1. WINDSOR UNIVERSITY SCHOOL OF MEDICINE
Cardio Vascular Physiology
Electrical activity
& Electrocardiography
Dr. Samuel Taiwo AlawodeVishal Surender.MD.

2. • The coordinated contractions of the heart result from electrical changes that take place in cardiac cells.
Intrinsic Conduction System
• Cardiac autorhythmic cells in the intrinsic conduction system generate action potentials that spread in waves to all the cardiac contractile cells. This action causes a coordinated heart contraction.
Gap Junctions
• Action potentials generated by autorhythmic cells create waves of depolarization that spread to contractile cells via gap junctions.
Gap Junctions
autorhythmic cell
contractile cells

3. Autorhythmic Cell Anatomy
1. Sodium Channels - allow sodium ions to enter the cell
2. Calcium Channels - allow calcium ions to enter the cell.
3. Potassium Channels - allow potassium ions to leave the cell.
. Sodium K+
Calcium
Gap Junction

4. Gap Junction

5. Action Potentials in Cardiac Autorhythmic Cells(ex:-SA node)
Myocardial Autorhythmic Cells
Generate action potentials spontaneously in the absence of input from the nervous system.
This ability results from their unstable membrane potential, which starts at -60 mV and slowly drifts upward toward threshold.
This unstable membrane potential is called a pacemaker potential rather than a resting membrane potential because it never "rests" at a constant value. Whenever a pacemaker potential depolarizes to threshold, the autorhythmic cell fires an action potential.

6. Regulation of the Heart Rate
HR is controlled by the ANS: both parasympathetic (PS) and sympathetic nerves.
The speed with which pacemaker cells depolarize determines the rate at which the heart contracts (the heart rate),SA node-Pacemaker.
The effects of the autonomic nervous system on heart rate are called chronotropic effects.

7. Contractile Cell Anatomy
• The cardiac contractile cell relies on the autorhythmic cell to generate an action potential and pass the impulse down the line before the cell can contract.
• Like the autorhythmic cell, it has ion transport channels, but they are slightly different.
• Gap junctions link autorhythmic and contractile cells, and link contractile cells with each other.
• Notice the sarcoplasmic reticulum (SR), which is a storage site for calcium. Channels within the SR membrane allow calcium ions to be released within the cell.
• The myofilaments are the contractile units of the cardiac muscle cell.
Fast Na+ K+
Slow Ca+ SR

8. Myocardial Contractile Cells
Action potential of a cardiac contractile cell
The action potentials of
myocardial contractile cells are similar in several ways to those of neurons and skeletal muscle.
The main difference between the action potential of the myocardial contractile cell and that of a skeletal muscle fiber or a neuron is that in the myocardial cell, there is a longer action potential due to Ca2+ entry.
Phase
Membrane channels
PX = Permeability to ion X
+20
-20
-40
-60
-80
-100
Membrane potential (mV)
100
200
300
Time (msec)
PK and PCa
PNa
Na+ channels open
Na+ channels close
Ca2+ channels open; fast K+ channels close
Ca2+ channels close; slow K+ channels open
Resting potential 1 2 3 4

9. Myocardial Contractile Cells
Phase 4: resting membrane potential. Myocardial contractile cells have a stable resting potential of about -90 mV.
Phase 0: depolarization. When a wave of depolarization moves into a contractile cell the membrane potential becomes more positive. Voltage-gated Na+ channels open, Na+ enter the cell and rapidly depolarize it. The membrane potential reaches about +20 mV before the Na1 channels close.
Phase
Membrane channels
PX = Permeability to ion X
+20
-20
-40
-60
-80
-100
Membrane potential (mV)
100
200
300
Time (msec)
PNa
Na+ channels open
Na+ channels close 1

10. Myocardial Contractile Cells
Phase 1 Initial Rapid Repolarization
The opening of the voltage gated
K + channels causes K + to flow out of the cell through the outward rectifier channel. This outward current starts to repolarize the cell. The membrane potential is partially
repolarized to just above zero.
Phase
Membrane channels
PX = Permeability to ion X
+20
-20
-40
-60
-80
-100
Membrane potential (mV)
100
200
300
Time (msec)
PK and PCa
PNa
Na+ channels open
Na+ channels close
Ca2+ channels open; fast K+ channels close 1 2

11. Myocardial Contractile Cells
Phase 2: the plateau.
Due to result of two events:
1)a decrease in K+ permeability and
2)an increase in Ca2t permeability.
The combination of Ca2+ influx and decreased K+ efflux causes the action potential to flatten out into a plateau
Phase
Membrane channels
PX = Permeability to ion X
+20
-20
-40
-60
-80
-100
Membrane potential (mV)
100
200
300
Time (msec)
PK and PCa
PNa
Na+ channels open
Na+ channels close
Ca2+ channels open; fast K+ channels close
Ca2+ channels close; slow K+ channels open 1 2 3

12. Phase 3: rapid repolarization
Phase 3: rapid repolarization. The plateau ends when Ca2+ channels close and K+ permeability increases once more.
The "slow" K1 channels responsible for this phase are similar to those in the neuron.
When the slow K+ channels open, K+ exits rapidly, returning the cell to its resting potential (phase 4).
Phase
Membrane channels
PX = Permeability to ion X
+20
-20
-40
-60
-80
-100
Membrane potential (mV)
100
200
300
Time (msec)
PK and PCa
PNa
Na+ channels open
Na+ channels close
Ca2+ channels open; fast K+ channels close
Ca2+ channels close; slow K+ channels open
Resting potential 1 2 3 4

13. The longer myocardial action potential helps pre­vent the sustained contraction called tetanus
The influx of Ca2' during phase 2 lengthens the total dura­tion of a myocardial action potential. A typical action potential in a neuron or skeletal muscle fiber lasts between 1 and 5 msec. In a contractile myocardial cell, the action potential typically lasts 200 msec or more. The longer myocardial action potential helps pre­vent the sustained contraction called tetanus. Prevention of tetanus in the heart is important because cardiac muscles must relax between contractions so the ventricles can fill with blood.
How does a longer action potential prevent tetanus? To understand this, compare the relationship between action po­tentials, refractory periods and contraction in skeletal and cardiac muscle cells . As you may re­call from Chapter 8, the refractory period is the time following an action potential during which a normal stimulus cannot trigger a second action potential. In skeletal muscle, the action potential (red curve) and refractory period (yellow background) are ending as contraction (blue curve) begins. For this reason, a second action potential fired immediately after the refractory period causes summation of the contractions. If a series of ac­tion potentials occurs in rapid succession, the sustained con­traction known as tetanus results

14. Electrical Conduction in Myocardial Cells
Electrical communication in the heart begins with an ac­tion potential in an autorhythmic cell. The depolarization spreads rapidly to adjacent cells through gap junctions in the intercalated disks (Fig •). The depolarization wave is fol­lowed by a wave of contraction that passes across the atria, then moves into the ventricles.
Figure 14-17

15. Electrical Conduction in Heart
THE CONDUCTING SYSTEM
OF THE HEART
SA node
AV node
Purkinje
fibers
Bundle branches
A-V bundle
Internodal
pathways
SA node depolarizes.
Electrical activity goes
rapidly to AV node via
internodal pathways.
Depolarization spreads
more slowly across
atria. Conduction slows
through AV node.
Depolarization moves
rapidly through ventricular
conducting system to the
apex of the heart.
Depolarization wave
spreads upward from
the apex. 1 4 5 3 2
Purple shading in steps 2–5 represents depolarization.
Why is it necessary to direct the electrical signals through the AV node? Why not allow them to spread downward from the atria? The answer lies in the fact that blood is pumped out of the ventricles through openings at the top of the chambers . If electrical signals from the atria were conducted directly into the ventricles, the ventricles would start contracting at the top.
Then blood would be squeezed downward and would become trapped in the bottom of the ventricles (think of squeezing a toothpaste tube at the top). The apex-to-base contraction squeezes blood toward the arterial openings at the base of the heart.
Why is it necessary to direct the electrical signals through the AV node? Why not allow them to spread downward from the atria?

16. Conduction of the Cardiac Action Potential

17. FIBRILLATION
If myocardial cells contract in a disorganized manner-fibrillation results.
Atrial fibrillation –Not a immediate emergency condition.
Ventricular fibrillation,- is an immediately life-threatening emergency.*
Ventricular fibrillation,- is an immediately life-threatening emergency because with­out coordinated contraction of the muscle fibers, the ventricles cannot pump enough blood to supply adequate oxygen to the brain.
Treatement-
electrical shock to the heart. The shock creates a depolarization that triggers action potentials in all cells simultaneously, coordinating them again.

18. Electrical Conduction
AV node
Direction of electrical signals
Delay the transmission of action potentials
SA node
Set the pace of the heartbeat at 70 bpm
AV node (50 bpm) and Purkinje fibers (25-40 bpm) can act as pacemakers under some conditions
The ejection of blood from the ventricles is aided by the spiral arrangement of the muscles in the walls . As these muscles contract, they pull the apex and base of the heart closer together, squeezing blood out the openings at the top of the ventricles.
A second function of the AV node is to delay the transmis­sion of action potentials slightly, allowing the atria to complete their contraction before ventricular contraction begins.
Why does the fastest pacemaker determine the pace of the heartbeat? Consider the following analogy. A group of people are playing "follow the leader" as they walk. Initially, everyone is walking at a different pace—some fast, some slow. When the game starts, everyone must match his or her pace to the pace of the person who is walking the fastest. The fastest person in the group is the SA node, walking at 70 steps per minute. Everyone else in the group (autorhythmic and contractile cells) sees that the SA node is fastest, and so they pick up their pace and follow the leader. In the heart, the cue to follow the leader is the electrical signal sent from the SA node to the other cells.
Now suppose the SA node gets tired and drops out of the group. The role of leader defaults to the next fastest person, the AV node, who is walking at a rate of 50 steps per minute. The group slows to match the pace of the AV node, but every­one is still following the fastest walker.
What happens if the group divides? Suppose that when they reach a corner, the AV node leader goes left but a renegade Purkinje fiber decides to go right. Those people who follow the AV node continue to walk at 50 steps per minute, but the peo­ple who follow the Purkinje fiber slow down to match his pace of 35 steps per minute. Now there are two leaders, each walk­ing at a different pace.
In the heart, the SA node is the fastest pacemaker and nor­mally sets the heart rate. If this node is damaged and cannot function, one of the slower pacemakers in the heart takes over. Heart rate then matches the rate of the new pacemaker. It is even possible for different parts of the heart to follow different pacemakers, just as the walking group split at the corner.

19. Complete heart block-
The conduction of electrical signals from the atria to the ventricles through the AV node is disrupted. The SA node fires at its rate of 70 beats per minute, but those signals never reach the ventricles. So the ventricles coordinate with their fastest pacemaker. Because ventricular autorhythmic cells discharge only about 35 times a minute, the rate at which the ventricles contract is much slower than the rate at which the atria contract.
If ventricular contraction is too slow to maintain adequate blood flow, it may be necessary for the heart's rhythm to be set artificially by a surgically implanted mechanical pacemaker. These battery-powered devices artificially stimulate the heart at a pre­determined rate.

20. Electrocardiography-ECG/EKG
Is a transthoracic interpretation of the electrical activity of the heart over time captured and externally recorded by skin electrodes. It is a noninvasive recording produced by an electrocardiographic device

21. Electrocardiography: Introduction
Body fluids are good conductors (the body is a volume conductor)
Fluctuations in potential (action potentials of myocardial fibers) can be recorded extracellularly with surface electrodes
placed on the skin
The record of these potential fluctuations during the cardiac cycle is the electrocardiogram (ECG).
The ECG provides information on: -
- Heart rate and rhythm The pattern of electrical activation of the atria and ventricles The approximate mass of tissue being activated Possible damage of the heart muscle Possible changes in the body’s electrolyte composition

22. Electrocardiography:
ECG is a complex recording representing the overall spread of activity throughout the heart during depolarization and repolarization.
The recording represents comparisons in voltage detected by electrodes at two different points on body surface, not the actual potential.

23. ECG graph paper Paper moves at a speed of 25mm/second At this speed
Each horizontal small cube represents 0.04 seconds
Each vertical small- 0.1 mv
Large cube- horizontal- 0.2 seconds
Large cube- vertically- 0.5 mv

25. Important features of the ECG are the P wave, the QRS complex and T wave.
Relevant intervals and segments are the PR interval, the RR interval, the QT segment and the ST segment.
ECG Paper
The ECG is recorded on calibrated paper. Refer to figure 1. The y-axis is voltage and 10 small
divisions represent 1 mV. (Note how much smaller these extracellular potentials are compared
with the amplitude of a single intracellular cardiac action potential (amplitude is ~ 120 mV). The
x-axis is time and a one division consisting of 5 smaller divisions represents 0.20 s. The actual
amplitude of the ECG signals depend on where the surface electrodes are actually placed.

26. P wave: Atrial depolarization as recorded from the surface of the
body
P – R interval: Time taken for the wave of depolarization to move through
the atria, AV node, bundle of His, Purkinje fibres to the
ventricular myocardium.
QRS complex: Depolarization of the ventricles.
ST segment: Marks the end of the QRS complex and the beginning of
the T wave. It occurs when the ventricular cells are in the
plateau phase of the action potential (i.e. there is no change
in potential occurring and so the ECG baseline is at zero
potential)
T wave: Repolarization of the ventricles (due to potential changes
occurring during phase 3 of the cardiac action potential)
Q – T interval: Period during which ventricular systole occurs
R – R interval: This time is usually used to calculate the heart rate.

27. Waves and normal values
P wave- Atrial depolarization
0.1 seconds
0.25 milli volts
PR interval- AV nodal delay
0.12 seconds- 0.2 seconds
QRS complex- ventricular depolarization
seconds

28. Normal Duration(s) Average Range Events on the heart during intervals
ECG intervals
Intervals
Normal Duration(s) Average Range
Events on the heart during intervals
PR interval1
Atrial depolarization and conduction through AV node
QRS duration
to 0.10
Ventricular depolarization and atrial repolarization
QT interval
to 0.43
Ventricular depolarization plus ventricular repolarization
ST interval (QT-QRS) …
Ventricular repolarization
1Measured from the beginning of the P wave to the beginning of the QRS complex 2Shortens as heart rate increases from average of 0.18 at a rate of 70 beats/min to 0.14 at a rate of 130 beats/min

29. Fig. 2. Principles of the bipolar recording of an action potential

30. Recording the Electrocardiogram. Basic concept
When the wave of depolarization moves toward the positive electrode, an upward deflection is recorded, whereas depolarization moving in the opposite direction produces a negative deflection

31. EKG RULES:
A wave of depolarization traveling toward a positive electrode results in a positive deflection in the ECG trace.
2) A wave of depolarization traveling away from a positive electrode results in a negative deflection.
3) A wave of repolarization traveling toward a positive electrode results in a negative deflection.
4) A wave of repolarization traveling away from a positive electrode results in a positive deflection.

32. EKG RULES: continued
5)A wave of depolarization or repolarization traveling perpendicular to an electrode axis results in a biphasic deflection of equal positive and negative voltages (i.e., no net deflection).
6) The instantaneous amplitude of the measured potentials depends upon the orientation of the positive electrode relative to the Mean QRS vector.
7)The voltage amplitude is directly related to the mass of tissue undergoing depolarization or repolarization.

34. Electrical Vectors
whose length and orientation reflect the size and position of the dipole. The vector arrow
In ECG, the potential differences arising in the heart are represented by electrical vectors
Electrical Vectors
size of the potential difference.
convention) points to the positive pole (of the dipole) and its length is a measure of the
itself reflects the cardiac dipole at that moment in time. The vector always (by
interventricular septum and anterior portion of the base are the first regions of the
It is a schematic diagram of the septum with the walls of the RV and LV. The
Look at the figure above.
ventricles to be depolarized. Depolarization of this part results in a dipole with the overall
diagram.
potential difference being in the direction indicated by the vector arrow on the right of the
mass than the RV and this causes leftward electrical forces to predominate over those
apex through the Purkinje fibres which are in the endocardium. The LV has a much larger
The wave of depolarization now spreads down the interventricular septum towards the
directed to the right so that the vector generated by depolarization of this area is pointing
ventricles. Activation proceeds from endocardium to epicardium. Again the left
The last regions of the ventricles to be depolarized are the bases of the right and left
downward and to the left.
What we have demonstrated are three mean QRS vectors which occur as the wave of
directed upwards.
ventricular forces predominate and the overall electrical vector is pointed to the left and
Each of the tail of the vectors is at zero potential. So if we put all the vector tails together
depolarization spreads from the septum to the apex and then to the base of the ventricles.
which can be averaged to
we get :
travels through the ventricles. It defines the mean electrical axis of the heart. Its direction
which represents the average electrical vector generated when a wave of depolarization
These 3 QRS vectors can be added together to generate the overall mean QRS vector,
How the polarity of the waveform depends on the position of the
Figure 3 Heart showing the direction of the mean electrical axis.
shows the general direction of the wave of depolarization is downward and to the left.
ECG
Figure 4 The effect of changing electrode position on the wave form reorded.
recording electrodes relative to the heart. 44
Figure 4 shows a mass of cardiac muscle that is partially depolarized. Three pairs of
simultaneously as shown above.
This is illustrated by recording from a mass of cardiac tissue with 3 pairs of electrodes
principles as before, the voltmeter on the your left records a negative potential, the one in
is how these three pairs of electrodes record different potentials. Using the same
recording electrodes have been placed on the skin over this muscle. What we want to see
the middle doesn’t record a potential at all, and the one on the right shows a positive
pairs of electrodes pick up different signals and what they pick up is entirely dependent
The important point illustrated here is although the event happening is the same, the 3
potential.
slightly different angle, and as a result picking up a slightly different picture of what is
ECG is done, up to 12 pairs of electrodes are used. Each “looking” at the heart from a
on where they are placed in relation to the cardiac tissue. In the clinical setting, when an
composite picture of the electrical activity of the heart.
happening. When the results from all twelve traces are seen, then the clinician obtains a
Fig. 11. The basic direction of electrical conduction through the heart

35. How the polarity of the waveform depends on the position of the recording electrodes relative to the heart.
Figure shows a mass of cardiac muscle that is partially depolarized. Three pairs of
recording electrodes have been placed on the skin over this muscle. What we want to see
is how these three pairs of electrodes record different potentials. Using the same
principles as before, the voltmeter on the your left records a negative potential, the one in
the middle doesn’t record a potential at all, and the one on the right shows a positive
potential.
The important point illustrated here is although the event happening is the same, the 3
pairs of electrodes pick up different signals and what they pick up is entirely dependent
on where they are placed in relation to the cardiac tissue. In the clinical setting, when an
ECG is done, up to 12 pairs of electrodes are used. Each “looking” at the heart from a
slightly different angle, and as a result picking up a slightly different picture of what is
happening. When the results from all twelve traces are seen, then the clinician obtains a
composite picture of the electrical activity of the heart.
The effect of changing electrode position on the wave form recorded.

36. EKG Leads
Leads are electrodes which measure the difference in electrical potential between either:
1. Two different points on the body (bipolar leads)
2. One point on the body and a virtual reference point with zero electrical potential, located in the center of the heart (unipolar leads)
Electrocardiographic Leads
The potentials generated by the heart can be picked up by 12 pairs of electrodes,
strategically located, with each pair “looking” at the heart from a slightly different angle.
By observing the recordings from the 12 leads, which can appear simultaneously on an
ECG machine, it is possible to detect many abnormalities in cardiac function.
Abnormalities of rhythm would be detected by all pairs of electrodes but abnormalities in
conduction, caused by an ischemic area of damage, might be picked up on some
recordings but not others.

37. EKG Leads The standard EKG has 12 leads: 3 Standard Bipolar Limb Leads
3 Augmented Unipolar Limb Leads
6 Precordial Leads
The axis of a particular lead represents the viewpoint from which it looks at the heart.

38. ECG recordings from Bipolar Limb Leads
In Lead I the negative terminal of the ECG machine is connected to the right arm and the
positive terminal to the left arm. This is simply just a convention so that
when depolarization spreads through the cardiac tissue an upward deflection will be
recorded from all three leads. Remember that upward deflections are recorded when the
wave of depolarization travels towards the positive electrode. Remember the direction of
the mean QRS vector.
Note that the largest amplitude positive deflection in each is the QRS complex. It is
bigger in Lead II simply because the axis of lead II is more in line with the direction of
ECG recordings from Bipolar Limb Leads

39. ECG recordings from Bipolar Limb Leads
Right arm
Left arm
In Lead I the negative terminal of the ECG machine is connected to the right arm and the
positive terminal to the left arm. This is simply just a convention so that
when depolarization spreads through the cardiac tissue an upward deflection will be
recorded from all three leads. Remember that upward deflections are recorded when the
wave of depolarization travels towards the positive electrode. Remember the direction of
the mean QRS vector.
Note that the largest amplitude positive deflection in each is the QRS complex. It is
bigger in Lead II simply because the axis of lead II is more in line with the direction of II
III
Left leg
ECG recordings from Bipolar Limb Leads

40. Einthoven’s Triangle ECG recordings from Bipolar Limb Leads -900 I
aVR
aVL
-300
-1500 I
+1800
Right arm 00
Left arm
III II
600
1200
In Lead I the negative terminal of the ECG machine is connected to the right arm and the
positive terminal to the left arm. This is simply just a convention so that
when depolarization spreads through the cardiac tissue an upward deflection will be
recorded from all three leads. Remember that upward deflections are recorded when the
wave of depolarization travels towards the positive electrode. Remember the direction of
the mean QRS vector.
Note that the largest amplitude positive deflection in each is the QRS complex. It is
bigger in Lead II simply because the axis of lead II is more in line with the direction of
+900
+aVF
Left leg
ECG recordings from Bipolar Limb Leads

41. Einthoven’s Triangle Lead I at the top of the triangle, is
hypothetical triangle created around the heart when electrodes are placed on both arms and the left leg .The sides of the triangle are numbered to correspond with the three leads ("leeds"), or pairs of electrodes.
ECG electrodes at­tached to both arms and the left leg form a triangle. Each two-electrode pair constitutes one lead (pronounced "leed"), and only one lead is active at a time. Lead I, for instance, has the negative electrode attached to the right arm and the positive electrode at­tached to the left arm.
Lead I at the top of the triangle, is
orientated horizontally across the chest. This angle is taken as zero.
Lead II is angled at 60 degrees to Lead I, and Lead III at roughly 120 degrees to Lead I.

42. Augmented Unipolar Limb Leads (aVR, aVL and aVF)
The three Unipolar augmented leads are termed unipolar leads because there is a single positive electrode that is referenced against a combination of the other limb electrodes.  The positive electrodes for these augmented leads are located on the left arm (aVL), the right arm (aVR), and the left leg (aVF).  In practice, these are the same electrodes used for leads I, II and III.  (The ECG machine does the actual switching and rearranging of the electrode designations). 

43. Augmented Unipolar Limb Leads (aVR, aVL and aVF)
Three unipolar limb leads are also used for recording ECGs. Each lead measures the potential difference between an exploring electrode and an “indifferent” electrode (V) assumed to be at zero potential. This indifferent electrode is constructed by connecting the electrodes on the right arm (R), left arm (L) and left leg or foot (F) together. This indifferent electrode is called V and is assumed to be at zero potential (since the sum of the potentials in all the leads cancel out).

44. Augmented limb leads Represented by aVR, aVF, aVR. a- augmented
V-unipolar
Last letter represents the part of body
aVR- between right arm and left arm+ left leg
aVL- between left arm and rt arm+ left leg
aVF- between left foot and rt arm+ lt arm

45. Precordial Leads
These are unipolar leads measuring the potential difference between an electrode placed on the chest and an indifferent electrode, again made up by connecting the RA, LA and LL electrodes (i.e. the V electrode). There are 6 locations to place the chest electrode and
so there are 6 chest electrodes (V1 – V6).
With the chest leads, if the chest electrode is in an area of positivity, which occurs if the wave of depolarization is approaching this electrode, then an upward deflection is recorded.
Adapted from:

46. Precordial Leads

47. Pre cordial leads V1- 4th intercoastal space, rt side sternal boarder
V2- 4th intercoastal space lt side of sternal boarder
V3- between V2 and V4
V4- 5th intercoastal space in the mid clavicular space
V5- 5th intercoastal space in the anterior axillary line
V6- 5th intercoastal space in the mid axillary line.

48. aVR, aVL, aVF (augmented limb leads)
Summary of Leads
Limb Leads
Precordial Leads
Bipolar
I, II, III
(standard limb leads) -
Unipolar
aVR, aVL, aVF (augmented limb leads)
V1-V6

49. Leads I, II and III have a QRS complex that is positive (upward deflection) because in all
three, the direction of electrical conduction is primarily towards the positive electrode.
The magnitude of the QRS complex will be largest in lead II because the mean QRS
vector of the heart is closer to the axis of Lead II than it is to Lead I or III. (Remember
figure 3).
In the augmented limb leads aVL and aVF the QRS complex is positive, again because
the positive electrode (left arm, left foot) is more aligned with the mean QRS vector. On
the other hand, aVR will have a negative QRS complex because the wave of
depolarization is moving away from the right arm (positive electrode).
In the precordial chest leads, V1 through to V4 QRS changes from negative to positive as
the positive electrode for each subsequent lead is more in line with the mean QRS vector
than the previous one. Leads V5 and V6 are most in line with the mean QRS vector so
their QRS complexes are positive

51. Situs Inversus with dextrocardia

52. Arrangement of Leads on the EKG

53. Anatomic Groups (Septum)

54. Anatomic Groups (Anterior Wall)

55. Anatomic Groups (Lateral Wall)

56. Anatomic Groups (Inferior Wall)

57. Anatomic Groups (Summary)

58. What to inspect in an ECG 1. Heart Rate
INTERPRETATION OF THE ELECTROCARDIOGRAM
What to inspect in an ECG
1. Heart Rate
2. Rhythm
3. Duration, segments and intervals.(P wave duration, PR interval,
QRS duration, QT interval)
4. Mean QRS Axis (mean electrical axis, mean QRS vector)
5. P wave abnormalities
Inspect the P waves in leads II and V1 for left atrial or right atrial enlargement.
Left atrial hypertrophy would result in a taller P wave in Lead II
RA hypertrophy – taller P wave in V1.
6. QRS wave abnormalities
7. ST segment / T wave abnormalities

59. Determining the Heart Rate Rule of 300
Take the number of “big boxes” between neighboring QRS complexes( R – R interval), and divide this by The result will be approximately equal to the rate
Although fast, this method only works for regular rhythms.
(300 / 6) = 50 bpm
(1500/30) = 50 bpm

60. What is the heart rate? (300 / ~ 4) = ~ 75 bpm (1500/20 ) = 75 bpm
(300 / ~ 4) = ~ 75 bpm
(1500/20 ) = 75 bpm

61. What is the heart rate? (300 / 1.5) = 200 bpm
Heart Rate < 60 beats / min  Bradycardia
Heart Rate > 100 beats / min Tachycardia

62. The Rule of 300 It may be easiest to memorize the following table:
# of big boxes
Rate 1
300 2
150 3
100 4 75 5 60 6 50

63. 2. Rhythm
Is the rhythm determined by the SA node pacemaker? i.e. is it a “sinus rhythm”?
If normal, the following should be present:
· The P wave should be upright in leads I, II and III.
· Each QRS complex should follow a P wave

64. Einthoven’s Triangle Lead I at the top of the triangle, is
hypothetical triangle created around the heart when electrodes are placed on both arms and the left leg .The sides of the triangle are numbered to correspond with the three leads ("leeds"), or pairs of electrodes.
ECG electrodes at­tached to both arms and the left leg form a triangle. Each two-electrode pair constitutes one lead (pronounced "leed"), and only one lead is active at a time. Lead I, for instance, has the negative electrode attached to the right arm and the positive electrode at­tached to the left arm.
Lead I at the top of the triangle, is
orientated horizontally across the chest. This angle is taken as zero.
Lead II is angled at 60 degrees to Lead I, and Lead III at roughly 120 degrees to Lead I.

65. All Limb Leads

66. The QRS Axis
The QRS axis represents the net overall direction of the heart’s electrical activity.
Abnormalities of axis can hint at:
Ventricular enlargement
Conduction blocks (i.e. hemiblocks)

67. The QRS Axis
By near-consensus, the normal QRS axis is defined as ranging from -30° to +90°.
-30° to -90° is referred to as a left axis deviation (LAD)
+90° to +180° is referred to as a right axis deviation (RAD)

68. Determining the Axis
The Quadrant Approach
The Geometric method.

69. Determining the Axis Predominantly Positive Predominantly Negative
Equiphasic

70. The Quadrant Approach
1. Examine the QRS complex in leads I and aVF to determine if they are predominantly positive or predominantly negative. The combination should place the axis into one of the 4 quadrants below.

71. The Quadrant Approach
2. In the event that LAD is present, examine lead II to determine if this deviation is pathologic. If the QRS in II is predominantly positive, the LAD is non-pathologic (in other words, the axis is normal). If it is predominantly negative, it is pathologic.

72. Quadrant Approach: Example 1
The Alan E. Lindsay ECG Learning Center
Negative in I, positive in aVF  RAD

73. Quadrant Approach: Example 2
The Alan E. Lindsay ECG Learning Center
Positive in I, negative in aVF  Predominantly positive in II 
Normal Axis (non-pathologic LAD)

74. QRS Axis Determination- Using the Hexaxial Diagram
 First find the isoelectric lead if there is one; i.e., the lead with equal forces in the positive and negative direction. Often this is the lead with the smallest QRS.  The QRS axis is perpendicular to that lead's orientation.  Since there are two perpendiculars to each isoelectric lead, chose the perpendicular that best fits the direction of the other ECG leads.

76. Applied physiology Myocardial infarction- Q wave Ischemia-
elevated ST segment
Ischemia-
ST depression

77. Heart block- First Degree AV Block
There is a slowing of conduction through the AV node. The P-R interval is unusually
long (> 0.20 s). However each P wave is followed by a QRS complex.

78. Second Degree Block
As the PR interval increases to > 0.25s, sometimes conduction through the AV node fails and a P wave does not result in a QRS complex. This is intermittent conduction failure with a subsequent loss of ventricular contraction and is typical of a second degree block. There are 3 types of Second Degree Block:
Mobitz type I
Mobitz type II
Bundle Branch Block
Mobitz Type I
The PR interval gradually lengthens from one cycle to the next until the AV node fails
completely and no QRS complex is seen. One usually seen every third or fourth atrial
beat failing to excite the ventricle (3 : 1 block or 4 : 1 block). The PR interval then
immediately resets to the original interval and the process begins again. Mobitz type 1 is
usually due to a conduction block in the AV node and is generally benign. It may be seen
in children, athletes or individuals with elevated vagal tone. No specific treatment is
needed for this condition.
Mobitz Type II
In this condition there is a sudden, unpredictable loss of AV conduction and loss of
ventricular activation and is usually due to a conduction block beyond the AV node (e.g.
bundle of His). The PR interval remains constant from beat to beat but every nth
ventricular depolarization is missing. In Figure 15 the first cardiac cycle is normal,
however the second P wave is not followed by a QRS or T. Instead, the ECG record is
flat until the third P wave arrives at the expected time, followed by a QRS and a T wave.
Figure 6 Second Degree Conduction Block
In other words every second QRS is dropped (2 : 1 block). Mobitz type II is more
dangerous than type I as it could lead to cardiac arrest. Treatment is generally to implant
a pacemaker.
Bundle Branch Block
When the HR exceeds a critical level, the ventricular conduction system fails – probably
because the conduction system does not have adequate time to repolarize. As a result the
impulse spreads slowly and inefficiently through the ventricles by going from one
myocyte to the next (since the conducting system is now no longer working properly
which is why it is called bundle branch block). As a result the QRS complex is widened.
Because this block impairs the coordinated spread of the action potentials through the
myocardium the resulting ventricular contractions may be weaker.

79. Complete Conduction Block:- Third Degree Block
In this condition no impulse goes through the AV node. The atria and the ventricles are now severed – electrically speaking – and each beats under control of its own pacemakers. This is also called AV dissociation. The atria have an inherent rhythm of 60
– 80 bpm and the P-P interval will be regular and consisten. The only ventricular pacemaker that are available to initiate ventricular contractions are the Purkinje fibres - their inherent rhythm is 20 – 40 bpm.
The R – R interval may be regular and consistent.
The P – P interval will be faster than the R – R interval and there is no relation between
the two. If the ventricular excitation starts within cells of the conducting system (like the
Purkinje cells) then the QRS complex appears normal, but if excitation starts somewhere
else in the ventricular myocardium the QRS complex will be abnormal. Third degree
block is a medical emergency since the CO, and hence the BP can be seriously
compromised. Treatment is to implant a pacemaker.
On an ECG, the complete block appears as regularly spaced P waves (since the SA node
properly triggers the atria), but the QRS and T waves may be irregular, with a low
frequency and bearing no fixed relationship to the P waves

80. Hypokalemia: Flattened T wave ST depression More prominent U wave
Arrhythmias caused by changes in Electrolyte Composition
Both Hypokalemia and Hyperkalemia can cause serious cardiac arrhythmias. This is not surprising considering how dependent the membrane potential is on extracellular K+ levels. To treat arrhythmias due to hyperkalemia calcium gluconate is infused. Ca++ has the opposite effects to K+ on the action potential.
Hypokalemia:
Flattened T wave
ST depression
More prominent U wave
Hyperkalemia:
Peaked T wave
Loss of P wave
Widened QRS

81. Leads I, II and III have a QRS complex that is positive (upward deflection) because in all
three, the direction of electrical conduction is primarily towards the positive electrode.
The magnitude of the QRS complex will be largest in lead II because the mean QRS
vector of the heart is closer to the axis of Lead II than it is to Lead I or III. (Remember
figure 3).
In the augmented limb leads aVL and aVF the QRS complex is positive, again because
the positive electrode (left arm, left foot) is more aligned with the mean QRS vector. On
the other hand, aVR will have a negative QRS complex because the wave of
depolarization is moving away from the right arm (positive electrode).
In the precordial chest leads, V1 through to V4 QRS changes from negative to positive as
the positive electrode for each subsequent lead is more in line with the mean QRS vector
than the previous one. Leads V5 and V6 are most in line with the mean QRS vector so
their QRS complexes are positive