deviation from
normal sinus rhythm is considered a cardiac arrhythmia. Thus, the first question in interpreting an ECG is
whether or not there is a sinus rhythm. A criterion for sinus rhythm is that P waves and QRS complexes
appear 1-to-1, thus implying that the P wave causes the QRS complex.[52]

Once sinus rhythm is established, or not, the second question is the rate. For a sinus rhythm, this is either
the rate of P waves or QRS complexes since they are 1-to-1. If the rate is too fast, then it is sinus
tachycardia, and if it is too slow, then it is sinus bradycardia.
If it is not a sinus rhythm, then determining the rhythm is necessary before proceeding with further
interpretation. Some arrhythmias with characteristic findings:

Absent P waves with "irregularly irregular" QRS complexes is the hallmark of atrial
fibrillation.
A "saw tooth" pattern with QRS complexes is the hallmark of atrial flutter.
A sine wave pattern is the hallmark of ventricular flutter.
Absent P waves with wide QRS complexes and a fast heart rate is ventricular tachycardia.

Determination of rate and rhythm is necessary in order to make sense of further interpretation.

Axis

The heart has several axes, but the most common by far is the axis
of the QRS complex (references to "the axis" imply the QRS axis).
Each axis can be computationally determined to result in a number
representing degrees of deviation from zero, or it can be
categorized into a few types.[61] Diagram showing how the polarity of
the QRS complex in leads I, II, and
The QRS axis is the general direction of the ventricular III can be used to estimate the
depolarization wavefront (or mean electrical vector) in the frontal heart's electrical axis in the frontal
plane. It is often sufficient to classify the axis as one of three types: plane.
normal, left deviated, or right deviated. Population data shows that
a normal QRS axis is from −30° to 105°, with 0° being along lead I
and positive being inferior and negative being superior (best understood graphically as the hexaxial
reference system).[62] Beyond +105° is right axis deviation and beyond −30° is left axis deviation (the third
quadrant of −90° to −180° is very rare and is an indeterminate axis). A shortcut for determining if the QRS
axis is normal is if the QRS complex is mostly positive in lead I and lead II (or lead I and aVF if +90° is the
upper limit of normal).[63]

The normal QRS axis is generally down and to the left, following the anatomical orientation of the heart
within the chest. An abnormal axis suggests a change in the physical shape and orientation of the heart or a
defect in its conduction system that causes the ventricles to depolarize in an abnormal way.[52]

Classification Angle Notes

Normal −30° to 105° Normal

May indicate left ventricular hypertrophy, left anterior fascicular block, or an
Left axis deviation −30° to −90°
old inferior STEMI

Right axis +105° to May indicate right ventricular hypertrophy, left posterior fascicular block, or
deviation +180° an old lateral STEMI

Indeterminate +180° to
Rarely seen; considered an 'electrical no-man's land'
axis −90°

The extent of a normal axis can be +90° or 105° depending on the source.

Amplitudes and intervals

All of the waves on an ECG tracing and the intervals between them
have a predictable time duration, a range of acceptable amplitudes
(voltages), and a typical morphology. Any deviation from the
normal tracing is potentially pathological and therefore of clinical
significance.[64]

For ease of measuring the amplitudes and intervals, an ECG is

printed on graph paper at a standard scale: each 1 mm (one small
box on the standard 25mm/s ECG paper) represents 40
milliseconds of time on the x-axis, and 0.1 millivolts on the y-
axis.[65]

Animation of a normal ECG wave

 Feature Description Pathology Duration

The P wave is typically upright in most leads except

The P wave represents
for aVR; an unusual P wave axis (inverted in other
depolarization of the atria.
leads) can indicate an ectopic atrial pacemaker. If the
Atrial depolarization spreads
P wave P wave is of unusually long duration, it may represent <80 ms
from the SA node towards the
atrial enlargement. Typically a large right atrium gives
AV node, and from the right
a tall, peaked P wave while a large left atrium gives a
atrium to the left atrium.
two-humped bifid P wave.

The PR interval is measured A PR interval shorter than 120 ms suggests that the
from the beginning of the P electrical impulse is bypassing the AV node, as in
wave to the beginning of the Wolf-Parkinson-White syndrome. A PR interval
PR QRS complex. This interval consistently longer than 200 ms diagnoses first 120 to
interval reflects the time the electrical degree atrioventricular block. The PR segment (the 200 ms
impulse takes to travel from portion of the tracing after the P wave and before the
the sinus node through the QRS complex) is typically completely flat, but may be
AV node. depressed in pericarditis.

If the QRS complex is wide (longer than 120 ms) it

The QRS complex represents
suggests disruption of the heart's conduction system,
the rapid depolarization of the
such as in LBBB, RBBB, or ventricular rhythms such
right and left ventricles. The
as ventricular tachycardia. Metabolic issues such as
ventricles have a large
QRS severe hyperkalemia, or tricyclic antidepressant 80 to 100
muscle mass compared to
complex overdose can also widen the QRS complex. An ms
the atria, so the QRS
unusually tall QRS complex may represent left
complex usually has a much
ventricular hypertrophy while a very low-amplitude
larger amplitude than the P
QRS complex may represent a pericardial effusion or
wave.
infiltrative myocardial disease.

The J-point is the point at The J-point may be elevated as a normal variant. The
which the QRS complex appearance of a separate J wave or Osborn wave at
J-point
finishes and the ST segment the J-point is pathognomonic of hypothermia or
begins. hypercalcemia.[66]

It is usually isoelectric, but may be depressed or

The ST segment connects
elevated with myocardial infarction or ischemia. ST
the QRS complex and the T
ST depression can also be caused by LVH or digoxin. ST
wave; it represents the period
segment elevation can also be caused by pericarditis, Brugada
when the ventricles are
syndrome, or can be a normal variant (J-point
depolarized.
elevation).

The T wave represents the Inverted T waves can be a sign of myocardial

repolarization of the ischemia, left ventricular hypertrophy, high intracranial
T wave ventricles. It is generally pressure, or metabolic abnormalities. Peaked T 160 ms
upright in all leads except waves can be a sign of hyperkalemia or very early
aVR and lead V1. myocardial infarction.

The QT interval is measured

from the beginning of the
A prolonged QTc interval is a risk factor for ventricular
Corrected QRS complex to the end of
tachyarrhythmias and sudden death. Long QT can
QT the T wave. Acceptable
arise as a genetic syndrome, or as a side effect of <440 ms
interval ranges vary with heart rate,
certain medications. An unusually short QTc can be
(QTc) so it must be corrected to the
seen in severe hypercalcemia.
QTc by dividing by the square
root of the RR interval.

The U wave is hypothesized

to be caused by the
repolarization of the A very prominent U wave can be a sign of
U wave interventricular septum. It
normally has a low amplitude, hypokalemia, hypercalcemia or hyperthyroidism.[67]
and even more often is
completely absent.
Limb leads and electrical conduction through the heart

Formation of limb waveforms during a pulse

The animation shown to the right illustrates how the path of electrical conduction gives rise to the ECG
waves in the limb leads. Recall that a positive current (as created by depolarization of cardiac cells)
traveling towards the positive electrode and away from the negative electrode creates a positive deflection
on the ECG. Likewise, a positive current traveling away from the positive electrode and towards the
negative electrode creates a negative deflection on the ECG.[68][69] The red arrow represents the overall
direction of travel of the depolarization. The magnitude of the red arrow is proportional to the amount of
tissue being depolarized at that instance. The red arrow is simultaneously shown on the axis of each of the
3 limb leads. Both the direction and the magnitude of the red arrow's projection onto the axis of each limb
lead is shown with blue arrows. Then, the direction and magnitude of the blue arrows are what theoretically
determine the deflections on the ECG. For example, as a blue arrow on the axis for Lead I moves from the
negative electrode, to the right, towards the positive electrode, the ECG line rises, creating an upward
wave. As the blue arrow on the axis for Lead I moves to the left, a downward wave is created. The greater
the magnitude of the blue arrow, the greater the deflection on the ECG for that particular limb lead.[70]

Frames 1–3 depict the depolarization being generated in and spreading through the Sinoatrial node. The SA
node is too small for its depolarization to be detected on most ECGs. Frames 4–10 depict the depolarization
traveling through the atria, towards the Atrioventricular node. During frame 7, the depolarization is
traveling through the largest amount of tissue in the atria, which creates the highest point in the P wave.
Frames 11–12 depict the depolarization traveling through the AV node. Like the SA node, the AV node is
too small for the depolarization of its tissue to be detected on most ECGs. This creates the flat PR
segment.[71]

Frame 13 depicts an interesting phenomenon in an over-simplified fashion. It depicts the depolarization as it

starts to travel down the interventricular septum, through the Bundle of His and Bundle branches. After the
Bundle of His, the conduction system splits into the left bundle branch and the right bundle branch. Both
branches conduct action potentials at about 1 m/s. Interestingly, however, the action potential starts traveling
down the left bundle branch about 5 milliseconds before it starts traveling down the right bundle branch, as
depicted by frame 13. This causes the depolarization of the interventricular septum tissue to spread from left
to right, as depicted by the red arrow in frame 14. In some cases, this gives rise to a negative deflection after
the PR interval, creating a Q wave such as the one seen in lead I in the animation to the right. Depending
on the mean electrical axis of the heart, this phenomenon can result in a Q wave in lead II as well.[72][73]
Following depolarization of the interventricular septum, the depolarization travels towards the apex of the
heart. This is depicted by frames 15–17 and results in a positive deflection on all three limb leads, which
creates the R wave. Frames 18–21 then depict the depolarization as it travels throughout both ventricles
from the apex of the heart, following the action potential in the Purkinje fibers. This phenomenon creates a
negative deflection in all three limb leads, forming the S wave on the ECG. Repolarization of the atria
occurs at the same time as the generation of the QRS complex, but it is not detected by the ECG since the
tissue mass of the ventricles is so much larger than that of the atria. Ventricular contraction occurs between
ventricular depolarization and repolarization. During this time, there is no movement of charge, so no
deflection is created on the ECG. This results in the flat ST segment after the S wave.[74]

Frames 24–28 in the animation depict repolarization of the ventricles. The epicardium is the first layer of
the ventricles to repolarize, followed by the myocardium. The endocardium is the last layer to repolarize.
The plateau phase of depolarization has been shown to last longer in endocardial cells than in epicardial
cells. This causes repolarization to start from the apex of the heart and move upwards. Since repolarization
is the spread of negative current as membrane potentials decrease back down to the resting membrane
potential, the red arrow in the animation is pointing in the direction opposite of the repolarization. This
therefore creates a positive deflection in the ECG, and creates the T wave.[75]

Ischemia and infarction

Ischemia or non-ST elevation myocardial infarctions (non-STEMIs) may manifest as ST depression or

inversion of T waves. It may also affect the high frequency band of the QRS.

ST elevation myocardial infarctions (STEMIs) have different characteristic ECG findings based on the
amount of time elapsed since the MI first occurred. The earliest sign is hyperacute T waves, peaked T
waves due to local hyperkalemia in ischemic myocardium. This then progresses over a period of minutes to
elevations of the ST segment by at least 1 mm. Over a period of hours, a pathologic Q wave may appear
and the T wave will invert. Over a period of days the ST elevation will resolve. Pathologic Q waves
generally will remain permanently.[76]

The coronary artery that has been occluded can be identified in an STEMI based on the location of ST
elevation. The left anterior descending (LAD) artery supplies the anterior wall of the heart, and therefore
causes ST elevations in anterior leads (V1 and V2 ). The LCx supplies the lateral aspect of the heart and
therefore causes ST elevations in lateral leads (I, aVL and V6 ). The right coronary artery (RCA) usually
supplies the inferior aspect of the heart, and therefore causes ST elevations in inferior leads (II, III and
aVF).[77]

Artifacts

An ECG tracing is affected by patient motion. Some rhythmic motions (such as shivering or tremors) can
create the illusion of cardiac arrhythmia.[78] Artifacts are distorted signals caused by a secondary internal or
external sources, such as muscle movement or interference from an electrical device.[79][80]

Distortion poses significant challenges to healthcare providers,[79] who employ various techniques[81] and
strategies to safely recognize[82] these false signals. Accurately separating the ECG artifact from the true
ECG signal can have a significant impact on patient outcomes and legal liabilities.[83]
Improper lead placement (for example, reversing two of the limb leads) has been estimated to occur in 0.4%
to 4% of all ECG recordings,[84] and has resulted in improper diagnosis and treatment including
unnecessary use of thrombolytic therapy.[85][86]

Diagnosis
Numerous diagnoses and findings can be made based upon electrocardiography, and many are discussed
above. Overall, the diagnoses are made based on the patterns. For example, an "irregularly irregular" QRS
complex without P waves is the hallmark of atrial fibrillation; however, other findings can be present as
well, such as a bundle branch block that alters the shape of the QRS complexes. ECGs can be interpreted
in isolation but should be applied – like all diagnostic tests – in the context of the patient. For example, an
observation of peaked T waves is not sufficient to diagnose hyperkalemia; such a diagnosis should be
verified by measuring the blood potassium level. Conversely, a discovery of hyperkalemia should be
followed by an ECG for manifestations such as peaked T waves, widened QRS complexes, and loss of P
waves. The following is an organized list of possible ECG-based diagnoses.[87]

Rhythm disturbances or arrhythmias:[88]

Atrial fibrillation and atrial flutter without rapid ventricular response

Premature atrial contraction (PACs) and premature ventricular contraction (PVCs)
Sinus arrhythmia
Sinus bradycardia and sinus tachycardia
Sinus pause and sinoatrial arrest
Sinus node dysfunction and bradycardia-tachycardia syndrome
Supraventricular tachycardia
Atrial fibrillation with rapid ventricular response
Atrial flutter with rapid ventricular response
AV nodal reentrant tachycardia
Atrioventricular reentrant tachycardia
Junctional ectopic tachycardia
Atrial tachycardia
Ectopic atrial tachycardia (unicentric)
Multifocal atrial tachycardia
Paroxysmal atrial tachycardia
Sinoatrial nodal reentrant tachycardia
Torsades de pointes (polymorphic ventricular tachycardia)
Wide complex tachycardia
Ventricular flutter
Ventricular fibrillation
Ventricular tachycardia (monomorphic ventricular tachycardia)
Pre-excitation syndrome
Lown–Ganong–Levine syndrome
Wolff–Parkinson–White syndrome
J wave (Osborn wave)
Heart block and conduction problems:

Aberration
Sinoatrial block: first, second, and third-degree
AV node
First-degree AV block
Second-degree AV block (Mobitz [Wenckebach] I and II)
Third-degree AV block or complete AV block
Right bundle
Incomplete right bundle branch block (IRBBB)
Complete right bundle branch block (RBBB)
Left bundle
Incomplete left bundle branch block (ILBBB)
Complete left bundle branch block (LBBB)
Left anterior fascicular block (LAFB)
Left posterior fascicular block (LPFB)
Bifascicular block (LAFB plus LPFB)
Trifascicular block (LAFP plus FPFB plus RBBB)
QT syndromes
Brugada syndrome
Short QT syndrome
Long QT syndromes, genetic and drug-induced
Right and left atrial abnormality

Electrolytes disturbances and intoxication:

Digitalis intoxication
Calcium: hypocalcemia and hypercalcemia
Potassium: hypokalemia and hyperkalemia
Serotonin Toxicity

Ischemia and infarction:

Wellens' syndrome (LAD occlusion)

de Winter T waves (LAD occlusion) [89]
ST elevation and ST depression
High Frequency QRS changes
Myocardial infarction (heart attack)
Non-Q wave myocardial infarction
NSTEMI
STEMI
Sgarbossa's criteria for ischemia with a LBBB

Structural:
 Acute pericarditis
Right and left ventricular hypertrophy
Right ventricular strain or S1Q3T3 (can be seen in pulmonary embolism)

History
In 1872, Alexander Muirhead is reported to have
attached wires to the wrist of a patient with fever to
obtain an electronic record of their heartbeat.[90]
In 1882, John Burdon-Sanderson working with frogs,
was the first to appreciate that the interval between
variations in potential was not electrically quiescent and
coined the term "isoelectric interval" for this period.[91]
In 1887, Augustus Waller[92] invented an ECG machine
consisting of a Lippmann capillary electrometer fixed to a
projector. The trace from the heartbeat was projected
An early commercial ECG device
onto a photographic plate that was itself fixed to a toy
(1911)
train. This allowed a heartbeat to be recorded in real
time.
In 1895, Willem Einthoven assigned the letters P, Q, R,
S, and T to the deflections in the theoretical waveform he
created using equations which corrected the actual
waveform obtained by the capillary electrometer to ECG from 1957
compensate for the imprecision of that instrument. Using
letters different from A, B, C, and D (the letters used for
the capillary electrometer's waveform) facilitated comparison when the uncorrected and
corrected lines were drawn on the same graph.[93] Einthoven probably chose the initial letter
P to follow the example set by Descartes in geometry.[93] When a more precise waveform
was obtained using the string galvanometer, which matched the corrected capillary
electrometer waveform, he continued to use the letters P, Q, R, S, and T,[93] and these letters
are still in use today. Einthoven also described the electrocardiographic features of a
number of cardiovascular disorders.
In 1897, the string galvanometer was invented by the French engineer Clément Ader.[94]
In 1901, Einthoven, working in Leiden, the Netherlands, used the string galvanometer: the
first practical ECG.[95] This device was much more sensitive than the capillary electrometer
Waller used.
In 1924, Einthoven was awarded the Nobel Prize in Medicine for his pioneering work in
developing the ECG.[96]
By 1927, General Electric had developed a portable apparatus that could produce
electrocardiograms without the use of the string galvanometer. This device instead
combined amplifier tubes similar to those used in a radio with an internal lamp and a moving
mirror that directed the tracing of the electric pulses onto film.[97]
In 1937, Taro Takemi invented a new portable electrocardiograph machine.[98]
In 1942, Emanuel Goldberger increases the voltage of Wilson's unipolar leads by 50% and
creates the augmented limb leads aVR, aVL and aVF. When added to Einthoven's three limb
leads and the six chest leads we arrive at the 12-lead electrocardiogram that is used
today.[99]
In the late 1940s Rune Elmqvist invented an inkjet printer - thin jets of ink deflected by
electrical potentials from the heart, with good frequency response and direct recording of
 ECG on paper - the device, called the Mingograf, was sold by Siemens Elema until the
1990s.[100]

Etymology

The word is derived from the Greek electro, meaning related to electrical activity; kardia, meaning heart;
and graph, meaning "to write".

See also
Signal-averaged electrocardiogram
Electrical conduction system of the heart
Electroencephalography
Electrogastrogram
Electropalatography
Electroretinography
Emergency medicine
Forward problem of electrocardiology
Heart rate
Heart rate monitor
KardiaMobile
Wireless ambulatory ECG

Notes
a. The version with '-K-', more commonly used in American English than in British English, is
an early-20th-century loanword from the German acronym EKG for Elektrokardiogramm
(electrocardiogram),[1] which reflects that German physicians were pioneers in the field at
the time. Today, AMA style and – under its stylistic influence – most American medical
publications use ECG instead of EKG.[2] The German term Elektrokardiogramm as well as
the English equivalent, electrocardiogram, consist of the New Latin/international scientific
vocabulary elements elektro- (cognate electro-) and kardi- (cognate 'cardi-'), the latter from
Greek kardia (heart).[3] The '-K-' version is more often retained under circumstances where
there may be verbal confusion between ECG and EEG (electroencephalography) due to
similar pronunciation.

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External links
The whole ECG course on 1 A4 paper ([Link]
[Link]) from ECGpedia ([Link] a wiki encyclopedia for a
course on interpretation of ECG ([Link]
Wave Maven – a large database of practice ECG questions ([Link]
aven/[Link]) provided by Beth Israel Deaconess Medical Center
PysioBank – a free scientific database with physiologic signals (here ecg) ([Link]
[Link]/physiobank/database/#ecg)
EKG Academy – free EKG lectures, drills and quizzes ([Link]
ECG Learning Center ([Link] created by Eccles Health Sciences
Library at University of Utah

Retrieved from "[Link]

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