Artificial pacemaker

From Wikipedia, the free encyclopedia

"Cardiac resynchronization therapy" and "CRT (Cardiac Resynchronization Therapy)" redirect

here. For the device termed a CRT-D, see Implanted cardiac resynchronization device. For other

uses, see Pacemaker (disambiguation).

A pacemaker, scale in centimeters

An artificial pacemaker with electrode for transvenous insertion. The body of the device is about

4 centimeters long, the electrode measures between 50 and 60 centimeters (20 to 24 inches).

A pacemaker (or artificial pacemaker, so as not to be confused with the heart's natural

pacemaker) is a medical device that uses electrical impulses, delivered by electrodes contacting

the heart muscles, to regulate the beating of the heart. The primary purpose of a pacemaker is to

maintain an adequate heart rate, either because the heart's native pacemaker is not fast enough, or

there is a block in the heart's electrical conduction system. Modern pacemakers are externally

programmable and allow the cardiologist to select the optimum pacing modes for individual

patients. Some combine a pacemaker and defibrillator in a single implantable device. Others

have multiple electrodes stimulating differing positions within the heart to improve

synchronisation of the lower chambers of the heart.

Contents

[hide]

1 History

2 Methods of pacing

o 2.1 Percussive pacing

o 2.2 Transcutaneous pacing

o 2.3 Epicardial pacing (temporary)

o 2.4 Transvenous pacing (temporary)

o 2.5 Permanent pacing

3 Basic function

4 Biventricular pacing (BVP)

5 Advancements in function

6 Considerations

o 6.1 Insertion

6.1.1 Pacemaker patient identification card

o 6.2 Living with a pacemaker

6.2.1 Periodic pacemaker checkups

6.2.2 Lifestyle considerations

6.2.3 Turning off the pacemaker

o 6.3 Privacy and security

o 6.4 Complications

7 Other devices with pacemaker function

8 See also

9 References

10 External links

History

The first implantable pacemaker

In 1958, Arne Larsson (1915-2001) became the first to receive an implantable pacemaker. He

had a total of 26 devices during his life and campaigned for other patients needing pacemakers.

In 1899, J A McWilliam reported in the British Medical Journal of his experiments in which

application of an electrical impulse to the human heart in asystole caused a ventricular

contraction and that a heart rhythm of 60-70 beats per minute could be evoked by impulses

applied at spacings equal to 60-70/minute.[1]

In 1926, Dr Mark C Lidwell of the Royal Prince Alfred Hospital of Sydney, supported by

physicist Edgar H Booth of the University of Sydney, devised a portable apparatus which

"plugged into a lighting point" and in which "One pole was applied to a skin pad soaked in

strong salt solution" while the other pole "consisted of a needle insulated except at its point, and

was plunged into the appropriate cardiac chamber". "The pacemaker rate was variable from

about 80 to 120 pulses per minute, and likewise the voltage variable from 1.5 to 120 volts" In

1928, the apparatus was used to revive a stillborn infant at Crown Street Women's Hospital,

Sydney whose heart continued "to beat on its own accord", "at the end of 10 minutes" of

stimulation.[2][3]

In 1932, American physiologist Albert Hyman, working independently, described an electro-

mechanical instrument of his own, powered by a spring-wound hand-cranked motor. Hyman

himself referred to his invention as an "artificial pacemaker", the term continuing in use to this

day.[4][5]

An apparent hiatus in publication of research conducted between the early 1930s and World War

II may be attributed to the public perception of interfering with nature by 'reviving the dead'. For

example, "Hyman did not publish data on the use of his pacemaker in humans because of adverse

publicity, both among his fellow physicians, and due to newspaper reporting at the time. Lidwell

may have been aware of this and did not proceed with his experiments in humans".[3]

An external pacemaker was designed and built by the Canadian electrical engineer John Hopps

in 1950 based upon observations by cardio-thoracic surgeon Wilfred Gordon Bigelow at Toronto

General Hospital . A substantial external device using vacuum tube technology to provide

transcutaneous pacing, it was somewhat crude and painful to the patient in use and, being

powered from an AC wall socket, carried a potential hazard of electrocution of the patient by

inducing ventricular fibrillation.

A number of innovators, including Paul Zoll, made smaller but still bulky transcutaneous pacing

devices in the following years using a large rechargeable battery as the power supply.[6]

In 1957, Dr. William L. Weirich published the results of research performed at the University of

Minnesota. These studies demonstrated the restoration of heart rate, cardiac output and mean

aortic pressures in animal subjects with complete heart block through the use of a myocardial

electrode. This effective control of postsurgical heart block proved to be a significant

contribution to decreasing mortality of open heart surgery in this time period.[7]

The development of the silicon transistor and its first commercial availability in 1956 was the

pivotal event which led to rapid development of practical cardiac pacemaking.

In 1958, engineer Earl Bakken of Minneapolis, Minnesota, produced the first wearable external

pacemaker for a patient of Dr. C. Walton Lillehei. This transistorised pacemaker, housed in a

small plastic box, had controls to permit adjustment of pacing heart rate and output voltage and

was connected to electrode leads which passed through the skin of the patient to terminate in

electrodes attached to the surface of the myocardium of the heart.

The first clinical implantation into a human of a fully implantable pacemaker was in 1958 at the

Karolinska Institute in Solna, Sweden, using a pacemaker designed by Rune Elmqvist and

surgeon Åke Senning, connected to electrodes attached to the myocardium of the heart by

thoracotomy. The device failed after three hours. A second device was then implanted which

lasted for two days. The world's first implantable pacemaker patient, Arne Larsson, went on to

receive 26 different pacemakers during his lifetime. He died in 2001, at the age of 86, outliving

the inventor as well as the surgeon.[8]

In 1959, temporary transvenous pacing was first demonstrated by Furman et al. in which the

catheter electrode was inserted via the patient's basilic vein.[9]

In February 1960, an improved version of the Swedish Elmqvist design was implanted in

Montevideo, Uruguay in the Casmu Hospital by Doctors Fiandra and Rubio. That device lasted

until the patient died of other ailments, 9 months later. The early Swedish-designed devices used

rechargeable batteries, which were charged by an induction coil from the outside.

Implantable pacemakers constructed by engineer Wilson Greatbatch entered use in humans from

April 1960 following extensive animal testing. The Greatbatch innovation varied from the earlier

Swedish devices in using primary cells (mercury battery) as the energy source. The first patient

lived for a further 18 months.

The first use of transvenous pacing in conjunction with an implanted pacemaker was by

Parsonnet in the USA,[10][11][12]

Lagergren in Sweden[13][14]

and Jean-Jaques Welti in France[15]

in

1962-63. The transvenous, or pervenous, procedure involved incision of a vein into which was

inserted the catheter electrode lead under fluoroscopic guidance, until it was lodged within the

trabeculae of the right ventricle. This method was to become the method of choice by the mid-

1960s.

World's first Lithium-iodide cell powered pacemaker. Cardiac Pacemakers Inc. 1972

The preceding implantable devices all suffered from the unreliability and short lifetime of the

available primary cell technology which was mainly that of the mercury battery.

In the late 1960s, several companies, including ARCO in the USA, developed isotope powered

pacemakers, but this development was overtaken by the development in 1971 of the lithium-

iodide cell by Wilson Greatbatch. Lithium-iodide or lithium anode cells became the standard for

future pacemaker designs.

A further impediment to reliability of the early devices was the diffusion of water vapour from

the body fluids through the epoxy resin encapsulation affecting the electronic circuitry. This

phenomenon was overcome by encasing the pacemaker generator in an hermetically sealed metal

case, initially by Telectronics of Australia in 1969 followed by Cardiac Pacemakers Inc of

Minneapolis in 1972. This technology, using titanium as the encasing metal, became the standard

by the mid-1970s.

Others who contributed significantly to the technological development of the pacemaker in the

pioneering years were Bob Anderson of Medtronic Minneapolis, J.G (Geoffrey) Davies of St

George's Hospital London, Barouh Berkovits and Sheldon Thaler of American Optical, Geoffrey

Wickham of Telectronics Australia, Walter Keller of Cordis Corp. of Miami, Hans Thornander

who joined previously mentioned Rune Elmquist of Elema-Schonander in Sweden, Janwillem

van den Berg of Holland and Anthony Adducci of Cardiac Pacemakers Inc.Guidant.

Methods of pacing

An ECG in a person with an atrial pacemaker. Note the circle around one of the sharp electrical

spike in the position were one would expect the P wave.

Percussive pacing

Percussive pacing, also known as transthoracic mechanical pacing, is the use of the closed fist,

usually on the left lower edge of the sternum over the right ventricle in the vena cava, striking

from a distance of 20 – 30 cm to induce a ventricular beat (the British Journal of Anesthesia

suggests this must be done to raise the ventricular pressure to 10 - 15mmHg to induce electrical

activity). This is an old procedure used only as a life saving means until an electrical pacemaker

is brought to the patient.[16]

Transcutaneous pacing

Main article: Transcutaneous pacing

Transcutaneous pacing (TCP), also called external pacing, is recommended for the initial

stabilization of hemodynamically significant bradycardias of all types. The procedure is

performed by placing two pacing pads on the patient's chest, either in the anterior/lateral position

or the anterior/posterior position. The rescuer selects the pacing rate, and gradually increases the

pacing current (measured in mA) until electrical capture (characterized by a wide QRS complex

with a tall, broad T wave on the ECG) is achieved, with a corresponding pulse. Pacing artifact on

the ECG and severe muscle twitching may make this determination difficult. External pacing

should not be relied upon for an extended period of time. It is an emergency procedure that acts

as a bridge until transvenous pacing or other therapies can be applied.

Epicardial pacing (temporary)

Main article: Epicardial

ECG rhythm strip of a threshold determination in a patient with a temporary (epicardial)

ventricular pacemaker. The epicardial pacemaker leads were placed after the patient collapsed

during aortic valve surgery. In the first half of the tracing, pacemaker stimuli at 60 beats per

minute result in a wide QRS complex with a right bundle branch block pattern. Progressively

weaker pacing stimuli are administered, which results in asystole in the second half of the

tracing. At the end of the tracing, distortion results from muscle contractions due to a (short)

hypoxic seizure. Because decreased pacemaker stimuli do not result in a ventricular escape

rhythm, the patient can be said to be pacemaker-dependent and needs a definitive pacemaker.

Temporary epicardial pacing is used during open heart surgery should the surgical procedure

create atrio ventricular block. The electrodes are placed in contact with the outer wall of the

ventricle (epicardium) to maintain satisfactory cardiac output until a temporary transvenous

electrode has been inserted.

Transvenous pacing (temporary)

Main article: Transvenous pacing

Transvenous pacing, when used for temporary pacing, is an alternative to transcutaneous pacing.

A pacemaker wire is placed into a vein, under sterile conditions, and then passed into either the

right atrium or right ventricle. The pacing wire is then connected to an external pacemaker

outside the body. Transvenous pacing is often used as a bridge to permanent pacemaker

placement. It can be kept in place until a permanent pacemaker is implanted or until there is no

longer a need for a pacemaker and then it is removed.

Permanent pacing

Right atrial and right ventricular leads as visualized under x-ray during a pacemaker implant

procedure. The atrial lead is the curved one making a U shape in the upper left part of the figure.

Permanent pacing with an implantable pacemaker involves transvenous placement of one or

more pacing electrodes within a chamber, or chambers, of the heart. The procedure is performed

by incision of a suitable vein into which the electrode lead is inserted and passed along the vein,

through the valve of the heart, until positioned in the chamber. The procedure is facilitated by

fluoroscopy which enables the physician or cardiologist to view the passage of the electrode

lead. After satisfactory lodgement of the electrode is confirmed the opposite end of the electrode

lead is connected to the pacemaker generator.

There are three basic types of permanent pacemakers, classified according to the number of

chambers involved and their basic operating mechanism:[17]

Single-chamber pacemaker. In this type, only one pacing lead is placed into a chamber of

the heart, either the atrium or the ventricle.[17]

Dual-chamber pacemaker. Here, wires are placed in two chambers of the heart. One lead

paces the atrium and one paces the ventricle. This type more closely resembles the

natural pacing of the heart by assisting the heart in coordinating the function between the

atria and ventricles.[17]

Rate-responsive pacemaker. This pacemaker has sensors that detect changes in the

patient's physical activity and automatically adjust the pacing rate to fulfill the body's

metabolic needs.[17]

The pacemaker generator is a hermetically sealed device containing a power source, usually a

lithium battery, a sensing amplifier which processes the electrical manifestation of naturally

occurring heart beats as sensed by the heart electrodes, the computer logic for the pacemaker and

the output circuitry which delivers the pacing impulse to the electrodes.

Most commonly, the generator is placed below the subcutaneous fat of the chest wall, above the

muscles and bones of the chest. However, the placement may vary on a case by case basis.

The outer casing of pacemakers is so designed that it will rarely be rejected by the body's

immune system. It is usually made of titanium, which is inert in the body. The whole thing will

not be rejected, and will be encapsulated by scar tissue, in the same way a piercing is.[citation needed]

Basic function

Modern pacemakers usually have multiple functions. The most basic form monitors the heart's

native electrical rhythm. When the pacemaker fails to sense a heartbeat within a normal beat-to-

beat time period, it will stimulate the ventricle of the heart with a short low voltage pulse. This

sensing and stimulating activity continues on a beat by beat basis.

The more complex forms include the ability to sense and/or stimulate both the atrial and

ventricular chambers.

The revised NASPE/BPEG generic code for antibradycardia pacing[18]

I II III IV V

Chamber(s)

paced

Chamber(s)

sensed

Response to

sensing Rate modulation Multisite pacing

O = None O = None O = None O = None O = None

A = Atrium A = Atrium T = Triggered R = Rate

modulation A = Atrium

V = Ventricle V = Ventricle I = Inhibited

V = Ventricle

D = Dual (A+V) D = Dual (A+V) D = Dual (T+I)

D = Dual

(A+V)

From this the basic ventricular "on demand" pacing mode is VVI or with automatic rate

adjustment for exercise VVIR - this mode is suitable when no synchronization with the atrial

beat is required, as in atrial fibrillation. The equivalent atrial pacing mode is AAI or AAIR which

is the mode of choice when atrioventricular conduction is intact but the natural pacemaker the

sinoatrial node is unreliable - sinus node disease (SND) or sick sinus syndrome. Where the

problem is atrioventricular block (AVB) the pacemaker is required to detect (sense) the atrial

beat and after a normal delay (0.1-0.2 seconds) trigger a ventricular beat, unless it has already

happened - this is VDD mode and can be achieved with a single pacing lead with electrodes in

the right atrium (to sense) and ventricle (to sense and pace). These modes AAIR and VDD are

unusual in the US but widely used in Latin America and Europe.[19][20]

The DDDR mode is most

commonly used as it covers all the options though the pacemakers require separate atrial and

ventricular leads and are more complex, requiring careful programming of their functions for

optimal results.

Biventricular pacing (BVP)

Three leads can be seen in this example of a cardiac resynchronization device: a right atrial lead

(solid black arrow), a right ventricular lead (dashed black arrow), and a coronary sinus lead (red

arrow). The coronary sinus lead wraps around the outside of the left ventricle, enabling pacing of

the left ventricle. Note that the right ventricular lead in this case has 2 thickened aspects that

represent conduction coils and that the generator is larger than typical pacemaker generators,

demonstrating that this device is both a pacemaker and a cardioverter-defibrillator, capable of

delivering electrical shocks for dangerously fast abnormal ventricular rhythms.

A biventricular pacemaker, also known as CRT (cardiac resynchronization therapy) is a type of

pacemaker that can pace both the septal and lateral walls of the left ventricle. By pacing both

sides of the left ventricle, the pacemaker can resynchronize a heart whose opposing walls do not

contract in synchrony, which occurs in approximately 25-50 % of heart failure patients. CRT

devices have at least two leads, one in the right ventricle to stimulate the septum, and another

inserted through the coronary sinus to pace the lateral wall of the left ventricle. Often, for

patients in normal sinus rhythm, there is also a lead in the right atrium to facilitate synchrony

with the atrial contraction. Thus, timing between the atrial and ventricular contractions, as well

as between the septal and lateral walls of the left ventricle can be adjusted to achieve optimal

cardiac function. CRT devices have been shown to reduce mortality and improve quality of life

in patients with heart failure symptoms; a LV ejection fraction less than or equal to 35% and

QRS duration on EKG of 120 msec or greater.[21][22][23]

CRT can be combined with an

implantable cardioverter-defibrillator (ICD).[24]

Advancements in function

X-ray image of installed pacemaker showing wire routing

A major step forward in pacemaker function has been to attempt to mimic nature by utilizing

various inputs to produce a rate-responsive pacemaker using parameters such as the QT interval,

pO2 - pCO2 (dissolved oxygen or carbon dioxide levels) in the arterial-venous system, physical

activity as determined by an accelerometer, body temperature, ATP levels, adrenaline, etc.

Instead of producing a static, predetermined heart rate, or intermittent control, such a pacemaker,

a 'Dynamic Pacemaker', could compensate for both actual respiratory loading and potentially

anticipated respiratory loading. The first dynamic pacemaker was invented by Dr. Anthony

Rickards of the National Health Hospital, London, UK, in 1982.[citation needed]

Dynamic pacemaking technology could also be applied to future artificial hearts. Advances in

transitional tissue welding would support this and other artificial organ/joint/tissue replacement

efforts. Stem cells may or may not be of interest to transitional tissue welding.

Many advancements have been made to improve the control of the pacemaker once implanted.

Many of these have been made possible by the transition to microprocessor controlled

pacemakers. Pacemakers that control not only the ventricles but the atria as well have become

common. Pacemakers that control both the atria and ventricles are called dual-chamber

pacemakers. Although these dual-chamber models are usually more expensive, timing the

contractions of the atria to precede that of the ventricles improves the pumping efficiency of the

heart and can be useful in congestive heart failure.

Rate responsive pacing allows the device to sense the physical activity of the patient and respond

appropriately by increasing or decreasing the base pacing rate via rate response algorithms.

The DAVID trials[25]

have shown that unnecessary pacing of the right ventricle can exacerbate

heart failure and increases the incidence of atrial fibrillation. The newer dual chamber devices

can keep the amount of right ventricle pacing to a minimum and thus prevent worsening of the

heart disease.

Considerations

Insertion

A pacemaker is typically inserted into the patient through a simple surgery using either local

anesthetic or a general anesthetic. The patient may be given a drug for relaxation before the

surgery as well. An antibiotic is typically administered to prevent infection.[26]

In most cases the

pacemaker is inserted in the left shoulder area where an incision is made below the collar bone

creating a small pocket where the pacemaker is actually housed in the patient's body. The lead or

leads (the number of leads varies depending on the type of pacemaker) are fed into the heart

through a large vein using a fluoroscope to monitor the progress of lead insertion. The Right

Ventricular lead would be positioned away from the apex (tip) of the right ventricle and up on

the inter ventricular septum, below the outflow tract, to prevent deterioration of the strength of

the heart. The actual surgery may take about 30 to 90 minutes.

Following surgery the patient should exercise reasonable care about the wound as it heals. There

is a followup session during which the pacemaker is checked using a "programmer" that can

communicate with the device and allows a health care professional to evaluate the system's

integrity and determine the settings such as pacing voltage output. The patient should have the

strength of their heart analyzed frequently with echocardiography, every 1 or 2 years, to make

sure the that placement of the right ventricular lead has not lead to weakening of the left

ventricle.

The patient may want to consider some basic preparation before the surgery. The most basic

preparation is that people who have body hair on the chest may want to remove the hair by

shaving or using a depilatory agent as the surgery will involve bandages and monitoring

equipment to be afixed to the body.

Since a pacemaker uses batteries, the device itself will need replacement as the batteries lose

power. Device replacement is usually a simpler procedure than the original insertion as it does

not normally require leads to be implanted. The typical replacement requires a surgery in which

an incision is made to remove the existing device, the leads are removed from the existing

device, the leads are attached to the new device, and the new device is inserted into the patient's

body replacing the previous device.

Pacemaker patient identification card

International pacemaker patient identification cards carry information such as; patient data

(among others, symptom primary, ECG, aetiology), pacemaker center (doctor, hospital), IPG

(rate, mode[disambiguation needed]

, date of implantation, MFG, type) and lead.[27][28]

Living with a pacemaker

Periodic pacemaker checkups

Two types of remote monitoring devices used by pacemaker patients

Once the pacemaker is implanted, it is periodically checked to ensure the device is operational

and performing appropriately. Depending on the frequency set by the following physician, the

device can be checked as often as is necessary. Routine pacemaker checks are typically done in-

office every six (6) months, though will vary depending upon patient/device status and remote

monitoring availability.

At the time of in-office follow-up, the device will be interrogated to perform diagnostic testing.

These tests include:

Sensing: the ability of the device to "see" intrinsic cardiac activity (Atrial and ventricular

depolarization).

Impedance: A test to measure lead integrity. Large and/or sudden increases in impedance

can be indicative of a lead fracture while large and/or sudden decreases in impedance can

signify a breach in lead insulation.

Threshold: this test confirms the minimum amount of energy (Both volts and pulse

width) required to reliably depolarize (capture) the chamber being tested. Determining

the threshold allows the Allied Professional, Representative, or Physician to program an

output that recognizes an appropriate safety margin while optimizing device longevity.

As modern pacemakers are "on-demand", meaning that they only pace when necessary, device

longevity is affected by how much it is utilized. Other factors affecting device longevity include

programmed output and algorithms (features) causing a higher level of current drain from the

battery.

An additional aspect of the in-office check is to examine any events that were stored since the

last follow-up. These are typically stored based on specific criteria set by the physician and

specific to the patient. Some devices have the availability to display intracardiac electrograms of

the onset of the event as well as the event itself. This is especially helpful in diagnosing the cause

or origin of the event and making any necessary programming changes.

Lifestyle considerations

A patient's lifestyle is usually not modified to any great degree after insertion of a pacemaker.

There are a few activities that are unwise such as full contact sports and activities that involve

intense magnetic fields.

The pacemaker patient may find that some types of everyday actions need to be modified. For

instance, the shoulder harness of a vehicle seatbelt may be uncomfortable if the harness should

fall across the pacemaker insertion site.

Any kind of an activity that involves intense magnetic fields should be avoided. This includes

activities such as arc welding possibly, with certain types of equipment,[29]

or maintaining heavy

equipment that may generate intense magnetic fields (such as an MRI (Magnetic Resonance

Imaging Machine)).

However, in February 2011 the FDA approved a new pacemaker device called the Revo MRI

SureScan which is the first to be proven safe for MRI use. There are several limitations to its use

including certain patients qualifications, body parts, and scan settings.

A 2008 U.S. study has found[30]

that the magnets in some portable music players, when placed

within an inch of pacemakers, may cause interference.

Some medical procedures may require the use of antibiotics to be administered before the

procedure. The patient should inform all medical personnel that they have a pacemaker. Some

standard medical procedures such as the use of Magnetic resonance imaging (MRI) may be ruled

out by the patient having a pacemaker.

In addition, according to the American Heart Association, some home devices have a remote

potential to cause interference by occasionally inhibiting a single beat. Cellphones available in

the United States (less than 3 watts) do not seem to damage pulse generators or affect how the

pacemaker works.[31]

Turning off the pacemaker

According to a consensus statement by the Heart Rhythm Society, it is legal and ethical to honor

requests by patients, or by those with legal authority to make decisions for patients, to deactivate

implanted cardiac devices. Lawyers say that the legal situation is similar to removing a feeding

tube. A patient has a right to refuse or discontinue treatment, including a pacemaker that keeps

him or her alive. Physicians have a right to refuse to turn it off, but they should refer the patient

to a physician who will.[32]

Some patients believe that hopeless, debilitating conditions like

strokes, in combination with dementia, can cause so much suffering to themselves and their

families that they would prefer not to prolong their lives with supportive measures, such as

cardiac devices.[33]

Privacy and security

Security and privacy concerns have been raised with pacemakers that allow wireless

communication. Unauthorized third parties may be able to read patient records contained in the

pacemaker, or reprogram the devices, as has been demonstrated by a team of researchers.[34]

The

demonstration worked at short range; they did not attempt to develop a long range antenna. The

proof of concept exploit helps demonstrate the need for better security and patient alerting

measures in remotely accessible medical implants.[34]

Complications

A possible complication of dual-chamber artificial pacemakers is pacemaker-mediated

tachycardia (PMT), a form of reentrant tachycardia. In PMT, the artificial pacemaker forms the

anterograde (atrium to ventricle) limb of the circuit and the atrioventricular (AV) node forms the

retrograde limb (ventricle to atrium) of the circuit.[35]

Treatment of PMT typically involves

reprogramming the pacemaker.[35]

Other devices with pacemaker function

Sometimes devices resembling pacemakers, called implantable cardioverter-defibrillators (ICDs)

are implanted. These devices are often used in the treatment of patients at risk from sudden

cardiac death. An ICD has the ability to treat many types of heart rhythm disturbances by means

of pacing, cardioversion, or defibrillation. Some ICD devices can distinguish between ventricular

fibrillation and ventricular tachycardia (VT), and may try to pace the heart faster than its intrinsic

rate in the case of VT, to try to break the tachycardia before it progresses to ventricular

fibrillation. This is known as fast-pacing, overdrive pacing, or anti-tachycardia pacing (ATP).

ATP is only effective if the underlying rhythm is ventricular tachycardia, and is never effective if

the rhythm is ventricular fibrillation.

NASPE / BPEG Defibrillator (NBD) code - 1993[36]

I II III IV

Shock

chamber

Antitachycardia pacing

chamber

Tachycardia

detection

Antibradycardia pacing

chamber

O = None O = None E = Electrogram O = None

A = Atrium A = Atrium H = Hemodynamic A = Atrium

V = Ventricle V = Ventricle

V = Ventricle

D = Dual

(A+V) D = Dual (A+V)

D = Dual (A+V)

Short form of the NASPE/BPEG Defibrillator (NBD) code[36]

ICD-S ICD with shock capability only

ICD-B ICD with bradycardia pacing as well as shock

ICD-T ICD with tachycardia (and bradycardia) pacing as well as shock

Magnetic resonance imaging

From Wikipedia, the free encyclopedia

(Redirected from Mri)

"MRI" redirects here. For other meanings of MRI or Mri, see MRI (disambiguation).

This article may be too technical for most readers to understand. Please help improve

this article to make it understandable to non-experts, without removing the technical

details. The talk page may contain suggestions. (January 2011)

Magnetic resonance imaging

Intervention

Sagittal MR image of the knee

ICD-10-PCS B?3?ZZZ

ICD-9: 88.91-88.97

MeSH D008279

OPS-301 code: 3-80...3-84

Para-sagittal MRI of the head, with aliasing artifacts (nose and forehead appear at the back of the

head)

Magnetic resonance imaging (MRI), nuclear magnetic resonance imaging (NMRI), or

magnetic resonance tomography (MRT) is a medical imaging technique used in radiology to

visualize detailed internal structures. MRI makes use of the property of nuclear magnetic

resonance (NMR) to image nuclei of atoms inside the body.

An MRI machine uses a powerful magnetic field to align the magnetization of some atoms in the

body, and radio frequency fields to systematically alter the alignment of this magnetization. This

causes the nuclei to produce a rotating magnetic field detectable by the scanner—and this

information is recorded to construct an image of the scanned area of the body.[1]:36

Strong

magnetic field gradients cause nuclei at different locations to rotate at different speeds. 3-D

spatial information can be obtained by providing gradients in each direction.

MRI provides good contrast between the different soft tissues of the body, which makes it

especially useful in imaging the brain, muscles, the heart, and cancers compared with other

medical imaging techniques such as computed tomography (CT) or X-rays. Unlike CT scans or

traditional X-rays, MRI uses no ionizing radiation.

Contents

[hide]

1 How MRI works

2 History

o 2.1 2003 Nobel Prize

3 Applications

o 3.1 Basic MRI scans

3.1.1 T1-weighted MRI

3.1.2 T2-weighted MRI

3.1.3 T*2-weighted MRI

3.1.4 Spin density weighted MRI

o 3.2 Specialized MRI scans

3.2.1 Diffusion MRI

3.2.2 Magnetization Transfer MRI

3.2.3 Fluid attenuated inversion recovery (FLAIR)

3.2.4 Magnetic resonance angiography

3.2.5 Magnetic resonance gated intracranial CSF dynamics (MR-GILD)

3.2.6 Magnetic resonance spectroscopy

3.2.7 Functional MRI

3.2.8 Real-time MRI

o 3.3 Interventional MRI

o 3.4 Radiation therapy simulation

3.4.1 Current density imaging

3.4.2 Magnetic resonance guided focused ultrasound

3.4.3 Multinuclear imaging

3.4.4 Susceptibility weighted imaging (SWI)

3.4.5 Other specialized MRI techniques

o 3.5 Portable instruments

o 3.6 MRI versus CT

o 3.7 Economics of MRI

4 Safety

o 4.1 Magnetic field

o 4.2 Radio frequency energy

o 4.3 Peripheral nerve stimulation (PNS)

o 4.4 Acoustic noise

o 4.5 Cryogens

o 4.6 Contrast agents

o 4.7 Pregnancy

o 4.8 Claustrophobia and discomfort

o 4.9 Guidance

o 4.10 The European Physical Agents Directive

5 Three-dimensional (3D) image reconstruction

o 5.1 The principle

o 5.2 3D rendering techniques

o 5.3 Image segmentation

6 See also

7 References

8 Further reading

9 External links

[edit] How MRI works

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removed. (September 2009)

Main article: Physics of Magnetic Resonance Imaging

The body is largely composed of water molecules. Each water molecule has two hydrogen nuclei

or protons. When a person is inside the powerful magnetic field of the scanner, the magnetic

moments of some of these molecules become aligned with the direction of the field. A radio

frequency transmitter is briefly turned on, producing a further varying electromagnetic field. The

photons of this field have just the right energy, known as the resonance frequency, to be

absorbed and flip the spin of the aligned protons in the body. The frequency at which the protons

resonate depends on the strength of the applied magnetic field. After the field is turned off, those

protons which absorbed energy revert to the original lower-energy spin-down state. Now a

hydrogen dipole has two spins, 1 high spin and 1 low. In low spin both dipole and field are in

parallel direction and in high spin case it is antiparallel. They release the difference in energy as

a photon, and the released photons are detected by the scanner as an electromagnetic signal,

similar to radio waves.

As a result of conservation of energy, the resonant frequency also dictates the frequency of the

released photons. The photons released when the field is removed have an energy — and

therefore a frequency — which depends on the energy absorbed while the field was active. It is

this relationship between field-strength and frequency that allows the use of nuclear magnetic

resonance for imaging. An image can be constructed because the protons in different tissues

return to their equilibrium state at different rates, which is a difference that can be detected. Five

different tissue variables — spin density, T1 and T2 relaxation times and flow and spectral shifts

can be used to construct images.[2]

By changing the settings on the scanner, this effect is used to

create contrast between different types of body tissue or between other properties, as in fMRI

and diffusion MRI.

The 3D position from which photons were released is learned by applying additional fields

during the scan. This is done by passing electric currents through specially-wound solenoids,

known as gradient coils. These fields make the magnetic field strength vary depending on the

position within the patient, which in turn makes the frequency of released photons dependent on

their original position in a predictable manner, and the original locations can be mathematically

recovered from the resulting signal by the use of inverse Fourier transform.

Contrast agents may be injected intravenously to enhance the appearance of blood vessels,

tumors or inflammation. Contrast agents may also be directly injected into a joint in the case of

arthrograms, MRI images of joints. Unlike CT, MRI uses no ionizing radiation and is generally a

very safe procedure. Nonetheless the strong magnetic fields and radio pulses can affect metal

implants, including cochlear implants and cardiac pacemakers. In the case of cochlear implants,

the US FDA has approved some implants for MRI compatibility. In the case of cardiac

pacemakers, the results can sometimes be lethal,[3]

so patients with such implants are generally

not eligible for MRI.

Since the gradient coils are within the bore of the scanner, there are large forces between them

and the main field coils, producing most of the noise that is heard during operation. Without

efforts to damp this noise, it can approach 130 decibels (dB) with strong fields [4]

(see also the

subsection on acoustic noise).

MRI is used to image every part of the body, and is particularly useful for tissues with many

hydrogen nuclei and little density contrast, such as the brain, muscle, connective tissue and most

tumors.

[edit] History

In the 1950s, Herman Carr reported on the creation of a one-dimensional MR image.[5]

Paul

Lauterbur expanded on Carr's technique and developed a way to generate the first MRI images,

in 2D and 3D, using gradients. In 1973, Lauterbur published the first nuclear magnetic resonance

image.[6][7]

and the first cross-sectional image of a living mouse was published in January 1974.[8]

Nuclear magnetic resonance imaging is a relatively new technology first developed at the

University of Nottingham, England. Peter Mansfield, a physicist and professor at the university,

then developed a mathematical technique that would allow scans to take seconds rather than

hours and produce clearer images than Lauterbur had.

Raymond Damadian's "Apparatus and method for detecting cancer in tissue."

In a 1971 paper in the journal Science,[9]

Dr. Raymond Damadian, an Armenian-American

physician, scientist, and professor at the Downstate Medical Center State University of New

York (SUNY), reported that tumors and normal tissue can be distinguished in vivo by nuclear

magnetic resonance ("NMR"). He suggested that these differences could be used to diagnose

cancer, though later research would find that these differences, while real, are too variable for

diagnostic purposes. Damadian's initial methods were flawed for practical use,[10]

relying on a

point-by-point scan of the entire body and using relaxation rates, which turned out to not be an

effective indicator of cancerous tissue.[11]

While researching the analytical properties of magnetic resonance, Damadian created the world's

first magnetic resonance imaging machine in 1972. He filed the first patent for an MRI machine,

U.S. patent #3,789,832 on March 17, 1972, which was later issued to him on February 5,

1974.[12]

As the National Science Foundation notes, "The patent included the idea of using NMR

to 'scan' the human body to locate cancerous tissue."[13]

However, it did not describe a method

for generating pictures from such a scan or precisely how such a scan might be done.[14]

Damadian along with Larry Minkoff and Michael Goldsmith, subsequently went on to perform

the first MRI body scan of a human being on July 3, 1977.[15][16]

These studies performed on

humans were published in 1977.[17][18]

In recording the history of MRI, Mattson and Simon (1996) credit Damadian with describing the

concept of whole-body NMR scanning, as well as discovering the NMR tissue relaxation

differences that made this feasible.

[edit] 2003 Nobel Prize

Reflecting the fundamental importance and applicability of MRI in medicine, Paul Lauterbur of

the University of Illinois at Urbana-Champaign and Sir Peter Mansfield of the University of

Nottingham were awarded the 2003 Nobel Prize in Physiology or Medicine for their "discoveries

concerning magnetic resonance imaging". The Nobel citation acknowledged Lauterbur's insight

of using magnetic field gradients to determine spatial localization, a discovery that allowed rapid

acquisition of 2D images. Mansfield was credited with introducing the mathematical formalism

and developing techniques for efficient gradient utilization and fast imaging. The actual research

that won the prize was done almost 30 years before, while Paul Lauterbur was at Stony Brook

University in New York.

The award was vigorously protested by Raymond Vahan Damadian, founder of FONAR

Corporation, who claimed that he invented the MRI,[7]

and that Lauterbur and Mansfield had

merely refined the technology.[19]

An ad hoc group, called "The Friends of Raymond Damadian",

took out full-page advertisements in the New York Times and The Washington Post entitled "The

Shameful Wrong That Must Be Righted", demanding that he be awarded at least a share of the

Nobel Prize.[20]

Also, even earlier, in the Soviet Union, Vladislav Ivanov filed (in 1960) a

document with the USSR State Committee for Inventions and Discovery at Leningrad for a

Magnetic Resonance Imaging device,[21]

although this was not approved until the 1970s.[22]

In a

letter to Physics Today, Herman Carr pointed out his own even earlier use of field gradients for

one-dimensional MR imaging.[23]

[edit] Applications

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removed. (September 2009)

In clinical practice, MRI is used to distinguish pathologic tissue (such as a brain tumor) from

normal tissue. One advantage of an MRI scan is that it is harmless to the patient. It uses strong

magnetic fields and non-ionizing radiation in the radio frequency range, unlike CT scans and

traditional X-rays, which both use ionizing radiation.

While CT provides good spatial resolution (the ability to distinguish two separate structures an

arbitrarily small distance from each other), MRI provides comparable resolution with far better

contrast resolution (the ability to distinguish the differences between two arbitrarily similar but

not identical tissues). The basis of this ability is the complex library of pulse sequences that the

modern medical MRI scanner includes, each of which is optimized to provide image contrast

based on the chemical sensitivity of MRI.

Effects of TR, TE, T1 and T2 on MR signal.

For example, with particular values of the echo time (TE) and the repetition time (TR), which are

basic parameters of image acquisition, a sequence takes on the property of T2-weighting. On a

T2-weighted scan, water- and fluid-containing tissues are bright (most modern T2 sequences are

actually fast T2 sequences) and fat-containing tissues are dark. The reverse is true for T1-

weighted images. Damaged tissue tends to develop edema, which makes a T2-weighted sequence

sensitive for pathology, and generally able to distinguish pathologic tissue from normal tissue.

With the addition of an additional radio frequency pulse and additional manipulation of the

magnetic gradients, a T2-weighted sequence can be converted to a FLAIR sequence, in which

free water is now dark, but edematous tissues remain bright. This sequence in particular is

currently the most sensitive way to evaluate the brain for demyelinating diseases, such as

multiple sclerosis.

The typical MRI examination consists of 5–20 sequences, each of which are chosen to provide a

particular type of information about the subject tissues. This information is then synthesized by

the interpreting physician.

[edit] Basic MRI scans

[edit] T1-weighted MRI

Main article: Spin-lattice relaxation time

T1-weighted scans are a standard basic scan, in particular differentiating fat from water - with

water darker and fat brighter[24]

use a gradient echo (GRE) sequence, with short TE and short TR.

This is one of the basic types of MR contrast and is a commonly run clinical scan. The T1

weighting can be increased (improving contrast) with the use of an inversion pulse as in an MP-

RAGE sequence. Due to the short repetition time (TR) this scan can be run very fast allowing the

collection of high resolution 3D datasets. A T1 reducing gadolinium contrast agent is also

commonly used, with a T1 scan being collected before and after administration of contrast agent

to compare the difference. In the brain T1-weighted scans provide good gray matter/white matter

contrast; in other words, T1-weighted images highlight fat deposition.

[edit] T2-weighted MRI

Main article: Spin-spin relaxation time

T2-weighted scans are another basic type. Like the T1-weighted scan, fat is differentiated from

water - but in this case fat shows darker, and water lighter. For example, in the case of cerebral

and spinal study, the CSF (cerebrospinal fluid) will be lighter in T2-weighted images. These

scans are therefore particularly well suited to imaging edema, with long TE and long TR. Because

the spin echo sequence is less susceptible to inhomogeneities in the magnetic field, these images

have long been a clinical workhorse.

[edit] T*

2-weighted MRI

T*

2 (pronounced "T 2 star") weighted scans use a gradient echo (GRE) sequence, with long TE and

long TR. The gradient echo sequence used does not have the extra refocusing pulse used in spin

echo so it is subject to additional losses above the normal T2 decay (referred to as T2′), these

taken together are called T*

2. This also makes it more prone to susceptibility losses at air/tissue boundaries, but can increase

contrast for certain types of tissue, such as venous blood.

[edit] Spin density weighted MRI

Spin density, also called proton density, weighted scans try to have no contrast from either T2 or

T1 decay, the only signal change coming from differences in the amount of available spins

(hydrogen nuclei in water). It uses a spin echo or sometimes a gradient echo sequence, with short

TE and long TR.

[edit] Specialized MRI scans

[edit] Diffusion MRI

Main article: Diffusion MRI

DTI image

Diffusion MRI measures the diffusion of water molecules in biological tissues.[25]

In an isotropic

medium (inside a glass of water for example), water molecules naturally move randomly

according to turbulence and Brownian motion. In biological tissues however, where the

Reynolds number is low enough for flows to be laminar, the diffusion may be anisotropic. For

example, a molecule inside the axon of a neuron has a low probability of crossing the myelin

membrane. Therefore the molecule moves principally along the axis of the neural fiber. If it is

known that molecules in a particular voxel diffuse principally in one direction, the assumption

can be made that the majority of the fibers in this area are going parallel to that direction.

The recent development of diffusion tensor imaging (DTI)[7]

enables diffusion to be measured in

multiple directions and the fractional anisotropy in each direction to be calculated for each voxel.

This enables researchers to make brain maps of fiber directions to examine the connectivity of

different regions in the brain (using tractography) or to examine areas of neural degeneration and

demyelination in diseases like Multiple Sclerosis.

Another application of diffusion MRI is diffusion-weighted imaging (DWI). Following an

ischemic stroke, DWI is highly sensitive to the changes occurring in the lesion.[26]

It is

speculated that increases in restriction (barriers) to water diffusion, as a result of cytotoxic edema

(cellular swelling), is responsible for the increase in signal on a DWI scan. The DWI

enhancement appears within 5–10 minutes of the onset of stroke symptoms (as compared with

computed tomography, which often does not detect changes of acute infarct for up to 4–6 hours)

and remains for up to two weeks. Coupled with imaging of cerebral perfusion, researchers can

highlight regions of "perfusion/diffusion mismatch" that may indicate regions capable of salvage

by reperfusion therapy.

Like many other specialized applications, this technique is usually coupled with a fast image

acquisition sequence, such as echo planar imaging sequence.

[edit] Magnetization Transfer MRI

Main article: Magnetization transfer

Magnetization transfer (MT) refers to the transfer of longitudinal magnetization from free water

protons to hydration water protons in NMR and MRI.

In magnetic resonance imaging of molecular solutions, such as protein solutions, two types of

water molecules, free (bulk) and hydration (bound), are found. Free water protons have faster

average rotational frequency and hence less fixed water molecules that may cause local field

inhomogeneity. Because of this uniformity, most free water protons have resonance frequency

lying narrowly around the normal proton resonance frequency of 63 MHz (at 1.5 teslas). This

also results in slower transverse magnetization dephasing and hence longer T2. Conversely,

hydration water molecules are slowed down by interaction with solute molecules and hence

create field inhomogeneities that lead to wider resonance frequency spectrum.

In free liquids, protons, which may be viewed classically as small magnetic dipoles, exhibit

translational and rotational motions. These moving dipoles disturb the surrounding magnetic

field however on long enough time-scales (which may be nanoseconds) the average field caused

by the motion of protons is zero. This is known as ―motional averaging‖ or narrowing and is

characteristic of protons moving freely in liquid. On the other hand, protons bound to

macromolecules, such as proteins, tend to have a fixed orientation and so the average magnetic

field in close proximity to such structures does not average to zero. The result is a spatial pattern

in the magnetic field that gives rise to a residual dipolar coupling (range of precession

frequencies) for the protons experiencing the magnetic field. The wide frequency distribution

appears as a broad spectrum that may be several kHz wide. The net signal from these protons

disappears very quickly, in inverse proportion to the width, due to the loss of coherence of the

spins, i.e. T2 relaxation. Due to exchange mechanisms, such as spin transfer or proton chemical

exchange, the (incoherent) spins bound to the macromolecules continually switch places with

(coherent) spins in the bulk media and establish a dynamic equilibrium.

Magnetization transfer: Although there is no measurable signal from the bound spins, or the

bound spins that exchange into the bulk media, their longitudinal magnetization is preserved and

may recover only via the relatively slow process of T1 relaxation. If the longitudinal

magnetization of just the bound spins can be altered, then the effect can be measured in the spins

of the bulk media due to the exchange processes. The magnetization transfer sequence applies

RF saturation at a frequency that is far off resonance for the narrow line of bulk water but still on

resonance for the bound protons with a spectral linewidth of kHz. This causes saturation of the

bound spins which exchange into the bulk water, resulting in a loss of longitudinal magnetization

and hence signal decrease in the bulk water. This provides an indirect measure of

macromolecular content in tissue. Implementation of magnetization transfer involves choosing

suitable frequency offsets and pulse shapes to saturate the bound spins sufficiently strongly,

within the safety limits of specific absorption rate for RF irradiation.

T1ρ (T1rho): Molecules have a kinetic energy that is a function of the temperature and is

expressed as translational and rotational motions, and by collisions between molecules. The

moving dipoles disturb the magnetic field but are often extremely rapid so that the average effect

over a long time-scale may be zero. However, depending on the time-scale, the interactions

between the dipoles do not always average away. At the slowest extreme the interaction time is

effectively infinite and occurs where there are large, stationary field disturbances (e.g. a metallic

implant). In this case the loss of coherence is described as a "static dephasing". T2* is a measure

of the loss of coherence in an ensemble of spins that include all interactions (including static

dephasing). T2 is a measure of the loss of coherence that excludes static dephasing, using an RF

pulse to reverse the slowest types of dipolar interaction. There is in fact a continuum of

interaction time-scales in a given biological sample and the properties of the refocusing RF pulse

can be tuned to refocus more than just static dephasing. In general, the rate of decay of an

ensemble of spins is a function of the interaction times and also the power of the RF pulse. This

type of decay, occurring under the influence of RF, is known as T1ρ. It is similar to T2 decay but

with some slower dipolar interactions refocused as well as the static interactions.

[edit] Fluid attenuated inversion recovery (FLAIR)

Main article: Fluid attenuated inversion recovery

Fluid Attenuated Inversion Recovery (FLAIR)[27]

is an inversion-recovery pulse sequence used

to null signal from fluids. For example, it can be used in brain imaging to suppress cerebrospinal

fluid (CSF) so as to bring out the periventricular hyperintense lesions, such as multiple sclerosis

(MS) plaques. By carefully choosing the inversion time TI (the time between the inversion and

excitation pulses), the signal from any particular tissue can be suppressed.

[edit] Magnetic resonance angiography

Magnetic Resonance Angiography

Main article: Magnetic resonance angiography

Magnetic resonance angiography (MRA) generates pictures of the arteries to evaluate them for

stenosis (abnormal narrowing) or aneurysms (vessel wall dilatations, at risk of rupture). MRA is

often used to evaluate the arteries of the neck and brain, the thoracic and abdominal aorta, the

renal arteries, and the legs (called a "run-off"). A variety of techniques can be used to generate

the pictures, such as administration of a paramagnetic contrast agent (gadolinium) or using a

technique known as "flow-related enhancement" (e.g. 2D and 3D time-of-flight sequences),

where most of the signal on an image is due to blood that recently moved into that plane, see also

FLASH MRI. Techniques involving phase accumulation (known as phase contrast angiography)

can also be used to generate flow velocity maps easily and accurately. Magnetic resonance

venography (MRV) is a similar procedure that is used to image veins. In this method, the tissue

is now excited inferiorly, while signal is gathered in the plane immediately superior to the

excitation plane—thus imaging the venous blood that recently moved from the excited plane.[28]

[edit] Magnetic resonance gated intracranial CSF dynamics (MR-GILD)

Magnetic resonance gated intracranial cerebrospinal fluid (CSF) or liquor dynamics (MR-GILD)

technique is an MR sequence based on bipolar gradient pulse used to demonstrate CSF pulsatile

flow in ventricles, cisterns, aqueduct of Sylvius and entire intracranial CSF pathway. It is a

method for analyzing CSF circulatory system dynamics in patients with CSF obstructive lesions

such as normal pressure hydrocephalus. It also allows visualization of both arterial and venous

pulsatile blood flow in vessels without use of contrast agents.[29][30]

Diastolic time data acquisition (DTDA). Systolic time data acquisition (STDA).

[edit] Magnetic resonance spectroscopy

Main article: In vivo magnetic resonance spectroscopy

Main article: Nuclear magnetic resonance spectroscopy

Magnetic resonance spectroscopy (MRS) is used to measure the levels of different metabolites in

body tissues. The MR signal produces a spectrum of resonances that correspond to different

molecular arrangements of the isotope being "excited". This signature is used to diagnose certain

metabolic disorders, especially those affecting the brain,[31]

and to provide information on tumor

metabolism.[32]

Magnetic resonance spectroscopic imaging (MRSI) combines both spectroscopic and imaging

methods to produce spatially localized spectra from within the sample or patient. The spatial

resolution is much lower (limited by the available SNR), but the spectra in each voxel contains

information about many metabolites. Because the available signal is used to encode spatial and

spectral information, MRSI requires high SNR achievable only at higher field strengths (3 T and

above).

[edit] Functional MRI

Main article: Functional magnetic resonance imaging

A fMRI scan showing regions of activation in orange, including the primary visual cortex (V1,

BA17).

Functional MRI (fMRI) measures signal changes in the brain that are due to changing neural

activity. The brain is scanned at low resolution but at a rapid rate (typically once every 2–3

seconds). Increases in neural activity cause changes in the MR signal via T*

2 changes;[33]

this mechanism is referred to as the BOLD (blood-oxygen-level dependent) effect.

Increased neural activity causes an increased demand for oxygen, and the vascular system

actually overcompensates for this, increasing the amount of oxygenated hemoglobin relative to

deoxygenated hemoglobin. Because deoxygenated hemoglobin attenuates the MR signal, the

vascular response leads to a signal increase that is related to the neural activity. The precise

nature of the relationship between neural activity and the BOLD signal is a subject of current

research. The BOLD effect also allows for the generation of high resolution 3D maps of the

venous vasculature within neural tissue.

While BOLD signal is the most common method employed for neuroscience studies in human

subjects, the flexible nature of MR imaging provides means to sensitize the signal to other

aspects of the blood supply. Alternative techniques employ arterial spin labeling (ASL) or weight

the MRI signal by cerebral blood flow (CBF) and cerebral blood volume (CBV). The CBV

method requires injection of a class of MRI contrast agents that are now in human clinical trials.

Because this method has been shown to be far more sensitive than the BOLD technique in

preclinical studies, it may potentially expand the role of fMRI in clinical applications. The CBF

method provides more quantitative information than the BOLD signal, albeit at a significant loss

of detection sensitivity.

[edit] Real-time MRI

Main article: Real-time MRI

Real-time MRI of a human heart at a resolution of 50 ms

[34]

Real-time MRI refers to the continuous monitoring (―filming‖) of moving objects in real time.

While many different strategies have been developed over the past two decades, a recent

development reported a real-time MRI technique based on radial FLASH and iterative

reconstruction that yields a temporal resolution of 20 to 30 milliseconds for images with an in-

plane resolution of 1.5 to 2.0 mm[35]

. The new method promises to add important information

about diseases of the joints and the heart. In many cases MRI examinations may become easier

and more comfortable for patients.

[edit] Interventional MRI

Main article: Interventional MRI

The lack of harmful effects on the patient and the operator make MRI well-suited for

"interventional radiology", where the images produced by a MRI scanner are used to guide

minimally invasive procedures. Of course, such procedures must be done without any

ferromagnetic instruments.

A specialized growing subset of interventional MRI is that of intraoperative MRI in which the

MRI is used in the surgical process. Some specialized MRI systems have been developed that

allow imaging concurrent with the surgical procedure. More typical, however, is that the surgical

procedure is temporarily interrupted so that MR images can be acquired to verify the success of

the procedure or guide subsequent surgical work.

[edit] Radiation therapy simulation

Because of MRI's superior imaging of soft tissues, it is now being utilized to specifically locate

tumors within the body in preparation for radiation therapy treatments. For therapy simulation, a

patient is placed in specific, reproducible, body position and scanned. The MRI system then

computes the precise location, shape and orientation of the tumor mass, correcting for any spatial

distortion inherent in the system. The patient is then marked or tattooed with points that, when

combined with the specific body position, permits precise triangulation for radiation

therapy.[citation needed]

[edit] Current density imaging

Current density imaging (CDI) endeavors to use the phase information from images to

reconstruct current densities within a subject. Current density imaging works because electrical

currents generate magnetic fields, which in turn affect the phase of the magnetic dipoles during

an imaging sequence.[citation needed]

[edit] Magnetic resonance guided focused ultrasound

In MRgFUS therapy, ultrasound beams are focused on a tissue—guided and controlled using MR

thermal imaging—and due to the significant energy deposition at the focus, temperature within

the tissue rises to more than 65 °C (150 °F), completely destroying it. This technology can

achieve precise ablation of diseased tissue. MR imaging provides a three-dimensional view of

the target tissue, allowing for precise focusing of ultrasound energy. The MR imaging provides

quantitative, real-time, thermal images of the treated area. This allows the physician to ensure

that the temperature generated during each cycle of ultrasound energy is sufficient to cause

thermal ablation within the desired tissue and if not, to adapt the parameters to ensure effective

treatment.[36]

[edit] Multinuclear imaging

Hydrogen is the most frequently imaged nucleus in MRI because it is present in biological

tissues in great abundance, and because its high gyromagnetic ratio gives a strong signal.

However, any nucleus with a net nuclear spin could potentially be imaged with MRI. Such nuclei

include helium-3, carbon-13, fluorine-19, oxygen-17, sodium-23, phosphorus-31 and xenon-129. 23

Na and 31

P are naturally abundant in the body, so can be imaged directly. Gaseous isotopes

such as 3He or

129Xe must be hyperpolarized and then inhaled as their nuclear density is too low

to yield a useful signal under normal conditions. 17

O and 19

F can be administered in sufficient

quantities in liquid form (e.g. 17

O-water) that hyperpolarization is not a necessity.[citation needed]

Multinuclear imaging is primarily a research technique at present. However, potential

applications include functional imaging and imaging of organs poorly seen on 1H MRI (e.g.

lungs and bones) or as alternative contrast agents. Inhaled hyperpolarized 3He can be used to

image the distribution of air spaces within the lungs. Injectable solutions containing 13

C or

stabilized bubbles of hyperpolarized 129

Xe have been studied as contrast agents for angiography

and perfusion imaging. 31

P can potentially provide information on bone density and structure, as

well as functional imaging of the brain.[citation needed]

[edit] Susceptibility weighted imaging (SWI)

Main article: Susceptibility weighted imaging

Susceptibility weighted imaging (SWI), is a new type of contrast in MRI different from spin

density, T1, or T2 imaging. This method exploits the susceptibility differences between tissues

and uses a fully velocity compensated, three dimensional, RF spoiled, high-resolution, 3D

gradient echo scan. This special data acquisition and image processing produces an enhanced

contrast magnitude image very sensitive to venous blood, hemorrhage and iron storage. It is used

to enhance the detection and diagnosis of tumors, vascular and neurovascular diseases (stroke

and hemorrhage, multiple sclerosis, Alzheimer's), and also detects traumatic brain injuries that

may not be diagnosed using other methods[37]

[edit] Other specialized MRI techniques

New methods and variants of existing methods are often published when they are able to produce

better results in specific fields. Examples of these recent improvements are T*

2-weighted turbo spin-echo (T2 TSE MRI), double inversion recovery MRI (DIR-MRI) or phase-

sensitive inversion recovery MRI (PSIR-MRI), all of them able to improve imaging of the brain

lesions.[38][39]

Another example is MP-RAGE (magnetization-prepared rapid acquisition with

gradient echo),[40]

which improves images of multiple sclerosis cortical lesions.[41]

[edit] Portable instruments

Portable magnetic resonance instruments are available for use in education and field research.

Using the principles of Earth's field NMR, they have no powerful polarizing magnet, so that such

instruments can be small and inexpensive. Some can be used for both EFNMR spectroscopy and

MRI imaging.[42]

The low strength of the Earth's field results in poor signal to noise ratios

(SNR), requiring long scan times to capture spectroscopic data or build up MRI images.

However, the extremely low noise floor of SQUID-based MRI detectors, and the low density of

thermal noise in the low-frequency operating range (tens of kiloHertz) may result in useable

SNR approaching that of mid-field conventional instruments. Further, the ultra-low field

technologies enable electron spin resonance detection, and potentially imaging, at safe operating

frequencies (NASA Technical Brief).

Research with atomic magnetometers have discussed the possibility for cheap and portable MRI

instruments without the large magnet.[43][44]

[edit] MRI versus CT

A computed tomography (CT) scanner uses X-rays, a type of ionizing radiation, to acquire

images, making it a good tool for examining tissue composed of elements of a higher atomic

number than the tissue surrounding them, such as bone and calcifications (calcium based) within

the body (carbon based flesh), or of structures (vessels, bowel). MRI, on the other hand, uses

non-ionizing radio frequency (RF) signals to acquire its images and is best suited for soft tissue

(although MRI can also be used to acquire images of bones, teeth[45]

and even fossils[46]

).

Contrast in CT images is generated purely by X-ray attenuation, while a variety of properties

may be used to generate contrast in MR images. By variation of scanning parameters, tissue

contrast can be altered to enhance different features in an image (see Applications for more

details). Both CT and MR images may be enhanced by the use of contrast agents. Contrast agents

for CT contain elements of a high atomic number, relative to tissue, such as iodine or barium,

while contrast agents for MRI have paramagnetic properties, such as gadolinium and manganese,

used to alter tissue relaxation times.

CT and MRI scanners are able to generate multiple two-dimensional cross-sections (slices) of

tissue and three-dimensional reconstructions. MRI can generate cross-sectional images in any

plane (including oblique planes). In the past, CT was limited to acquiring images in the axial (or

near axial) plane. The scans used to be called Computed Axial Tomography scans (CAT scans).

However, the development of multi-detector CT scanners with near-isotropic resolution, allows

the CT scanner to produce data that can be retrospectively reconstructed in any plane with

minimal loss of image quality. For purposes of tumor detection and identification in the brain,

MRI is generally superior.[47][48]

However, in the case of solid tumors of the abdomen and chest,

CT is often preferred as it suffers less from motion artifacts. Furthermore, CT usually is more

widely available, faster, less expensive, and may be less likely to require the person to be sedated

or anaesthetized as a result of being less enclosed and noisy, and therefore less psychologically

intimidating.

MRI is also best suited for cases when a patient is to undergo the exam several times

successively in the short term, because, unlike CT, it does not expose the patient to the hazards

of ionizing radiation.

[edit] Economics of MRI

The examples and perspective in this article deal primarily with the United States and

do not represent a worldwide view of the subject. Please improve this article and

discuss the issue on the talk page. (September 2011)

MRI equipment is expensive. 1.5 tesla scanners often cost between US$1 million and US$1.5

million. 3.0 tesla scanners often cost between US$2 million and US$2.3 million. Construction of

MRI suites can cost up to US$500,000, or more, depending on project scope.

Looking through an MRI scanner.

MRI scanners have been significant sources of revenue for healthcare providers in the US. This

is because of favorable reimbursement rates from insurers and federal government programs.

Insurance reimbursement is provided in two components, an equipment charge for the actual

performance of the MRI scan and professional charge for the radiologist's review of the images

and/or data. In the US Northeast, an equipment charge might be $3,500 and a professional charge

might be $350 [49]

although the actual fees received by the equipment owner and interpreting

physician are often significantly less and depend on the rates negotiated with insurance

companies or determined by governmental action as in the Medicare Fee Schedule. For example,

an orthopedic surgery group in Illinois billed a charge of $1,116 for a knee MRI in 2007 but the

Medicare reimbursement in 2007 was only $470.91.[50]

Many insurance companies require

preapproval of an MRI procedure as a condition for coverage.

In the US, the Deficit Reduction Act of 2005 significantly reduced reimbursement rates paid by

federal insurance programs for the equipment component of many scans, shifting the economic

landscape. Many private insurers have followed suit.[citation needed]

[edit] Safety

A number of features of MRI scanning can give rise to risks.

These include:

Powerful magnetic fields

Cryogenic liquids

Noise

Claustrophobia

In addition, in cases where MRI contrast agents are used, these also typically have associated

risks.

[edit] Magnetic field

Most forms of medical or biostimulation implants are generally considered contraindications for

MRI scanning. These include pacemakers, vagus nerve stimulators, implantable cardioverter-

defibrillators, loop recorders, insulin pumps, cochlear implants, deep brain stimulators and

capsules retained from capsule endoscopy. Patients are therefore always asked for complete

information about all implants before entering the room for an MRI scan. Several deaths have

been reported in patients with pacemakers who have undergone MRI scanning without

appropriate precautions.[citation needed]

To reduce such risks, implants are increasingly being

developed to make them able to be safely scanned,[51]

and specialized protocols have been

developed to permit the safe scanning of selected implants and pacing devices. Cardiovascular

stents are considered safe, however.[52]

Ferromagnetic foreign bodies such as shell fragments, or metallic implants such as surgical

prostheses and aneurysm clips are also potential risks. Interaction of the magnetic and radio

frequency fields with such objects can lead to trauma due to movement of the object in the

magnetic field or thermal injury from radio-frequency induction heating of the object.[citation needed]

Titanium and its alloys are safe from movement from the magnetic field.

In the United States a classification system for implants and ancillary clinical devices has been

developed by ASTM International and is now the standard supported by the US Food and Drug

Administration:

MR Safe sign

MR-Safe — The device or implant is completely non-magnetic, non-electrically

conductive, and non-RF reactive, eliminating all of the primary potential threats during

an MRI procedure.

MR Conditional sign

MR-Conditional — A device or implant that may contain magnetic, electrically

conductive or RF-reactive components that is safe for operations in proximity to the MRI,

provided the conditions for safe operation are defined and observed (such as 'tested safe

to 1.5 teslas' or 'safe in magnetic fields below 500 gauss in strength').

MR Unsafe sign

MR-Unsafe — Nearly self-explanatory, this category is reserved for objects that are

significantly ferromagnetic and pose a clear and direct threat to persons and equipment

within the magnet room.

The very high strength of the magnetic field can also cause "missile-effect" accidents, where

ferromagnetic objects are attracted to the center of the magnet, and there have been incidences of

injury and death.[53][54]

To reduce the risks of projectile accidents, ferromagnetic objects and

devices are typically prohibited in proximity to the MRI scanner and patients undergoing MRI

examinations are required to remove all metallic objects, often by changing into a gown or

scrubs and ferromagnetic detection devices are used by some sites[55][56]

There is no evidence for biological harm from even very powerful static magnetic fields[57]

[edit] Radio frequency energy

A powerful radio transmitter is needed for excitation of proton spins. This can heat the body to

the point of risk of hyperthermia in patients, particularly in obese patients or those with

thermoregulation disorders[citation needed]

. Several countries have issued restrictions on the

maximum specific absorption rate that a scanner may produce.

[edit] Peripheral nerve stimulation (PNS)

The rapid switching on and off of the magnetic field gradients is capable of causing nerve

stimulation. Volunteers report a twitching sensation when exposed to rapidly switched fields,

particularly in their extremities[58]

.[59]

The reason the peripheral nerves are stimulated is that the

changing field increases with distance from the center of the gradient coils (which more or less

coincides with the center of the magnet).[60]

Note however that when imaging the head, the heart

is far off-center and induction of even a tiny current into the heart must be avoided at all

costs.[citation needed]

Although PNS was not a problem for the slow, weak gradients used in the early

days of MRI, the strong, rapidly switched gradients used in techniques such as EPI, fMRI,

diffusion MRI, etc. are indeed capable of inducing PNS. American and European regulatory

agencies insist that manufacturers stay below specified dB/dt limits (dB/dt is the change in field

per unit time) or else prove that no PNS is induced for any imaging sequence. As a result of

dB/dt limitation, commercial MRI systems cannot use the full rated power of their gradient

amplifiers.

[edit] Acoustic noise

Switching of field gradients causes a change in the Lorentz force experienced by the gradient

coils, producing minute expansions and contractions of the coil itself. As the switching is

typically in the audible frequency range, the resulting vibration produces loud noises (clicking or

beeping). This is most marked with high-field machines[61]

and rapid-imaging techniques in

which sound intensity can reach 120 dB(A) (equivalent to a jet engine at take-off),[62]

and

therefore appropriate ear protection is essential for anyone inside the MRI scanner room during

the examination.[63]

[edit] Cryogens

As described in Physics of Magnetic Resonance Imaging, many MRI scanners rely on cryogenic

liquids to enable superconducting capabilities of the electromagnetic coils within. Though the

cryogenic liquids used are non-toxic, their physical properties present specific hazards.

An unintentional shut-down of a superconducting electromagnet, an event known as "quench",

involves the rapid boiling of liquid helium from the device. If the rapidly expanding helium

cannot be dissipated through an external vent, sometimes referred to as 'quench pipe', it may be

released into the scanner room where it may cause displacement of the oxygen and present a risk

of asphyxiation.[64]

Oxygen deficiency monitors are usually used as a safety precaution. Liquid helium, the most

commonly used cryogen in MRI, undergoes near explosive expansion as it changes from liquid

to a gaseous state. The use of an oxygen monitor is important to ensure that oxygen levels safe

for patient/physicians. Rooms built in support of superconducting MRI equipment should be

equipped with pressure relief mechanisms[65]

and an exhaust fan, in addition to the required

quench pipe.

Because a quench results in rapid loss of cryogens from the magnet, recommissioning the

magnet is expensive and time-consuming. Spontaneous quenches are uncommon, but a quench

may also be triggered by equipment malfunction, improper cryogen fill technique, contaminants

inside the cryostat, or extreme magnetic or vibrational disturbances.

[edit] Contrast agents

Main article: MRI contrast agent

The most commonly used intravenous contrast agents are based on chelates of gadolinium. In

general, these agents have proved safer than the iodinated contrast agents used in X-ray

radiography or CT. Anaphylactoid reactions are rare, occurring in approx. 0.03–0.1%.[66]

Of

particular interest is the lower incidence of nephrotoxicity, compared with iodinated agents,

when given at usual doses—this has made contrast-enhanced MRI scanning an option for

patients with renal impairment, who would otherwise not be able to undergo contrast-enhanced

CT.[67]

Although gadolinium agents have proved useful for patients with renal impairment, in patients

with severe renal failure requiring dialysis there is a risk of a rare but serious illness, nephrogenic

systemic fibrosis, that may be linked to the use of certain gadolinium-containing agents. The

most frequently linked is gadodiamide, but other agents have been linked too.[68]

Although a

causal link has not been definitively established, current guidelines in the United States are that

dialysis patients should only receive gadolinium agents where essential, and that dialysis should

be performed as soon as possible after the scan to remove the agent from the body

promptly.[69][70]

In Europe, where more gadolinium-containing agents are available, a

classification of agents according to potential risks has been released.[71][72]

Recently a new

contrast agent named gadoxetate, brand name Eovist (US) or Primovist (EU), was approved for

diagnostic use: this has the theoretical benefit of a dual excretion path.[73]

[edit] Pregnancy

No effects of MRI on the fetus have been demonstrated.[74]

In particular, MRI avoids the use of

ionizing radiation, to which the fetus is particularly sensitive. However, as a precaution, current

guidelines recommend that pregnant women undergo MRI only when essential. This is

particularly the case during the first trimester of pregnancy, as organogenesis takes place during

this period. The concerns in pregnancy are the same as for MRI in general, but the fetus may be

more sensitive to the effects—particularly to heating and to noise. However, one additional

concern is the use of contrast agents; gadolinium compounds are known to cross the placenta and

enter the fetal bloodstream, and it is recommended that their use be avoided.

Despite these concerns, MRI is rapidly growing in importance as a way of diagnosing and

monitoring congenital defects of the fetus because it can provide more diagnostic information

than ultrasound and it lacks the ionizing radiation of CT. MRI without contrast agents is the

imaging mode of choice for pre-surgical, in-utero diagnosis and evaluation of fetal tumors,

primarily teratomas, facilitating open fetal surgery, other fetal interventions, and planning for

procedures (such as the EXIT procedure) to safely deliver and treat babies whose defects would

otherwise be fatal.

[edit] Claustrophobia and discomfort

Due to the construction of some MRI scanners, they can be potentially unpleasant to lie in. Older

models of closed bore MRI systems feature a fairly long tube or tunnel. The part of the body

being imaged must lie at the center of the magnet, which is at the absolute center of the tunnel.

Because scan times on these older scanners may be long (occasionally up to 40 minutes for the

entire procedure), people with even mild claustrophobia are sometimes unable to tolerate an MRI

scan without management. Modern scanners may have larger bores (up to 70 cm) and scan times

are shorter. This means that claustrophobia is less of an issue, and many patients now find MRI

an innocuous and easily tolerated procedure.[citation needed]

Nervous patients may still find the following strategies helpful:

Advance preparation

o visiting the scanner to see the room and practice lying on the table

o visualization techniques

o chemical sedation

o general anesthesia

Coping while inside the scanner

o holding a "panic button"

o closing eyes as well as covering them (e.g. washcloth, eye mask)

o listening to music on headphones or watching a movie, using mirror-glasses and a

projection screen or via a Head-mounted display, while in the machine.

Alternative scanner designs, such as open or upright systems, can also be helpful where these are

available. Though open scanners have increased in popularity, they produce inferior scan quality

because they operate at lower magnetic fields than closed scanners. However, commercial 1.5

tesla open systems have recently become available, providing much better image quality than

previous lower field strength open models.[75]

For babies and young children chemical sedation or general anesthesia are the norm, as these

subjects cannot be instructed to hold still during the scanning session. Obese patients and

pregnant women may find the MRI machine to be a tight fit. Pregnant women may also have

difficulty lying on their backs for an hour or more without moving.

[edit] Guidance

Safety issues, including the potential for biostimulation device interference, movement of

ferromagnetic bodies, and incidental localized heating, have been addressed in the American

College of Radiology's White Paper on MR Safety, which was originally published in 2002 and

expanded in 2004. The ACR White Paper on MR Safety has been rewritten and was released

early in 2007 under the new title ACR Guidance Document for Safe MR Practices.

In December 2007, the Medicines in Healthcare product Regulation Agency (MHRA), a UK

healthcare regulatory body, issued their Safety Guidelines for Magnetic Resonance Imaging

Equipment in Clinical Use.

In February 2008, the Joint Commission, a US healthcare accrediting organization, issued a

Sentinel Event Alert #38, their highest patient safety advisory, on MRI safety issues.

In July 2008, the United States Veterans Administration, a federal governmental agency serving

the healthcare needs of former military personnel, issued a substantial revision to their MRI

Design Guide, which includes physical or facility safety considerations.

[edit] The European Physical Agents Directive

The European Physical Agents (Electromagnetic Fields) Directive is legislation adopted in

European legislature. Originally scheduled to be required by the end of 2008, each individual

state within the European Union must include this directive in its own law by the end of 2012.

Some member nations passed complying legislation and are now attempting to repeal their state

laws in expectation that the final version of the EU Physical Agents Directive will be

substantially revised prior to the revised adoption date.

The directive applies to occupational exposure to electromagnetic fields (not medical exposure)

and was intended to limit workers’ acute exposure to strong electromagnetic fields, as may be

found near electricity substations, radio or television transmitters or industrial equipment.

However, the regulations impact significantly on MRI, with separate sections of the regulations

limiting exposure to static magnetic fields, changing magnetic fields and radio frequency energy.

Field strength limits are given, which may not be exceeded. An employer may commit a criminal

offense by allowing a worker to exceed an exposure limit, if that is how the Directive is

implemented in a particular member state.

The Directive is based on the international consensus of established effects of exposure to

electromagnetic fields, and in particular the advice of the European Commissions's advisor, the

International Commission on Non-Ionizing Radiation Protection (ICNIRP). The aims of the

Directive, and the ICNIRP guidelines it is based on, are to prevent exposure to potentially

harmful fields. The actual limits in the Directive are very similar to the limits advised by the

Institute of Electrical and Electronics Engineers, with the exception of the frequencies produced

by the gradient coils, where the IEEE limits are significantly higher.

Many Member States of the EU already have either specific EMF regulations or (as in the UK) a

general requirement under workplace health and safety legislation to protect workers against

electromagnetic fields. In almost all cases the existing regulations are aligned with the ICNIRP

limits so that the Directive should, in theory, have little impact on any employer already meeting

their legal responsibilities.

The introduction of the Directive has brought to light an existing potential issue with

occupational exposures to MRI fields. There are at present very few data on the number or types

of MRI practice that might lead to exposures in excess of the levels of the Directive.[76][77]

There

is a justifiable concern amongst MRI practitioners that if the Directive were to be enforced more

vigorously than existing legislation, the use of MRI might be restricted, or working practices of

MRI personnel might have to change.

In the initial draft a limit of static field strength to 2 T was given. This has since been removed

from the regulations, and whilst it is unlikely to be restored as it was without a strong

justification, some restriction on static fields may be reintroduced after the matter has been

considered more fully by ICNIRP. The effect of such a limit might be to restrict the installation,

operation and maintenance of MRI scanners with magnets of 2 T and stronger. As the increase in

field strength has been instrumental in developing higher resolution and higher performance

scanners, this would be a significant step back. This is why it is unlikely to happen without

strong justification.

Individual government agencies and the European Commission have now formed a working

group to examine the implications on MRI and to try to address the issue of occupational

exposures to electromagnetic fields from MRI.

[edit] Three-dimensional (3D) image reconstruction

[edit] The principle

Because contemporary MRI scanners offer isotropic, or near isotropic, resolution, display of

images does not need to be restricted to the conventional axial images. Instead, it is possible for a

software program to build a volume by 'stacking' the individual slices one on top of the other.

The program may then display the volume in an alternative manner.

[edit] 3D rendering techniques

Surface rendering

A threshold value of greyscale density is chosen by the operator (e.g. a level that

corresponds to fat). A threshold level is set, using edge detection image processing

algorithms. From this, a 3-dimensional model can be constructed and displayed on

screen. Multiple models can be constructed from various different thresholds, allowing

different colors to represent each anatomical component such as bone, muscle, and

cartilage. However, the interior structure of each element is not visible in this mode of

operation.

Volume rendering

Surface rendering is limited in that it only displays surfaces that meet a threshold density,

and only displays the surface closest to the imaginary viewer. In volume rendering,

transparency and colors are used to allow a better representation of the volume to be

shown in a single image - e.g. the bones of the pelvis could be displayed as semi-

transparent, so that even at an oblique angle, one part of the image does not conceal

another.

[edit] Image segmentation

Where different structures have similar threshold density, it can become impossible to separate

them simply by adjusting volume rendering parameters. The solution is called segmentation, a

manual or automatic procedure that can remove the unwanted structures from the image.

Electrocardiography

From Wikipedia, the free encyclopedia

(Redirected from Ecg)

"ECG" redirects here. For other uses, see ECG (disambiguation).

Not to be confused with echocardiogram, electromyogram, electroencephalogram, or EEG.

Electrocardiography

Intervention

Image showing a patient connected to the 10

electrodes necessary for a 12-lead ECG

ICD-9-CM 89.52

MeSH D004562

12 Lead EKG of a 26-year-old male.

Electrocardiography (ECG or EKG from the German Elektrokardiogramm) is a transthoracic

(across the thorax or chest) interpretation of the electrical activity of the heart over a period of

time, as detected by electrodes attached to the outer surface of the skin and recorded by a device

external to the body.[1]

The recording produced by this noninvasive procedure is termed an

electrocardiogram (also ECG or EKG).

The etymology of the word is derived from the Greek electro, because it is related to electrical

activity, kardio, Greek for heart, and graph, a Greek root meaning "to write". In English

speaking countries, medical professionals often write EKG (the abbreviation for the German

word elektrokardiogramm) in order to avoid confusion with EEG in emergency situations where

background noise is high.[citation needed]

Most EKGs are performed for diagnostic or research purposes on human hearts, but may also be

performed on animals, usually for research.

Contents

[hide]

1 Function

2 History

3 EKG graph paper

o 3.1 Layout

4 Leads

o 4.1 Placement of electrodes

4.1.1 Additional electrodes

o 4.2 Limb leads

o 4.3 Unipolar vs. bipolar leads

o 4.4 Augmented limb leads

o 4.5 Precordial leads

5 Waves and intervals

6 Vectors and views

o 6.1 Axis

o 6.2 Clinical lead groups

7 Filter selection

8 Indications

9 Some pathological entities which can be seen on the ECG

o 9.1 Electrocardiogram heterogeneity

10 See also

11 References

12 External links

[edit] Function

The EKG device detects and amplifies the tiny electrical changes on the skin that are caused

when the heart muscle depolarizes during each heartbeat. At rest, each heart muscle cell has a

charge across its outer wall, or cell membrane. Reducing this charge towards zero is called

depolarization, which activates the mechanisms in the cell that cause it to contract. During each

heartbeat a healthy heart will have an orderly progression of a wave of depolarisation that is

triggered by the cells in the sinoatrial node, spreads out through the atrium, passes through

"intrinsic conduction pathways" and then spreads all over the ventricles. This is detected as tiny

rises and falls in the voltage between two electrodes placed either side of the heart which is

displayed as a wavy line either on a screen or on paper. This display indicates the overall rhythm

of the heart and weaknesses in different parts of the heart muscle.

Usually more than 2 electrodes are used and they can be combined into a number of pairs (For

example: Left arm (LA), right arm (RA) and left leg (LL) electrodes form the three pairs

LA+RA, LA+LL, and RA+LL). The output from each pair is known as a lead. Each lead is said

to look at the heart from a different angle. Different types of EKGs can be referred to by the

number of leads that are recorded, for example 3-lead, 5-lead or 12-lead EKGs (sometimes

simply "a 12-lead"). A 12-lead EKG is one in which 12 different electrical signals are recorded at

approximately the same time and will often be used as a one-off recording of an EKG,

traditionally printed out as a paper copy. 3- and 5-lead EKGs tend to be monitored continuously

and viewed only on the screen of an appropriate monitoring device, for example during an

operation or whilst being transported in an ambulance. There may or may not be any permanent

record of a 3- or 5-lead EKG, depending on the equipment used.

It is the best way to measure and diagnose abnormal rhythms of the heart,[2]

particularly

abnormal rhythms caused by damage to the conductive tissue that carries electrical signals, or

abnormal rhythms caused by electrolyte imbalances.[3]

In a myocardial infarction (MI), the EKG

can identify if the heart muscle has been damaged in specific areas, though not all areas of the

heart are covered.[4]

The EKG cannot reliably measure the pumping ability of the heart, for

which ultrasound-based (echocardiography) or nuclear medicine tests are used. It is possible for

a human or other animal to be in cardiac arrest but still have a normal EKG signal (a condition

known as pulseless electrical activity).

[edit] History

Alexander Muirhead is reported to have attached wires to a feverish patient's wrist to obtain a

record of the patient's heartbeat while studying for his Doctor of Science (in electricity) in 1872

at St Bartholomew's Hospital.[5]

This activity was directly recorded and visualized using a

Lippmann capillary electrometer by the British physiologist John Burdon Sanderson.[6]

The first

to systematically approach the heart from an electrical point-of-view was Augustus Waller,

working in St Mary's Hospital in Paddington, London.[7]

His electrocardiograph machine

consisted of a Lippmann capillary electrometer fixed to a projector. The trace from the heartbeat

was projected onto a photographic plate which was itself fixed to a toy train. This allowed a

heartbeat to be recorded in real time. In 1911 he still saw little clinical application for his work.

Einthoven's ECG device

An initial breakthrough came when Willem Einthoven, working in Leiden, Netherlands, used the

string galvanometer that he invented in 1903.[8]

This device was much more sensitive than both

the capillary electrometer that Waller used and the string galvanometer that had been invented

separately in 1897 by the French engineer Clément Ader.[9]

Rather than using today's self-

adhesive electrodes Einthoven's subjects would immerse each of their limbs into containers of

salt solutions from which the EKG was recorded.

Einthoven assigned the letters P, Q, R, S and T to the various deflections, and described the

electrocardiographic features of a number of cardiovascular disorders. In 1924, he was awarded

the Nobel Prize in Medicine for his discovery.[10]

Though the basic principles of that era are still in use today, there have been many advances in

electrocardiography over the years. The instrumentation, for example, has evolved from a

cumbersome laboratory apparatus to compact electronic systems that often include computerized

interpretation of the electrocardiogram.[11]

[edit] EKG graph paper

One second of ECG graph paper

The output of an ECG recorder is a graph (or sometimes several graphs, representing each of the

leads) with time represented on the x-axis and voltage represented on the y-axis. A dedicated

ECG machine would usually print onto graph paper which has a background pattern of 1mm

squares (often in red or green), with bold divisions every 5 mm in both vertical and horizontal

directions.

It is possible to change the output of most ECG devices but it is standard to represent each mV

on the y axis as 1 cm and each second as 25 mm on the x-axis (that is a paper speed of 25 mm/s).

Faster paper speeds can be used, for example, to resolve finer detail in the ECG. At a paper

speed of 25 mm/s, one small block of ECG paper translates into 40 ms. Five small blocks make

up one large block, which translates into 200 ms. Hence, there are five large blocks per second.

A calibration signal may be included with a record. A standard signal of 1 mV must move the

stylus vertically 1 cm, that is, two large squares on ECG paper.

[edit] Layout

By definition, a 12-lead ECG will show a short segment of the recording of each of the 12-leads.

This is often arranged in a grid of 4 columns by three rows, the first columns being the limb

leads (I,II and III), the second column the augmented limb leads (aVR, aVL and aVF) and the

last two columns being the chest leads (V1-V6). It is usually possible to change this layout so it

is vital to check the labels to see which lead is represented. Each column will usually record the

same moment in time for the three leads and then the recording will switch to the next column

which will record the heart beats after that point. It is possible for the heart rhythm to change

between the columns of leads.

Each of these segments is short, perhaps 1-3 heart beats only, depending on the heart rate and it

can be difficult to analyse any heart rhythm that shows changes between heart beats. To help

with the analysis it is common to print one or two "rhythm strips" as well. This will usually be

lead II (which shows the electrical signal from the atrium, the P-wave, well) and shows the

rhythm for the whole time the ECG was recorded (usually 5–6 seconds). Some ECG machines

will print a second lead II along the very bottom of the paper in addition to the output described

above. This printing of Lead II is continuous from start to finish of the process.

The term "rhythm strip" may also refer to the whole printout from a continuous monitoring

system which may show only one lead and is either initiated by a clinician or in response to an

alarm or event.

[edit] Leads

The term "lead" in electrocardiography causes much confusion because it is used to refer to two

different things. In accordance with common parlance the word lead may be used to refer to the

electrical cable attaching the electrodes to the ECG recorder. As such it may be acceptable to

refer to the "left arm lead" as the electrode (and its cable) that should be attached at or near the

left arm. There are usually ten of these electrodes in a standard "12-lead" ECG.

Alternatively (and some would say properly, in the context of electrocardiography) the word lead

may refer to the tracing of the voltage difference between two of the electrodes and is what is

actually produced by the ECG recorder. Each will have a specific name. For example "Lead I"

(lead one) is the voltage between the right arm electrode and the left arm electrode, whereas

"Lead II" (lead two) is the voltage between the right limb and the feet. (This rapidly becomes

more complex as one of the "electrodes" may in fact be a composite of the electrical signal from

a combination of the other electrodes (see later). Twelve of this type of lead form a "12-lead"

ECG

To cause additional confusion the term "limb leads" usually refers to the tracings from leads I, II

and III rather than the electrodes attached to the limbs.

[edit] Placement of electrodes

Ten electrodes are used for a 12-lead ECG. The electrodes usually consist of a conducting gel,

embedded in the middle of a self-adhesive pad onto which cables clip. Sometimes the gel also

forms the adhesive.[12]

They are labeled and placed on the patient's body as follows:[13][14]

Proper placement of the limb electrodes, color coded as recommended by the American Heart

Association (a different colour scheme is used in Europe). Note that the limb electrodes can be

far down on the limbs or close to the hips/shoulders, but they must be even (left vs right).[15]

. * Note that when exercise stress tests are performed, limb leads may be placed on the trunk to

avoid artifacts while ambulatory (arm leads moved sub-clavicularly and leg leads medial to and

above the iliac crest).

12 leads

Electrode

label (in the

USA)

Electrode placement

RA On the right arm, avoiding thick muscle.

LA In the same location that RA was placed, but on the left arm.

RL On the right leg, lateral calf muscle

LL In the same location that RL was placed, but on the left leg.

V1 In the fourth intercostal space (between ribs 4 & 5) just to the right of the

sternum (breastbone).

V2 In the fourth intercostal space (between ribs 4 & 5) just to the left of the sternum.

V3 Between leads V2 and V4.

V4

In the fifth intercostal space (between ribs 5 & 6) in the mid-clavicular line (the

imaginary line that extends down from the midpoint of the clavicle

(collarbone)).

V5

Horizontally even with V4, but in the anterior axillary line. (The anterior axillary

line is the imaginary line that runs down from the point midway between the

middle of the clavicle and the lateral end of the clavicle; the lateral end of the

collarbone is the end closer to the arm.)

V6 Horizontally even with V4 and V5 in the midaxillary line. (The midaxillary line

is the imaginary line that extends down from the middle of the patient's armpit.)

[edit] Additional electrodes

The classical 12-lead ECG can be extended in a number of ways in an attempt to improve its

sensitivity in detecting myocardial infarction involving territories not normally "seen" well. This

includes an rV4 lead which uses the equivalent landmarks to the V4 but on the right side of the

chest wall and extending the chest leads onto the back with a V7, V8 and V9.

[edit] Limb leads

In both the 5- and 12-lead configuration, leads I, II and III are called limb leads. The electrodes

that form these signals are located on the limbs—one on each arm and one on the left

leg.[16][17][18]

The limb leads form the points of what is known as Einthoven's triangle.[19]

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

electrode:

I = LA − RA.

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

(RA) electrode:

II = LL − RA.

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

electrode:

III = LL − LA.

Simplified electrocardiograph sensors designed for teaching purposes at e.g. high school level

are generally limited to three arm electrodes serving similar purposes.[20]

[edit] Unipolar vs. bipolar leads

There are two types of leads: unipolar and bipolar. Bipolar leads have one positive and one

negative pole.[21]

In a 12-lead ECG, the limb leads (I, II and III) are bipolar leads. Unipolar leads

also have two poles, as a voltage is measured; however, the negative pole is a composite pole

(Wilson's central terminal, or WCT) made up of signals from lots of other electrodes.[22]

In a 12-

lead ECG, all leads besides the limb leads are unipolar (aVR, aVL, aVF, V1, V2, V3, V4, V5, and

V6).

Wilson's central terminal VW is produced by connecting the electrodes, RA; LA; and LL,

together, via a simple resistive network, to give an average potential across the body, which

approximates the potential at infinity (i.e. zero):

[edit] Augmented limb leads

Leads aVR, aVL, and aVF are augmented limb leads (after their inventor Dr. Emanuel

Goldberger known collectively as the Goldberger's leads). They are derived from the same three

electrodes as leads I, II, and III. However, they view the heart from different angles (or vectors)

because the negative electrode for these leads is a modification of Wilson's central terminal. This

zeroes out the negative electrode and allows the positive electrode to become the "exploring

electrode". This is possible because Einthoven's Law states that I + (−II) + III = 0. The equation

can also be written I + III = II. It is written this way (instead of I − II + III = 0) because

Einthoven reversed the polarity of lead II in Einthoven's triangle, possibly because he liked to

view upright QRS complexes. Wilson's central terminal paved the way for the development of

the augmented limb leads aVR, aVL, aVF and the precordial leads V1, V2, V3, V4, V5 and V6.

Lead augmented vector right (aVR) has the positive electrode (white) on the right arm.

The negative electrode is a combination of the left arm (black) electrode and the left leg

(red) electrode, which "augments" the signal strength of the positive electrode on the

right arm:

Lead augmented vector left (aVL) has the positive (black) electrode on the left arm. The

negative electrode is a combination of the right arm (white) electrode and the left leg

(red) electrode, which "augments" the signal strength of the positive electrode on the left

arm:

Lead augmented vector foot (aVF) has the positive (red) electrode on the left leg. The

negative electrode is a combination of the right arm (white) electrode and the left arm

(black) electrode, which "augments" the signal of the positive electrode on the left leg:

The augmented limb leads aVR, aVL, and aVF are amplified in this way because the signal is

too small to be useful when the negative electrode is Wilson's central terminal. Together with

leads I, II, and III, augmented limb leads aVR, aVL, and aVF form the basis of the hexaxial

reference system, which is used to calculate the heart's electrical axis in the frontal plane. The

aVR, aVL, and aVF leads can also be represented using the I and II limb leads:

[edit] Precordial leads

The electrodes for the precordial leads (V1, V2, V3, V4, V5 and V6) are placed directly on the

chest. Because of their close proximity to the heart, they do not require augmentation. Wilson's

central terminal is used for the negative electrode, and these leads are considered to be unipolar

(recall that Wilson's central terminal is the average of the three limb leads. This approximates

common, or average, potential over the body). The precordial leads view the heart's electrical

activity in the so-called horizontal plane. The heart's electrical axis in the horizontal plane is

referred to as the Z axis.

[edit] Waves and intervals

Schematic representation of normal ECG

Animation of a normal ECG wave.

Detail of the QRS complex, showing ventricular activation time (VAT) and amplitude.

A typical ECG tracing of the cardiac cycle (heartbeat) consists of a P wave, a QRS complex, a T

wave, and a U wave which is normally visible in 50 to 75% of ECGs.[23]

The baseline voltage of

the electrocardiogram is known as the isoelectric line. Typically the isoelectric line is measured

as the portion of the tracing following the T wave and preceding the next P wave.

Feature Description Duration

RR

interval

The interval between an R wave and the next R wave . Normal resting

heart rate is between 60 and 100 bpm 0.6 to 1.2s

P wave

During normal atrial depolarization, the main electrical vector is

directed from the SA node towards the AV node, and spreads from the

right atrium to the left atrium. This turns into the P wave on the ECG.

80ms

PR

interval

The PR interval is measured from the beginning of the P wave to the

beginning of the QRS complex. The PR interval reflects the time the

electrical impulse takes to travel from the sinus node through the AV

node and entering the ventricles. The PR interval is therefore a good

estimate of AV node function.

120 to 200ms

PR

segment

The PR segment connects the P wave and the QRS complex. This

coincides with the electrical conduction from the AV node to the

bundle of His to the bundle branches and then to the Purkinje Fibers.

This electrical activity does not produce a contraction directly and is

merely traveling down towards the ventricles and this shows up flat on

the ECG. The PR interval is more clinically relevant.

50 to 120ms

QRS

complex

The QRS complex reflects the rapid depolarization of the right and left

ventricles. They have a large muscle mass compared to the atria and so

the QRS complex usually has a much larger amplitude than the P-wave.

80 to 120ms

J-point

The point at which the QRS complex finishes and the ST segment

begins. Used to measure the degree of ST elevation or depression

present.

N/A

ST

segment

The ST segment connects the QRS complex and the T wave. The ST

segment represents the period when the ventricles are depolarized. It is

isoelectric.

80 to 120ms

T wave

The T wave represents the repolarization (or recovery) of the ventricles.

The interval from the beginning of the QRS complex to the apex of the

T wave is referred to as the absolute refractory period. The last half of

the T wave is referred to as the relative refractory period (or vulnerable

period).

160ms

ST

interval

The ST interval is measured from the J point to the end of the T wave. 320ms

QT

interval

The QT interval is measured from the beginning of the QRS complex to

the end of the T wave. A prolonged QT interval is a risk factor for

ventricular tachyarrhythmias and sudden death. It varies with heart rate

and for clinical relevance requires a correction for this, giving the QTc.

300 to

430ms[citation

needed]

U wave

The U wave is hypothesized to be caused by the repolarization of the

interventricular septum. They normally have a low amplitude, and even

more often completely absent. They always follow the T wave and also

follow the same direction in amplitude. If they are too prominent we

suspect hypokalemia, hypercalcemia or hyperthyroidism usually. [24]

J wave

The J wave, elevated J-Point or Osborn Wave appears as a late delta

wave following the QRS or as a small secondary R wave . It is

considered pathognomonic of hypothermia or hypocalcemia.[25]

There were originally four deflections, but after the mathematical correction for artifacts

introduced by early amplifiers, five deflections were discovered. Einthoven chose the letters P,

Q, R, S, and T to identify the tracing which was superimposed over the uncorrected labeled A, B,

C, and D.[26]

In intracardiac electrocardiograms, such as can be acquired from pacemaker sensors, an

additional wave that can be seen is the H deflection, which reflects the depolarization of the

bundle of His.[27]

The H-V interval, in turn, is the duration from the beginning of the H deflection

to the earliest onset of ventricular depolarization recorded in any lead.[28]

[edit] Vectors and views

Graphic showing the relationship between positive electrodes, depolarization wavefronts (or

mean electrical vectors), and complexes displayed on the ECG.

Interpretation of the ECG relies on the idea that different leads (by which we mean the ECG

leads I,II,III, aVR, aVL, aVF and the chest leads) "view" the heart from different angles. This

has two benefits. Firstly, leads which are showing problems (for example ST segment elevation)

can be used to infer which region of the heart is affected. Secondly, the overall direction of travel

of the wave of depolarisation can also be inferred which can reveal other problems. This is

termed the cardiac axis . Determination of the cardiac axis relies on the concept of a vector

which describes the motion of the depolarisation wave. This vector can then be described in

terms of its components in relation to the direction of the lead considered. One component will

be in the direction of the lead and this will be revealed in the behaviour of the QRS complex and

one component will be at 90 degrees to this (which will not). Any net positive deflection of the

QRS complex (i.e. height of the R-wave minus depth of the S-wave) suggests that the wave of

depolarisation is spreading through the heart in a direction that has some component (of the

vector) in the same direction as the lead in question.

[edit] Axis

Diagram showing how the polarity of the QRS complex in leads I, II, and III can be used to

estimate the heart's electrical axis in the frontal plane.

The heart's electrical axis refers to the general direction of the heart's depolarization wavefront

(or mean electrical vector) in the frontal plane. With a healthy conducting system the cardiac

axis is related to where the major muscle bulk of the heart lies. Normally this is the left ventricle

with some contribution from the right ventricle. It is usually oriented in a right shoulder to left

leg direction, which corresponds to the left inferior quadrant of the hexaxial reference system,

although −30° to +90° is considered to be normal. If the left ventricle increases its activity or

bulk then there is said to be "left axis deviation" as the axis swings round to the left beyond -30°,

alternatively in conditions where the right ventricle is strained or hypertrophied then the axis

swings round beyond +90° and "right axis deviation" is said to exist. Disorders of the conduction

system of the heart can disturb the electrical axis without necessarily reflecting changes in

muscle bulk.

Normal −30° to

90° Normal Normal

Left axis

deviation

−30° to

−90°

May indicate left anterior fascicular

block or Q waves from inferior MI.

Left axis deviation is considered

normal in pregnant women and

those with emphysema.

Right axis

deviation

+90° to

+180°

May indicate left posterior fascicular

block, Q waves from high lateral MI,

or a right ventricular strain pattern.

Right deviation is considered

normal in children and is a

standard effect of dextrocardia.

Extreme right

axis deviation

+180°

to −90°

Is rare, and considered an 'electrical

no-man's land'.

The hexaxial reference system showing the orientation of each lead. For example, if the bulk of

heart muscle is oriented at +60 degrees with respect to the SA node, lead II will show the

greatest deflection and aVL the least.

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

block.

[edit] Clinical lead groups

There are twelve leads in total, each recording the electrical activity of the heart from a different

perspective, which also correlate to different anatomical areas of the heart for the purpose of

identifying acute coronary ischemia or injury. Two leads that look at neighbouring anatomical

areas of the heart are said to be contiguous (see color coded chart). The relevance of this is in

determining whether an abnormality on the ECG is likely to represent true disease or a spurious

finding.

Diagram showing the contiguous leads in the same color

Category Color on

chart Leads Activity

Inferior

leads Yellow

Leads II,

III and

aVF

Look at electrical activity from the vantage point of the inferior

surface (diaphragmatic surface of heart).

Lateral

leads Green

I, aVL,

V5 and V6

Look at the electrical activity from the vantage point of the

lateral wall of left ventricle.

The positive electrode for leads I and aVL should be

located distally on the left arm and because of which,

leads I and aVL are sometimes referred to as the high

lateral leads.

Because the positive electrodes for leads V5 and V6 are

on the patient's chest, they are sometimes referred to as

the low lateral leads.

Septal

leads Orange V1 and V2

Look at electrical activity from the vantage point of the septal

wall of the ventricles (interventricular septum).

Anterior

leads Blue V3 and V4

Look at electrical activity from the vantage point of the anterior

surface of the heart (sternocostal surface of heart).

In addition, any two precordial leads that are next to one another are considered to be contiguous.

For example, even though V4 is an anterior lead and V5 is a lateral lead, they are contiguous

because they are next to one another.

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

cardiac cycle.

Lead aVR offers no specific view of the left ventricle. Rather, it views the inside of the

endocardial wall to the surface of the right atrium, from its perspective on the right shoulder.

[edit] Filter selection

Modern ECG monitors offer multiple filters for signal processing. The most common settings are

monitor mode and diagnostic mode. In monitor mode, the low frequency filter (also called the

high-pass filter because signals above the threshold are allowed to pass) is set at either 0.5 Hz or

1 Hz and the high frequency filter (also called the low-pass filter because signals below the

threshold are allowed to pass) is set at 40 Hz. This limits artifact for routine cardiac rhythm

monitoring. The high-pass filter helps reduce wandering baseline and the low-pass filter helps

reduce 50 or 60 Hz power line noise (the power line network frequency differs between 50 and

60 Hz in different countries). In diagnostic mode, the high-pass filter is set at 0.05 Hz, which

allows accurate ST segments to be recorded. The low-pass filter is set to 40, 100, or 150 Hz.

Consequently, the monitor mode ECG display is more filtered than diagnostic mode, because its

passband is narrower.[29]

[edit] Indications

Symptoms generally indicating use of electrocardiography include:

Cardiac murmurs [30]

Syncope or collapse[30]

Seizures[30]

Perceived cardiac dysrhythmias[30]

Symptoms of myocardial infarction. See Electrocardiography in myocardial infarction

It is also used to assess patients with systemic disease as well as monitoring during anesthesia

and critically ill patients.[30]

[edit] Some pathological entities which can be seen on the

ECG

Shortened QT

interval Hypercalcemia, some drugs, certain genetic abnormalities.

Prolonged QT

interval Hypocalcemia, some drugs, certain genetic abnormalities.

Flattened or

inverted T waves

Coronary ischemia, hypokalemia, left ventricular hypertrophy, digoxin

effect, some drugs.

Hyperacute T waves Possibly the first manifestation of acute myocardial infarction, where T

waves become more prominent, symmetrical, and pointed.

Prominent U waves Hypokalemia.

[edit] Electrocardiogram heterogeneity

This section may require cleanup to meet Wikipedia's quality standards. (Consider

using more specific cleanup instructions.) Please help improve this section if you can. The

talk page may contain suggestions. (March 2010)

Electrocardiogram (ECG) heterogeneity is a measurement of the amount of variance between

one ECG waveform and the next. This heterogeneity can be measured by placing multiple ECG

electrodes on the chest and by then computing the variance in waveform morphology across the

signals obtained from these electrodes. Recent research suggests that ECG heterogeneity often

precedes dangerous cardiac arrhythmias.

In the future, implantable devices may be programmed to measure and track heterogeneity.

These devices could potentially help ward off arrhythmias by stimulating nerves such as the

vagus nerve, by delivering drugs such as beta-blockers, and if necessary, by defibrillating the

heart.[31]