30.03.15

Cardiac Function Assessment

via Electrocardiography, Phonocardiography and 2D Echocardiography

Conducted by: MinChul Park, Thomas Michael Allen Nairn and Hadassah Patchigalla (Class 14661:

Group A5)

Aims

1. To record an electrocardiogram and phonocardiogram and use these recordings to:

a) Determine the link between electrical activity in the heart and the sequence of events in cardiac

cycle

b) Investigate a cause of variation in the ECG recording

c) Investigate the relationship between the ECG recording, the heart sounds and the pulse as

measured at the carotid sinus

2. To analyse data obtained by echocardiogram to determine changes in ventricular function

following myocardial infarction

Introduction

The cardiac cycle is the sequence of events that occurs in the heart during one heartbeat, mainly

involving diastole (filling) and systole (contraction) of the atria and ventricles on the left and right

sides of the heart (Tortora & Derrickson, 2006). The specific sequence of events in the cardiac

cycle can be represented in a graphical form by recording the electrical activity that occurs

simultaneously in the heart to produce each contraction and relaxation (and so each subsequent

movement of blood from the heart to the systemic or pulmonary circulation).

The electrical activity that occurs in the heart is the constant firing of action potentials, originating

from the sinoatrial node, which spread throughout cardiac muscle cells to initiate depolarisation

and the corresponding contraction of cardiac myocytes, muscle fibres and tissue (Boron &

Boulpaep, 2009). This electric current generated in the heart with each cardiac cycle can be

detected at the surface of the body (i.e. the skin) because the extracellular fluid of the body acts

as a volume conductor, and it is this property that is used in the creation of an electrocardiogram

(ECG), a graphical representation of the depolarisation and repolarisation of the heart muscle

(Tortora & Derrickson, 2006).

The ECG is recorded using four electrodes placed on both arms and both legs of the subject (six

more electrodes are placed at strategic points on the subject's chest to record a standard 12-lead

ECG, but this experiment obtains only a 6-lead ECG). Leads are created between sets of two

electrodes and are used to measure the potential difference (voltage) between them, thus

measuring the potential difference between two points of the body and so the conduction of

electrical activity within the heart. This is achieved as a potential difference between two

electrodes is created only when an action potential spreads through the cells of the myocardium

causing depolarisation of part of the muscle while the rest remains polarised (Klabunde, 2004). A

wave of depolarisation spreading towards a positive electrode will produce a positive ECG

deflection, and a wave of depolarisation moving away from a positive electrode will produce a

negative ECG deflection (conversely, a wave of repolarisation moving towards a positive electrode

will produce a negative ECG deflection, and a wave of repolarisation moving away from a positive

electrode will produce a positive ECG deflection) (Klabunde, 2004).

Therefore, as waves of depolarisation spread throughout the heart from the SA node to the atria,

AV node, bundle of His, Purkinje fibres and the ventricles, voltages will be recorded between pairs

of electrodes as positive or negative deflections from the isoelectric voltage (or baseline voltage)

on the ECG and the direction in which it spreads will be shown by the leads that produce a

positive deflection on the ECG.

The standard leads used to record the ECG in the frontal plane are the bipolar limb leads and the

augmented unipolar leads, which represent the potential difference between two limbs and

between one limb and an average of the other two limbs respectively. The limb leads are: lead I -

positive electrode at left arm, negative at right arm; lead II - positive at left leg, negative at right

arm; lead III - positive at left leg, negative at left arm. The augmented leads measure the potential

difference between one limb electrode (defined as positive) and the heart (defined as negative).

The augmented leads are: lead aVR - positive at right arm; aVL - positive at left arm; aVF - positive

at left leg (Boron & Boulpaep, 2009). These six leads can also be represented in Einthoven's

triangle used for vector analysis, as used in this experiment.

The position of the electrodes and the combination of leads created between them allows

multiple perspectives and therefore recordings to be created of the same electrical activity in the

heart - that is, each lead represents a different segment of the heart over which the voltage

difference is measured, and so the deflections recorded will differ depending on which lead is

aligned with the direction of the electrical activity of the heart (Boron & Boulpaep, 2009). This in

turn depends on the location and orientation of the heart within the thoracic cavity, as discussed

below.

In a standard ECG, the P wave represents right and left atrial depolarisation; the QRS complex

represents right and left ventricular depolarisation; the T wave represents repolarisation of both

ventricles. The P-T segment reflects spread of electrical activity from the atria to the ventricles,

however the depolarisation of the structures between the two chambers is not shown on the ECG

as the deflections are extremely small (Boron & Boulpaep, 2009).

A phonocardiogram is the recording of the heart sounds associated with the closing of the

atrioventricular and semilunar valves using a digital stethoscope or a microphone (as used in this

experiment). The closure of the valves does not itself produce the heart sound; instead the

vibrations in the ventricular wall produced by the closure are recorded by the microphone. The

two major heart sounds that can be easily attained by phonocardiography are the first heart

sound produced by the closing of the AV (mitral and tricuspid) valves, and the second heart

sound produced by the closure of the semilunar (aortic and pulmonary) valves (Boron &

Boulpaep, 2009).

An echocardiogram is the recording of the interior image of the heart using ultrasound waves.

Echocardiography is used to assess ventricular function as the imaging technique shows various

aspects of the heart in motion such as heart size, shape and the volume and velocity of blood

ejected from the ventricles (Tortora & Derrickson, 2012). Images of the heart shape gives

knowledge of how the ventricles act in a healthy heart and how it fails to pump properly in a

damaged heart. In this experiment a patient who had an anteroseptal myocardial infarction (MI) is

assessed (blockage of the coronary arteries ultimately resulting in cardiac myocyte deaths in the

anterior region of the interventricular wall) (Tortora & Derrickson, 2012). Using echocardiography,

evidence for akinesis (no heart wall movement during systole) and dyskinesis (heart wall

bulging/curving during systole) (MEDSCI 205 Laboratory Manual, 2015).

Method

For all ECG recordings the subject was lying supine, palms upturned and breathing normally.

Electrodes were placed on the subject's lower left and right forearms, lower left leg, and a

grounding electrode was placed on the lower right leg (note that this electrode was not used in

any lead configuration for recording the ECG). The labelled lead wires were attached to each

respective electrode to enable recordings to be made for leads I, II, III, aVR, aVL and aVF.

The voltage output (in millivolts) was recorded using the Chart software as an output graph

showing voltage deflections over the time period (in seconds).

Part A:

Experiment A: The ECG was recorded using lead II with subject:

a) Breathing normally for 30s; then

b) Breathing deeply, taking approximately 10s per inhalation and exhalation cycle, for 30s

Heart rate of the subject was then calculated by LabChart during normal breathing, inhalation and

exhalation and recorded.

Experiment B: A short segment of ECG was recorded for each of leads I, II, III, aVR, aVL, aVF. The

recording for each lead was made for the duration of 4 cardiac cycles, and the recording from the

output of the electrodes was paused in between each recording to allow the lead input to be

adjusted.

For each of the six leads, the magnitude of the peak positive and peak negative deflections within

the QRS complex were measured (in millivolts). This was achieved by setting the baseline

recording of the ECG as 0mV, then using the Chart software to measure the change in voltage

between the baseline and each of: the peak positive deflection (the R deflection in all but the aVR

recording) and the peak negative deflection (the Q deflection in all but the aVR recording).

The net deflection of the QRS complex (in mV) was calculated as follows:

Net deflection (mV) = peak positive (mV) + peak negative (mV)

E.G. Net deflection of lead I (mV) = 0.667mV + (-0.029mV)

= 0.638mV

The net deflection of each of leads I, II and III were then used for an Einthoven's triangle analysis

in order to produce a vector representation of electrical activity in the heart during the QRS

complex of the ECG. The Einthoven's triangle was produced as follows:

The scale used for the Einthoven's triangle analysis was 1mV = 5cm and the centre of each side

of the triangle set as 0mV. The net deflection was converted to cm and marked on the side of the

triangle representing each of leads I, II and III in a positive or negative direction, depending on

the direction of each lead (as shown in Fig. 1). For example:

The length of each line segment was calculated as follows:

Length of line segment (cm) = net deflection (mV) X 5cm

E.G. Length of lead II segment (cm) = 1.133mV X 5cm

= 5.665cm (in a positive direction)

This was calculated for leads I, II and III and a resultant vector produced by connecting

perpendicular lines from all three line segments drawn. The resultant vector can be seen in the

Einthoven's triangle produced (see Fig. 1, below).

Three axes of symmetry were then drawn through the triangle, representing each of leads aVR, aVL

and aVF. To predict the magnitudes (in mV) of each of these leads during the QRS complex, lines

perpendicular to each of the axes of symmetry were drawn from the tip of the resultant vector.

The length of each line segment from the point of intersection of the axes, the centre of the

triangle, was then measured (in cm) and used to calculate the predicted values for the net

deflection of each lead (in mV).

The length of each line segment was used to calculate the predicted net deflection as follows:

Magnitude of net deflection (mV) = length of line segment (cm) / 5cm

E.G. Magnitude of lead aVF net deflection (mV) = 6.5cm / 5cm

= 1.30mV

The predicted values for the augmented leads were then compared to those measured during

ECG recording (see Table 2 of the results section).

Part B:

A stethoscope was used for auscultation to investigate where in the chest wall the heart beat was

able to be heard clearly. A microphone was then taped over this point on the subject's chest in

order to record each heart sound. A segment of ECG was then recorded using lead II

simultaneously with the output from the microphone. This enabled graphs to be produced using

Chart software to allow correlation of the heart sounds with the electrical activity of the heart.

The carotid pulse was then found and a segment of ECG and phonocardiogram recorded

simultaneously. The timing of the pulse was synchronized with these recordings by the pressing

of the "enter" key every time the pulse was felt to produce a mark on the graph. These three

recordings were then combined to produce a graph of the ECG, phonocardiogram and timing of

the pulse (as presented in Results, below). D1D2L

Part C:

The end diastolic and end systolic volumes for both 1 week and 3 months post-MI were

calculated by measuring the length and diameters given by the 2 dimensional (2D) representation

of the left ventricle and then using the following formula:

Volume = 5𝜋

24D1D2L

D1 = calculated using long axis apical 4 view

D2 = calculated using long axis apical 2 view

L = length of the heart from the base to apex

LVEDV = Left Ventricular End Diastolic Volume

LVESV = Left Ventricular End Systolic Volume

Stroke Volume (SV) = LVEDV – LVESV

Ejection Fraction (EF) = (SV / LVEDV) X 100

The EFs of both 1 week and 3 months post-MI were then compared to assess ventricular function.

Further analysis was conducted by examining ventricular cavity curvature during systole and

diastole to see signs of akinesis and dyskinesis. Also, numerical changes in ventricular volume was

calculated using the given echocardiogram.

Results

Part A: Electrocardiography

Chart 1: ECG recording from Lead 2 when breathing normally.

The heart rate shows a cycle of increase and decrease over time which is shown more

prominently in Chart 2. The highest heart rate recorded is 81.0 bpm and the lowest heart rate

recorded is 63.8 bpm.

Mean heart rate from LabChart = 70.7 bpm

Chart 2: ECG recording from Lead 2 when breathing deeply and slowly.

ECG recording when breathing deeply and slowly is much different from Chart 1. Chart 2 displays

a clear cyclic pattern of the increase and decrease in heart rate with respect to inhalation and

exhalation. The time in which the subject began inhalation was marked by “in” and exhalation was

marked by “out”. The time taken for both inhalation and exhalation was above 10 seconds. The

highest heart rate recorded was 78.0 bpm and the lowest heart rate recorded was 59.3 bpm. Thus,

Chart 2 indicates that the effect of ventilation on changes in heart rate is large as deep and slow

inhalation results in marked increase in heart rate (almost 20 bpm from lowest).

Mean heart rate from LabChart = 68.7 bpms

Chart 3: ECG recordings of standard limb leads and augmented limb leads.

From left to right, the ECG recordings show Lead 1, 2, 3, aVR, aVL and aVF. The heart rate is

relatively constant with some minor anomalous peaks in Lead 1 and aVR. Plainly the ECG

recordings for each lead is different indicating that each lead observes the heart’s electrical

activity from various viewpoints. The largest deflections were seen in Lead 3 and the smallest

deflections were seen in Lead 1. Chart 3 was used to generate Table 1 which in turn was used to

produce Einthoven’s Triangle diagram and thus Table 2.

Lead Peak positive deflection

(mV)

Peak negative deflection

(mV)

Net deflection;

Peak positive and negative (mV)

I 0.2887 -0.2194 +0.0693

II 1.3980 -0.2650 +1.1330

III 1.3519 -0.2569 +1.0950

aVR 0.4831 -0.5844 -0.1013

aVL 0.1219 -0.4050 -0.2831

aVF 1.1294 -0.1875 +0.9419

Table 1: Standard and Augmented Limb Leads – QRS deflections

For each measurement as per the methods section, the highest deflection was recorded and the

lowest deflection was recorded for positive and negative deflections respectively. Leads I, II, III and

aVF show a net positive deflection but aVR and aVL show a net negative deflection.

Figure 1: Einthoven’s Triangle Analysis using values from Table 1.

The writings in red represent the augmented limb Leads and writings in blue represent the

standard limb leads (the bipolar leads: I, II and III). The dotted lines represent diagrammatic

construction lines used to derive the resultant vector and the 3 augmented limb lead line

segments in cm. The lengths of augmented limb lead line segments were converted to its

corresponding value in millivolts using the scale 1mV = 5cm. The angle of QRS axis deviation was

measured to be (with a protractor) 88˚.

The predicted augmented limb leads are written in red which is recorded in Table 2.

The resultant QRS vector is 1.30mV in magnitude and its direction is shown in Figure 1. The

resultant vector is leaning slightly to the left side.

Lead Measured Magnitude (mV) Predicted Magnitude (mV) Error (mV)

aVR -0.10 -0.72 0.62

aVL -0.28 -0.58 0.30

aVF +0.94 +1.30 0.36

Table 2: Measured and predicted values of the augmented limb leads from Table 1 and Figure 1.

The measured values show concordance with their respective predicted values in terms of their

directions. However, in terms of their magnitudes all 3 leads show disagreement. The errors are

large with the largest error calculated to be 0.62 mV.

Part B: Auscultation and Phonocardiography

Figure 2: Integrated diagram of Electrocardiogram, Phonocardiogram and Heart rate.

The above shows a short segment of simultaneous recordings made from LabChart of

Electrocardiogram, Phonocardiogram and Heart rate outlining their relationships with one another.

From experimental data, segment showing their relationships the best was chosen. The first heart

sound usually described as “lubb,” is heard immediately after the QRS complex and the second

heart sound usually described as “dubb,” is heard immediately after the T wave. By observation,

the first heart sound is definitely louder than the second heart sound. But it appears the dubb

sound is longer in duration compared to the lubb sound. The decreasing purple line shows a

decrease in heart rate indicating that the subject must have been exhaling.

Part C: Echocardiographic Analysis of Left Ventricular Function

Figure 3: Scanned

document copy of 2D

Echocardiograms of

heart 1 week post-MI

and 3 months post-MI.

What is clearly different

between the Baseline

and the heart 3 months

post-MI is the shape of

the heart during systole

and diastole. The

immediately noticeable

observation is cardiac

dilatation. Compared to

the Baseline image, the

3 months post-MI

image display increased

ventricular size. The

second observation is

the remarkable

difference in changes in

heart shape (between

End Diastole and End

Systole). While the

Baseline image shows

an obvious change in

heart shape at End

Systole, the heart 3

months post-MI shows

little change in heart

shape at End Systole (illustrating akinesis). There is no bulging of the heart wall during systole

which was seen in the Baseline image therefore 3 months post-MI does not show dyskinesis.

Figure 4: Scanned document copy

of Quantitative analysis of

Ventricular volumes comparing

heart 1 week post-MI and 3

months post-MI.

As per the method, Figure 3

shows quantitative analysis of left

ventricular function. The workings

for calculating LVEDV, LVESV, SV

and EF are all shown above. The

LVEDV and LVESV are greater in

volume in the heart 3 months

post-MI but SV and EF are greater

in the heart 1 week post-MI.

Calculation indicates, the LVEDV 3

months after MI has increased by

19.2% supporting observation

made in Figure 3 – cardiac

dilatation. 3 months after MI the

heart’s EF is not even 20% which

is less than half of the EF of heart

1 week after MI. The end result of

the analysis is that the heart 3

months post-MI has much lower

EF than the heart 1 week post-MI

(difference of 30%). Thus

myocardial infarction

compromises the heart’s ability to

pump with high EF.

Discussion

Part A: Electrocardiography

Charts 1 and 2 both show the cyclic patterns of the increase and decrease in heart rate as the

subject inhales and exhales respectively. Chart 2 shows a more prominent cyclic nature of the

changes in heart rate than Chart 1.

Inspiration causes an increase in heart rate. During inspiration, the intrathoracic (intrapleural)

volume increases because of the activities of external intercostals and diaphragm. The volume has

increased therefore by Boyle’s law the intrathoracic pressure must decrease (Tortora & Derrickson,

2012). This leads to increased venous return to the right ventricles. Known as the Bainbridge

reflex, increased venous return to the right atrium stretches low pressure B fibres during atrial

filling which causes tachycardia. Note that this reflex is limited to the more important

parasympathetic and sympathetic nerve activity to the sinoatrial node (baroreflex). Therefore, it is

when the heart is at its baseline activity that the Bainbridge reflex can be seen the best. This

explains why the subject was told to lie down, be quiet and be relaxed.

Expiration causes a decrease in heart rate. The increased venous return to the right atrium

ultimately means increased blood volume to the left atrium and thus the left ventricle. The left

ventricle ejects increased volume of blood. The high pressure baroreceptors present in the aortic

arch are stretched more and increases their rate of firing. Sympathetic activity is decreased

(decreased firing from rostral ventrolateral medulla) and vagal activity is increased (increased

firing from nucleus ambiguus) which decreases heart rate.

The central concept behind Chart 3 is different leads observe the heart from various viewpoints.

All 6 leads in Chart 6 show different deflections in their magnitudes and directions and in the

following section, the concepts behind this will be discussed.

In electrocardiography the measured deflection depends on 3 factors: a) Magnitude of charges, b)

orientation of dipole and electrodes and c) distance between dipole and electrodes (MEDSC 205

Lecture Manual, 2015).

Magnitude of charge (dipole) refers to the magnitude of deflection. In all the 6 leads, the QRS

complex (ventricular depolarisation) is greater in magnitude than the P wave (atrial

depolarisation). Ventricular muscle mass is greater than atrial muscle mass thus the magnitude of

depolarisation/deflection must be greater for the ventricles.

The orientation of dipole and electrodes refers to the degree of alignment between the direction

and magnitude of dipole activity and electrode positioning (line of measurement). This idea is

shown well in Leads 1 and 2. Considering the QRS complex it can seem odd that one Lead shows

such minimal deflection while the other displays a clear deflection. The explanation to this is that

Lead 2 (Left Leg – Right Arm) is better aligned with the mean direction of QRS complex compared

to Lead 1 (Left Arm – Right Arm). Therefore, Lead 2 records the magnitude of mean QRS complex

better than Lead 1 and projects it on lead axis. Figure 3 shows Lead 3 having the largest positive

deflection indicating Lead 3 aligns with the mean QRS electrical activity the best. This second

concept is perhaps the most important out of the 3 as viewing the 3 dimensional (3D) heart in a

3D volume conductor (body) requires different leads viewing the heart in different electrical

perspectives. Indeed, the clinical 12-Lead ECG uses 12 different leads all viewing the heart in

different perspectives. Overall, all the Leads used in the experiment differ in their magnitudes and

directions of deflection because of this concept of different electrical viewpoints.

Next Einthoven’s triangle analysis was conducted to generate the resultant QRS vector and

predicted magnitudes of the augmented limb leads.

Figure 1 shows the resultant QRS vector (drawn in blue) of magnitude 1.30mV is leaning to the

left side. To determine whether the resultant vector is normal, left axis deviated or right axis

deviated the Figure below has been included.

Figure 5: Normal QRS axis and right and left axis deviation (LeGrice, 2015).

The resultant QRS vector of angle 88˚ is within -30˚ and +110˚; the normal range of QRS axis.

Overall, Figure 1 shows the mean dipole direction of the QRS complex of angle 88˚ with respect

to the horizontal line (0˚) with magnitude 1.30mV.

Comparing the measured and predicted magnitudes of the augmented limb leads indicates the

directions are concordant but the magnitudes are not. The errors are found to be quite large as

well. This infers the Einthoven’s triangle should not be used for detailed analysis of

electrocardiology but more as a general guide of the electrical activity behind cardiac function.

The Einthoven Triangle analysis could be improved by computer based method rather than

manual drawing by hand which can have large human random errors.

Part B: Auscultation and Phonocardiography

Figure 6: The Wigger’s diagram (Guyton & Hall, 2010).

The integrated approach of explaining cardiac activity using electrocardiography and

phonocardiography is useful since the 2 cardiograms show the relationship between the

mechanical and electrical activities of the heart. The results show that the first heart sound is

immediately after the QRS complex and second heart sound is immediately after the T wave.

The QRS complex and T wave represents ventricular depolarisation (thus ventricular systole) and

repolarisation (thus ventricular diastole) respectively. At the QRS complex the ventricles go

through systole and during systole the atrioventricular valves (AV: mitral and tricuspid) close as

seen in introduction. When the valves close up the vibrations from blood turbulence in the

ventricular wall causes the first heart sound “lubb”. Similar series of events happen to semilunar

valves during ventricular diastole (aortic and pulmonary valves).

During iso-volumetric contraction (IVC), the mitral valves actually closes 20-30ms before the

tricuspid valves close. This is because the pressure in the left ventricle at IVC is much greater than

the pressure in the right ventricle and the left ventricle actually contracts before the right (Boron

& Boulpaep, 2005). Normally, the sounds provided by the closure of the 2 valves will be heard as

one but through careful auscultation, the sounds can be distinguished. This is the splitting of the

first heart sound (MEDSCI 205 Laboratory Manual, 2015).

There is also the splitting of the second heart sound (also called physiological splitting). Like the

mitral and tricuspid valves, the aortic and pulmonary valves open and close at different times.

Upstream and downstream regions from the aortic valve is under high pressure compared to the

pulmonary valve because the right ventricle is weaker than the left (Johnson, 1998). Therefore

having lower pressure regions both upstream and downstream, the pulmonary valve opens before

aortic valve and closes after aortic valve. This difference in valve closure timing is further

enhanced by deep inspiration (negative intrathoracic pressure) which increases venous return and

thus the EDV of the right ventricle. There is more blood to eject and more time is required for the

right ventricle, further delaying the closure of the pulmonary valve (Boron & Boulpaep, 2005).

The first heart sound was louder than the second. The physiology behind this observation lies in

the volume of blood associated with blood turbulence. The first heart sound was caused by

turbulence of blood within the ventricles whereas the second heart sound was caused by

turbulence of blood within the aorta and pulmonary artery. Blood volume in the ventricles is

greater than the blood volume in both the great arteries. Magnitude of blood turbulence is

greater within the ventricles (because the blood volume is high) therefore the lubb heart sound is

greater than the dubb heart sound.

Medical literature adds, the duration of first heart sound should be greater than the second

(Tortora & Derrickson, 2012). However experimental results do not give support for this. Figure 2

shows the second heart sound is actually longer in duration than the first. One possible

explanation behind this is that the second heart sound indicated in Figure 2 actually contains the

third heart sound as well. Looking at Figure 6, the 3rd heart sound (S3), is before the P wave and

after the T wave. The laboratory environment in which phonocardiography was conducted had

high background noise level. Therefore, it would not be surprising to categories S3 with the

second heart sound since the background noise level makes sound distinction difficult.

Part C: Echocardiographic Analysis of Left Ventricular Function

Results from Figures 3 and 4 have made it clear that myocardial infarction leads to an increase in

left ventricular end diastolic volume and decrease in stroke volume which leads to large decrease

in ejection fraction.

Anteroseptal myocardial infarction, as introduced previously is the cardiac myocyte deaths in the

anterior region of the interventricular wall from coronary artery blockage. The deaths of cardiac

myocytes will mean there are less number of myocytes available for contraction. When the heart

contracts the amount of blood ejected decreases. This means end systolic volume will increase

which in turn decreases stroke volume. The increase in end systolic volume will increase the

preload of the heart (new blood from the atria plus the remaining blood which have not been

ejected). Increase in preload increases pressure exerted on ventricular walls and causes

detachments of the points where cardiac myocytes are linked to its neighbour – dilatation. Dilated

heart has normal heart muscle mass but increased ventricular chamber diameter. Degree of

contractility of the heart remains the same but there is increased volume of blood to eject

therefore ejection fraction decreases.

Note it is heart dilatation that is discussed not heart hypertrophy. In cardiac hypertrophy, the

heart gains muscle mass thus its ventricular walls are thickened. 2D echocardiogram does not give

evidence for thickening of the ventricular walls. Indeed, Figure 3 does not show thickening of

ventricular walls as the lines representing them remains the same in their thickness.

Discussing Figure 3 qualitatively, the results give evidence for akinesis (little to no heart wall

movement in systole) of the heart 3 months post-MI but does not for dyskinesis (bulging of the

heart in systole). In a dilated heart, there is increased preload and therefore pressure. Thus, the

heart cannot contract to the same degree as it did before myocardial infarction – little heart wall

movement. Since there is little heart movement, it follows that there is minimal change in heart

shape. This is shown again in Figure 3. Compared to the heart 1 week post-MI, the heart 3

months post-MI shows little changes in ventricular curvature. For the heart 3 months post-MI the

heart at the end systolic volume appears to be almost the same in shape as the heart in end

diastolic volume, displaying lack of dyskinesis.

Although varying from textbook to textbook, one source suggests ejection fractions of a healthy

heart and diseased heart are 0.6 and 0.5 respectively. A severely damaged heart, thus associated

with high mortality has ejection fraction of 0.3 (Johnson, 1998). Figure 4 gives the EF of the heart

3 months post-MI as 19.6% = 0.2. Therefore the patient with this heart is at a high risk of death

associated with the heart.

Conclusion

Overall, electrocardiogram and phonocardiogram were recorded successfully. The recording were

used to discuss the relationship between ventilation and heart rate as well as heart sounds and

cardiac electrical activity. Different leads were used to view the heart in different perspectives

electrically which was the central concept of the laboratory. The Einthoven’s triangle analysis was

conducted to derive the resultant QRS vector and its angle. 2D Echocardiogram was analysed to

discuss ventricular function between heart 1 week post-MI and 3 months post-MI.

References

Boron, W.F. & Boulpaep, E.L. (2009). Medical Physiology. 2nd ed. Philadelphia, PA: Elsevier Inc.

Boron, W.F. & Boulpaep, E.L. (2005). Medical Physiology. Updated ed. Philadelphia, PA: Elsevier Inc.

Tortora, G. J. & Derrickson, B. (2006). Principles of Anatomy and Physiology. 11th ed. Hoboken, NJ:

John Wiley & Sons Inc.

Tortora, G. J. & Derrickson, B. (2012). Principles of Anatomy and Physiology. 13th ed. United States

of America: John Wiley & Sons, Inc.

Kalbunde CVS Reference, 2004

MEDSCI 205 Laboratory Manual (2015). Laboratory 3: Electrocardiography, Auscultation,

Phonocardiography and 2D Echocardiography.

MEDSC 205 Lecture Manual (2015). Cardiac and Vascular Function.

Johnson, L. (1998). Essential Medical Physiology. United States of America: Lippincott-Raven

Guyton & Hall. (2010). Textbook of Medical Physiology. 12th ed. Philadelphia: Saunders

LeGrice, I. (2015). Unpublished MEDSCI 205 Lecture Handout.