Blood type

Blood type (or blood group) is determined, in part, by the ABO blood group antigens present
on red blood cells.

A blood type (also called a blood group) is a classification of blood based on the presence or
absence of inherited antigenic substances on the surface of red blood cells (RBCs). These
antigens may be proteins, carbohydrates, glycoproteins, or glycolipids, depending on the
blood group system. Some of these antigens are also present on the surface of other types of
cells of various tissues. Several of these red blood cell surface antigens can stem from one
allele (or very closely linked genes) and collectively form a blood group system.[1] Blood
types are inherited and represent contributions from both parents. A total of 30 human blood
group systems are now recognized by the International Society of Blood Transfusion (ISBT).
[2]

Many pregnant women carry a fetus with a blood type different from their own, and the
mother can form antibodies against fetal RBCs. Sometimes these maternal antibodies are
IgG, a small immunoglobulin, which can cross the placenta and cause hemolysis of fetal
RBCs, which in turn can lead to hemolytic disease of the newborn, an illness of low fetal
blood counts that ranges from mild to severe.[3]

Blood group systems

A complete blood type would describe a full set of 30 substances on the surface of RBCs, and
an individual's blood type is one of the many possible combinations of blood-group antigens.
[2]
Across the 30 blood groups, over 600 different blood-group antigens have been found,[4]
but many of these are very rare, some being found mainly in certain ethnic groups.

Almost always, an individual has the same blood group for life, but very rarely an
individual's blood type changes through addition or suppression of an antigen in infection,
malignancy, or autoimmune disease.[5][6][7][8] Another more common cause in blood type
change is a bone marrow transplant. Bone-marrow transplants are performed for many
leukemias and lymphomas, among other diseases. If a person receives bone marrow from
someone who is a different ABO type (e.g., a type A patient receives a type O bone marrow),
the patient's blood type will eventually convert to the donor's type.

Some blood types are associated with inheritance of other diseases; for example, the Kell
antigen is sometimes associated with McLeod syndrome.[9] Certain blood types may affect
susceptibility to infections, an example being the resistance to specific malaria species seen in
individuals lacking the Duffy antigen.[10] The Duffy antigen, presumably as a result of natural
selection, is less common in ethnic groups from areas with a high incidence of malaria.[11]

ABO blood group system

ABO blood group system: diagram showing the carbohydrate chains that determine the ABO
blood group

The ABO system is the most important blood-group system in human-blood transfusion. The
associated anti-A and anti-B antibodies are usually Immunoglobulin M, abbreviated IgM,
antibodies. ABO IgM antibodies are produced in the first years of life by sensitization to
environmental substances such as food, bacteria, and viruses. The O in ABO is often called 0
(zero, or null) in other languages.[12]

Phenotype Genotype
A AA or AO
B BB or BO
AB AB
O OO

Rh blood group system

The Rh system is the second most significant blood-group system in human-blood transfusion
with currently 50 antigens. The most significant Rh antigen is the D antigen, because it is the
most likely to provoke an immune system response of the five main Rh antigens. It is
common for D-negative individuals not to have any anti-D IgG or IgM antibodies, because
anti-D antibodies are not usually produced by sensitization against environmental substances.
However, D-negative individuals can produce IgG anti-D antibodies following a sensitizing
event: possibly a fetomaternal transfusion of blood from a fetus in pregnancy or occasionally
a blood transfusion with D positive RBCs.[13] Rh disease can develop in these cases.[14] Rh
negative blood types are much less in proportion of Asian populations (0.3%) than they are in
White (15%).[15] In the table below, the presence or absence of the Rh antigens is signified by
the + or - sign, so that for example the A- group does not have any of the Rh antigens.

ABO and Rh distribution by country

Blood group B has its highest frequency in Northern India and neighboring Central Asia, and
its incidence diminishes both towards the west and the east, falling to single digit percentages
in Spain.[47][48] It is believed to have been entirely absent from Native American and
Australian Aboriginal populations prior to the arrival of Europeans in those areas.[48][49]

Blood group A is associated with high frequencies in Europe, especially in Scandinavia and
Central Europe, although its highest frequencies occur in some Australian Aborigine
populations and the Blackfoot Indians of Montana.[50][51]

Other blood group systems

The International Society of Blood Transfusion currently recognizes 30 blood-group systems

(including the ABO and Rh systems).[2] Thus, in addition to the ABO antigens and Rh
antigens, many other antigens are expressed on the RBC surface membrane. For example, an
individual can be AB, D positive, and at the same time M and N positive (MNS system), K
positive (Kell system), Lea or Leb negative (Lewis system), and so on, being positive or
negative for each blood group system antigen. Many of the blood group systems were named
after the patients in whom the corresponding antibodies were initially encountered.

Clinical significance
Transfusion medicine is a specialized branch of hematology that is concerned with the study
of blood groups, along with the work of a blood bank to provide a transfusion service for
blood and other blood products. Across the world, blood products must be prescribed by a
medical doctor (licensed physician or surgeon) in a similar way as medicines.

Main symptoms of acute hemolytic reaction due to blood type mismatch.[52][53]

Much of the routine work of a blood bank involves testing blood from both donors and
recipients to ensure that every individual recipient is given blood that is compatible and is as
safe as possible. If a unit of incompatible blood is transfused between a donor and recipient, a
severe acute hemolytic reaction with hemolysis (RBC destruction), renal failure and shock is
likely to occur, and death is a possibility. Antibodies can be highly active and can attack
RBCs and bind components of the complement system to cause massive hemolysis of the
transfused blood.

Patients should ideally receive their own blood or type-specific blood products to minimize
the chance of a transfusion reaction. Risks can be further reduced by cross-matching blood,
but this may be skipped when blood is required for an emergency. Cross-matching involves
mixing a sample of the recipient's serum with a sample of the donor's red blood cells and
checking if the mixture agglutinates, or forms clumps. If agglutination is not obvious by
direct vision, blood bank technicians usually check for agglutination with a microscope. If
agglutination occurs, that particular donor's blood cannot be transfused to that particular
recipient. In a blood bank it is vital that all blood specimens are correctly identified, so
labeling has been standardized using a barcode system known as ISBT 128.

The blood group may be included on identification tags or on tattoos worn by military
personnel, in case they should need an emergency blood transfusion. Frontline German
Waffen-SS had blood group tattoos during World War II.

Rare blood types can cause supply problems for blood banks and hospitals. For example
Duffy-negative blood occurs much more frequently in people of African origin,[54] and the
rarity of this blood type in the rest of the population can result in a shortage of Duffy-
negative blood for these patients. Similarly for RhD negative people, there is a risk associated
with travelling to parts of the world where supplies of RhD negative blood are rare,
particularly East Asia, where blood services may endeavor to encourage Westerners to donate
blood.[55]

Hemolytic disease of the newborn (HDN)

A pregnant woman can make IgG blood group antibodies if her fetus has a blood group
antigen that she does not have. This can happen if some of the fetus' blood cells pass into the
mother's blood circulation (e.g. a small fetomaternal hemorrhage at the time of childbirth or
obstetric intervention), or sometimes after a therapeutic blood transfusion. This can cause Rh
disease or other forms of hemolytic disease of the newborn (HDN) in the current pregnancy
and/or subsequent pregnancies. If a pregnant woman is known to have anti-D antibodies, the
Rh blood type of a fetus can be tested by analysis of fetal DNA in maternal plasma to assess
the risk to the fetus of Rh disease.[56] One of the major advances of twentieth century
medicine was to prevent this disease by stopping the formation of Anti-D antibodies by D
negative mothers with an injectable medication called Rho(D) immune globulin.[57][58]
Antibodies associated with some blood groups can cause severe HDN, others can only cause
mild HDN and others are not known to cause HDN.[3]

Blood products

To provide maximum benefit from each blood donation and to extend shelf-life, blood banks
fractionate some whole blood into several products. The most common of these products are
packed RBCs, plasma, platelets, cryoprecipitate, and fresh frozen plasma (FFP). FFP is
quick-frozen to retain the labile clotting factors V and VIII, which are usually administered to
patients who have a potentially fatal clotting problem caused by a condition such as advanced
liver disease, overdose of anticoagulant, or disseminated intravascular coagulation (DIC).

Units of packed red cells are made by removing as much of the plasma as possible from
whole blood units.

Clotting factors synthesized by modern recombinant methods are now in routine clinical use
for hemophilia, as the risks of infection transmission that occur with pooled blood products
are avoided.

Red blood cell compatibility

 Blood group AB individuals have both A and B antigens on the surface of their
RBCs, and their blood plasma does not contain any antibodies against either A or B
antigen. Therefore, an individual with type AB blood can receive blood from any
group (with AB being preferable), but can donate blood only to another type AB
individual.
 Blood group A individuals have the A antigen on the surface of their RBCs, and
blood serum containing IgM antibodies against the B antigen. Therefore, a group A
individual can receive blood only from individuals of groups A or O (with A being
preferable), and can donate blood to individuals with type A or AB.
 Blood group B individuals have the B antigen on the surface of their RBCs, and
blood serum containing IgM antibodies against the A antigen. Therefore, a group B
individual can receive blood only from individuals of groups B or O (with B being
preferable), and can donate blood to individuals with type B or AB.
 Blood group O (or blood group zero in some countries) individuals do not have either
A or B antigens on the surface of their RBCs, but their blood serum contains IgM
anti-A and anti-B antibodies against the A and B blood group antigens. Therefore, a
group O individual can receive blood only from a group O individual, but can donate
blood to individuals of any ABO blood group (i.e., A, B, O or AB). If anyone needs a
blood transfusion in an emergency, and if the time taken to process the recipient's
blood would cause a detrimental delay, O Negative blood can be issued.

RBC Compatibility chart

In addition to donating to the same blood group; type O blood donors can give to A, B and
AB; blood donors of types A and B can give to AB.
 Red blood cell compatibility table[59][60]
Donor[1]
Recipient[1]
O− O+ A− A+ B− B+ AB− AB+
O−
O+
A−
A+
B−
B+
AB−
AB+

Table note
1. Assumes absence of atypical antibodies that would cause an incompatibility between donor and recipient
blood, as is usual for blood selected by cross matching.

An Rh D-negative patient who does not have any anti-D antibodies (never being previously
sensitized to D-positive RBCs) can receive a transfusion of D-positive blood once, but this
would cause sensitization to the D antigen, and a female patient would become at risk for
hemolytic disease of the newborn. If a D-negative patient has developed anti-D antibodies, a
subsequent exposure to D-positive blood would lead to a potentially dangerous transfusion
reaction. Rh D-positive blood should never be given to D-negative women of child bearing
age or to patients with D antibodies, so blood banks must conserve Rh-negative blood for
these patients. In extreme circumstances, such as for a major bleed when stocks of D-negative
blood units are very low at the blood bank, D-positive blood might be given to D-negative
females above child-bearing age or to Rh-negative males, providing that they did not have
anti-D antibodies, to conserve D-negative blood stock in the blood bank. The converse is not
true; Rh D-positive patients do not react to D negative blood.

This same matching is done for other antigens of the Rh system as C, c, E and e and for other
blood group systems with a known risk for immunization such as the Kell system in
particular for females of child-bearing age or patients with known need for many
transfusions.

Plasma compatibility
Plasma compatibility chart
In addition to donating to the same blood group; plasma from type AB can be given to A, B
and O; plasma from types A, B and AB can be given to O.

Recipients can receive plasma of the same blood group, but otherwise the donor-recipient
compatibility for blood plasma is the converse of that of RBCs: plasma extracted from type
AB blood can be transfused to individuals of any blood group; individuals of blood group O
can receive plasma from any blood group; and type O plasma can be used only by type O
recipients.

Plasma compatibility table[60]

Donor[1]
Recipient
O A B AB
O
A
B
AB

Table note
1. Assumes absence of strong atypical antibodies in donor plasma

Rh D antibodies are uncommon, so generally neither D negative nor D positive blood contain
anti-D antibodies. If a potential donor is found to have anti-D antibodies or any strong
atypical blood group antibody by antibody screening in the blood bank, they would not be
accepted as a donor (or in some blood banks the blood would be drawn but the product would
need to be appropriately labeled); therefore, donor blood plasma issued by a blood bank can
be selected to be free of D antibodies and free of other atypical antibodies, and such donor
plasma issued from a blood bank would be suitable for a recipient who may be D positive or
D negative, as long as blood plasma and the recipient are ABO compatible.[citation needed]..

Universal donors and universal recipients

A hospital corpsman with the Blood Donor Team from Portsmouth Naval Hospital takes
samples of blood from a donor for testing

With regard to transfusions of packed red blood cells, individuals with type O Rh D negative
blood are often called universal donors, and those with type AB Rh D positive blood are
called universal recipients; however, these terms are only generally true with respect to
possible reactions of the recipient's anti-A and anti-B antibodies to transfused red blood cells,
and also possible sensitization to Rh D antigens. One exception is individuals with hh antigen
system (also known as the Bombay phenotype) who can only receive blood safely from other
hh donors, because they form antibodies against the H antigen present on all red blood cells.
[61][62]

Blood donors with particularly strong anti-A, anti-B or any atypical blood group antibody are
excluded from blood donation. The possible reactions of anti-A and anti-B antibodies present
in the transfused blood to the recipients RBCs need not be considered, because a relatively
small volume of plasma containing antibodies is transfused.
By way of example: considering the transfusion of O Rh D negative blood (universal donor
blood) into a recipient of blood group A Rh D positive, an immune reaction between the
recipient's anti-B antibodies and the transfused RBCs is not anticipated. However, the
relatively small amount of plasma in the transfused blood contains anti-A antibodies, which
could react with the A antigens on the surface of the recipients RBCs, but a significant
reaction is unlikely because of the dilution factors. Rh D sensitization is not anticipated.

Additionally, red blood cell surface antigens other than A, B and Rh D, might cause adverse
reactions and sensitization, if they can bind to the corresponding antibodies to generate an
immune response. Transfusions are further complicated because platelets and white blood
cells (WBCs) have their own systems of surface antigens, and sensitization to platelet or
WBC antigens can occur as a result of transfusion.

With regard to transfusions of plasma, this situation is reversed. Type O plasma, containing
both anti-A and anti-B antibodies, can only be given to O recipients. The antibodies will
attack the antigens on any other blood type. Conversely, AB plasma can be given to patients
of any ABO blood group due to not containing any anti-A or anti-B antibodies.

Blood group genotyping

In addition to the current practice of serologic testing of blood types, the progress in
molecular diagnostics allows the increasing use of blood group genotyping. In contrast to
serologic tests reporting a direct blood type phenotype, genotyping allows the prediction of a
phenotype based on the knowledge of the molecular basis of the currently known antigens.
This allows a more detailed determination of the blood type and therefore a better match for
transfusion, which can be crucial in particular for patients with needs for many transfusions
to prevent allo-immunization.[63][64]

History
The two most significant blood group systems were discovered by Karl Landsteiner during
early experiments with blood transfusion: the ABO group in 1901[65] and in co-operation with
Alexander S. Wiener the Rhesus group in 1937.[66] Development of the Coombs test in 1945,
[67]
the advent of transfusion medicine, and the understanding of hemolytic disease of the
newborn led to discovery of more blood groups, and now 30 human blood group systems are
recognized by the International Society of Blood Transfusion (ISBT),[2] and across the 30
blood groups, over 600 different blood group antigens have been found;[4] many of these are
very rare or are mainly found in certain ethnic groups. Blood types have been used in forensic
science and were formerly used to demonstrate impossibility of paternity (e.g., a type AB
man cannot be the father of a type O infant), but both of these uses are being replaced by
genetic fingerprinting, which provides greater certainty.[68]
 Electrocardiography
Electrocardiography
Intervention

Image showing a patient connected to the 10

electrodes necessary for a 12-lead ECG

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.
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).

History
Alexander Muirhead is reported to have attached wires to a feverish patient's wrist to obtain a
record of the patient's heartbeat while studying for his Doctor of Science (in electricity) in
1872 at St Bartholomew's Hospital.[5] This activity was directly recorded and visualized using
a Lippmann capillary electrometer by the British physiologist John Burdon Sanderson.[6] The
first to systematically approach the heart from an electrical point-of-view was Augustus
Waller, working in St Mary's Hospital in Paddington, London.[7] His electrocardiograph
machine consisted of a Lippmann capillary electrometer fixed to a projector. The trace from
the heartbeat was projected onto a photographic plate which was itself fixed to a toy train.
This allowed a heartbeat to be recorded in real time. In 1911 he still saw little clinical
application for his work.
Einthoven's ECG device

An initial breakthrough came when Willem Einthoven, working in Leiden, Netherlands, used
the string galvanometer that he invented in 1903.[8] This device was much more sensitive than
both the capillary electrometer that Waller used and the string galvanometer that had been
invented separately in 1897 by the French engineer Clément Ader.[9] Rather than using
today's self-adhesive electrodes Einthoven's subjects would immerse each of their limbs into
containers of salt solutions from which the EKG was recorded.

Einthoven assigned the letters P, Q, R, S and T to the various deflections,Naming of the

Waves in the ECG 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]

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.

Layout

By definition, a 12-lead ECG will show a short segment of the recording of each of the 12-
leads. This is often arranged in a grid of 4 columns by three rows, the first columns being the
limb leads (I,II and III), the second column the augmented limb leads (aVR, aVL and aVF)
and the last two columns being the chest leads (V1-V6). It is usually possible to change this
layout so it is vital to check the labels to see which lead is represented. Each column will
usually record the same moment in time for the three leads and then the recording will switch
to the next column which will record the heart beats after that point. It is possible for the
heart rhythm to change between the columns of leads.

Each of these segments is short, perhaps 1-3 heart beats only, depending on the heart rate and
it can be difficult to analyse any heart rhythm that shows changes between heart beats. To
help with the analysis it is common to print one or two "rhythm strips" as well. This will
usually be lead II (which shows the electrical signal from the atrium, the P-wave, well) and
shows the rhythm for the whole time the ECG was recorded (usually 5–6 seconds). Some
ECG machines will print a second lead II along the very bottom of the paper in addition to
the output described above. This printing of Lead II is continuous from start to finish of the
process.

The term "rhythm strip" may also refer to the whole printout from a continuous monitoring
system which may show only one lead and is either initiated by a clinician or in response to
an alarm or event.

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.

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 In the same location that RA was placed, but on the left arm.
RL On the right leg, lateral calf muscle
LL In the same location that RL was placed, but on the left leg.
In the fourth intercostal space (between ribs 4 & 5) just to the right of the
V1
sternum (breastbone).
In the fourth intercostal space (between ribs 4 & 5) just to the left of the
V2
sternum.
V3 Between leads V2 and V4.
In the fifth intercostal space (between ribs 5 & 6) in the mid-clavicular line
V4 (the imaginary line that extends down from the midpoint of the clavicle
(collarbone)).
V5 Horizontally even with V4, but in the anterior axillary line. (The anterior
 axillary line is the imaginary line that runs down from the point midway
between the middle of the clavicle and the lateral end of the clavicle; the
lateral end of the collarbone is the end closer to the arm.)
Horizontally even with V4 and V5 in the midaxillary line. (The midaxillary
V6 line is the imaginary line that extends down from the middle of the patient's
armpit.)

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.

Limb leads

In both the 5- and 12-lead configuration, leads I, II and III are called limb leads. The
electrodes that form these signals are located on the limbs—one on each arm and one on the
left leg.[16][17][18] The limb leads form the points of what is known as Einthoven's triangle.[19]

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

I = LA − RA.
 Lead II is the voltage between the (positive) left leg (LL) electrode and the right arm
(RA) electrode:

II = LL − RA.
 Lead III is the voltage between the (positive) left leg (LL) electrode and the left arm
(LA) electrode:

III = LL − LA.

Simplified electrocardiograph sensors designed for teaching purposes at e.g. high school level
are generally limited to three arm electrodes serving similar purposes.[20]

Unipolar vs. bipolar leads

There are two types of leads: unipolar and bipolar. Bipolar leads have one positive and one
negative pole.[21] In a 12-lead ECG, the limb leads (I, II and III) are bipolar leads. Unipolar
leads also have two poles, as a voltage is measured; however, the negative pole is a
composite pole (Wilson's central terminal, or WCT) made up of signals from lots of other
electrodes.[22] In a 12-lead ECG, all leads besides the limb leads are unipolar (aVR, aVL,
aVF, V1, V2, V3, V4, V5, and V6).

Wilson's central terminal VW is produced by connecting the electrodes, RA; LA; and LL,
together, via a simple resistive network, to give an average potential across the body, which
approximates the potential at infinity (i.e. zero):
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 V 1,
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:
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.

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
0.6 to 1.2s
interval resting heart rate is between 60 and 100 bpm
During normal atrial depolarization, the main electrical vector is
directed from the SA node towards the AV node, and spreads from
P wave 80ms
the 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.
QRS The QRS complex reflects the rapid depolarization of the right and 80 to 120ms
complex left ventricles. They have a large muscle mass compared to the atria
and so the QRS complex usually has a much larger amplitude than
 the P-wave.
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 80 to 120ms
segment
is isoelectric.
The T wave represents the repolarization (or recovery) of the
ventricles. The interval from the beginning of the QRS complex to
T wave the apex of the T wave is referred to as the absolute refractory 160ms
period. The last half of 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
320ms
interval wave.
The QT interval is measured from the beginning of the QRS
complex to the end of the T wave. A prolonged QT interval is a risk 300 to
QT
factor for ventricular tachyarrhythmias and sudden death. It varies 430ms[citation
interval needed]
with heart rate 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 more often completely absent. They always follow the T wave
U 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]

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.

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.
 −30° to
Normal Normal Normal
90°
Left axis deviation is considered
Left axis −30° to May indicate left anterior fascicular
normal in pregnant women and
deviation −90° block or Q waves from inferior MI.
those with emphysema.
May indicate left posterior fascicular
Right deviation is considered
Right axis +90° to block, Q waves from high lateral
normal in children and is a
deviation +180° MI, or a right ventricular strain
standard effect of dextrocardia.
pattern.
Extreme right +180° to Is rare, and considered an 'electrical
axis deviation −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.

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
Yellow III and
leads inferior surface (diaphragmatic surface of heart).
aVF
Look at the electrical activity from the vantage point of the
lateral wall of left ventricle.
 The positive electrode for leads I and aVL should be
located distally on the left arm and because of which,
Lateral I, aVL, V5 leads I and aVL are sometimes referred to as the high
Green
leads and V6 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 Look at electrical activity from the vantage point of the
Orange V1 and V2
leads septal wall of the ventricles (interventricular septum).
Anterior Look at electrical activity from the vantage point of the
Blue V3 and V4
leads anterior surface of the heart (sternocostal surface of heart).

In addition, any two precordial leads that are next to one another are considered to be
contiguous. For example, even though V4 is an anterior lead and V5 is a lateral lead, they are
contiguous because they are next to one another.

Wiggers diagram, showing a normal ECG curve synchronized with other major events during
the cardiac cycle.

Lead aVR offers no specific view of the left ventricle. Rather, it views the inside of the
endocardial wall to the surface of the right atrium, from its perspective on the right shoulder.

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 pass band is narrower.[29]

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]

Some pathological entities which can be seen on the ECG

Shortened QT
Hypercalcemia, some drugs, certain genetic abnormalities.
interval
Prolonged QT
Hypocalcemia, some drugs, certain genetic abnormalities.
interval
Flattened or Coronary ischemia, hypokalemia, left ventricular hypertrophy, digoxin
inverted T waves 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.

Electrocardiogram heterogeneity

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]
Artificial respiration
Artificial respiration is the act of assisting or stimulating respiration, a metabolic process
referring to the overall exchange of gases in the body by pulmonary ventilation, external
respiration, and internal respiration.[1] Assistance takes many forms, but generally entails
providing air for a person who is not breathing or is not making sufficient respiratory effort
on their own[2] (although it must be used on a patient with a beating heart or as part of
cardiopulmonary resuscitation to achieve the internal respiration).

Pulmonary ventilation (and hence external respiration) is achieved through manual

insufflation of the lungs either by the rescuer blowing into the patient's lungs, or by using a
mechanical device to do so. This method of insufflation has been proved more effective than
methods which involve mechanical manipulation of the patient's chest or arms, such as the
Silvester method.[3] It is also known as Expired Air Resuscitation (EAR), Expired Air
Ventilation (EAV), mouth-to-mouth resuscitation, rescue breathing or colloquially the
kiss of life.

Artificial respiration is a part of most protocols for performing cardiopulmonary resuscitation

(CPR)[4][5] making it an essential skill for first aid. In some situations, artificial respiration is
also performed separately, for instance in near-drowning and opiate overdoses. The
performance of artificial respiration in its own is now limited in most protocols to health
professionals, whereas lay first aiders are advised to undertake full CPR in any case where
the patient is not breathing sufficiently.

Mechanical ventilation involves the use of a mechanical ventilator to move air in and out of
the lungs when an individual is unable to breathe on his or her own, for example during
surgery with general anesthesia or when an individual is in a coma.

Insufflations

Mouth-to-mouth insufflation

Insufflation, also known as 'rescue breaths' or 'ventilations', is the act of mechanically

forcing air into a patient's respiratory system. This can be achieved via a number of methods,
which will depend on the situation and equipment available. All methods require good airway
management to perform, which ensures that the method is effective. These methods include:

 Mouth to mouth - This involves the rescuer making a seal between their mouth and
the patient's mouth and 'blowing', to pass air into the patient's body
  Mouth to nose - In some instances, the rescuer may need or wish to form a seal with
the patient's nose. Typical reasons for this include maxillofacial injuries, performing
the procedure in water or the remains of vomit in the mouth
 Mouth to mouth and nose - Used on infants (usually up to around 1 year old), as this
forms the most effective seal
 Mouth to mask – Most organisations recommend the use of some sort of barrier
between rescuer and patient to reduce cross infection risk. One popular type is the
'pocket mask'. This may be able to provide higher tidal volumes than a Bag Valve
Mask.[6]
 Bag valve mask (BVM) - This is a simple device manually operated by the rescuer,
which involves squeezing a bag to expel air into the patient.
 Mechanical resuscitator - An electric unit designed to breathe for the patient

Adjuncts to insufflation

A CPR pocket mask, with carrying case

Most training organisations recommend that in any of the methods involving mouth to
patient, that a protective barrier is used, to minimise the possibility of cross infection (in
either direction).[7]

Barriers available include pocket masks and keyring-sized face shields. These barriers are an
example of Personal Protective Equipment to guard the face against splashing, spraying or
splattering of blood or other potentially infectious materials.

These barriers should provide a one-way filter valve which lets the air from the rescuer
deliver to the patient while any substances from the patient (e.g. vomit, blood) cannot reach
the rescuer. Many adjuncts are single use, though if they are multi use, after use of the
adjunct, the mask must be cleaned and autoclaved and the filter replaced.

The CPR mask is the preferred method of ventilating a patient when only one rescuer is
available. Many feature 18mm inlets to support supplemental oxygen, which increases the
oxygen being delivered from the approximate 17% available in the expired air of the rescuer
to around 40-50%.

Tracheal intubation is often used for short term mechanical ventilation. A tube is inserted
through the nose (nasotracheal intubation) or mouth (orotracheal intubation) and advanced
into the trachea. In most cases tubes with inflatable cuffs are used for protection against
leakage and aspiration. Intubation with a cuffed tube is thought to provide the best protection
against aspiration. Tracheal tubes inevitably cause pain and coughing. Therefore, unless a
patient is unconscious or anesthetized for other reasons, sedative drugs are usually given to
provide tolerance of the tube. Other disadvantages of tracheal intubation include damage to
the mucosal lining of the nasopharynx or oropharynx and subglottic stenosis.

In an emergency a Cricothyrotomy can be used by health care professionals, where an airway

is inserted through a surgical opening in the cricothyroid membrane. This is similar to a
tracheostomy but a cricothyrotomy is reserved for emergency access. This is usually only
used when there is a complete blockage of the pharynx or there is massive maxillofacial
injury, preventing other adjunts being used.[8]

Efficiency of mouth to patient insufflation

Normal atmospheric air contains approximately 21% oxygen when created in. After gaseous
exchange has taken place in the lungs, with waste products (notably carbon dioxide) moved
from the bloodstream to the lungs, the air being exhaled by humans normally contains around
17% oxygen. This means that the human body utilises only around 19% of the oxygen
inhaled, leaving over 80% of the oxygen available in the exhalatory breath.[9]

This means that there is more than enough residual oxygen to be used in the lungs of the
patient, which then crosses the cell membrane to form oxyhemoglobin.

Oxygen

Typical view of resuscitation in progress with a BVM in use

The efficiency of artificial respiration can be greatly increased by the simultaneous use of
oxygen therapy. The amount of oxygen available to the patient in mouth to mouth is around
16%. If this is done through a pocket mask with an oxygen flow, this increases to 40%
oxygen. If a Bag Valve Mask or mechanical respirator is used with an oxygen supply, this
rises to 99% oxygen. The greater the oxygen concentration, the more efficient the gaseous
exchange will be in the lungs.