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Good sources:

http://www.practicalclinicalskills.com

Suggested reading:
Mohrman and Heller 8th Edition: http://www.amazon.com/Cardiovascular-
Physiology-Lange-Medical-Books/dp/0071793119
Free access via the link:
http://accessmedicine.mhmedical.com/content.aspx?bookid=843&sectionid=487796
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Good resource:
https://www.youtube.com/watch?v=9TRYM7IdnDY

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Online resources: (the underlined words are hyperlinks):

EKGpedia: http://en.ecgpedia.org/wiki/Main_Page

Combines ECG and heart sounds – http://www.bioscience.org/atlases/heart/

Up-To-Date (Accessible through Electronic Resources, Ross Library)


ECG Tutorial part 1; ECG Tutorial part 2; Myocardial action potential
and arrhythmias

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When the heart cells are at rest, the outer surface of the cells are positive relative to
the inside, which are more negative. However, as an action potential spreads
throughout the cardiac tissues, the outer surface of the cell changes from positive to
negative. It is this change in surface charge that is recorded in an ECG as this is
conducted via the extracellular fluid to the surface of the skin. Electrodes placed on
the surface of the body can detect the movement of electrical activity, or the spread
of electrical activity throughout the heart. The magnitude of the signals is however
much smaller than what is occurring at the cellular level in the heart.

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As the action potential (in blue) spreads from left to right the volt meter now records
a difference in potential.

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See Slide

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See Slide

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There are three standard limb leads (I, II, III) which are bipolar (see figure above).
•Lead I has the positive electrode on the left arm
•Lead II has the positive electrode on the left leg
•Lead III has the positive electrode on the left leg

This arrangement creates a triangle with the heart in the centre. This is known as
Einthoven’s triangle. Willem Einthoven (born May 21st 1860- September 29th 1927
was a Dutch doctor and Physiologist. He invented the first practical
electrocardiogram (ECG or EKG) in 1903 and received the Nobel Prize for Medicine
in 1924.

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P wave associated with atrial depolarization which then leads to the contraction of
the atria.
PQ (aka PR interval) interval includes the time for atrial depolarization as well as
the time for the passage of the action potential through the AV nodal tissue
QRS reflects Ventricular depolarization following which ventricular contraction
occurs.
The ST segment reflects the period of time that the ventricles are fully depolarized
during the plateau phase of the ventricular action potential.
The T wave represents ventricular repolarization.
The QT interval represents the period of time from the beginning of ventricular
depolarization to the end of ventricular repolarization.

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The P wave is the first positive (upward) deflection, and represents depolarization of the atrium. This
is the electrical event which initiates contraction of the atria, and its duration (approx 80 ms) reflects
the time required for atrial depolarization to occur. The right atrium depolarizes first followed by the
left atrium, so the first third of the P wave = RA depolarization, the 2nd third = RA and LA
depolarization and the final third, LA depolarization. Therefore in conditions leading to right or left
atrial hypertrophy (which occurs as a consequence of valvular disease) the P wave will be increased
in magnitude. So for example in left atrial hypertrophy the final 3rd of the P wave will be increased in
magnitude .
The P wave is followed by a period of electrical neutrality called the PR segment. This segment
represents the time required for conduction of an action potential through the AV Node. Remember
that the PR segment is different from the P-R interval (see later). The important factor to analyze for
‘segments’ on the ECG is any change from the isoelectric line (e.g. elevation or depression) while the
important thing to analyze for ‘intervals’ is their duration.
The PR interval therefore includes the P-wave (spread of excitation through the atria) and the PR
segment, and is the time required for the wave of depolarization to move from the SA Node through
the atria, through the AV node enter the His-Purkinje system. The normal PR interval is 0.12 to 0.20
seconds. The PR interval shortens when heart rate increases and lengthens when heart rate
decreases. If this interval is greater than 0.20 seconds, this usually indicates an AV conduction block
(in the AV Node or Bundle of His).

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See Slide Text

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The QRS interval reflects the time required for ventricular depolarization through
the cardiac myocytes. This is the electrical event which initiates ventricular
contraction. The normal duration is less than 0.10 seconds. Atrial repolarization is
occurring at this time but is obscured by the greater signal arising from the electrical
activity of the ventricles.

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As the epicardial AP is shorter than the Endocardial one (more Ito) , repolarization
proceeds from epi to endo (see lecture 1)

• Greater expression of Ito in epicardium


• Gives marked phase 1 repolarization and spike and dome configuration in
epicardium
• Epicardial APs are shorter in duration than Endocardial Aps
• Depolarization spreads Endo to Epi
• Repolarization spreads Epi to Endo

If ventricular excitation is not a result of the spread of electrical activity via the His-
Purkinje system, then abnormalities in QRS configuration are caused and this leads
to abnormalities in the configuration of the T-wave also.

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The P-Q and P-R intervals are effectively interchangeable but in the USA, P-R
interval is most commonly used. Paradoxically, the PR interval is not the measure
from the beginning of P wave to the R peak, but to the end of the P-R segment as in
the P-Q interval.

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The ECG is a very useful diagnostic tool and many conditions can be diagnosed due to
changes in ECG waveform.
ST segment elevation (by 2 or more small squares): This is commonly seen in cases of
acute myocardial infarction (full wall thickness) and also seen in acute pericarditis. This is
caused by changes in the electrical properties of myocytes within the infarct area and the
generation of injury currents as a consequence. ST elevation in groups of leads helps
identify the location of the infarct- e.g. ST elevation in leads II, III and avF which are the
inferior group of leads, suggests an inferior MI (see later slides).
ST segment depression: It is often a sign of myocardial hypoxia/ischemia, of which
coronary insufficiency is a major cause. Other ischemic heart diseases causing ST
depression include: during angina attacks, subendocardial ischemia or even infarction (i.e.
not full wall thickness) . Subendocardial means an infarct that does not affect the full
thickness of the left ventricular wall. In contrast, ST segment elevation is associated with
transmural (or full thickness) ischemia.

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Normal QT interval is generally less than 400 ms at rest. Prolongation of QT e.g. in
Long QT syndrome (LQTS) where a QT interval of >450 ms is measured,
predisposes the heart to ventricular arrhythmias. LQT comes in many forms and
the 3 most common forms are caused by mutations in genes which leads to
abnormalities in Ion channel function in channels involved in the generation of the
ventricular action potential. These channels include gain of function in the sodium
current (INa) responsible for the fast upstroke of the ventricular action potential
(LQT3) as well as loss of function in potassium channels IKs (LQT1) and IKr
(LQT2) due to gene mutations which delay the repolarization phase in ventricular
tissue.

As heart rate increases the Q-T interval shortens in normal individuals and so you
can correct for the effects of heart rate by using a variety of strategies e.g. Bazett’s
formula: QTC = QT / √ R-R interval (in s) which takes the measured QT interval
which is divided by the square root of the R-R interval to give a corrected QT
interval or QTc and is considered prolonged if >450 ms in men and 470 ms in
women. See ECG 2 lecture.

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The electrocardiogram (ECG) reflects the electrical activity of the heart recorded on
the surface of the body. Recordings from 10 different wires placed at specific
locations on the body constitute a normal 12 lead ECG. An individual connected to
an ECG recorder is illustrated in the figure to the left.
Don’t think of Leads as wires, think of a lead as an electrical view through the
heart.
Limb leads are made up of 4 leads placed on the extremities: left and right wrist; left
and right ankle.
The lead connected to the right ankle is a neutral lead, like you would find in an
electric plug. It is there to complete an electrical circuit and plays no role in the ECG
waveforms at the different viewpoints.

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The 12 ECG leads should be considered as electrical viewpoints

The electrodes are placed on the left and right wrists and the Left foot, with a
neutral on the right foot. However, because each limb serves as an electrical
conductor connected to the trunk, the limb electrodes in effect record from each
shoulder and the pelvis, thus forming a triangle around the heart- Einthoven’s
Triangle. Each lead “looks” at the electrical activity of the heart from a directional
‘viewpoint’ (vector) that depends upon the positioning of the electrodes and how the
electrodes are interconnected with each other.

No matter which lead is being used to "look" at the heart, the electrode doing the
looking is always a single positive electrode. However, the "other" electrode could
be a single electrode or a number of other electrodes joined together to form a
reference point (as the negative). The viewpoint of each can be calculated from all
these influences.

Pairs of limb electrodes can be connected across a voltmeter in three different


combinations, called the bipolar limb leads (I, II and III). When the left arm signal is
connected to the positive terminal of the voltmeter with the right arm as the
negative, this is called Lead I. The Lead II view is created by feeding the signal from
the left leg into the positive electrode of the voltmeter and using the right arm signal
as the negative. Finally, if the left leg is positive and left arm negative, that gives
you Lead III.

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The augmented limb lead views are created as follows: The electrical signal from
two of the limb electrodes is simultaneously fed into the negative terminal of the
voltmeter, thereby producing an average signal which is located roughly in the
centre of the chest. If you then compare the signal from the foot with the averaged
signal from the other two limb wires (aVR and AVL) then that gives a view at 90
degrees to the horizontal and creates the view aVF with the positive terminal
pointing towards the feet.

If you then make the left arm the positive electrode and combine the signals from
the left leg (aVF) and right arm (aVR) as the negative, then this creates another
view aVL at an angle of -30 degrees to the horizontal.

Finally If you then make the right arm the positive electrode and combine the
signals from the left leg (aVF) and left arm (aVL) as the negative, then this creates
another view aVR at an angle of -150 degrees to the horizontal.

So from these 4 wires (including the neutral), 6 different electrical views of the heart
are created.

NOTE: for example viewpoint aVR has its +ve end at -150 degrees and its negative
end at +30 degrees- don’t mix up the angles (e.g. -150 degrees, +ve end of aVR)
with which is the positive end of a viewpoint.

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There are six precordial leads, aka “chest leads”, which are unipolar (V1 to V6).
They only have positive electrodes, as depicted on the image. These leads are
placed along an arc on the chest beginning just to the right of the sternum and
proceeding under the left arm as shown in the figure above. The precordial leads
see a “wraparound view” of the heart from the horizontal (transverse) plane through
the heart.
These unipolar positive electrodes use a zero reference point as a negative, which
is generated by the sum of the three limb electrodes (right arm, left arm and left leg)
connected to a central terminal through three large resistors (e.g. 5000 Ohms-
Wilson’s Central Terminal). The net effect is a potential difference of close to zero
that lies as a point source at the center of Einthoven’s triangle.

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Understanding the QRS deflections in the precordial leads.
Because initial ventricular depolarization is from left to right across the ventricular septum,
therefore in V1, the spread of electrical activity is initially towards the V1 electrode giving a
small upward deflection but then as the larger mass of the left ventricle depolarizes, the
main vector for the spread of excitation is then away from the V1 electrode giving a large
negative deflection before the wave of depolarization moves up the walls of the heart
leading to a return of the deflection to the isoelectric point. You will see as you progress
from V1 to V4, the electrodes become closer to aligning with the orientation of the
interventricular septum of the heart and in this example V4 is almost situated opposite the
apex of the heart (very much like lead II) so that the spread of excitation down the septum
is spreading directly towards V4. So you will see that the R wave is becoming
progressively more positive and the V4 tracing is very similar to the Lead II waveform.
Tracings from leads V5 and V6 are almost opposite in polarity from V1 because they are
viewing opposite sides of the heart. Leads V2-V4 are intermediate owing to their electrode
placement.
As the orientation of the heart differs between individuals (and in pathological conditions),
then the waveforms recorded will differ slightly depending on which of the 6 precordial
leads is most closely oriented with the apex of the heart But there should always be a
progression from a negative QRS through to a positive QRS as you go from V1-V6. In
summary, the chest leads provide a different view of the electrical activity within the
heart. Therefore, the waveform recorded is different for each lead compared to the limb
leads.

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So V1 and 2 are viewing the anterior and septal portion of the heart (including Right Ventricle
and anterior septum) , V3 and 4 the anterior and apical section of the heart and V5 and 6 the
lateral part of the heart (Left Ventricle).
Images taken from : http://www.cvphysiology.com/Arrhythmias/A013c.htm

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The ECG trace covers 10 seconds of time. The upper 3 sets of traces show 2.5
seconds from each of the 12 leads and the bottom 3 traces in this example
duplicate some chosen leads- in this example V1, Lead II and V5 over a 10 second
period, this is commonly called the ECG rhythm strip.

NOTE:
Any downward deflection immediately following the P-R segment is denoted as a Q
wave (e.g. in Lead 2) which normally is followed by an upward R wave
An upward deflection following the P-R segment is denoted as an R wave: see V1
which is then followed by a deep S wave which goes strongly negative to the
isoelectric line or look at V5 which has a tall R wave and only a very small S wave.

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This slide shows how the leads are grouped together. The table above separates
the leads into Inferior, Lateral, Anterior and Septal groups. So for example if you
saw ST elevation in a group of leads e.g. Leads II, III and aVF, that would be
indicative of an acute Inferior infarct. In such a condition, you would also see
reciprocal ST depression in leads looking the other way- for example aVL as this
looks away from lead III, if the inferior leads display ST elevation.

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ST elevation in groups of leads helps identify the location of an infarct- e.g. ST
elevation in leads II, III and avF which are the inferior group of leads, suggests an
acute inferior MI.

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