Electrocardiography

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"ECG" and "EKG" redirect here. For other uses, see ECG (disambiguation) and EKG (disambiguation).

Not to be confused with other types of electrography or with echocardiography.

Method to record the electrical activity of the heart through passive electrodes placed over the skin.

Electrocardiography

ECG of a heart in normal sinus rhythm

ICD-10-PCS R94.31

ICD-9-CM 89.52

MeSH D004562

MedlinePlus 003868

[edit on Wikidata]

Electrocardiography is the process of producing an electrocardiogram (ECG or EKG[a]). It is a graph of

voltage versus time of the electrical activity of the heart[4] 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 and ventricular tachycardia), inadequate coronary artery blood flow (such as myocardial
ischemia and myocardial infarction), and electrolyte disturbances (such as hypokalemia and
hyperkalemia).

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.[5]

There are three main components to an ECG: the P wave, which represents the depolarization of the
atria; the QRS complex, which represents the depolarization of the ventricles; and the T wave, which
represents the repolarization of the ventricles.[6]

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.[6] 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.[7] 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.[8]

Contents

1 Medical uses

1.1 Screening

2 Electrocardiograph machines

3 Electrodes and leads

3.1 Limb leads

3.2 Augmented limb leads

3.3 Precordial leads

3.4 Specialized leads

3.5 Lead locations on an ECG report

3.6 Contiguity of leads

4 Electrophysiology

5 Interpretation

5.1 Theory
5.2 Background grid

5.3 Rate and rhythm

5.4 Axis

5.5 Amplitudes and intervals

5.6 Limb leads and electrical conduction through the heart

5.7 Ischemia and infarction

5.8 Artifacts

6 Diagnosis

7 History

7.1 Etymology

8 See also

9 Notes

10 References

11 External links

Medical uses[edit]

Normal 12-lead ECG

A 12-lead ECG of a 26-year-old male with an incomplete RBBB

The overall goal of performing an ECG is to obtain information about the electrical function 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:[citation needed]

Chest pain or suspected myocardial infarction (heart attack), such as ST elevated myocardial infarction
(STEMI)[9] or non-ST elevated myocardial infarction (NSTEMI)[10]

Symptoms such as shortness of breath, murmurs,[11] 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

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.

Cardiac stress testing

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,[11] 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.

Screening[edit]
A woman undergoing an ECG

Evidence does not support the use of ECGs among those without symptoms or at low risk of
cardiovascular disease as an effort for prevention.[12][13][14] 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,[15] 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.[citation needed]

Electrocardiograph machines[edit]

An EKG sensor

Electrocardiographs are recorded by machines that consist of a set of electrodes connected to a central
unit.[16] 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.[17] These smaller devices often rely on only two electrodes to deliver a single lead I.[18]
Portable six-lead devices are also available.

Recording an ECG is a safe and painless procedure.[19] 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 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 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.[20]

Electrodes and leads[edit]

Proper placement of the limb electrodes. The limb electrodes can be far down on the limbs or close to
the hips/shoulders as long as they are placed symmetrically.[21]

Placement of the precordial electrodes

Electrodes are the actual conductive pads attached to the body surface.[22] 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, respectively.[citation needed]

Commonly, 10 electrodes attached to the body are used to form 12 ECG leads, with each lead measuring
a specific electrical potential difference (as listed in the table below).[23]

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).[24]

In medical settings, the term leads is also sometimes used to refer to the electrodes themselves,
although this is technically incorrect.[citation needed]

The 10 electrodes in a 12-lead ECG are listed below.[25]

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.[26] 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.[citation
needed]

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:

V W = 1 3 ( R A + L A + L L ) {\displaystyle V_{W}={\frac {1}{3}}(RA+LA+LL)}

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.[27]

Limb leads[edit]

The limb leads and augmented limb leads (Wilson's central terminal is used as the negative pole for the
latter in this representation)
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.[28][29][30] The limb leads form the points of what is
known as Einthoven's triangle.[31]

Lead I is the voltage between the (positive) left arm (LA) electrode and right arm (RA) electrode:

I = L A − R A {\displaystyle I=LA-RA}

Lead II is the voltage between the (positive) left leg (LL) electrode and the right arm (RA) electrode:

I I = L L − R A {\displaystyle II=LL-RA}

Lead III is the voltage between the (positive) left leg (LL) electrode and the left arm (LA) electrode:

I I I = L L − L A {\displaystyle III=LL-LA}

Augmented limb leads[edit]

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:

a V R = R A − 1 2 ( L A + L L ) = 3 2 ( R A − V W ) {\displaystyle aVR=RA-{\frac {1}{2}}(LA+LL)={\frac {3}{2}}

(RA-V_{W})}

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:
a V L = L A − 1 2 ( R A + L L ) = 3 2 ( L A − V W ) {\displaystyle aVL=LA-{\frac {1}{2}}(RA+LL)={\frac {3}{2}}

(LA-V_{W})}

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:

a V F = L L − 1 2 ( R A + L A ) = 3 2 ( L L − V W ) {\displaystyle aVF=LL-{\frac {1}{2}}(RA+LA)={\frac {3}{2}}(LL-

V_{W})}

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.[citation
needed]

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.[32]

Precordial leads[edit]

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.[33]

Specialized leads[edit]

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. A Lewis lead (requiring an electrode at
the right sternal border in the second intercostal space) can be used to study pathological rhythms
arising in the right atrium.[citation needed]

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).[34] 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.[35] It can also evaluate the risk in people with Wolff-Parkinson-White syndrome,
as well as terminate supraventricular tachycardia caused by re-entry.[35]

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.[citation needed]
Lead locations on an ECG report[edit]

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.[citation needed]

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.[citation needed]

Contiguity of leads[edit]

Diagram showing the contiguous leads in the same color in the standard 12-lead layout

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.[citation needed]

Category Leads Activity

Inferior Leads II, III Look at electrical activity from the vantage point of the inferior surface
leads and aVF (diaphragmatic surface of heart)

Lateral I, aVL, V5 Look at the electrical activity from the vantage point of the lateral wall of left
leads and V6 ventricle

Look at electrical activity from the vantage point of the septal surface of the
Septal leads V1 and V2
heart (interventricular septum)

Anterior Look at electrical activity from the vantage point of the anterior wall of the
V3 and V4
leads 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.

Electrophysiology[edit]
Main article: Cardiac 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.[citation needed]

Interpretation[edit]

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.[citation needed]

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.[citation needed]

Theory[edit]

QRS is upright in a lead when its axis is aligned with that lead's vector
Schematic representation of a normal ECG

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:

depolarization of the heart towards the positive electrode produces a positive deflection

depolarization of the heart away from the positive electrode produces a negative deflection

repolarization of the heart towards the positive electrode produces a negative deflection

repolarization of the heart away from the positive 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.

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[edit]
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:

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.

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[edit]

In a normal heart, the heart rate is the rate in 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. 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]).[citation needed]

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.[citation needed]

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[edit]

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.[citation needed]

The QRS axis is the general direction of the ventricular depolarization wavefront (or mean electrical
vector) in the frontal plane. It is often sufficient to classify the axis as one of three types: 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).[36] 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).[citation needed]

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.[citation
needed]

Classification Angle Notes

Normal −30° to 105° Normal

May indicate left ventricular hypertrophy, left anterior fascicular block,

Left axis deviation −30° to −90°
or an old inferior STEMI

Right axis +105° to May indicate right ventricular hypertrophy, left posterior fascicular
deviation +180° block, or 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[edit]

Animation of a normal ECG wave

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.[citation needed]

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 ECG paper) represents 40 milliseconds of time on the
x-axis, and 0.1 millivolts on the y-axis.[citation needed]

Feature Description Pathology Duration

The P wave is typically upright in most leads

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

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

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

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

The J-point may be elevated as a normal variant.

The J-point is the point at which
The appearance of a separate J wave or Osborn
J-point the QRS complex finishes and
wave at the J-point is pathognomonic of
the ST segment begins.
hypothermia or hypercalcemia.[37]

It is usually isoelectric, but may be depressed or

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

Inverted T waves can be a sign of myocardial

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

The QT interval is measured

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

U wave The U wave is hypothesized to A very prominent U wave can be a sign of

be caused by the repolarization hypokalemia, hypercalcemia or
of the interventricular septum. It hyperthyroidism.[38]
normally has a low amplitude,
 and even more often is
completely absent.

Limb leads and electrical conduction through the heart [edit]

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.[39][40] 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.[citation needed]

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.[41]
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.[42][43]

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.

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.[44]

Ischemia and infarction[edit]

Main article: Electrocardiography in myocardial 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.[45]

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).[citation needed]

Artifacts[edit]

An ECG tracing is affected by patient motion. Some rhythmic motions (such as shivering or tremors) can
create the illusion of cardiac arrhythmia.[46] Artifacts are distorted signals caused by a secondary
internal or external sources, such as muscle movement or interference from an electrical device.[47][48]

Distortion poses significant challenges to healthcare providers,[47] who employ various techniques[49]
and strategies to safely recognize[50] these false signals.[medical citation needed] Accurately separating
the ECG artifact from the true ECG signal can have a significant impact on patient outcomes and legal
liabilities.[51][unreliable medical source?]

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,[52] and has resulted in improper diagnosis and treatment including
unnecessary use of thrombolytic therapy.[53][54]

Diagnosis[edit]

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.
[citation needed]

Rhythm disturbances or arrhythmias:[citation needed]

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

Complete right bundle branch block (RBBB)

Left bundle

Complete left bundle branch block (LBBB)

Incomplete left bundle branch block

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) [55]

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[edit]

An early commercial ECG device (1911)

ECG from 1957

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.[56]

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.[57]

In 1887, Augustus Waller[58] invented an ECG machine consisting 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 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 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.[59] Einthoven probably chose the
initial letter P to follow the example set by Descartes in geometry.[59] 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,[59] 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.[60]

In 1901, Einthoven, working in Leiden, the Netherlands, used the string galvanometer: the first practical
ECG.[61] 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.[62]
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.[63]

In 1937, Taro Takemi invented a new portable electrocardiograph machine.[64]

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.[65]

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.[66]

Etymology[edit]

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

See also[edit]

Electrical conduction system of the heart

Electrogastrogram

Electropalatography

Electroretinography

Heart rate

Heart rate monitor

Emergency medicine

Forward problem of electrocardiology

Notes[edit]

^ 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[edit]

Wikimedia Commons has media related to ECG.

The whole ECG course on 1 A4 paper from ECGpedia, a wiki encyclopedia for a course on interpretation
of ECG

Wave Maven – a large database of practice ECG questions provided by Beth Israel Deaconess Medical
Center

PysioBank – a free scientific database with physiologic signals (here ecg)

EKG Academy – free EKG lectures, drills and quizzes

ECG Learning Center created by Eccles Health Sciences Library at University of Utah

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v

Tests and procedures involving the heart

Cardiac surgery  · Interventional cardiology  · Cardiology diagnostic tests and procedures  · Cardiac
imaging

Surgery Heart valves Valve repair

and septa
Valvulotomy

Mitral valve repair

Valvuloplasty

aortic

mitral

Valve replacement

Aortic valve repair

Aortic valve replacement

Ross procedure

Percutaneous aortic valve replacement

Mitral valve replacement

Percutaneous pulmonary valve implantation

production of septal defect in heart

enlargement of existing septal defect

Atrial septostomy

Balloon septostomy

creation of septal defect in heart

Blalock–Hanlon procedure

shunt from heart chamber to blood vessel

atrium to pulmonary artery

Fontan procedure
 left ventricle to aorta

Rastelli procedure

right ventricle to pulmonary artery

Sano shunt

compound procedures

for transposition of the great vessels

Arterial switch operation

Mustard procedure

Senning procedure

for univentricular defect

Norwood procedure

Kawashima procedure

shunt from blood vessel to blood vessel

systemic circulation to pulmonary artery shunt

Blalock–Taussig shunt

SVC to the right PA

Glenn procedure

Cardiac vessels CHD

Angioplasty

Bypass/Coronary artery bypass

MIDCAB

Off-pump CAB

TECAB

Coronary stent

Bare-metal stent

Drug-eluting stent

Bentall procedure

Valve-sparing aortic root replacement

 LeCompte maneuver

Pericardium

Pericardiocentesis

Pericardial window

Pericardiectomy

Myocardium

Cardiomyoplasty

Dor procedure

Septal myectomy

Ventricular reduction

Alcohol septal ablation

Other
Conduction system

Maze procedure

Cox maze and minimaze

Catheter ablation

Cryoablation

Radiofrequency ablation

Pacemaker insertion

Left atrial appendage occlusion

Cardiotomy

Heart transplantation

Tests Electrophysiology

Electrocardiography

Vectorcardiography

Holter monitor

Implantable loop recorder

Cardiac stress test

 Bruce protocol

Electrophysiology study

Cardiac imaging

Angiocardiography

Echocardiography

TTE

TEE

Myocardial perfusion imaging

Cardiovascular MRI

Ventriculography

Radionuclide ventriculography

Cardiac catheterization/Coronary catheterization

Cardiac CT

Cardiac PET

sound

Phonocardiogram

Impedance cardiography

Function tests Ballistocardiography

Cardiotocography

Cardioversion
Pacing
Transcutaneous pacing

Category

show

e
Medical test: Electrodiagnosis

Electrocardiography

Heart Vectorcardiography

Magnetocardiography

Electroencephalography (Intracranial EEG,

Central nervous system stereoelectroencephalography)

Magnetoencephalography

Electromyography (Facial electromyography)

Peripheral nervous system
Nerve conduction study

Ears Electrocochleography

Electronystagmography

Eyes Electrooculography

Electroretinography

Electrogastrogram

Magnetogastrography
Digestive system
Electrogustometry

Electro-olfactography

show

Physiology of the cardiovascular system

Cardiac output Cardiac cycle

Cardiac output
Heart
Heart rate

Stroke volume
 Stroke volume

End-diastolic volume

End-systolic volume

Afterload

Preload

Frank–Starling law

Cardiac function curve

Venous return curve

Wiggers diagram

Pressure volume diagram

Fractional shortening = (End-diastolic

dimension

End-systolic dimension) / End-diastolic

dimension
Ultrasound
Aortic valve area calculation

Ejection fraction

Cardiac index

Cardiac pacemaker

Chronotropic (Heart rate)

Dromotropic (Conduction velocity)

Heart rate
Inotropic (Contractility)

Bathmotropic (Excitability)

Lusitropic (Relaxation)

Conduction Conduction system

Cardiac electrophysiology

Action potential

cardiac

atrial
 ventricular

Effective refractory period

Pacemaker potential

Electrocardiography

P wave

PR interval

QRS complex

QT interval

ST segment

T wave

U wave

Hexaxial reference system

Central venous

Right

atrial

ventricular

pulmonary artery
Chamber pressure
wedge

Left

atrial

ventricular

Aortic

Other Ventricular remodeling

Compliance

Vascular system/ Vascular resistance

Blood flow
Hemodynamics Pulse

Perfusion
 Pulse pressure

Systolic

Diastolic

Blood pressure Mean arterial pressure

Jugular venous pressure

Portal venous pressure

Critical closing pressure

Baroreflex

Kinin–kallikrein system

Renin–angiotensin system

Vasoconstrictors

Vasodilators

Autoregulation

Regulation of BP Myogenic mechanism

Tubuloglomerular feedback

Cerebral autoregulation

Paraganglia

Aortic body

Carotid body

Glomus cell

GND: 4014280-2

LCCN: sh85042098
Authority control
MA: 2780040984

NDL: 00571014

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Coronary artery disease (CAD), also called coronary heart disease (CHD), ischemic heart disease (IHD), or
simply heart disease, involves the reduction of blood flow to the heart muscle due to build-up of plaque
(atherosclerosis) in the arteries of the heart. It is the most common of the cardiovascular diseases. Types
include stable angina, unstable angina, myocardial infarction, and sudden cardiac death. A common
symptom is chest pain or discomfort which may travel into the shoulder, arm, back, neck, or jaw.
Occasionally it may feel like heartburn. Usually symptoms occur with exercise or emotional stress, last
less than a few minutes, and improve with rest. Shortness of breath may also occur and sometimes no
symptoms are present. In many cases, the first sign is a heart attack. Other complications include heart
failure or an abnormal heartbeat.