Equipment*Packet:*Electrocardiograph*UMDNS*#:.11407..Date*of*Creation:.October.14,.2015.Creator:.Complied.by.Cassandra.Stanco.for*Engineering.World.Health.(EWH)***Equipment*Packet*Contents:*This.packet.contains.information.about.the.operation,.maintenance,.and.repair.of.electrocardiograms...Part*I:*External*From*the*Packet:** 1. An*Introduction*to*Electrocardiographs*(ECG):*.PowerPoint.*Part*II:*Included*in*this*Packet:** 1. Operation*and*Use:*a. Brief.Overview:.Electrocardiographs,.(ECG).(p..3).b. Introduction.to.the.Heart.(p..4O15).c. Introduction.to.Laboratory.Electrocardiography.(p.16O23).d. Operation.and.Use.of.Electrocardiograms.(p..24O27).2. Diagrams*and*Schematics:*a. Figure.1:.ECG.Quick.Reference.Card.(p..29O30).b. Figure.2:.The.Heart.and.Electrocardiogram.Readings.(p..31)*c. Figure.3:.Instrumentation.Amplifier.(p..32)*d. Figure.4:.Block.Diagram.of.a.Electrocardiograph.Machine.(p..33)*3. Preventative*Maintenance*and*Safety:*a. Electrocardiograph.Preventative.Maintenance.(p..35O37)*b. Electrocardiograph.Calibration.(p..38O40)*4. Troubleshooting*and*Repair:**a. Electrocardiogram.(ECG).Troubleshooting.Flowchart.(p..42O45)*b. Electrocardiogram.(ECG).Troubleshooting.Table.(p..46O47)*5. Resources*for*More*Information:*a. Resources.for.More.Information.(p..49)*b. Bibliography.(p..50O51)** .** *
1. Operation*and*Use*of*Electrocardiographs*(ECG)****Featured*in*this*Section:****.ECGpedia.org,.“Basics.”.Wikipedia..Retrieved.from:.http://en.ecgpedia.org/wiki/Basics.*Malkin,.Robert..Medical(Instrumentation(in(the(Developing(World..Engineering.World.Health,.2006...*Wikipedia..“Heart.”.Wikipedia,.p..1O13..Retrieved.from:.https://en.wikipedia.org/wiki/Heart... WHO..“Electrocardiograph,.ECG.”.From.the.publication:.Core(Medical(Equipment..Geneva,.Switzerland,.2011... **.* ** *
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Reproduced with Permission from ECRI Institute’s Healthcare Product Comparison System.
© Copyright GMDN Agency 2011. GMDN codes and device names are reproduced with permission from the GMDN Agency.
Health problem addressed
Electrocardiographs detect the electrical signals associated
with cardiac activity and produce an ECG, a graphic record of
the voltage versus time. They are used to diagnose and assist in
treating some types of heart disease and arrhythmias, determine
a patient’s response to drug therapy, and reveal trends or
changes in heart function. Multichannel electrocardiographs
record signals from two or more leads simultaneously and
are frequently used in place of single-channel units. Some
electrocardiographs can perform automatic measurement and
interpretation of the ECG as a selectable or optional feature.
ECG units consist of the ECG unit, electrodes, and cables. The 12-lead
system includes three different types of leads: bipolar, augmented
or unipolar, and precordial. Each of the 12 standard leads presents
a different perspective of the heart’s electrical activity; producing
ECG waveforms in which the P waves, QRS complex, and T
waves vary in amplitude and polarity. Single-channel ECGs record
the electric signals from only one lead confi guration at a time,
although they may receive electric signals from as many as 12 leads.
Noninterpretive multichannel electrocardiographs only record the
electric signals from the electrodes (leads) and do not use any
internal procedure for their interpretation. Interpretive multichannel
electrocardiographs acquire and analyze the electrical signals.
Principles of operation
Electrocardiographs record small voltages of about one millivolt
(mV) that appear on the skin as a result of cardiac activity. The
voltage differences between electrodes are measured; these
differences directly correspond to the heart’s electrical activity.
Each of the 12 standard leads presents a different perspective of the
heart’s electrical activity; producing ECG waveforms in which the P
waves, QRS complex, and T waves vary in amplitude and polarity.
Other lead confi gurations include those of the Frank system and
Cabrera leads. The Frank confi guration measures voltages from
electrodes applied to seven locations—the forehead or neck, the
center spine, the midsternum, the left and right midaxillary lines,
a position halfway between the midsternum and left midaxillary
electrodes, and the left leg.
After the electrodes are attached to the patient, the user selects
automatic or manual lead switching, signal sensitivity, frequency-
response range, and chart speed. In some units, the operator can
choose the lead groupings, their sequence, and the recording
duration for each group. In standard 12-lead tracings, signals from
each group of leads (i.e., bipolar, augmented, precordial) can be
recorded for 2.5 seconds. For a rhythm strip, one lead (usually lead
II) is recorded for a full 12 seconds.
Because electrocardiographs have electrical
safety standards that are well established and
adhered to by all major manufacturers, few
problems are associated with their use. Of
these, the most common is artifact or noise
(e.g., broken electrode wires, poor electrode
cleaning or improper application, poor skin
preparation, patient movement, baseline
drift, and interference). Incorrect placement
of ECG leads can cause an abnormality to
be overlooked. Chest wall thickness can also
affect diagnostic accuracy.
Use and maintenance
User(s): Physicians, nurses, other medical staff
Maintenance: Biomedical or clinical engineer/
technician, medical staff, manufacturer/
Training: Initial training by manufacturer,
operator’s manuals, user’s guide
Environment of use
Settings of use: Hospital (all areas), family
medicine practices and other medical offi ces
Requirements: Uninterruptible power source,
battery backup, appropriate electrodes
Product specifi cations
Approx. dimensions (mm): 120 x 400 x 350
Approx. weight (kg): 6
Consumables: Batteries, cables, electrodes
Price range (USD): 975 - 6,000
Typical product life time (years): 10
Shelf life (consumables): 1-2 years for
Types and variations
Portable, cart, desktop, tabletop
Electrocardiographs, Multichannel, Interpretive
Electrocardiographs, Multichannel, Interpretive,
Electrocardiographs, Multichannel, Noninterpretive
Electrocardiographs, Multichannel, Noninterpretive,
Interpretive multichannel electrocardiograph
Other common names:
Computer-assisted electrocardiographs; interpretive ECG machines; interpretive electrocardiographs; automated
electrocardiographs; EKG machines; Electrocardiograph multichannel;
The heart is a muscular organ found in all animals with a
circulatory system (including all vertebrates), that is responsible
for pumping blood throughout the blood vessels by repeated,
rhythmic contractions. The term cardiac (as in cardiology) means
"related to the heart" and comes from the Greek καρδιά, kardia,
The vertebrate heart is composed of cardiac muscle, which is an
involuntary striated muscle tissue found only within this organ.
The average human heart, beating at 72 beats per minute, will beat
approximately 2.5 billion times during an average 66 year lifespan,
and weighs approximately 250 to 300 grams (9 to 11 oz) in
females and 300 to 350 grams (11 to 12 oz) in males.
In invertebrates that possess a circulatory system, the heart is typically a tube or small sac and pumps fluid that
contains water and nutrients such as proteins, fats, and sugars. In insects, the "heart" is often called the dorsal tube
and insect "blood" is almost always not oxygenated since they usually respirate (breathe) directly from their body
surfaces (internal and external) to air. However, the hearts of some other arthropods (including spiders and
crustaceans such as crabs and shrimp) and some other animals pump hemolymph, which contains the copper-based
protein hemocyanin as an oxygen transporter similar to the iron-based hemoglobin in red blood cells found in
The mammalian heart is derived from embryonic mesoderm germ-layer cells that differentiate after gastrulation into
mesothelium, endothelium, and myocardium. Mesothelial pericardium forms the outer lining of the heart. The inner
lining of the heart, lymphatic and blood vessels, develop from endothelium. Myocardium develops into heart
From splanchnopleuric mesoderm tissue, the cardiogenic plate develops cranially and laterally to the neural plate. In
the cardiogenic plate, two separate angiogenic cell clusters form on either side of the embryo. Each cell cluster
coalesces to form an endocardial tube continuous with a dorsal aorta and a vitteloumbilical vein. As embryonic
tissue continues to fold, the two endocardial tubes are pushed into the thoracic cavity, begin to fuse together, and
complete the fusing process at approximately 21 days.
At 21 days after conception, the human heart begins beating at 70 to
80 beats per minute and accelerates linearly for the first month of
The human embryonic heart begins beating at around
21 days after conception, or five weeks after the last
normal menstrual period (LMP). The first day of the
LMP is normally used to date the start of the gestation
(pregnancy). It is unknown how blood in the human
embryo circulates for the first 21 days in the absence of
a functioning heart. The human heart begins beating at
a rate near the mother’s, about 75-80 beats per minute
The embryonic heart rate (EHR) then accelerates
approximately 100 BPM during the first month of
beating, peaking at 165-185 BPM during the early 7th
week, (early 9th week after the LMP). This acceleration
is approximately 3.3 BPM per day, or about 10 BPM
every three days, which is an increase of 100 BPM in
the first month. After 9.1 weeks after the LMP, it decelerates to about 152 BPM (+/-25 BPM) during the 15th
week post LMP. After the 15th week, the deceleration slows to an average rate of about 145 (+/-25 BPM) BPM, at
term. The regression formula, which describes this acceleration before the embryo reaches 25 mm in crown-rump
length, or 9.2 LMP weeks, is: Age in days = EHR(0.3)+6. There is no difference in female and male heart rates
The structure of the heart varies among the different branches of the animal kingdom. (See Circulatory system.)
Cephalopods have two "gill hearts" and one "systemic heart". In vertebrates, the heart lies in the anterior part of the
body cavity, dorsal to the gut. It is always surrounded by a pericardium, which is usually a distinct structure, but may
be continuous with the peritoneum in jawless and cartilaginous fish. Hagfishes, uniquely among vertebrates, also
possess a second heart-like structure in the tail.
Structure diagram of the human heart. Blue components indicate de-oxygenated blood
pathways and red components indicate oxygenated pathways.
The heart is enclosed in a
double-walled sac called the
pericardium. The superficial part of
this sac is called the fibrous
pericardium. This sac protects the
heart, anchors its surrounding
structures, and prevents overfilling of
the heart with blood. It is located
anterior to the vertebral column and
posterior to the sternum. The size of
the heart is about the size of a fist and
has a mass of between 250 grams and
350 grams. The heart is composed of
three layers, all of which are rich with
blood vessels. The superficial layer,
called the visceral layer, the middle
layer, called the myocardium, and the
third layer which is called the
endocardium. The heart has four
chambers, two superior atria and two inferior ventricles. The atria are the receiving chambers and the ventricles are
the discharging chambers. The pathway of blood through the heart consists of a pulmonary circuit and a systemic
circuit. Blood flows through the heart in one direction, from the atrias to the ventricles, and out of the great arteries,
or the aorta for example. This is done by four valves which are the tricuspid atrioventricular valve, the mitral
atrioventicular valve, the aortic semilunar valve, and the pulmonary semilunar valve.
Primitive fish have a four-chambered heart; however, the chambers are arranged sequentially so that this primitive
heart is quite unlike the four-chambered hearts of mammals and birds. The first chamber is the sinus venosus, which
collects de-oxygenated blood, from the body, through the hepatic and cardinal veins. From here, blood flows into the
atrium and then to the powerful muscular ventricle where the main pumping action takes place. The fourth and final
chamber is the conus arteriosus which contains several valves and sends blood to the ventral aorta. The ventral aorta
delivers blood to the gills where it is oxygenated and flows, through the dorsal aorta, into the rest of the body. (In
tetrapods, the ventral aorta has divided in two; one half forms the ascending aorta, while the other forms the
In the adult fish, the four chambers are not arranged in a straight row but, instead, form an S-shape with the latter
two chambers lying above the former two. This relatively simpler pattern is found in cartilaginous fish and in the
more primitive ray-finned fish. In teleosts, the conus arteriosus is very small and can more accurately be described as
part of the aorta rather than of the heart proper. The conus arteriosus is not present in any amniotes which
presumably having been absorbed into the ventricles over the course of evolution. Similarly, while the sinus venosus
is present as a vestigial structure in some reptiles and birds, it is otherwise absorbed into the right atrium and is no
In double circulatory systems
In amphibians and most reptiles, a double circulatory system is used but the heart is not completely separated into
two pumps. The development of the double system is necessitated by the presence of lungs which deliver
oxygenated blood directly to the heart.
In living amphibians, the atrium is divided into two separate chambers by the presence of a muscular septum even
though there is only a single ventricle. The sinus venosus, which remains large in amphibians but connects only to
the right atrium, receives blood from the vena cavae, with the pulmonary vein by-passing it entirely to enter the left
In the heart of lungfish, the septum extends part-way into the ventricle. This allows for some degree of separation
between the de-oxygenated bloodstream destined for the lungs and the oxygenated stream that is delivered to the rest
of the body. The absence of such a division in living amphibian species may be at least partly due to the amount of
respiration that occurs through the skin in such species; thus, the blood returned to the heart through the vena cavae
is, in fact, already partially oxygenated. As a result, there may be less need for a finer division between the two
bloodstreams than in lungfish or other tetrapods. Nonetheless, in at least some species of amphibian, the spongy
nature of the ventricle seems to maintain more of a separation between the bloodstreams than appears the case at first
glance. Furthermore, the conus arteriosus has lost its original valves and contains a spiral valve, instead, that divides
it into two parallel parts, thus helping to keep the two bloodstreams separate.
The heart of most reptiles (except for crocodilians; see below) has a similar structure to that of lungfish but, here, the
septum is generally much larger. This divides the ventricle into two halves but, because the septum does not reach
the whole length of the heart, there is a considerable gap near the openings to the pulmonary artery and the aorta. In
practice, however, in the majority of reptilian species, there appears to be little, if any, mixing between the
bloodstreams, so the aorta receives, essentially, only oxygenated blood.
The fully-divided heart
Human heart removed from a 64-year-old male.
Archosaurs, (crocodilians, birds), and mammals show complete
separation of the heart into two pumps for a total of four heart
chambers; it is thought that the four-chambered heart of archosaurs
evolved independently from that of mammals. In crocodilians, there
is a small opening, the foramen of Panizza, at the base of the arterial
trunks and there is some degree of mixing between the blood in each
side of the heart; thus, only in birds and mammals are the two streams
of blood - those to the pulmonary and systemic circulations - kept
entirely separate by a physical barrier.
In the human body, the heart is usually situated in the middle of the
thorax with the largest part of the heart slightly offset to the left,
although sometimes it is on the right (see dextrocardia), underneath
the sternum. The heart is usually felt to be on the left side because the
left heart (left ventricle) is stronger (it pumps to all body parts). The
left lung is smaller than the right lung because the heart occupies
more of the left hemithorax. The heart is fed by the coronary
circulation and is enclosed by a sac known as the pericardium; it is
also surrounded by the lungs. The pericardium comprises two parts: the fibrous pericardium, made of dense
Surface anatomy of the human heart. The heart is
-A point 9 cm to the left of the midsternal line (apex of
-The seventh right sternocostal articulation
-The upper border of the third right costal cartilage
1 cm from the right sternal line
-The lower border of the second left costal cartilage
2.5 cm from the left lateral sternal line.
fibrous connective tissue, and a double membrane structure
(parietal and visceral pericardium) containing a serous fluid to
reduce friction during heart contractions. The heart is located in
the mediastinum, which is the central sub-division of the thoracic
cavity. The mediastinum also contains other structures, such as the
esophagus and trachea, and is flanked on either side by the right
and left pulmonary cavities; these cavities house the lungs.
The apex is the blunt point situated in an inferior (pointing down
and left) direction. A stethoscope can be placed directly over the
apex so that the beats can be counted. It is located posterior to the
5th intercostal space just medial of the left mid-clavicular line. In
normal adults, the mass of the heart is 250-350 g (9-12 oz), or
about twice the size of a clenched fist (it is about the size of a
clenched fist in children), but an extremely diseased heart can be
up to 1000 g (2 lb) in mass due to hypertrophy. It consists of four
chambers, the two upper atria and the two lower ventricles.
Blood flow diagram of the human heart. Blue components indicate
de-oxygenated blood pathways and red components indicate
Image showing the conduction system of the heart
In mammals, the function of the right
side of the heart (see right heart) is to
collect de-oxygenated blood, in the
right atrium, from the body (via
superior and inferior vena cavae) and
pump it, via the right ventricle, into the
lungs (pulmonary circulation) so that
carbon dioxide can be dropped off and
oxygen picked up (gas exchange). This
happens through the passive process of
diffusion. The left side (see left heart)
collects oxygenated blood from the
lungs into the left atrium. From the left
atrium the blood moves to the left
ventricle which pumps it out to the
body (via the aorta). On both sides, the
lower ventricles are thicker and
stronger than the upper atria. The
muscle wall surrounding the left
ventricle is thicker than the wall
surrounding the right ventricle due to
the higher force needed to pump the
blood through the systemic circulation.
Starting in the right atrium, the blood
flows through the tricuspid valve to the
right ventricle. Here, it is pumped out
the pulmonary semilunar valve and
travels through the pulmonary artery to
the lungs. From there, oxygenated
blood flows back through the
pulmonary vein to the left atrium. It
then travels through the mitral valve to
the left ventricle, from where it is
pumped through the aortic semilunar
valve to the aorta. The aorta forks and
the blood is divided between major arteries which supply the upper and lower body. The blood travels in the arteries
to the smaller arterioles and then, finally, to the tiny capillaries which feed each cell. The (relatively) deoxygenated
blood then travels to the venules, which coalesce into veins, then to the inferior and superior venae cavae and finally
back to the right atrium where the process began.
The heart is effectively a syncytium, a meshwork of cardiac muscle cells interconnected by contiguous cytoplasmic
bridges. This relates to electrical stimulation of one cell spreading to neighboring cells.
Some cardiac cells are self-excitable, contracting without any signal from the nervous system, even if removed from
the heart and placed in culture. Each of these cells have their own intrinsic contraction rhythm. A region of the
human heart called the sinoatrial node, or pacemaker, sets the rate and timing at which all cardiac muscle cells
contract. The SA node generates electrical impulses, much like those produced by nerve cells. Because cardiac
muscle cells are electrically coupled by inter-calated disks between adjacent cells, impulses from the SA node spread
rapidly through the walls of the artria, causing both artria to contract in unison. The impulses also pass to another
region of specialized cardiac muscle tissue, a relay point called the atrioventricular node, located in the wall
between the right artrium and the right ventricle. Here, the impulses are delayed for about 0.1s before spreading to
the walls of the ventricle. The delay ensures that the artria empty completely before the ventricles contract.
Specialized muscle fibers called Purkinje fibers then conduct the signals to the apex of the heart along and
throughout the ventricular walls. The Purkinje fibres form conducting pathways called bundle branches. This entire
cycle, a single heart beat, lasts about 0.8 seconds. The impulses generated during the heart cycle produce electrical
currents, which are conducted through body fluids to the skin, where they can be detected by electrodes and recorded
as an electrocardiogram (ECG or EKG). The events related to the flow or blood pressure that occurs from the
beginning of one heartbeat to the beginning of the next can be referred to a cardiac cycle.
The SA node is found in all amniotes but not in more primitive vertebrates. In these animals, the muscles of the heart
are relatively continuous and the sinus venosus coordinates the beat which passes in a wave through the remaining
chambers. Indeed, since the sinus venosus is incorporated into the right atrium in amniotes, it is likely homologous
with the SA node. In teleosts, with their vestigial sinus venosus, the main centre of coordination is, instead, in the
atrium. The rate of heartbeat varies enormously between different species, ranging from around 20 beats per minute
in codfish to around 600 in hummingbirds.
Cardiac arrest is the sudden cessation of normal heart rhythm which can include a number of pathologies such as
tachycardia, an extremely rapid heart beat which prevents the heart from effectively pumping blood, fibrillation,
which is an irregular and ineffective heart rhythm, and asystole, which is the cessation of heart rhythm entirely.
Cardiac tamponade is a condition in which the fibrous sac surrounding the heart fills with excess fluid or blood,
suppressing the heart's ability to beat properly. Tamponade is treated by pericardiocentesis, the gentle insertion of the
needle of a syringe into the pericardial sac (avoiding the heart itself) on an angle, usually from just below the
sternum, and gently withdrawing the tamponading fluids.
History of discoveries
A preserved human heart with a visible gunshot wound
The valves of the heart were discovered by a physician of
the Hippocratean school around the 4th century BC.
However, their function was not properly understood
then. Because blood pools in the veins after death, arteries
look empty. Ancient anatomists assumed they were filled
with air and that they were for transport of air.
Philosophers distinguished veins from arteries but
thought that the pulse was a property of arteries
themselves. Erasistratos observed the arteries that were
cut during life bleed. He described the fact to the
phenomenon that air escaping from an artery is replaced
with blood which entered by very small vessels between
veins and arteries. Thus he apparently postulated
capillaries but with reversed flow of blood.
The 2nd century AD, Greek physician Galenos (Galen)
knew that blood vessels carried blood and identified
venous (dark red) and arterial (brighter and thinner)
blood, each with distinct and separate functions. Growth
and energy were derived from venous blood created in the
liver from chyle, while arterial blood gave vitality by
containing pneuma (air) and originated in the heart. Blood flowed from both creating organs to all parts of the body
where it was consumed and there was no return of blood to the heart or liver. The heart did not pump blood around,
the heart's motion sucked blood in during diastole and the blood moved by the pulsation of the arteries themselves.
Galen believed that the arterial blood was created by venous blood passing from the left ventricle to the right through
'pores' in the inter ventricular septum while air passed from the lungs via the pulmonary artery to the left side of the
heart. As the arterial blood was created, 'sooty' vapors were created and passed to the lungs, also via the pulmonary
artery, to be exhaled.
The first major scientific understanding of the heart was put forth by the medieval Arab polymath Ibn Al-Nafis,
regarded as the father of circulatory physiology. He was the first physician to correctly describe pulmonary
circulation, the capillary and coronary circulations. Prior to this, Galen's theory was widely accepted, and
improved upon by Avicenna. Al-Nafis rejected the Galen-Avicenna theory and corrected many wrong ideas that
were put forth by it, and also adding his new found observations of pulse and circulation to the new theory. His
major observations include (as surmised by Dr. Paul Ghalioungui):
1. "Denying the existence of any pores through the interventricular septum."
2. "The flow of blood from the right ventricle to the lungs where its lighter parts filter into the pulmonary vein to
mix with air."
3. "The notion that blood, or spirit from the mixture of blood and air, passes from the lung to the left ventricle, and
not in the opposite direction."
4. "The assertion that there are only two ventricles, not three as stated by Avicenna."
5. "The statement that the ventricle takes its nourishment from blood flowing in the vessels that run in its substance
(i.e. the coronary vessels) and not, as Avicenna maintained, from blood deposited in the right ventricle."
6. "A premonition of the capillary circulation in his assertion that the pulmonary vein receives what comes out of
the pulmonary artery, this being the reason for the existence of perceptible passages between the two."
Ibn Al-Nafis also corrected Galen-Avicenna assertion that heart has a bone structure through his own observations
and wrote the following criticism on it:
"This is not true. There are absolutely no bones beneath the heart as it is positioned right in the middle of the
chest cavity where there are no bones at all. Bones are only found at the chest periphery not where the heart is
For more recent technological developments, see Cardiac surgery.
Obesity, high blood pressure, and high cholesterol can increase the risk of developing heart disease. However, fully
half the amount of heart attacks occur in people with normal cholesterol levels. Heart disease is a major cause of
death (and the number one cause of death in the Western World).
Of course one must also consider other factors such as lifestyle, for instance the amount of exercise one undertakes
and their diet, as well as their overall health (mental and social as well as physical).   
• Cardiac cycle
• Heart disease
• Human heart
• Electrical conduction system of the heart
• Trauma triad of death
• Langendorff Heart
• Atlas of Human Cardiac Anatomy  - Endoscopic views of beating hearts - Cardiac anatomy
• Heart contraction and blood flow (animation) 
• Heart Disease 
• eMedicine: Surgical anatomy of the heart 
• Interactive 3D heart  This realistic heart can be rotated, and all its components can be studied from any angle.
• Heart Information 
• Oath of Awareness  Heart disease awareness site
• SmartyMaps: Interactive Overview of the Human Heart 
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 (http:/ / www. islamset. com/ isc/ nafis/ drpaul. html) Dr. Paul Ghalioungui (1982), "The West denies Ibn Al Nafis's contribution to the
discovery of the circulation", Symposium on Ibn al-Nafis, Second International Conference on Islamic Medicine: Islamic Medical
Organization, Kuwait (cf.) The West denies Ibn Al Nafis's contribution to the discovery of the circulation
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International Society for the History of Islamic Medicine 1: 22–28.
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Islamic Medicine: Islamic Medical Organization, Kuwait (cf. Ibn ul-Nafis has Dissected the Human Body, Encyclopedia of Islamic World).
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 Division of Vital Statistics; Arialdi M. Miniño, M.P.H., Melonie P. Heron, Ph.D., Sherry L. Murphy, B.S., Kenneth D. Kochanek, M.A.
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 White House News. "American Heart Month, 2007" (http:/ / georgewbush-whitehouse. archives. gov/ news/ releases/ 2007/ 02/ 20070201-2.
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 National Statistics Press Release (http:/ / www. statistics. gov. uk/ pdfdir/ hsq0506. pdf) 25 May 2006
 http:/ / www. vhlab. umn. edu/ atlas/ index. shtml
 http:/ / www. nhlbi. nih. gov/ health/ dci/ Diseases/ hhw/ hhw_pumping. html
 http:/ / www. heart. org. in/
 http:/ / www. emedicine. com/ ped/ topic2902. htm
 http:/ / thevirtualheart. org/ anatomyindex. html
 http:/ / www. pharmacyproductinfo. com/ Heart. html
 http:/ / www. oathofawareness. org/
 http:/ / smartymaps. com/ map. php?s=humanHeart
Article Sources and Contributors 11
Article Sources and Contributors
Heart Source: http://en.wikipedia.org/w/index.php?oldid=359401921 Contributors: *crups*, 16@r, 210.50.203.xxx, 2D Backfire Master, 2enable, 2v11, 334a, 3dscience, A. B., A8UDI,
AHands, Aaron Brenneman, Abcmmmm, Abonilla, Academic Challenger, Accarpenter, Adam7davies, Adambro, Adashiel, Adi4094, AdjustShift, Ae77, Aetylus, Aff123a, AgentPeppermint,
Agüeybaná, Ahoerstemeier, Aircorn, Aka042, Akanemoto, Aksi great, Alansohn, Alberto Orlandini, Alesnormales, Alex.tan, AlexandKevin, Alexius08, AlexiusHoratius, Alexyu1, Algormortis,
Alison, AliveFreeHappy, Allen4names, Alpha 4615, Alpha Omicron, Alphachimp, Altenmann, Alucardxt, AmiDaniel, Amicon, Amplitude101, Anaxial, Andr987, Andre Engels, Andrea105,
AndreasPraefcke, Andrewa, Andrewpmk, Andy85719, AndyZ, Andycjp, Anetode, Angela, AngryParsley, Anirvan, Anjelelsy, Anonymi, Anonymous101, Anonymousboy04, Antandrus, Antonio
Lopez, Ap, Apokryltaros, Arakunem, Arbitrarily0, Arcadian, Arcenciel, ArielGold, Arun Philip, Aryeh, Asaunders135, Ascorbic, Asterion, AstroPig7, Astronaut97, Atomic Cosmos, AuburnPilot,
Avono, AxelBoldt, Ayla, Az1568, AzaToth, Babyblack, Backslash Forwardslash, Barfooz, Baseball Bugs, Baswellbrat408, Batman n' robin, Beastinwith, Beetstra, Benpayne2004, Bensaccount,
Bernard the Varanid, BesselDekker, Bhadani, Bielle, BigBadUglyBugFacedBabyEatingO'Brian, Bigboithecoolest, BillyWagner13BS, Bisqwit, Biŋhai, BjarteSorensen, Bkonrad, Blanchardb,
BlueAg09, Bluezy, Bmicomp, Bob f it, Bobbo, Bobdoc, Bobisbob, Bobo192, Bobthesmall, Bodnotbod, Bogey97, Bomac, Bomberzboy, Bongwarrior, Bookfairy12, Bowserxxx, Bradjamesbrown,
Brandmeister, Brian the Editor, Brim, Bringerofrain, Brusegadi, Bryan Derksen, Bth, Bubbyreallystinks, Buillon sexycat798, Burntsauce, Bushcarrot, Caesura, Calco blue, Calebe,
California123123, Calmer Waters, Calor, Caltas, Can't sleep, clown will eat me, Canderson7, CanisRufus, Capricorn42, Cardiac Morph, CardinalDan, Carlsotr, Carlwev, Caspian, Catgut,
Cbrown1023, Cburnett, Cd.dolata, Celithemis, Chaldor, Chasingsol, Cheddon, Chizeng, Chris bonney, Christal1999, CliffC, Closedmouth, Cmichael, Coatbutton, Coffee, Cogorno, Cometstyles,
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monster under your bed, DaL33T, Dadude3320, Dalillama, Damicatz, DanD, Danny beaudoin, Danny32797, Dantecubed, Dark jedi requiem, Darth Panda, DaveJ7, David Henderson, DavidCary,
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Drivenapart, Drmies, Droid392, Drypelia, DuBose, Dungodung, Dureo, Dynaflow, E!, ESkog, EarthPerson, Ebyabe, Ec5618, Ed g2s, Edsuom, Edward321, Effeietsanders, Either way, Ejay,
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Eukesh, Evercat, Everyking, Evil Monkey, Excirial, Facts707, FaerieInGrey, Faggyass17, Fahadsadah, Fairychild, Faithlessthewonderboy, Faradayplank, Farosdaughter, Farside, Fastily,
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ZooFari, Zurishaddai, Zvika, Zzuuzz, 2252 anonymous edits
Image Sources, Licenses and Contributors
File:heart.jpg Source: http://en.wikipedia.org/w/index.php?title=File:Heart.jpg License: Creative Commons Attribution-Sharealike 2.5 Contributors: Heikenwaelder Hugo,
File:EHR-BBII.jpg Source: http://en.wikipedia.org/w/index.php?title=File:EHR-BBII.jpg License: unknown Contributors: Bek the Conqueror, Brighterorange, Bsadowski1, Diberri, DuBose,
MithrandirMage, Vinsfan368, 5 anonymous edits
File:Heart diagram-en.svg Source: http://en.wikipedia.org/w/index.php?title=File:Heart_diagram-en.svg License: Creative Commons Attribution-Sharealike 3.0 Contributors: User:ZooFari
File:Humhrt2.jpg Source: http://en.wikipedia.org/w/index.php?title=File:Humhrt2.jpg License: unknown Contributors: User:Ewen
File:Surface anatomy of the heart.png Source: http://en.wikipedia.org/w/index.php?title=File:Surface_anatomy of the_heart.png License: Public Domain Contributors: Mikael Häggström
File:Heart diagram blood flow en.svg Source: http://en.wikipedia.org/w/index.php?title=File:Heart_diagram_blood_flow_en.svg License: Creative Commons Attribution-Sharealike 3.0
image:ConductionsystemoftheheartwithouttheHeart.png Source: http://en.wikipedia.org/w/index.php?title=File:ConductionsystemoftheheartwithouttheHeart.png License: Creative
Commons Attribution-Sharealike 3.0 Contributors: User:Madhero88
File:Gunshot heart.jpg Source: http://en.wikipedia.org/w/index.php?title=File:Gunshot_heart.jpg License: Public Domain Contributors: National Institutes of Health, Health & Human
Creative Commons Attribution-Share Alike 3.0 Unported
http:/ / creativecommons. org/ licenses/ by-sa/ 3. 0/
4/15/13 Basics - ECGpedia
Author(s) I.A.C. van der Bilt , MD
Moderator I.A.C. van der Bilt , MD
some notes about authorship
A short ECG registration of
normal heart rhythm (sinus
An example of a normal ECG.
Click on the Image for an
«Introduction Step 1: Rhythm»
1 How do I begin to read an ECG?
2 What does the ECG register?
3 The ECG represents the sum of the action potentials of millions of
4 The electric discharge of the heart
5 The different ECG waves
6 The history of the ECG
7 The ECG electrodes
7.1 The Extremity Leads
7.2 The Chest Leads
8 ECG variants
9 Color coding of the ECG leads
10 Special Leads
11 Ladder diagram
12 Technical Problems
How do I begin to read an ECG?
Click on the ECG to see an enlargement. Where do you start
when interpreting an ECG?
On the top left are the patient's information, name, sex and
date of birth
At the right of that are below each other the Frequency, the
conduction times (PQ,QRS,QT/QTc), and the heart axis
(P-top axis, QRS axis and T-top axis)
Farther to the right is the interpretation of the ECG written
(this may be missing in a 'fresh' ECG, but later the
interpretation of the cardiologist or computer will be added)
Down left is the 'paper speed' (25 mm/s on the horizontal
axis), the sensitivity (10mm/mV) and the filter's frequency
(40Hz, filters noise from eg. lights).
There is a calibration. At the beginning of every lead is a vertical block that shows with what amplitude a 1 mV signal is drawn. So
the height and depth of these signals are a measurement for the voltage. If this is not set at 10 mm, there is something wrong with the
Finally we have the ECG leads themselves.These will be discussed below.
Note that the layout is different for each machine, but most machines will show the information above somewhere.
What does the ECG register?
4/15/13 Basics - ECGpedia
Ion currents of the cardiomyocytes
The heart consists of approximately 300 billion cells
In rest the heart cells are negatively charged. Through
the depolarization by surrounding cells they become
positively charged and they contract.
An electrocardiogram (ECG or EKG) is a register of the heart's electrical activity.
Just like skeletal muscles, heart muscles are electrically stimulated to contract. This stimulation is also called activation or excitation.
Cardiac muscles are electrically charged at rest. The inside of the cell is negatively charged relative to the outside (resting potential). If the
cardiac muscle cells are electrically stimulated, they depolarize (the resting potential changes from negative to positive) and contract. The
electrical activity of a single cell can be registered as the action potential. As the electrical impulse spreads through the heart, the electrical
field changes continually in size and direction. The ECG is a graph of these electrical cardiac signals.
The ECG represents the sum of the action potentials of millions of cardiomyocytes
The individual action potentials of the individual cardiomyocytes are averaged. The final result, which is shown on the ECG, is actually the
average of billions of microscopic electrical signals.
During the depolarization, sodium ions stream into the cell. Subsequently, the calcium ions stream into the cell. These calcium ions cause the
actual muscular contraction.
Finally the potassium ions stream out of the cell. During repolarization the ion concentration returns to its precontraction state. On the ECG,
an action potential wave coming toward the electrode is shown as a positive (upwards) signal. Here the ECG electrode is represented as an
4/15/13 Basics - ECGpedia
The conduction system of the heart
The origin of the different waves on the ECG
The QRS complex is formed by the sum of the electric
avtivity of the inner (endocardial) and the outer
Example of the different QRS configurations
sinoatrial node (SA node) contains the fastest physiological pacemaker cells of
the heart; therefore, they determine the heart rate. First the atria depolarize
and contract. After that the ventricles depolarize and contract. The electrical signal
between the atria and the ventricles goes from the sinus node via the atria to the AV-node (atrioventricular transition) to the His bundle and
subsequently to the right and left bundle branches, which end in a dense network of Purkinje fibers. The depolarization of the heart results in
an electrical force which has a direction and magnitude; an electrical vector. This vector changes every millisecond of the depolarization. In
the animation vectors for atrial depolarization, ventricular depolarization and ventricular repolarization are shown.
The different ECG waves
The P wave is the result
of the atrial
depolarization starts in
the SA (sinoatrial) node.
The signal produced by
pacemaker cells in the
SA node is conducted to
the right and left atria.
repolarization is not
visible on the ECG (but
can be visible during
atrial infarction and
The QRS complex is
the average of the
depolarization waves of
the inner (endocardial)
and outer (epicardial)
cardiomyocytes. As the endocardial cardiomyocytes depolarize slightly earlier
than the outer layers, a typical QRS pattern occurs (figure).
The T wave represents the repolarization of the ventricles. There is no cardiac
muscle activity during the T wave.
One heart beat consists of an atrial depolarization --> atrial contraction --> p-
wave, ventricular depolarization --> ventricular contraction --> ORS-complex
and the resting phase (including the repolarization during the T-wave) between two heart beats.
Have a look at this [animation of the heart cycle (http://www-medlib.med.utah.edu/kw/pharm/hyper_heart1.html) ]
4/15/13 Basics - ECGpedia
The limb leads
The chest leads
The origin of the U wave is unknown. This wave possibly results from "afterdepolarizations" of the ventricles.
The letters "Q", "R" and "S" are used to describe the QRS complex
Q: the first negative deflection after the p-wave. If the first deflection is not negative, the Q is absent.
R: the positive deflection
S: the negative deflection after the R-wave
Small print letters (q, r, s) are used to describe deflections of small amplitude. For example: qRS = small q, tall R, deep S.
R`: is used to describe a second R-wave (as in a right bundle branch block)
See figure for some examples of this.
The history of the ECG
A concise history of the ECG is presented in a different chapter.
The ECG electrodes
Electrical activity going through the heart can be measured by external (skin)electrodes. The
electrocardiogram (ECG) registers these activities from electrodes which have been attached onto
different places on the body. In total, twelve leads are calculated using ten electrodes.
The ten electrodes are:
The four extremity electrodes:
LA - left arm
RA - right arm
N - neutral, on the right leg (= electrical earth, or point zero, to which the electrical
current is measured)
F - foot, on the left leg
It makes no difference whether the electrodes are attached proximal or distal on the extremities.
However, it is best to be uniform in this. (eg. do not attach an electrode on the left shoulder and one
on the right wrist).
The six chest electrodes:
V1 - placed in the 4th intercostal space, right of the sternum
V2 - placed in the 4th intercostal space, left of the sternum
V3 - placed between V2 and V4
V4 - placed 5th intercostal space in the nipple line. Official recommendations are to place V4 under the breast in women.
V5 - placed between V4 and V6
V6 - placed in the midaxillary line on the same height as V4 (horizontal line from V4, so not necessarily in the 5th intercostal
With the use of these 10 electrodes, 12 leads can be derived. There are 6 extremity leads and 6 precordial leads.
The Extremity Leads
The extremity leads are:
I from the right to the left arm
II from the right arm to the left leg
III from the left arm to the left leg
4/15/13 Basics - ECGpedia
An easy rule to remember: lead I + lead III = lead II This is done with the use of the height or depth, independent of the wave (QRS, P of
T). Example: if in lead I, the QrS complex is 3 mm in height and in lead III 9mm, the height of the QRS-complex in lead II is 12mm.
Other extremity leads are:
AVL points to the left arm
AVR points to the right arm
AVF points to the feet
The capital A stands for "augmented" and V for "voltage".
(aVR + aVL + aVF = 0)
The Chest Leads
The precordial, or chest leads, (V1,V2,V3,V4,V5 and V6) 'observe' the depolarization wave in the frontal plane.
Example: V1 is close to the right ventricle and the right atrium. Signals in these areas of the heart have the largest signal in this lead. V6 is
the closest to the lateral wall of the left ventricle.
Besides the standard 12 lead ECG a couple of variants are in use:
The 3 channel ECG uses 3 or 4 ECG electrodes. Red is on the right, yellow on the left arm, green on the left leg ('sun shines on the
grass') and black on the right leg. These basic leads yield enough information for rhythm-monitoring. For determination of ST
elevation, these basic leads are inadequate as there is no lead that gives (ST) information about the anterior wall. ST changes
registered during 3-4 channel ECG monitoring should prompt acquisition of a 12 lead ECG.
The 5 channel ECG uses 4 extremitiy leads and 1 precordial lead. This improves ST segment accuracy, but is still inferior to a 12
In vector electrocardiography the movement of electrical acitivity of the P, QRS and T wave is described. Additional X,Y and Z
leads are recorded. Vector electrocardiography is rarely used nowadays, but is sometimes useful in a research setting.
In body surface mapping several arrays are used to accurately map the cardiac electrical wavefront as it moves over de body
surface. With this information the electrical acitivity of the heart can be calculated. This is sometimes used in a research setting.
Color coding of the ECG leads
Two systems for ECG lead color coding are used: the AHA (American Heart Association) system and the IEC (International
Electrotechnical Commission) system:
4/15/13 Basics - ECGpedia
Leads V7,V8 and V9 can be
helpful in the diagnosis of
posterior myocardial infarction
Changed lead positions of leads
V3 and V5 to increase the
sensitiviy to 'catch' a Brugada
pattern on the ECG.
A patient with atrial fibrillation
with a 'Lewis Lead' positioning of
the leads. Compared with the
normal lead configuration, the
atrial signal is enlarged. Although
some parts have a 'sawtooth'
appearance consistent with atrial
flutter, the rhythm is atrial
fibrillation as there is a changing
pattern in the atrial activity.
The same patient with a normal
lead configuration. The rhythm is
atrial fibrillation. The atrial activity
in lead V1 is organized probably
due to a organisation of electrical
activity after it enters the right
atrial appendage, close to lead V1.
AHA (American Heart Association) IEC (International Electrotechnical Commission)
Location Inscription Colour Inscription Colour
Right Arm RA White R Red
Left Arm LA Black L Yellow
Right Leg RL Green N Black
Left Leg LL Red F Green
Chest V1 Brown/Red C1 White/Red
Chest V2 Brown/Yellow C2 White/Yellow
Chest V3 Brown/Green C3 White/Green
Chest V4 Brown/Blue C4 White/Brown
Chest V5 Brown/Orange C5 White/Black
Chest V6 Brown/Purple C6 White/Violet
Throughout history extra
lead positions have been
tried. Most are rarely used
in practice, but they can
deliver very valuable
diagnostic clues in specific
Leads to improve diagnosis
in right ventricular en
In case of an inferior wall
infarct, extra leads may be
1. On a right-sided ECG, V1 and V2 remain on the same place. V3 to
V6 are placed on the same place but mirrored on the chest. So V4 is in
the middle of the right clavicle. The ECG should be marked as a Right-
sided ECG. V4R (V4 but right sided) is a sensitive lead for diagnosing
right ventricular infarctions.
2. Leads V7-V8-V9 can be used to diagnose a posterior infarct. After
V6, leads are placed towards the back. See the chapter Ischemia for
other ways of diagnosing posterior infarction.
Leads to improve detection of atrial rhyhtm:
In wide complex tachycardia, good detection of atrial rhythm and atrio-ventricular
dissociation can be very helpful in the diagnosis process. An esophagal ECG electrode
placed close to the atria can be helpful. Another, less invasive, method is the Lewis
Lead. This is recorded by changing the limb electrodes, placing the right arm electrode in the second intercostal space and the
left arm electrode in the fourth intercostal space, both to the right of the sternum. Furthermore gain is increased to 20mm/mV
and paper speed to 50mm/sec.
Lead positioning to enhance detection of Brugada syndrome
4/15/13 Basics - ECGpedia
A ladder diagram is a diagram to explain arrhythmias. The figure shows a simple ladder diagram for normal sinus rhythm, followed by av-
nodal extrasystole. The origin of impulse formation (sinus node for the first two beats and AV junction for the third beat) and the conduction
in the heart are shown.
Also read the chapter about Technical Problems. That will help you recognize electrical disturbances and lead reversals.
1. Kligfield P, Gettes LS, Bailey JJ, Childers R, Deal BJ, Hancock EW, van Herpen G, Kors JA, Macfarlane P, Mirvis DM,
Pahlm O, Rautaharju P, Wagner GS, Josephson M, Mason JW, Okin P, Surawicz B, and Wellens H. Recommendations for
the standardization and interpretation of the electrocardiogram: part I: The electrocardiogram and its technology: a
scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council
on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society: endorsed by
the International Society for Computerized Electrocardiology. Circulation 2007 Mar 13; 115(10) 1306-24.
4. Rodrigues de Holanda-Miranda W, Furtado FM, Luciano PM, and Pazin-Filho A. Lewis lead enhances atrial activity
detection in wide QRS tachycardia. J Emerg Med 2012 Aug; 43(2) e97-9. doi:10.1016/j.jemermed.2009.08.057
5. Du Bois-Reymond, E. Untersuchungen über thierische Elektricität. Reimer, Berlin: 1848.
6. Hoffa M, Ludwig C. 1850. Einige neue versuche uber herzbewegung. Zeitschrift Rationelle Medizin, 9: 107-144
7. Waller AD. A demonstration on man of electromotive changes accompanying the heart's beat. J Physiol (London)
8. Einthoven W. Le telecardiogramme. Arch Int de Physiol 1906;4:132-164
9. Einthoven W. Über die Form des menschlichen Electrocardiogramms. Pfügers Archiv maart 1895, pagina 101-123
10. Marey EJ. Des variations electriques des muscles et du couer en particulier etudies au moyen de l'electrometre de M
Lippman. Compres Rendus Hebdomadaires des Seances de l'Acadamie des sciences 1876;82:975-977
11. Márquez MF, Colín L, Guevara M, Iturralde P, and Hermosillo AG. Common electrocardiographic artifacts mimicking
arrhythmias in ambulatory monitoring. Am Heart J 2002 Aug; 144(2) 187-97. pmid:12177632.
12. Hurst JW. Naming of the waves in the ECG, with a brief account of their genesis. Circulation 1998 Nov 3; 98(18)
Retrieved from "http://en.ecgpedia.org/index.php?title=Basics&oldid=16592"
4/15/13 Basics - ECGpedia
This page was last modified on 3 February 2013, at 21:34.
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Medical Instruments in the Developing World Malkin
2.5.1 Clinical Use and Principles of Operation
An ECG amplifier, (EKG is a German term that is widely used), is an amplifier with from three to
ten inputs combined to show from one to twelve traces (leads) of cardiac electrical activity. Each
input amplifies the signal from two or more electrodes placed on the skin.
If the ECG is being used to monitor a patient’s condition, then usually three to five wires are
connected to the patient and a low resolution ECG waveform and the heart rate are continuously
displayed and observed by the physician. Monitoring devices will include alarms for significant
changes in rhythm or waveform. If the ECG is being used as a diagnostic tool, then typically six
to ten wires are connected to the patient and one or two cardiac cycles are displayed, or printed,
in high resolution.
Most ECG machines in the developing world are of the monitoring type. For these, three or four
patient cable leads are directly connected to the patient's extremities: right leg (RL – not always
used), right arm (RA), left leg (LL), and left arm (LA). If the machine is reasonably modern, it
will have a color code marked on the leads. However, the color code is different in Europe, and
developing world hospitals often have a mixture of European and American donations. So, the
color code is of little value. A fifth connection marked “C” is often present, but rarely used and
may be left unconnected in most cases. A switch on the front will change the display to monitor
the difference between different electrode pairs: I, II, III, aVr, aVl, aVf, and V. The table below
shows the active electrodes for each switch setting. The RL lead, if present, is always active, as
it is used as a ground, either driven or passive, to reduce noise. If the RL lead is not present,
then one of the unused leads is being used as the reference.
This image shows typical ECG
images from all the most
common leads. The square
pulse is 1 mV in height. Most
developing world systems only
display leads I, II and III, with
some adding aVR, aVL and aVF.
Equipment found in the OR, ICU and ER
SWITCH SETTING ELECTRODES USED
Lead I LA, RA
Lead II LL, RA
Lead III LL, LA
Lead aVr RA, LA, LL
Lead aV1 RA, LA, LL
Lead aVf RA, LA, LL
Lead V C, RA, LA, LL (rarely used)
The terminology can get confusing between inputs, which have wires which are called leads by
the engineer, and inputs, corresponding to clinically significant features, which are also called
leads by the clinical staff. Using the term clinically, there are limb leads and modified limb leads.
Limb leads have the electrodes placed on the limbs, typically wrists and just above the ankles.
Modified limb leads have the electrodes placed on the shoulders and just above the patient’s
waist. Limb leads are used only for monitoring. For diagnostic purposes, there are 12-lead ECG
machines, with electrodes connected at specific spots across the chest, in addition to the
modified limb leads. In addition to the six leads already mentioned (Leads I, II, III, aVR, aVL
and aVF) the 12-lead machine will display V1, V2, V3, V4, V5 and V6, a total of 12 leads.
To operate, the machine should first be switched on. Then, the device should be connected to
the patient via the appropriate series of electrodes. After a few seconds, the device should begin
to record the ECG. In some cases, a start button must be pushed. Some of the 12-lead ECG’s
require a series of user inputs to record the patient’s name, gender and other factors.
All inputs are isolated from the power supply of the amplifier by an isolation transformer. This
prevents any power supply fault from putting voltage on the electrodes and potentially giving an
electrical shock to the patient. Also each input has a diode, resistor or spark gap circuit that will
short any high voltage/high current pulses to ground so the amplifier is not damaged by, for
example, defibrillation. The input impedance of an ECG amplifier is typically 100 megaohms.
Amplifiers, both those used for monitoring and diagnostics, have a switching mechanism that
selects the waveform (lead) to be displayed. The switch may be rotary, pushbutton or flat panel.
On some recorders there is an automatic button which switches the output through all leads
depending upon the mode. On some units there is a calibrate position on the switch which,
when selected, displays a 1 mV signal. The 1 mV calibration signal is used to confirm the gain of
the amplifier and is a good way to do a quick check to see if the amplifier is properly functioning.
If the output shows the 1 mV signal the amplifier is working.
The standard gain of an ECG amplifier is about 1,000 cm/V, meaning that a 1 mV signal on the
body surface creates a 1 cm deflection of the display device. However, some amplifiers have an
automatic gain control and some may have switches with settings like 0.25 (gain of 250), 0.5
(gain of 500), 1.0 (gain of 1,000 Standard) 3.0 (gain of 3,000) and 5.0 (gain of 5,000). As with
any amplifier, saturation can become a problem, even at the lowest gain setting. This is common
when the patient is small, a neonate or a thin, athletic adult. A distorted waveform, usually with
some peaks or valleys or, in the worst case, a flat line at the top or bottom of the display will
result. There also can be a voltage offset caused by the electrodes placed on the patient. This
offset voltage can move the base line up or down and can cause temporary saturation of the
ECG amplifiers have two frequency responses that are selectable, monitor and diagnostic. The
monitor frequency response for long-term observation of the patient’s ECG, as in intensive care,
is 0.5 to 35 Hz. Many of the monitors in the developing world do not observe modern
standardization of the frequency ranges. Therefore, the monitoring frequency range may range
Medical Instruments in the Developing World Malkin
as high as 50 Hz. The diagnostic frequency response is from 0.1 to 100 Hz, or up to 150 Hz,
with or without a notch filter to remove 50 or 60 Hz power line noise.
There are many different types of electrodes used to connect the patient to the monitor. These
electrodes range from short to long-term use. Monitoring electrodes are single use items with a
central column of conductive material surrounded by a plastic foam or paper tape disc or square
to hold the conductive column in place. At the top of the conductive column is a snap that the
lead wire is attached to, that goes to the patient cable that goes to the amplifier (figure 2.6.2).
These electrodes cost between $0.05 and $0.11 each. They cannot be cleaned or otherwise
reused. As these electrodes age, the conductive column will dry out, rendering the electrode
There are non-disposable alternatives for monitoring. The most common is the plate electrode
that is held on to the patient with a rubber belt. Between the electrode and the patient’s skin a
conductive gel is placed to assure good electrical contact. However, this gel is not critical. A
saline soaked gauze, or even a few drops of water, may improve the recording quality. If plate
electrodes are in use they should be checked and cleaned on every inspection.
For diagnostic ECG recordings, the most common electrodes are multiuse. The “Welch cup” is
the most common of these. This is a cup-shaped, silver-coated electrode with a suction bulb on
the top. Corrosion is a common problem as is the lack of suction as the suction bulb ages. It is
not unusual to find the suction bulb full of conductive gel and fungus has been known to grow in
There are two general methods of displaying the ECG waveforms, electronically or on paper. The
most common form of electronic display is on a screen or CRT. The size of the display and the
type of phosphor used in the manufacture of the CRT can enter into the quality of the waveform.
The presentation of the ECG trace can be in the same format as a paper/chart presentation with
the newest data closest to the left edge of the display, often called a moving or solid trace
display. Some manufactures use an ERASE BAR presentation, sometimes called a stationary
trace. In this presentation the waveform is stationary and a blank space, or bar, moves across
the CRT with the newest data being to the left of the space/bar.
The other common method of waveform presentation is on paper. The size and shape of the
paper varies between manufacturers. There are four general types of paper used for waveform
presentation, ink, clay, wax and chemical/thermal. Each has specific benefits and problems.
Ink paper has a shiny surface, with grid lines pre-printed. They can be single sheet or
continuous strip, roll or z-fold, or a continuous strip that can do a single sheet. In most cases
there are many channels of waveform presented with one or more ECG lead configurations per
channel. The marking of the leads is done with alpha characters or dots and dashes. If the stylus
is not properly maintained there can be blotching or smudging on the waveforms. Wax
paper is for hot stylus recordings. It is rare. Thermal paper is the most common paper. It
comes in rolls and z-folds. Its distinguishing feature, in most cases, is the lack of grid lines.
Thermal paper looks like, and essential is, thermal fax paper. The chart speeds on most
Disposable ECG electrodes look
something like large buttons.
However, they are often reused in
the developing world, making them a
constant source of problems.
Equipment found in the OR, ICU and ER
recorders and electronic displays are 25 and 50 mm/sec. Some may have additional speeds.
When the chart speed is 25 mm/sec each mm on the horizontal axis is 0.04 seconds.
2.5.2 Common Problems
By far the most common call to engineering is simple user error. ECG’s are common donations in
the developing world, but the manuals are not. Even when the manuals are delivered with the
machines, they are often in a language that the staff does not speak. Even when the staff can
read the manual, they often don’t. Modern ECG recorders can present a myriad of buttons and
controls and can be quite confusing. For all of these reasons, if the machine turns on, the first
thing to suspect is user error in the operation of the machine.
A common problem in older machines is getting the correct rate. The heart-rate meter may not
have an automatic gain control. In these cases, the user may not realize that they have to adjust
the gain for the rate to read correctly.
User error can extend beyond the operation of the machine. Though the positioning of the
electrodes is the doctor or nurse’s job, when done poorly, it can result in a call to engineering.
The most typical symptom is a saturated ECG or an ECG distorted by power line noise. A few
points to remember for electrode placement are: 1) electrodes should not be placed on scar
tissue, 2) electrodes should not be placed over a lot of body hair, 3) electrodes placed closer than
2 inches from each other may not record a clear signal, and 4) if more than one device requires
that electrodes be placed on the patient they may interfere with each other. Switching to
different leads, repositioning electrodes and shaving the skin may resolve these problems.
After the electrode the weakest link in an ECG system is the lead wires. The patient cable should
last for many years. However, abusive use can lead to wire breakage. Before rejecting a lead
wire, try a different wire from another machine to confirm that this is the cause. Lead wires
often look to be in poor condition because of tape residue on the cable. This residue can be
removed using alcohol or other solvents.
If the lead wire is at fault, replacement is the preferred option. However, lead wires can be
repaired in some cases. To find the faulty wire, for each position on the patient selector switch,
wiggle the patient cord at its end, in the middle where the five leads fan out, and at the machine
plug end. A break will be evidenced by a violent deflection on the display. If the break is in the
last, typically quite thin, part of the lead, this can be cut and soldered in the standard fashion, as
the last dozen inches are typically unshielded wire. If there is a shield, be sure to reconnect it as
The most common problem is in the connection to the main cord, or the connection to the
machine. This wire contains potentially two or three layers before the conductor. If the violent
deflections occur when the patient cable is wiggled at its plug end, and this occurs with several
lead sets, then the socket is broken. As replacement sockets are nearly impossible to find in the
developing world, you must consider rebuilding the socket (a time consuming, and often
unrewarding venture), or consider permanently soldering the lead set to the machine, if the
hospital desperately needs that ECG.
2.*Diagrams*and*Schematics*of*Electrocardiographs*(ECG)****Featured*in*this*Section:***Cromwell,.L...et..al..“Fig..5.1..Block.Diagram.of.an.ECG.Machine.”.From.the.publication.Biomedical.Instrumentation.and.Measurements..Prentice.Hall.(1973),.pg..155.***Carlson,.S..“Citizen.Science—DIY..ECGs.”.Make:..Posted.march.25,.2013..Retrieved.from:.http://makezine.com/2013/03/25/citizenOscienceOdiyOecgs/.. *ECGpedia.org,.“ECG.Reference.Card.”.Wikipedia..Retrieved.from:.http://www.ecgpedia.org/A4/ECGpedia_on_1_A4En.pdf.. *.......Openstax.College..“The.Cardiac.Cycle,.Fig..40.14.”.From.the.publication:.Biology..Rice.University:.2013,.pgs..1205..* * *
Before you start
Check name, date, time, paperspeed (25 mm/sec), scale (10 mm/mV).
Continue with the 7+2 step-plan.
Step 1: Rhythm
Sinus rhythm(SR) (60-100/min): every P wave is followed by a QRS
Narrow QRS tachycardias (QRS<120ms; >100/min) are always
supraventricular tachycardias (SVT):
> 100/min. Eg. Fever / Psych. stress / Cardiomyopathy
Atrial fibrillation (AFIB): irregular
t Permanent = chronic.
t Persisting = recurring after
chemical / electrical cardioversion
t Paroxysmal = comes and goes
spontaneously: SR AFIB SR
Atrial flutter: flutter waves on baseline.
Often regular 300 / min with a 2:1, 3:1 or
AVNRT: AV nodal re-entry tachycardia.
Regular, 180-250 / min. P in QRS complex
(resulting in RsR’ in V1), often young
patients and paroxysmal. Valsalva / carotid massage / adenosine can
Wide complex tachycardias (QRS>120ms): possible risk of sudden death,
always consult with cardiologist.
Ventricular tachycardia. Arguments for VT (Brugada criteria): fusion
(sudden narrow beat), absence of RS precordialy, RS > 100ms, AV
dissociation, atypical LBBB. Typically in older patient with previous MI.
Unconscious? proceed to immediate defibrillation.
SVT with aberrancy. Typical in younger patient. How was the QRS
duration / shape on a previous non-tachycardic ECG?
Ventricular fibrillation = no QRS-complexes, but chaotic ECG-pattern,
like ‘noise’ mechanical cardiac arrest resuscitate. If patient is
conscious it probably is noise.
Bradycardia (<60/min). Consider stop / reduce beta-blocker / digoxin / Ca-
antagonist. Asymptomatic sinusbradycardia with a normal blood pressure in
general doesn’t require treatment.
t 1st degree AV-block: prolonged PQ-interval (> 200ms)
t 2nd degree AV-block type I (Wenkebach): PQ interval increases
until 1 QRS complex is blocked. Good prognosis.
t 2nd degree AV-block type II (Mobitz): PQ interval is normal,
but not every P wave is followed by QRS. Requires pacemaker.
t 3rd degree AV-block = complete block. AV dissociation: no
relationship between P waves and QRS. Requires pacemaker.
t Ventriculair escape rhythm: wide complex rhythm < 40/min;
dangerous. Consult cardiologist. Ischemia? Severe electrolyte shift?
Step 2: Heart rate
Count the number of large grids between two QRS complexes: 1 box in
between = 300/min, 2=150/min - 100 - 75 - 60 - 50 - 40. Or use methods at the
bottom of this page.
Step 3: Conduction intervals (PQ, QRS, QT)
Normal: PQ <200ms (5 small squares), QRS < 120ms
(3 squares), QTc < 450 ms, < 460 ms, preferably
measured in lead II or lead V5.
PQ > 200ms = AV block (above)
PQ < 120ms + delta-wave = Wolff-Parkinson-White syndrome (WPW), risk of a circus
movement tachycardias (= AVRT: AV re-entry tachycardia)
QRS > 120ms = wide QRS complex, check V1:
t Left Bundle Branch Block (LBBB)
Latest activity towards the left, away from
V1, so QRS ends negatively in V1.
New LBBB? Consider ischemia.
t Right Bundle Branch Block (RBBB)
RsR’ (rabbit ear) latest activity rightwards,
(on average) positive in V1
t Intraventricular conduction delay=
if it’s not LBBB nor RBBB
QTc > 450ms: consider: hypokalemia, post myocardial
infarction, long QT syndrome, medication (full list on
torsades.org). Risk of torsade de pointes deteriorating
into ventricular fibrillation (risk increases especially >500ms).
Step 4: Heart axis
Heart axis: vector of the average electrical activity. Normal between –30˚ and +90 .̊
Expecially axis deviation compared to previous ECG is relevant.
Normal hart axis: QRS positive in II and AVF
Left axis: AVF and II negative. Eg. left anterior fascicular block (LAFB), LVH.
Right axis. I negative, AVF positive. Eg. pulmonary embolism, COPD.
Step 5: P wave morphology
Normal P wave: positive in I and II, bifasic in V1, similar shape in every beat.Otherwise
consider ectopic atrial rhythm.
Left atrial enlargement: terminal negative part in V1 > 1mm2. e.g. mitral-regurgitation.
Right atrial enlargement P>2.5mm high in II, III, AVF and / or P>1.5mm in V1. e.g. COPD
Step 6: QRS morphology
Pathologic Q waves? Old myocardial infarction (see ischemia)
Left ventricular hypertrophy (LVH): R in V5/V6 + S in V1 > 35 mm.
Seen in e.g. hypertension, aortic valve stenosis.
R wave progression: R increases V1-V5. R>S beyond V3
Microvoltages (<5mm in extremity leads): E.g. cardiomyopathy, tamponade, obesity,
Wide QRS complex (QRS > 120ms): see Step 3
Step 7: ST morphology
ST elevation: consider ischemia, pericarditis, LVH,
benign ST elevation, ‘early repolarisation’
ST depression: can be reciprocal in ischemie, strain
pattern in LVH, digoxin intoxication
Negative T wave: (not in the same direction as the
QRS complex) consider (subendocardial) ischemia,
Flat T wave (<0.5 mm): aspecific
Step +1: Compare with previous ECG
New LBBB? Change in axis?. New pathologic Q waves? Reduced R wave height?
Step +2: Conclusion (1 sentence)
Example: Sinustachycardia with ST elevation in the chest leads with a trifascicular
block consistent with an acute anterior myocardial infarction
Acute myocardial infarction (AMI): symptoms (chest pain, vagal response), ECG
consistent with transmural ischemia (ST elevations (+reciprocal depressions), new
LBBB, sometimes already pathologic Q waves), sometimes already elevated cardiac
markers for AMI (Troponin / CKMB). ’Time is muscle’. If you suspect AMI consult
cardiologist immediately (< 5 min.)
ST-elevation points at the infarcted area:
t Anterior: V1-V4. Coronary territory: LAD. sometimes tachycardia
t Inferior: II, III, AVF. Coronary: 80% RCA (bradycardia, elevation III>II;
depression in I and / or AVL), otherwise RCX (in 20%).
t Right ventricular MI: ST in V1 and V4R. IV fluids if hypotensive
t Posterior: high R wave and ST depressie in V1-V3
t Lateral: elevation in I, AVL, V6. Coronary: LAD (Diagonal branch)
t Left main: diffuse ST depression with ST elevation in AVR. Very high
risk of cardiogenic shock
Reciprocal depression: depression in reciprocal territory (e.g. ST depression in II, III,
AVF during anterior MI).
IPL-infarction: inferior-posterior-lateral. They frequently come together
Pathologic Q-wave (any Q in V1-V3 or Q width > 30ms in I, II, AVL, V4-V6; minimal in 2
contiguous leads, minimal depth 1 mm): previous MI. Leads III and AVR may have a Q
wave, which is non-pathological.
VPB (ventricular premature beat, VES: ventricular extrasystole, PVC,
Premature ventr. contr.). QRS > 120ms. Seen in 50% of healthy men. Increased
risk of arrhythmias if: complex form, very frequent occurence (> 30 / hour) or R on T.
Consider: Ischemia? Previous MI? Cardiomyopathy?
PAC (premature atrial contraction, AES): abnormal P wave, mostly narrow (normal)
Pericarditis: ST elevation in all leads. PTA depression
in II (between the end of the P wave and the
beginning of Q wave)
Hyperkalemia: tall T waves. QRS wide, flat P
Hypokalemia: QT prolongs, U wave, torsade
Hypocalcemia: ST prolongs, ‘normal’ T
Hypercalcemia: QT short, high T
Digoxin-intoxication: sagging ST depressions
Pulmonary embolism: sinustachycardia, deep S in
I, Q wave and negative T in III, negative T V1-V3, right
axis, sometimes RBBB
Chest lead positioning: V1= 4th intercostal space
right (IC4R), V2=IC4L, V3=between V2 en V4, V4=IC5
in midclavicular line, V5=between V4 and V6, V6= same height as V4 in axillary line. To
register V4R, use V3 in the right mid-clavicular line.
QT intervalPQ interval
How to measure ST elevation?
Heart rate = 10 times number of QRS complexes within these 15 cm ( = 6 seconds x 25 mm/sec) 1st R 300 150 100 75 60 50/min
Heartrate: measure 2 cardiac cycles
200 120 86 67 55
Maximal QTc per given heart rate:
what QT value at what heart rate
results in a QTc of 450ms?
50/min: QT 493ms
60/min: QT 450ms
70/min: QT 417ms
80/min: QT 390ms
90/min: QT 367ms
100/min: QT 349ms
Normal sinus rhythm. Every P wave is followed by a
QRS complex. Heart rate between 60 -100 /min.
Ventricular Premature Beat (VPB)
RBB B, Right Bundle Branch Block
LBB B, Left Bundle Branch Block
( W olff-P arkinson-Whi te).
Atrium flutter met 6:1 b lok.
Atrium fibrille ren met h oge k amerf requenti e.
A V -nodale re-entry ta c h y ca rdie
V entricular tachycardia
Acute anterior MI. ST-elevation in V1-V5, I and A VL.
R ecip rocal ST-dep ression in II, III and A V F .
Acute infero-posterior MI. ST-elevation in II, III
and A V F . R ecip rocal ST-dep ression in I, A VL, V1-V5
Color scheme to facilitate MI localisation. The colors mark contiguous
leads. Example: (see above): ST elevation in II, III, AVF
acute inferior MIP athol ogic Q wave, sign of a previous MI
Delta wave and short PQ interval in WP W -synd rome
aVR Left Main
Left Ventricular Hypertrophy (LVH, R in V5/V6 + S in V1 > 35 mm)
AV nodal re-entry tachycardia
AV re-entry tachycardia
(re-entry throught accessory bundle
as in WPW )
(often around tricuspid valve annulus)
Supraventricular tachycardias (’cherchez le P’)
large square = 5 mm = 0.20 sec small square = 1 mm = 0.04 sec
retrograde P wave in QRS
retrograde P between QRS
different P wave
3.*Preventative*Maintenance*and*Safety*of*Electrocardiographs*(ECG)****Featured*in*this*Section:*****Developing.World.Healthcare.Technologies.Laboratory,.“ECG.Monitor:.How.To.Use.”.DHT(Lab,.Duke.University,.2006... *Cooper,.Justin.and.Alex.Dahinten.for.EWH..“Electrocardiogram.(ECG).Preventative.Maintenance.”.From.the.publication:..Medical(Equipment(Troubleshooting(Flowchart(Handbook..Durham,.NC:.Engineering.World.Health,.2013..* ** *
• Clean&casing&• Clean&electrodes&and&inspect&for&corrosion&or&adhered&debris&after&each&use&• Inspect&insulation&for&defects&and&debris&• Inspect&cables&for&defects,&replace&if&necessary&• If&battery7powered,®ularly&check&batteries&to&prevent&corrosion&• Re7stock&and&refill&ink&and&paper&as&needed&&Electrode!Guide!Proper&Placement&of&12&Lead&ECG&For&the&4&extremity&electrodes&placement:&
• L&or&LA&is&placed&on&the&left&arm&• R&or&RA&is&placed&on&the&right&arm&• N&7&neutral,&on&the&right&leg&(=&electrical&earth,&or&point&zero,&to&which&the&electrical¤t&is&measured)&• F&7&foot,&on&the&left&leg&• It&does¬&matter&whether&the&electrodes&are&placed&on&the&bottoms&or&tops&of&extremities,&but&be&consistent.&Place&electrodes&in&similar&spots&on&extremities.&(eg.&do¬&attach&an&electrode&on&the&left&shoulder&and&one&on&the&right&wrist).&Also,&avoid&bony&parts&such&as&elbows&or&knees.&&&&For&the&6&chest&electrodes&placement:&
• V1&is&placed&to&the&right&of&the&sternum&in&the&4th&intercostal&space.&• V2&is&placed&to&the&left&of&the&sternum&in&the&4th&intercostal&space&
• V3&is&placed&between&V2&and&V4&• V4&is&placed&in&the&5th&intercostal&space&on&the&nipple&line.&Place&V4&beneath&the&breast&in&women.&• V5&is&placed&between&V4&and&V6&• V6&is&placed&in&the&midaxillary&line&on&the&same&height&as&V4&on&the&horizontal&line&from&V4&(not&necessarily&in&the&5th&intercostal&space)&&Common&lead&misplacements:&
1. Shave&body&hair&before&application,&if&in&excess.&2. Avoid&placing&electrodes&on&any&burn&or&scar&tissue.&3. Make&sure&electrodes&have&some&sort&of&conductive&gel&between&skin&and&metal&contact.&4. Make&sure&electrode&is&firmly&attached&to&skin.&Apply&tape,&if&necessary.&5. If&steps&174&struggle,&use&a&light&skin&abrasive&such&as&sand&paper.&6. Reapply&conducting&gel&every&couple&of&hours&to&avoid&skin&irritation&and&loss&of&signal.&&
Knowledge Domain: Mechanical
Skill: ECG Monitor
Tools and Parts Required:
1) ECG that requires calibration
2) A test patient
3) Alcohol swab
4) Watch that counts seconds
Electrocardiographs (ECGs) monitor the electrical activity of the heart. ECGs are used
to detect heart attacks or diagnose abnormal heart rhythms. ECGs are found in
ambulances, intensive care units, and other healthcare facilities. Sometimes ECGs also
have an apnea monitor. Apnea monitors detect changes in breathing.
Identification and Diagnosis
ECG monitors should be calibrated about every six months, as part of preventative
1. Turn the machine on. Depress the “1 millivolt” or
a. For analog machines: Check that the stylus has
deflected 10 small squares, similar to the picture at
b. For electric machines: Insure that a square wave
form appears when the button is pressed. The wave should resemble the
picture at right.
2. Find someone who will be your test patient.
3. Clean the test patient’s chest with an alcohol swab. Attach the electrodes and
leads to the patient. Follow the ECG manual for electrode placement. Use the
pictures below as a guide. The number of electrodes you will attach depends if
the ECG is made for 3-lead (monitoring) or 12-lead (diagnostic) use. 3-lead
ECG’s generally have four connections to the patient. 12-lead ECG’s have ten
connections to the patient.
4. Check the ECG heart rate measurement
- Find the patient’s pulse. You can find the pulse in two places. The radial pulse
is on the inside of the wrist. The carotid pulse is between the windpipe and
large muscle in the neck. Place two fingers on one of these areas. Press
lightly until you feel a pulse. Do not use your thumb to take pulse.
- Using a watch to time 30 seconds, count the heartbeats. Multiply the number
of heartbeats by 2. This is the patient’s heart rate.
- Compare the calculated heart rate to the ECG’s reading. The ECG reading
should match within 2 beats per minute.
5. Check the alarms*
- Set the maximum heart rate by navigating through the machine’s menus** to
an option resembling “alarm limits.” Set the maximum heart rate on the ECG
machine below your patient’s heart rate. The high heart rate (tachycardia)
alarm should sound.
- Set the minimum rate alarm on the ECG machine above your patient’s heart
rate. The low heart rate (bradycardia) alarm should sound.
- Remove the wires from the patient. The electrode-off (or lead-off) alarm on
the ECG machine should sound.
If the ECG has an apnea monitor, follow this procedure:
6. Attach the electrodes to the patient following the picture guide and the ECG
7. Check the breathing rate
- Count how many breaths are taken over 1 minute.
- Compare the calculated breathing rate to the ECG machine’s reading. The
ECG machine’s reading should be within 1 breath per minute.
8. Check the alarms
- Set the maximum breathing rate on the ECG apnea monitor below your
patient’s breathing rate. The high breathing (hyperventilation) alarm should
- Set the minimum breathing rate on the ECG apnea monitor above your
patient’s breathing rate. The low breathing (hypoventilation) alarm should
- Instruct the patient to hold his breath. The apnea alarm should sound.
*Note: Not all ECG monitors have all alarms.
** Menus for different device models may differ.
Calibrate your ECG with a partner. Your instructor must verify your work before you
Preventative Maintenance and Calibration
Always calibrate every medical device before returning it to use.
4.*Troubleshooting*and*Repair*of*Electrocardiographs*(ECG)****Featured*in*this*Section:****Cooper,.Justin.and.Alex.Dahinten.for.EWH..“Electrocardiogram.(ECG).Troubleshooting.Flowchart.”.From.the.publication:.Medical(Equipment(Troubleshooting(Flowchart(Handbook..Durham,.NC:.Engineering.World.Health,.2013....Strengthening.Specialised.Clinical.Services.in.the.Pacific..User(Care(of(Medical(Equipment:(A(first(line(maintenance(guide(for(end(users..(2015).. ** *
Description*#! Text-Box! Comments!1! Begin:!ECG!flowchart! Start!diagnostic!process!for!a!work!order!on!an!ECG!
2! Does!ECG!power!on?! Lights,!displays,!and!sounds!are!indications!that!device!is!powered!on.!Also,!check!the!power!cords!for!continuity.!See!BTA!skills!on!Connections.!
3! Troubleshoot!power!supply!(separate!flowchart)! ECG’s!have!an!AC!to!DC!power!supply.!See!Flowchart!on!Power!Supply,!and!BTA!skills!on!Power!Supply.!
4! Change!battery!if!necessary.! If!there!is!a!battery,!test!its!ability!to!receive!and!hold!a!charge.!See!BTA!skills!on!Batteries.!5! Does!screen!turn!on?! No!obvious!brightness!or!color!change!on!display!screen?!6! Check!brightness!level.! If!possible,!raise!brightness!level!of!screen.!
7! Check!internal!connections.! Check!for!obvious!wiring!issues!such!as!damaged!or!disconnected!wires.!See!BTA!skills!for!Connections!and!Electrical!Simple.!8! Go!to!begin.! Return!to!box!1,!Begin:!ECG!
9! Is!“Lead!off”!light!on?! “Lead!off”!light!will!likely!be!near!display!window.!It!indicates!that!there!is!a!bad!connection!somewhere!between!the!patient!electrodes!and!the!machine.!(1)!See!BTA!skills!for!Electrical!Simple.!
10! Are!the!electrodes!in!working!condition?! Check!for!damage!or!corrosion!to!the!electrode!or!electrode!insulation.!
11! Replace!electrodes!or!adjust!their!placement.! See!electrode!guide!below!for!replacement!of!electrodes!as!well!as!electrode!placement!and!a!conducting!gel!recipe.!If!possible,!attach!a!patient!simulator!to!the!patient!cables.!If!proper!signal!with!simulator,!electrodes!are!non[functional.!
12! Check!connections.! If!possible,!attach!patient!simulator!to!patient!cables,!if!no!signal!replace!cables.!Ensure!proper!connections!between!ECG!and!electrodes!and!ensure!patient!is!not!moving.!Make!sure!electrode!has!proper!contact!with!patient’s!skin.!(1)!See!BTA!skills!for!Electrical!Simple.!13! Go!to!Begin.! Return!to!box!1,!Begin:!ECG!
14! Does!lead!print!as!square!wave?! Does!one!or!more!lead!display!as!a!square!wave?!(1)!15! Is!there!a!wandering!baseline?! Does!display!show!an!unsteady!baseline!signal?!
17! Are!leads/electrodes!in!working!condition?! Check!for!damage!or!corrosion!to!the!electrode!or!electrode!insulation.!If!possible,!attach!a!patient!simulator!to!the!patient!cables.!If!proper!signal!with!simulator,!electrodes!are!non[functional.!
18! Replace!or!repair!intermittent!leads/electrodes!or!adjust!their!placement.! See!electrode!guide!below!for!replacement!of!electrodes!as!well!as!electrode!placement!and!a!conducting!gel!recipe.!
19! Check!connections.! If!possible,!attach!patient!simulator!to!patient!cables,!if!no!signal!replace!cables.!Ensure!proper!connections!between!ECG!and!electrodes!and!ensure!patient!is!not!moving.!Make!sure!electrode!has!proper!contact!with!patient’s!skin.!(1)!See!BTA!skills!for!Electrical!Simple.!
20! Fix!muscular!interference.! Make!sure!patient!is!comfortable!and!not!tense,!if!possible!turn!on!muscular!filter.!!See!user’s!manual!for!instructions!on!muscular!filter.!(1)!
21! Fix!AC!interference.! Verify!that!patient!is!not!touching!any!metal.!Verify!power!cable!is!not!touching!patient!cable.!If!possible,!turn!on!AC!filter!according!to!instructions!in!user’s!manual.!Also,!try!running!on!battery!power,!if!possible.!(1)!See!BTA!skills!on!Power!Supply!and!Electrical!Simple.!22! Unexpected!ECG!morphology?! Does!display!show!an!unexpected!ECG!morphology?!
23! Reference!electrode!guide.! Check!electrode!guide!below,!particularly!on!lead!placement!to!ensure!proper!location.!
24! Check!connections.! If!possible,!attach!patient!simulator!to!patient!cables,!if!no!signal!replace!cables.!Ensure!proper!connections!between!ECG!and!electrodes!and!ensure!patient!is!not!moving.!Make!sure!electrode!has!proper!contact!with!patient’s!skin.!(1)!See!BTA!skills!for!Electrical!Simple.!
25! Is!there!a!printer!problem?! Does!printer!not!print!or!print!output!that!does!not!match!display!
26! Refer!to!printer!guide!! Use!Printer!flowchart!to!determine!possible!problems!with!printer!output.!?!If!it!is!an!analog!ECG!machine,!the!stylus!heat!and!pressure!can!cause!poor!trace!display.!Refer!to!the!service!manual!or!online!documentation.!27! Go!to!Begin! Return!to!box!1,!Begin:!ECG!
28! Check!connections! If!possible,!attach!patient!simulator!to!patient!cables,!if!no!signal!replace!cables.!Ensure!proper!connections!between!ECG!and!electrodes!and!ensure!patient!is!not!moving.!Make!sure!electrode!has!proper!contact!with!patient’s!skin.!(1)!See!BTA!skills!for!Electrical!Simple.!
29! ECG!is!working!properly.! Return!the!machine!to!service!via!the!appropriate!clinical!personnel.!
User Care of Medical Equipment – First line maintenance for end users
Troubleshooting – ECG Machines
Fault Possible Cause Solution
ECG traces have artefacts or
base line drift
Check for good connection of reference
Try with battery power only. If the
recording improves then problem is with
earthing. Check the earthing
Power the machine from another outlet
with proper electrical earth
ECG traces have artefacts in
one or more traces, but not in
Improper electrode connection
with patient or problem with
the ECG cable
Check the patient cable continuity with
continuity tester. Replace cable if found
Check the electrodes expiration date
Check patient skin preparation
Check limb electrodes and chest
electrodes for damage, replace if
Paper feed not advancing
Incorrect paper loading
Use instructions to reload paper
Printing not clear or not
Printing head problem
Adjust the printing head temperature or
Clean the printing head with head
cleaner. If no improvement, replace the
Check the paper roller and replace if not
The machine shuts down after
a few minutes while on
Problem with battery or
Recharge the unit overnight
If there is no improvement then replace
the battery (if accessible)
If still no improvement, refer to
User Care of Medical Equipment – First line maintenance for end users
User Care Checklist – ECG Machines
9 Clean off dust with dry cloth
9 Wipe gel off reusable electrodes after every use
9 Check that battery charge indicator, power indicator and
patient cable connector indicators are working
9 Check operation of machine before use using 1mV pulse
9 Check the baseline of the ECG recording is steady
9 Check the printing is clear and replace dust cover
9 Clean the printing head, electrodes and connectors
9 Check all cables are not bent, knotted or damaged
9 Replace any damaged electrical plugs, sockets or cables
9 Check all knobs, switches and indicators are tightly fitted
9 Check the operation of recordings with 1mV pulse button
9 Check battery power can operate the equipment
Every six months
Biomedical Technician check required
5.*Resources*for*More*Information*Electrocardiographs*(ECG)****Featured*in*this*Section:***. ECGpedia.org,.“Welcome.to.ECGpedia.”.Wikipedia..Retrieved.from:.http://en.ecgpedia.org/.**. ...WHO..“Electrocardiograph.Machine.and.Stethoscopes.”.From.the.publication:.Maintenance(and(Repair(of(Laboratory,(Diagnostic(Imaging(and(Hospital(Equipment,.WHO,.1996..... * *...
*Resources*for*More*Information:..**Internal*Resources*at*library.ewh.org:*For*more*information*about*ECG’s,*please*see*the*following*resources*in*the*BMET*Library!*.1. WHO..“Electrocardiograph.Machine.and.Stethoscopes.”.From.the.publication:.Maintenance(and(Repair(of(Laboratory,(Diagnostic(Imaging(and(Hospital(Equipment,.WHO,.1996....External*Resources*for*More*Information:*2. ECGpedia:.This.website.is.a.comprehensive,.openOsource.resource.about..the.use,.operation,.and.theory.behind.electrocardiograms..This.website.includes.videos,.a.textbook,.case.studies,.and.an.ECG.course..ECGpedia.org,.“Welcome.to.ECGpedia.”.Wikipedia..Retrieved.from:.http://en.ecgpedia.org/.• ECGpedia*Homepage:.http://en.ecgpedia.org/.• ECG*Textbook:.http://en.ecgpedia.org/wiki/Textbook.• ECG*Videos:*http://en.ecgpedia.org/.• ECG*Cases*and*Examples:.http://en.ecgpedia.org/wiki/Cases_and_Examples.......