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
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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 electromechanical 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 ke 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 mid1960s.

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 lithiumiodide 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-tobeat 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 Chamber(s) paced

II Chamber(s) sensed

III Response to sensing

IV

Rate modulation

Multisite pacing

O = None

O = None

O = None

O = None R = Rate modulation

O = None

A = Atrium

A = Atrium

T = Triggered

A = Atrium

V = Ventricle

V = Ventricle

I = Inhibited

V = Ventricle D = Dual (A+V)

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

D = Dual (T+I)

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 inoffice 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 Shock chamber

II Antitachycardia pacing chamber

III Tachycardia detection

IV Antibradycardia pacing chamber

O = None A = Atrium

O = None A = Atrium

E = Electrogram

O = None

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 ICD-9: MeSH OPS-301 code: B?3?ZZZ 88.91-88.97 D008279 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 scannerand 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

4.9 Guidance 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

o o

[edit] How MRI works

This section does not cite any references or sources. Please help improve this section by adding citations to reliable sources. Unsourced material may be challenged and 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

This section does not cite any references or sources. Please help improve this section by adding citations to reliable sources. Unsourced material may be challenged and 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 T1weighted 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 520 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 MPRAGE 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 510 minutes of the onset of stroke symptoms (as compared with computed tomography, which often does not detect changes of acute infarct for up to 46 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. T1 (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 T1. 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 planethus 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 23 seconds). Increases in neural activity cause changes in the MR signal via T* [33] 2 changes; 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 inplane 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 tissueguided and controlled using MR thermal imagingand 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 31P 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. 17O and 19F can be administered in sufficient quantities in liquid form (e.g. 17O-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 13C or stabilized bubbles of hyperpolarized 129Xe have been studied as contrast agents for angiography and perfusion imaging. 31P 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 phasesensitive 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 cardioverterdefibrillators, 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. 0.030.1%.[66] Of particular interest is the lower incidence of nephrotoxicity, compared with iodinated agents, when given at usual dosesthis 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 effectsparticularly 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 semitransparent, 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 MeSH 89.52 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 Clment Ader.[9] Rather than using today's selfadhesive 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 56 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 Electrode placement USA) RA On the right arm, avoiding thick muscle. LA RL LL In the same location that RA was placed, but on the left arm. On the right leg, lateral calf muscle In the same location that RL was placed, but on the left leg.

V1 V2 V3 V4

In the fourth intercostal space (between ribs 4 & 5) just to the right of the sternum (breastbone). In the fourth intercostal space (between ribs 4 & 5) just to the left of the sternum. Between leads V2 and 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)). 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.) 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.)

V5

V6

[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 limbsone 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 12lead 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 The interval between an R wave and the next R wave . Normal resting 0.6 to 1.2s interval heart rate is between 60 and 100 bpm During normal atrial depolarization, the main electrical vector is P wave directed from the SA node towards the AV node, and spreads from the 80ms right atrium to the left atrium. This turns into the P wave on the ECG. 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 PR electrical impulse takes to travel from the sinus node through the AV 120 to 200ms interval node and entering the ventricles. The PR interval is therefore a good estimate of AV node function. The PR segment connects the P wave and the QRS complex. This coincides with the electrical conduction from the AV node to the PR bundle of His to the bundle branches and then to the Purkinje Fibers. 50 to 120ms segment 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. The QRS complex reflects the rapid depolarization of the right and left QRS ventricles. They have a large muscle mass compared to the atria and so 80 to 120ms complex the QRS complex usually has a much larger amplitude than the P-wave. The point at which the QRS complex finishes and the ST segment J-point begins. Used to measure the degree of ST elevation or depression N/A present. The ST segment connects the QRS complex and the T wave. The ST ST segment represents the period when the ventricles are depolarized. It is 80 to 120ms segment isoelectric. 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 T wave is referred to as the absolute refractory period. The last half of 160ms the T wave is referred to as the relative refractory period (or vulnerable period). ST The ST interval is measured from the J point to the end of the T wave. 320ms interval The QT interval is measured from the beginning of the QRS complex to 300 to QT the end of the T wave. A prolonged QT interval is a risk factor for 430ms[citation interval ventricular tachyarrhythmias and sudden death. It varies with heart rate needed] and for clinical relevance requires a correction for this, giving the QTc. The U wave is hypothesized to be caused by the repolarization of the interventricular septum. They normally have a low amplitude, and even U wave 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] The J wave, elevated J-Point or Osborn Wave appears as a late delta J wave 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 Left axis deviation Right axis deviation 30 to Normal 90 30 to May indicate left anterior fascicular 90 block or Q waves from inferior MI. Normal Left axis deviation is considered normal in pregnant women and those with emphysema.

May indicate left posterior fascicular Right deviation is considered +90 to block, Q waves from high lateral MI, normal in children and is a +180 or a right ventricular strain pattern. standard effect of dextrocardia.

Extreme right +180 Is rare, and considered an 'electrical axis deviation to 90 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 Color on Category Leads Activity chart Leads II, Inferior Look at electrical activity from the vantage point of the inferior Yellow III and leads surface (diaphragmatic surface of heart). aVF Look at the electrical activity from the vantage point of the lateral wall of left ventricle.

Lateral leads

Green

I, aVL, V5 and V6

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 Anterior leads

Orange Blue

Look at electrical activity from the vantage point of the septal wall of the ventricles (interventricular septum). Look at electrical activity from the vantage point of the anterior V3 and V4 surface of the heart (sternocostal surface of heart). V1 and V2

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 Prolonged QT interval Flattened or inverted T waves Hypercalcemia, some drugs, certain genetic abnormalities. Hypocalcemia, some drugs, certain genetic abnormalities.

Coronary ischemia, hypokalemia, left ventricular hypertrophy, digoxin effect, some drugs. Possibly the first manifestation of acute myocardial infarction, where T Hyperacute T waves 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]