LAB X
Electrocardiography
Electrocardiography is a procedure to evaluate the electrical activity of the heart.
Electrocardiography results in the production of an electrocardiograph (EKG) or a graphic
representation of the electrical activity of the heart. The EKG demonstrates a very organized and
reproducible sequence of electrical events that occur within the heart. Examination of this sequence of
electrical events can be useful to determine if the mechanical events (pumping of blood) of the heart
are also occurring in the proper manner (see Appendix 6-1). Abnormal electrical events in the EKG
may result in abnormal mechanical events which could compromise cardiac output and normal
delivery of oxygen. In this lab we will examine the normal function of the electrical activity of the
heart and some of the diagnostic measures that can be used to determine normal cardiac function.
Review appendix pages 6 and 14-20 as you read this lab.
When examining an EKG it is important to remember that the sequence of events represents a very
complex compound action potential. Every cell in the myocardium is depolarizing and then
repolarizing. In order to produce a productive contraction, some of the myocardial cells need to be
stimulated sooner than others. The heart has three important anatomical and physiological properties
that can account for this very reproducible event.
1) Automaticity - The cell membranes of most of the myocardial cells, especially pacemaker cells
(such as the SA and AV nodes) , have an increased permeability to sodium. These "leaky
membranes" allow sodium ions to gradually leak into the interior of the myocardial cell,
resulting in a slow depolarization of the membrane. Because of the presence of voltage gated
calcium channels, if the membrane depolarizes enough, the calcium channels open and allow
an influx of calcium, causing further depolarization. Thus, as sodium and then calcium ions
leak in, the membrane depolarizes and eventually reaches threshold. Once the cell reaches
threshold an action potential will occur, and will ultimately result in depolarization and
contraction of cardiac muscle cells. Therefore the heart has the ability to stimulate itself
without any outside influence (i.e. it automatically depolarizes itself). Thus, unlike skeletal
muscle, no neural input is required to initiate cardiac muscle contractions. The heart is
innervated by both branches of the autonomic nervous system. However, these serve to
increase the rate of depolarization (sympathetic nervous system) or decrease the rate of
depolarization (parasympathetic nervous system), resulting in an increase or decrease in heart
rate.
2) Functional Syncytium - Due to the presence of gap junctions, specialized proteins located in
the intercalated discs between cardiac muscle cells, once one cell in the heart reaches threshold
a wave of depolarization and repolarization will spread from cell to cell through the entire
myocardium. This arrangement allows the heart to function collectively. However, the heart
contains a fibrous skeleton, which separates the upper atria from the lower ventricles. How
does the impulse move from the atria to the ventricles?
3) Conduction System – (see Appendix 7-1) Within the myocardium is specialized muscle tissue
that exhibits very rapid conduction ability. This tissue is arranged in such a way to allow the
impulse to be rapidly distributed to different parts of the heart at different times. This system is
responsible for the order and timing of the electrical (and contraction) events within the heart.
Sino-atrial Node (SA), Internodal and Interatrial Bands, Atrioventricular Node (AV), The
Common AV Bundle (of HIS), Right and Left Bundle Branches and the Purkinje Fibers.
Each portion of the conduction system exhibits the property of automaticity. The SA node usually
spontaneously depolarizes at a rate of about 70 times per minute. Each segment of the conduction
system spontaneously depolarizes at a progressively slower rate If the SA node stopped having action
Lab X - 1
potentials, or if each part of the heart was dissected and studied separately, the atrial muscle cells
would depolarize approximately 60 times per minute. In the absence of SA node, or atrial muscle
initiation of depolarization in the heart the AV node could take over as the pacemaker. The AV node
depolarizes at an inherent rate of approximately 50 times per minute. The purkinje fibers could take
over as the pacemaker for the ventricles if the SA node, and AV node failed to take over as the
pacemaker. The purkinje fibers depolarize at an inherent rate of about 30 times per minute. The
inherent rate of depolarization in the ventricles is about 25 times per minute. Due to the arrangement
of the myocardial cell in a functional syncytium the cell that reaches threshold first will control the
rest. Thus, since the SA node normally depolarizes first, it usually serves as the pacemaker of the
heart, depolarizing around 70 times per minute in an average individual.
If some other cell in the heart should depolarize before the SA node it would become the
pacemaker, at least for that beat of the heart. For example, if a myocardial cell in the atria should
happen to depolarize before the SA node, it would result in a premature beat. If the premature beat is
initiated in the atria, they are referred to as premature atrial contractions (PAC). If a premature beat is
initiated in the ventricles they are referred to as premature ventricular contractions (PVC). These (atrial
or ventricular myocardial) cells that initiate a heart beat, but that are not normally the pacemaker are
referred to as ectopic foci. These PAC’s and PVC’s alter the normal cardiac cycle and therefore result
in an abnormal electrical rhythm. An abnormal heart rhythm is referred to as an arrhythmia. The
normal electrical rhythm of the heart is referred to as Normal sinus rhythm.
In addition to the myocardial properties listed above it is also important to understand that cardiac
muscle cells (myocardial cells) do not produce a “typical” action potential. This is due to the presence
of slow calcium channels in the myocardium. These channels are opened at the point of stimulus like
the sodium channels; however, they open much slower and remain open much longer. This produces a
plateau phase in the action potential immediately following depolarization. As the slow calcium
channels close the potassium channels open and the cell repolarizes. The end result is an action
potential that usually is 0.25 to 0.3 seconds in duration, much slower than typical skeletal muscle. This
long action potential results in an extended refractory period. This accounts for the inability of the
heart to be tetanized (as we will see in our cardiac cycle lab).
The normal function of these features results in the following sequence of electrical events in the
myocardium (see diagram and Appendix 7-2).
R
J-point
P
T
Q
S
P wave - Represents depolarization of the myocardial cells in the atria, initiated by the SA node. If an
impulse starts in the ventricles (e.g. PVC) then there will not be a P wave prior to the QRS.
QRS complex - Represents depolarization of the myocardial cells in the ventricles. This also happens
to coincide with the part of the cardiac cycle when the myocardial cells in the atria are
repolarizing. The impulse is slightly delayed at the AV node before entering the ventricles
through the Common AV Bundle.
J-point – Is the end of the QRS complex and the beginning of the ST segment.
T wave - Represents repolarization of the myocardial cells in the ventricles.
U wave - If present, it represents repolarization of purkinje fibers and/or the ventricular septum.
Lab X - 2
Isoelectric line - Is the flat parts of the EKG, for example between the T and P waves or between the
P wave and the QRS complex.
R-R interval - The RR interval represents the amount of time between heart beats. Thus, the RR
interval is heart rate dependent. When heart rate increases, RR interval decreases and the
opposite is true when heart rate decreases. In fact, most of our methods for determining
heart rate from the EKG are dependent on measureing the RR interval. For example if there
is 0.6 seconds between beats, and there are 60 seconds per minute, then the heart rate would
be 100 beats per minute [(60 sec/minute / (0.6 sec/beat)]. The RR interval is measured from
the peak of one QRS complex (R wave) to the peak of the next QRS complex. Heart rate
must be assessed in order to determine the subject’s electrical rhythm. If all intervals are
normal and all waves are present and if the subject’s heart rate is between 60 and 100 beats
per minute, then they are in normal sinus rhythm. Individuals with sinus arrhythmia have an
RR interval that varies with the respiratory cycle. Thus, it is necessary to measure the RR
interval several places across the EKG. If a subject’s heart rate is over 100 beats per minute
they are said to be in sinus tachycardia. If their heart rate is below 60 beats per minute they
are said to be in sinus bradycardia. Recall from human physiology that the sympathetic
nervous system causes an increase in heart rate and the parasympathetic nervous system
causes a decrease in heart rate. What effect would the sympathetic and parasympathetic
nervous system have on the RR interval?
PR interval - This interval represents the time delay between the depolarization of the atria and the
ventricles and is measured from the beginning of the P wave to the beginning of the QRS
complex (not to the R wave as its name implies). This interval normally lasts 0.12 and 0.20
seconds. It is used to evaluate the function of the AV node. For example, if the PR interval
is greater than 0.2 seconds every beat the subject has a first degree AV block, and represents
a slowing of action potential propagation across the AV node. There are several types of
“AV blocks” that are clinically significant that will be discussed later. There are a few
conditions that reduce the duration of the PR interval. One of the more common conditions
that results in a short PR interval (< 0.12 seconds) is Wolf-Parkinson-White Syndrome
(WPW), which is a result of an accessory pathway for the impulse to get from the atria to the
ventricles (thus the impulse gets to the ventricles without being “delayed” at the AV node).
This also results in a gradual upslope in the QRS complex called a delta wave (ventricles
start depolarizing before going from AV Node and through the rest of the ventricular
conduction system).
QRS interval - This interval represents the time for the impulse to be distributed over the entire
ventricular myocardium. This interval usually lasts between 0.08 and 0.12 seconds.
QT interval - This interval represents the total time between the beginning of ventricular
depolarization and the end of ventricular repolarization. It is measured from the beginning
of the QRS complex to the end of the T wave. At a heart rate of 70 beats per minute it is
usually about 0.35 seconds in duration, but the duration of the QT interval is very heart rate
dependent. The lower the heart rate is, the longer the QT interval. Individuals with a
mutation in one of several potassium ion channel genes may have long QT syndrome, which
increases the possibility of sudden cardiac death (SCD). There are, however, other causes of
long QT intervals, including: hyperkalemia, hypocalcemia, and mitral valve prolapsed, to
name a few. Because the QT interval is heart rate dependent, it is helpful to calculate a
corrected QT interval (QTc), which should be approximately 0.44sec ±0.02 seconds:
QTc = QT interval / RR interval
Lab X - 3
ST segment - Is the segment between the J point (the end of the QRS complex) and the beginning of
the T wave. If this segment is significantly below the isoelectric line it is called ST segment
depression and it suggests that part of the subject’s myocardium is not getting enough
oxygen (myocardial ischema). This segment is also frequently elevated (ST segment
elevation) above the isoelectric line in the early stages of a myocardial infarction. The ST
segment is discussed in detail in the next lab.
If you have assessed each of these intervals (see Appendix 7-2) and have assessed each of the
different waveforms on your subjects EKG, you can identify your subject’s rhythm (Appendix 7-3 to
7-6). That is, is their heart in a normal, regular electrical rhythm (normal sinus rhythm) or do they
have an abnormal rhythm (an arrhythmia). When abnormal electrical rhythms are present the subject
is said to have an arrhythmia (sometimes called a dysrhythmia). A very common arrhythmia occurs in
conjunction with respiration. During inspiration the large veins in the thoracic cavity fill with blood
and during expiration this blood is forced into the heart. If there is an increase filling of there will be
an increase in heart rate, this is called the Bainbridge reflex. Therefore heart rate is frequently seen to
increase and decrease during the respiratory cycle and is referred to as a Sinus arrhythmia. To
determine if your subject has sinus arrhythmia, measure the interval between two consecutive R
waves. Compare this interval with the next 5-8 R-R intervals; are they all the same or do they differ?
If the RR intervals are not all the same, your subject has sinus arrhythmia. In general, arrhythmias can
be grouped into four basic areas (Appendix 7-3 to 7-6).
a) abnormal pacemaker function
- Sinus arrhythmia
b) ectopic focus (originating from some point other than the SA node)
- PACs, PVCs
c) conduction system blocks
- Atrioventricular (1st, 2nd and 3rd degree) and bundle branch blocks
d) abnormal conduction pathways
- flutter and fibrillation patterns
Recording the electrical activity of the heart
EKGs are usually recorded on a standardized EKG paper resembling graph paper with red
lines. On EKG paper, each of the vertical thick red lines is separated from each other by a horizontal
distance of 5mm and represents a time of 0.2 seconds. Each thin red line is separated by a horizontal
distance of 1mm and represents 0.04 seconds. Thus, the PR interval, which is usually 0.12 to 0.2
seconds long, is usually 3 to 5 “small boxes” across and the QRS interval (0.08 to 0.12 seconds
normally) is 2-3 “small boxes” across. A vertical distance of 10mm usually represents a deflection of
1mV on a standard EKG tracing.
The electrical activity of the heart is recorded from the body by surface electrodes. The
combination of two or more electrodes is used to evaluate the timing and the direction of the electrical
activity. Each combination of electrodes is called and EKG lead. In each of the limb leads one
electrode is designated as positive (+) and one is designated as negative (-). In each of the augmented
voltage leads one electrode is designated as positive (+) and two electrodes are designated as negative
(-). The precordial leads (also called chest leads) are unipolar; they only have a single electrode,
which is a positive (+) electrode. If the wave of depolarization (the spread of electrical activity) is
moving toward the (+) electrode, it results in an upward deflection of the recording (see figure below).
A wave of depolarization moving away from the (+) electrode causes a downward deflection in the
recording. The opposite is true for a wave of repolarization.
Lab X - 4
(+)
(-)
(+)
Depolarization
(-)
Depolarization
EKG
EKG
recording
recording
If the wave of depolarization is in some other direction the corresponding graphic
representation may appear as one of the following.
(+)
(-)
The mean electrical axis (the average direction of the wave of depolarization) of the heart is
from the base toward the apex (down and to the left side of the subject). Thus, in limb lead II, because
the electrical activity is spreading from towards the positive electrode (Left leg), the QRS complex is
generally very positive (upwards). The mean electrical axis gives us a relative indicator of the direction
and magnitude of the electrical activity in the heart. Remember that in a normal human heart as the
electrical impulse goes from the SA node to the AV node to the Common bundle to the right and left
bundle branches to the Purkinje fibers and then into the ventricular myocardium the wave of
depolarization tends to go from the right atrium towards the apex of the heart.
Base
LA
RA
LV
RV
Apex
Looking at the mean electrical axis of an individual’s heart can give us valuable information
about possible hypertrophy and/or infarction of part of the myocardium. If the myocardium is
hypertrophied, the increase in the size of the myocardium in the hypertrophied area causes a relative
increase in the electrical activity of that area. This means that the mean electrical axis will tend to shift
towards hypertrophy due to this increase in electrical activity. On the other hand if the myocardium is
necrotic (dead) in a particular area, such as is the case after a myocardial infarction, because these cells
are no longer living they do not depolarize when an action potential reaches them. The result of this
lack of electrical activity is that the mean electrical axis will tend to shift away from infarction.
Other situations and conditions can alter the mean electrical axis. The mean electrical axis of
individuals who are severely obese or pregnant may be shifted to the left. The reason for this is that
the fatty deposits or the fetus are pushing up on the diaphragm, which is in turn pushing the apex of the
heart towards the left. It is also not uncommon in tall thin individuals to see a difference in mean
electrical axis between the supine and standing positions. The cause of this difference is that when the
individual is lying down many of the abdominal contents push up on the diaphragm, and thus on the
heart. When they stand up the heart shifts back.
Lab X - 5
Utilizing these concepts and placing surface electrodes on standard areas of the body we can
produce standard lead configuration with reproducible waveforms. The placement of electrodes in
different arrangements allows for different views of the same electrical event. Some leads provide
better information than others regarding a specific area of the heart. For this reason several lead
combinations are frequently used to give a comprehensive evaluation of the electrical activity of the
heart. A 12 lead EKG is a standard procedure that uses the combination of 10 different electrodes to
provide 12 different lead configurations. We will be using a standard 12 lead EKG in today's lab. A
standard 12 lead EKG includes: three limb leads, three augmented voltage leads, and six precordial
leads.
The limb lead configuration is based on Einthoven's Triangle. This triangle surrounds the heart
and is made up of three electrodes placed on the right and left arm and the left leg (an electrode is also
placed on the right leg to serve as a ground wire). Combinations of these three electrodes can be used
to produce six different views of the heart in the frontal plane. Limb leads I, II and III are
demonstrated in the following diagram. It is very important to note what
electrodes make up each of these leads and which electrode is positive or negative in each lead.
(-)
I
(+)
RA
LA
(-)
(-)
II
III
(+)
(+)
LL
The other three leads on the frontal plane are produced by combining two electrode locations to
make the negative component of the lead. These leads are referred to as augmented voltage (AV)
leads. There names correspond to the single electrode that is positive. AVR - the right arm is positive
and the left arm and left leg are negative. AVL the left arm is positive and the right arm and left leg
are negative, and in AVF (F is for the left foot or leg) the left leg is positive and the right and left arms
are negative. By combining two electrodes to serve as the negative pole of the lead reference of the
lead goes half way between the two electrodes.
RA
LA
AVR
AVL
AVF
LL
Lab X - 6
The combination of all six frontal leads allows the heart to be evaluated from six different angles or
views.
III
AVL
I
AVR
II
AVF
The six precordial leads, or chest leads, are said to be on the horizontal plane relative to the
heart. They are arranged at various positions around the chest and are named V1 through V6. V1 and
V2 are frequently referred to as the right chest leads. V5 and V6 are frequently referred to as the left
chest leads, although they are also sometimes referred to as lateral chest leads, or apical chest leads
because they are located near the apex of the heart. V3 and V4 are approximately over the anterior
wall of the heart and the interventricular septum.
Ischemia, Infarction, and graded exercise testing (GXT)/ stress testing
It has been demonstrated by many researchers that exercise can assume an important role in the
prevention of CAD by reducing the incidence of certain risk factors. In addition, exercise appears to
exert an independent beneficial effect on the body, which tends to increase one’s tolerance to
cardiovascular disease. Additionally, results of recent research seem to indicate that active people
suffer fewer heart attacks. It is generally accepted that physically active people have a higher rate of
survival from heart attacks.
Despite all of the recent awareness and interest in physical exercise among people of the world
there continues to be a cultural trend toward physical inactivity for most residents of industrialized
nations. Physicians and allied health personnel, in the past, have tended to ignore the value of properly
prescribed exercise as one mode of treatment for a variety of diseases or maladies associated directly
or indirectly with inactivity. By becoming more familiar with the area of exercise and testing in
general, perhaps you will not be quite as hesitant in prescribing exercise as a treatment when your
evaluation indicates under activity as a contributing factor. Additionally, there are some risks involved
in beginning an exercise program, particularly if it is a vigorous exercise program. These risks are
even greater for older individuals, and those individuals who are at increased risk of developing CAD.
Thus, one purpose of exercise stress testing is to determine what intensity of exercise is safe (if any)
for an individual to perform.
Exercise stress testing has become an integral diagnostic tool for the physician to diagnose and
reveal cardiac abnormalities. It is one of the first tests performed in addition to a medical examination
if a person is thought to have CAD. Other tests may be required, depending on the outcome of a 12lead EKG monitored GXT. The position statement made by the American Heart Association’s
Committee on Exercise emphasizes understanding both the risks of exercise and the roles of exercise
testing and exercise prescription to promote safe exercise programs.
Lab X - 7
“For the sedentary individual there is serious risk in the sudden, unregulated and injudicious
use of strenuous exercise. But it is a risk that can be minimized and perhaps even eliminated through
proper preliminary testing and the individualized prescribing of exercise programs.”
Stress tests are performed for several reasons including:
1.To diagnose the presence of CAD in symptomatic and asymptomatic individuals
2.To determine if a patient is ready for discharge after an MI, or after surgery such as PTCA
(Angioplasty, percutaneous transluminal angioplasty) or CABG (Bypass
surgery, coronary artery bypass graft)
3.To determine if a patient is ready to return to normal activities after being discharged
after an MI, PTCA, or CABG
4.To determine physical working capacity (aerobic capcity)
5.To assess the safety of exercise
6.To evaluate the progress of a known disease state
7.To evaluate the effectiveness of treatment (drug, exercise, surgery).
We will concentrate most of our efforts today on discussing the use of stress testing for the
diagnosis of CAD. There are several EKG changes that may be indicative CAD. Most notable are
changes that occur to the ST segment (see Appendix 8-3 and 8-4). The segment of an EKG between
the S-wave and the T-wave. The most frequent electrocardiographic signs of myocardial ischemia are
inverted T-waves in leads that normally have upright T-waves, and more frequently, ST-segment
depression. ST segment depression may occur in several forms (see figure in Appendix), listed here
from least bad to worst: upsloping, horizontal, and downsloping ST-segment depression. It should be
noted that ST segment depression is not always indicative of myocardial ischemia. A stress test
performed where significant ST-segment depression is present, but the person does not really have
CAD is called a false positive test. Likewise, the absence of ST-segment changes that are indicative of
CAD during a graded exercise test does not necessarily mean that the person doesn’t have CAD. A
GXT that is negative for signs of CAD when the person actually does have CAD (usually defined
conclusively by significant reduction in coronary blood flow as determined by an angiogram) is called
a false negative test.
ST-segment elevation may be indicative of myocardial injury or an acute myocardial infarction.
The transition from myocardial injury to myocardial infarction is also characterized by a widening, and
in some cases deepening of the Q-waves. Remember, myocardial ischemia is indicative of CAD, a
myocardial infarction (MI) is one possible consequence of CAD. A MI may be caused by other
mechanisms not directly associated with CAD.
Because of the possibility for false positive and false negative tests it is important to optimize
the validity and reliability of the stress test. Several things can be done to improve the accuracy of the
test for diagnostic purposes, for example, proper instructions (preferably written) should be provided to
the patient several days prior to the test. For example, the patients should not eat or exercise in the
hours preceding the test. Remember, the EKG is only one thing to consider when determining if the
test was positive for CAD or not. For instance, a failure of heart rate or systolic blood pressure to
increase during the exercise test are considered abnormal responses. Additionally, a drop in SBP may
be indicative of poor ventricular contractility (which is associated with heart failure, for example). It
should be recorded if the patient experienced angina, and if so how intense (painful) was the angina. It
should also be noted if the patient exhibited any dyspnea (shortness of breath, SOB)? All risk factors
must also be taken into account. If the person had a high pre-test probability of having CAD, based
upon risk factors and sign/symptoms of CAD, then ST-segment changes are likely to be indicative of a
true positive test. Additionally, the worse the ST-depression, the more likely it is to be indicative of
CAD.
Lab X - 8
To increase the objectivity in determining if the ST segment changes are significant, a set of
criteria should be used in order to maximize the accuracy of the stress test for diagnosis CAD. One
example of such criteria requires that you first find the “J-point” which is the point that demarcates the
end of the S-wave. It has been suggested that a good place to measure ST-segment changes is 0.08
seconds (2 small boxes) after the J-point (2 small boxes after the J-point on standard EKG paper). If
the ST-segment is depressed more than 1mm (one small box) at 0.08 seconds after the J-point, and the
ST depression is horizontal or downsloping, then this may be indicative of CAD. If the ST-segment
depression is upsloping, it has been suggested that the ST-segment should be depressed 1.5mm below
the isoelectric line for it to be considered truly indicative of CAD. This does not mean that a test
should be stopped as soon as the ST-depression reaches 1-1.5mm. If the test is being performed for the
diagnosis of CAD, then the greater the ST-depression 1) the more likely it is to be a “true” positive
test, and 2) the worse the ischemia. If the ST depression reaches 2mm, and continues to be worsening,
then the test should be stopped.
Lab X - 9
LABORATORY PROCEDURES
We will be recording 12 lead EKGs today from each person in the class. They require
electrode placement on the right arm, left arm and the left leg (the right leg is also used for a ground)
as well as various locations around the chest. Please note that for exercise measurements, the locations
of the limb electrodes are modified to the anterior shoulder just below the clavicle (avoiding muscle
mass) for the arm electrodes and the lower left intercostal space for the left leg electrode. Before
placement of electrodes, attachment sites should be rubbed thoroughly with an alcohol prep pad until
the skin is slightly reddened. It may be necessary to shave small areas around the chest for placement
of the chest electrodes. This will improve the electrical conductivity of your leads. Every student will
be given a printout of both a rhythm strip and a 12 lead EKG recording. The difference between a
rhythm strip and a 12 lead EKG is that a rhythm strip records the same lead or leads all the way across
the EKG paper. A 12 lead EKG records information from all 12 leads across the EKG paper divided
into short, 2.5 second periods so that all 12 leads can fit on one page. In this course we will always
analyze the EKG in the following order.
Analyze the EKG in the following order:
A.
B.
C.
D.
E.
Determine HR
Determine Rhythm (see below)
Determine Axis
Determine if there are any signs of hypertrophy
Determine if there is any evidence of ischemia or infarction
I. Site preparation and electrode placement.
The placement of the chest leads is fairly standard. However, the placement of the electrodes for
the limb and augmented voltage leads are slightly different depending on whether you are
performing a resting or exercising EKG. We will be using the exercise placement of these
electrodes. Prior to placing the electrodes on the subject prepare the skin with an alcohol prep pad,
and by shaving if necessary. Allow the alcohol on the skin to dry before placing the electrodes on
the skin. After the electrodes are attached to your subject's body, attach the electrical cords from
the EKG machine to the surface electrodes. The following are the locations of the 10 electrodes
used in a 12 lead EKG.
Ground (or "reference") electrode
RL – placed on the lowest right intercostal space, approximately mid-clavicular
Limb electrodes
RA - placed half way across the right clavicle in the sub-clavicular fossa
LA - placed half way across the left clavicle in the sub-clavicular fossa
LL - placed on the lowest left intercostal space, approximately mid-clavicular
Chest electrodes*
V1 - right sternal border in the 4th intercostal space
V2 - left sternal border in the 4th intercostal space
V3 - mid way between V2 & V4
V4 - mid clavicular in the left 5th intercostal space
V5 - mid way between V4 & V6 (around the left anterior axillary line, 5th intercostal space)
V6 - left mid axillary line in the 5th intercostal space (or mid axillary and even with V4)
*The placement of some or all the chest electrodes may need to be slightly modified in women to
avoid placing the electrodes over the fleshy part of the breast.
Lab X - 10
II. Printing the EKG.
Print off a single sheet rhythm strip and a 12 lead EKG for each subject.
III. Evaluating the EKG
After preparing the subject, hooking the subject up, and printing both a rhythm strip and a 12 lead
EKG, use the following steps to evaluate the EKG.
A. Determine the Heart Rate in beats per minute. Use the following four methods.
1. Count QRS complexes that are found in a 6 second interval and multiply by 10, this will
give you the approximate HR. This method is especially good if there is an arrhythmia.
2. Determine the amount of time between beats – count the number of small boxes between
QRS complexes and multiply by 0.04 seconds/box. 60 seconds divided by the amount of
time between beats will give you the HR.
3. Count the number of small boxes between QRS complexes (RR interval). 1,500 divided by
this number will give you the HR.
4. Count big boxes between QRS complexes to determine HR as follows:
boxes
rate
boxes
rate
1
300
4
75
2
150
5
60
3
100
6
50
B. Determining the electrical Rhythm of the heart and measuring intervals. (see Appendix for
examples of arrythmias).
1. RR interval and HR
a. Is Heart Rate normal?  Normal Sinus Rhythm, Bradycardia, or Tachycardia
b. Is RR interval (and thus HR) consistently the same from beat to beat? If not
check for sinus arrhythmia or PACs
2. Presence or absence of normally observed waves
a. Is there a P before each QRS?  if not check for PVCs, atrial fibrillation, 2 or 3 AV
blocks
b. Is there a QRS after each P wave?  if not check for 2 or 3 AV blocks, atrial
flutter
c. If P, Q, R, S, and T waves are all absent  check for ventricular fibrillation or
ventricular tachycardia
3. PR interval
a. Is PR interval normal? Is PR interval always normal?  if not check for WolfParkinson-White syndrome or 1, 2 or 3 AV blocks
4. QRS interval
a. Is QRS interval normal? Is QRS interval always normal?  if not check for PVCs
or bundle branch block
5. QT interval. Determine the QT interval and calculate the corrected QT interval. Is it
approximately 0.44 seconds?
C. Determine electrical axis
We will determine the mean electrical axis of the heart in two steps. See the electrical axis
worksheet to assist you with this part of the EKG analysis.
1. The first step is to determine which “quadrant” the mean electrical axis lies in. This will
allow us to know within 90 degrees the direction of the the mean electrical axis. This can
easily be determined by observing leads I and AVF. Observe each lead and determine if
the QRS complex is more above the isoelectric line (positive) or more below the isoelectric
Lab X - 11
line (negative). Lead I is horizontal relative to the heart (and the subject’s body) and is
positive on the left side of the body, if the QRS complex in this lead is more positive, then
most of the electrical activity is going to the left (normal quadrant or left axis deviation) and
if the QRS is more negative, then most of the electrical activity is going toward the right
(right axis deviation or extreme right axis deviation). Lead AVF is vertical relative to the
heart (and the subject’s body) and is positive at the subject’s left foot. If the QRS complex
in AVF is more positive, then most of the electrical activity is going down towards the
subject’s feet (normal quadrant or right axis deviation) and if the QRS is more negative,
then most of the electrical activity is going upwards (left or extreme right axis deviation).
Thus, based on using only these two leads you can determine which quadrant the mean
electrical axis lies in.
2. The second step in determining the mean electrical axis will allow us to determine the
direction of the mean electrical axis to the nearest 30 degrees. This step requires you to
look at all three limb leads and all three augmented voltage leads. Looking at these six
leads, you need to find the most isoelectric lead. The most isoelectric lead is the lead
whose QRS complex has closest to a net deflection of zero. To determine the net deflection
of the QRS complex you simply count the number of small boxes from the isoelectric line
to the peak of the QRS complex (the number of positive boxes) and count the number of
small boxes from the isoelectric line to the bottom of the QRS complex (the number of
negative boxes). The net deflection of the QRS complex is determined by adding the
number of positive and negative boxes. For example, if the QRS complex in AVL goes up
6 small boxes from the isoelectric line (+6) and goes down 6 small boxes from the
isoelectric line (-6), then the net deflection is zero. The significance of the most isoelectric
lead is that it lies approximately perpendicular to the mean electrical axis of the heart. You
can also think of it as the lead where there is just about as much electrical activity going
away from the positive electrode as there is going towards the positive electrode.
Once you have determined the most isoelectric lead, you go perpendicular from that
lead (in the direction of the quadrant that you determined above) to determine the mean
electrical axis. For example, if AVL is the most isoelectric lead and the subject’s mean
electrical axis is in the normal quadrant, their mean electrical axis is 60 (see electrical axis
worksheet below).
D. Determine if there is any evidence of myocardial hypertrophy
Several laboratory methods are available for assessing signs of myocardial hypertrophy. For
example, echocardiography can be used to directly take measurements of the heart's walls or
chambers. Assessing myocardial hypertrophy with EKGs is somewhat imperfect because it
only allows for an indirect assessment of myocardial hypertrophy. Myocardial hypertrophy
specifically relates to the size of the heart wall or chamber and EKGs do not provide direct
measurements of heart size or heart dimensions. However, EKGs can provide some indirect
evidence of cardiac hypertrophy. In this course we will only discuss the most common type of
cardiac (or myocardial) hypertrophy; left ventricular hypertrophy. The following are
considered electrocardiographic indicators of left ventricular hypertrophy.
1. A large, deep S wave in V1 and a large, tall R wave in V5. It has been suggested that if the
depth (in mm) of the S wave in V1 plus the height (in mm) of the R wave in V5 totals
greater than 35mm, then the subject may have left ventricular hypertrophy.
2. Asymmetric, inverted T waves in V5 or V6
3. Left axis deviation with a slightly widened QRS complex.
E. Determine if there is any evidence of myocardial ischemia/infarction. Look at all leads for
evidence of ST segment depression, ST segment elevation, or large Q waves.
Lab X - 12
IV. Demonstration and review of arrhythmias using the arrhythmia generator.
We will use an arrhythmia generator to demonstrate common types of arrhythmias after you have
determined your heart rate using several methods, determined your rhythm, your mean electrical
axis, and evaluated your EKG for signs of left ventricular hypertrophy. It is possible that this will
need to be completed during the next lab time. Review the arrhythmias in your Appendix to begin
your familiarization with these arrhythmias.
V. Evaluate sample EKGs provided by your instructor. Evaluate each for:
1. Heart Rate (measure several places each and use at least two methods)
2. Rhythm (what rhythm are they in, are there any arrhythmias)
A. To answer this you will need to note if all wave forms are present and measure each interval
in several locations
3. Axis (what quadrant are they in, what is their mean electrical axis)?
4. Hypertrophy (is there any evidence of Left Ventricular Hypertrophy?)
5. Ischemia/infarction (is there any evidence of ischemia or infarction – must look at all leads)
Lab X - 13
Data sheet
I. Draw and label a sketch of the location of the electrodes used in a 12 lead EKG. Next to your
figure write a brief description of the location of each.
1. How do we get a 12 lead EKG when using only 10 electrodes?
2. Draw Einthoven’s triangle and label the electrodes, leads, and indicate what electrodes are
+ or – in each lead.
3. What part(s) of the heart are roughly under each of the precordial leads. (you may answer
by drawing a picture)
Lab X - 14
II. Print a Rhythm Strip and a 12 Lead EKG.
III. Evaluating the EKG
A. Heart Rate. From the EKG determine heart rate using each of the four methods described
above. Take several measurements on each recording.
Heart rates _______ _______ _______ _______ _______ _______
_______ _______ _______
average heart rate = _______
B. Rhythm. Assess your subject's electrical rhythm using the methods listed above.
1. RR interval and HR.
a. Are these normal and regular or abnormal/irregular?
b. If these are abnormal, what arrhythmia(s) does your subject have?
2. Presence or absence of normally observed waves
a. Is there a P before each QRS?
b. Is there a QRS after each P wave?
c. Are P, Q, R, S, and T waves all present?
d. Based on this information, does your subject appear to have any arrhythmias?
3. PR interval
a. Is PR interval normal? And is PR interval always normal?
b. If not what arrhythmia(s) does your subject have?
4. QRS interval
a. Is QRS interval normal? Is QRS interval always normal?
b. If not what arrhythmia(s) does your subject have?
4. QT interval. What is the QT interval? What is the QTc? Is QTc ~0.44 seconds?
C. Axis. Determine your subject's mean electrical axis using the worksheet on the next page.
1. What quadrant is your subject's mean electrical axis in?
2. What is the most isoelectric lead?
3. What is your subject's mean electrical axis?
4. If your subject's mean electrical axis is outside of the normal range, what are possible reasons for
this abnormality?
Lab X - 15
Electrical Axis worksheet
LAD
AVF mostly LLI mostly +
ERAD
AVF mostly LLI mostly -
I
RAD
AVF mostly +
LLI mostly -
Normal
AVF mostly +
LLI mostly +
AVF
-90
-120
-60
III
-150
-30
AVL
180
I
0
II
AVR
150
30
II
AVF
60
120
90
Normal
Quadrant
Left Axis
Deviation
Right Axis
Deviation
Extreme Right
Axis Deviation
AVF = 0°
III = + 30°
AVL = + 60°
I
= + 90°
AVF = 0°
II = - 30°
AVR = - 60°
I
= - 90°
I
= + 90°
AVR = + 120°
II
= + 150°
AVF = + 180°
I
= - 90°
AVL = - 120°
III = - 150°
AVF = - 180°
Lab X - 16
D. Hypertrophy. Determine if there is any evidence of left ventricular hypertrophy? What evidence can
be used to determine if there is any evidence of LVH? What criteria can be used to evaluate LVH?
E. Ischemia/Infarction. Determine if there is any evidence of ischemia or infarction? What evidence
can be used to determine if there is any evidence of ischemia/infarction? Where do you look? What
criteria can be used to evaluate ischemia?
IV. Demonstration and review of arrhythmias using the arrhythmia generator.
We will use an arrhythmia generator to demonstrate common types of arrhythmias after you have
determined your heart rate using several methods, determined your rhythm, your mean electrical
axis, and evaluated your EKG for signs of left ventricular hypertrophy. It is possible that this will
need to be completed during the next lab time. Review the arrhythmias in your Appendix to begin
your familiarization with these arrhythmias.
We will cover the following rhythms and arrhythmias (see Appendix for examples):
A. Normal Sinus Rhythm (NSR)
B. Sinus Tachycardia
C. Sinus Bradycardia
D. Sinus Arrhythmia
E. Premature Ventricular Contractions (PVCs)
1. Unifocal
2. Multifocal
3. R on T PVCs
4. Ventricular bigemini
F. Premature Atrial Contractions (PACs)
G. AV blocks
1. 1st degree AV block
2. 2nd degree AV block type I (Wenchebach syndrome)
3. 3rd degree AV block (complete heart block)
H. Bundle Branch Blocks
I. Atrial Fibrillation
J. Atrial Flutter
K. Ventricular tachycardia
L. Ventricular fibrillation
Lab X - 17
V. Evaluate sample EKGs provided by your instructor. Evaluate each for:
A. EKG A
1. Heart Rate (measure several places each and use at least two methods)
2. Rhythm (what rhythm are they in, are there any arrhythmias). To answer this you will need to
note if all wave forms are present and measure each interval in several locations
3. Axis (what quadrant are they in, what is their mean electrical axis)?
4. Hypertrophy (is there any evidence of Left Ventricular Hypertrophy?)
5. Ischemia/infarction (is there any evidence of ischemia or infarction – must look at all leads)
B. EKG B
1. Heart Rate (measure several places each and use at least two methods)
2. Rhythm (what rhythm are they in, are there any arrhythmias). To answer this you will need to
note if all wave forms are present and measure each interval in several locations
3. Axis (what quadrant are they in, what is their mean electrical axis)?
4. Hypertrophy (is there any evidence of Left Ventricular Hypertrophy?)
5. Ischemia/infarction (is there any evidence of ischemia or infarction – must look at all leads)
Lab X - 18
C. EKG C
1. Heart Rate (measure several places each and use at least two methods)
2. Rhythm (what rhythm are they in, are there any arrhythmias). To answer this you will need to
note if all wave forms are present and measure each interval in several locations
3. Axis (what quadrant are they in, what is their mean electrical axis)?
4. Hypertrophy (is there any evidence of Left Ventricular Hypertrophy?)
5. Ischemia/infarction (is there any evidence of ischemia or infarction – must look at all leads)
D. EKG D
1. Heart Rate (measure several places each and use at least two methods)
2. Rhythm (what rhythm are they in, are there any arrhythmias). To answer this you will need to
note if all wave forms are present and measure each interval in several locations
3. Axis (what quadrant are they in, what is their mean electrical axis)?
4. Hypertrophy (is there any evidence of Left Ventricular Hypertrophy?)
5. Ischemia/infarction (is there any evidence of ischemia or infarction – must look at all leads)
Lab X - 19
Study questions
1. What are normal values for PR, QRS, QT, and RR intervals? Which of these are heart rate
dependent?
2. What intervals would you expect to change during exercise?
3. What arrhythmias are associated with abnormal PR intervals? How can you tell the difference
between these arrhythmias?
4. What arrhythmias are associated with abnormal QRS intervals? How can you tell the difference
between these arrhythmias?
5. Name the major life-threatening arrhythmias.
6. What is an ectopic focus? What arrhythmias are examples of ectopic foci?
7. Name several factors that affect mean electrical axis?
8. Explain in your own words how to determine mean electrical axis.
9. Explain in your own words each of the methods of determining heart rate.
10. What arrhythmia would be expected to occur in normal subjects during exercise?
Lab X - 20
11. The ____________________ branch of the autonomic nervous system could cause bradycardia,
whereas the ____________________ branch of the autonomic nervous system could cause
tachycardia.
12. What is sinus arrhythmia? What causes it?
13. What part of the EKG would be most affected by myocardial ischemia?
14. What are the characteristics of the following arrhythmias?
a. PAC
b. Atrial tachycardia
c. Atrial flutter
d. Atrial fibrillation
e. Unifocal PVCs
f. Ventricular tachycardia
g. Ventricular fibrillation
h. First Degree AV block
i. Second Degree AV block
j. Third Degree AV block
k. Bundle Branch Block
l. Multifocal PVCs
m. R on T PVC’s
n. Sinus arrhythmia
15. Which of the above are immediately life threatening? Why/how are these life threatening?
16.
Which of the above might you expect to happen on occasion in normal, healthy individuals?
Lab X - 21
17. Name and describe the location of each of the ten electrodes that are used to record a 12-lead
EKG.
18. What criteria are used to determine if ST segment changes are indicative of CAD?
19. Explain how the following terms are inter-related: atherosclerosis, coronary artery disease,
myocardial oxygen demand, rate pressure product, myocardial ischemia, angina pectoris, and
ST segment depression.
20. What is the basis for using graded exercise testing to diagnose CAD?
Lab X - 22