Effects of psychological stress on the heart of college students and ECG readings: QRS

Complex

Prepared By Vivian Sanni-Thomas

Partner; Kyle Sultzer

Principle of Physiology Laboratory

Richard Stockton College

Introduction
Stress is a natural way for our body to deal with any danger or situation we come across (Kristen
[date unknown]). Stress can be psychological, environmental, physical or emotional (Harvard
Mental Health Letter, March 2011). Psychological stress can also be mental or emotional
response to stressful situation. The hypothalamus, found in the brain activates the pituitary
glands and adrenal medulla by using HPA (Hypothalamus-Pituitary-Adrenal) axis and SAM
(Sympathetic -Adrenal-Medulla) axis when responding to short or long term stress. The SAM
axis is activated by short term stress response (fight or flight response), which secrets adrenaline
into the bloodstream by stimulating the adrenal medulla. Adrenaline makes the heart beat faster,
increases blood pressure, increases breath, increases blood sugar and sharpens our senses. HPA
axis on the other hand is activated during long term response by releasing corticotrophin
hormones (CRH) to stimulate the pituitary gland to secrete adrenocorticotropic hormones
(ACTH). ACTH triggers adrenal glands (cortex) to release cortisol which in turn, suppresses our
immune system. Cortisol raises blood sugar levels to prolong stress and the parasympathetic
nervous system brings the body to normal after stress. Prolong activation of stress response can
lead to health risk (Harvard Mental Health Letter, March 2011).
This experiment was done to study the effects of psychological stress on students heart. A
normal heart uses sinoatrail node (SA node) found at the atrium to create its own electrical signal
which start contraction of the heart muscles to help start a heartbeat. Apart from the circulatory
system which controls the heart rate and blood pressure, autonomic nervous system can also
control the heart rate and blood pressure as well. Autonomic nervous system has two

components; sympathetic and parasympathetic. The fibers of the sympathetic which are linked to
SA nodes when stimulated cause increase in heart rate, conduction velocity, and contraction. The
parasympathetic nervous system, also linked to the SA nodes, decreases the heart rate and
conduction velocity when stimulated (Rhodes and Bell 2012). Since both cardiovascular system
and autonomic nervous system influence the hearts electrical activity, ECG can be used for this
experiment.
An electrocardiogram (ECG or EKG) is a test used to record the electrical activity of the heart.
(Silverthorn 2013). This is done by placing electrodes on the skin to detect and magnify the
electrical changes that occur during heart muscle contraction on every heartbeat. The heart has
both left and right chambers called Atria and a lower chamber called the Ventricle. The right
atrium uses its SA nodes to generate an electrical signal to spread through the atria walls
resulting in atria contraction (P wave on the ECG readings, which should not be more than 0.11
seconds). The electrical signal then travels through atrioventricular node (AV node) before it gets
to the ventricles. AV nodes help to delay contraction of ventricles whiles the atria is working (Q
wave and end of P wave on the ECG readings). Ventricles use bundle of HIS-Purkinje fibers to
send signals through its muscular wall resulting in contraction (QRS complex on the ECG
readings, which should not be more than 0.10 seconds). The ventricles repolarize (S-T segment
on the ECG), then the ventricles then relax (T wave on the ECG readings). R to R interval is the
rate the heart is beating per minute (normal heart rate is between 60 and 80 BPM, after exercise
is 155 BPM) (Silverthorn 2013). ECG readings can be affected by conditions like diseases,
condition of the heart, age, medications taking etc. The aim of this experiment was to study the
effects of psychological stress on students heart irrespective of the any conditions.

Prior studies predicted that people with coronary disease when subjected to acute psychological
stress will increase in ECG abnormalities like QT dispersion. The studies concluded that QT
dispersion increased due to changes in JT dispersion (rather than QRS dispersion) (James et al
2000) . Other studies also indicated that people with chronic stress like post traumatic stress
disorder (PTSD) and depression may have high risk of cardiovascular disorder. This can be
dysfunction of the autonomic nervous system due to increase heart rate and blood pressure which
can result in ECG abnormalities. Thus, it was concluded that people with PTSD and depression
showed elevated rates of ECG abnormalities compared to people who did not have these
conditions (Khazaie et al. 2013).
Based on the previous results, since increases in heart rate and blood pressure can lead to
cardiovascular disorder with time, we expected students who report high or chronic levels of
psychological stress to have changes in the heart as well as its ECG readings in PR intervals,
QRS complex BPM (R-R) compared to those who have low or acute psychological stress levels.
Hopefully at the end of this experiment, knowing the effects of psychological stress on students
heart will help manage stress and avoid health risks for students.

Methods
This experiment was to find out if students stressors like academic
work, family matters, peer pressure, future success and financial troubles
can contribute to changes in heart rate using electrocardiogram readings; PR
interval and R-R interval. An ECG and survey data were acquired from 32
students population (39% of the student population was male, 61% female)
with ages mostly between 18 and 25 years old; only a few above 30 years

old. The gender balance in the sample was proportional to that of the college
population from which the sample was drawn. Survey questionnaires were
given to each student and rankings were assigned on a 1-5 response scale
where 1= never and 5= very often. To establish two treatment groups,
all the response scale score of the answered questionnaire were summed
and divided by the class population to get an average number of 46.
Numbers that fell below the average was given to students with low level
stress and above the average was assigned to students with high level
stress. A 3-lead electrocardiogram (ECG) test was recorded on two different
experiments; the first recordings were when students were resting before
exercises whiles the second one was after performing the exercise. There
were some conditions that might affect the ECG readings. For example, like
activities level before the recording, medications taken, etc
A Biopac lab manual procedures for ECG 1 was followed by using a 3-lead
ECG; white, black and red lead. These leads were attached to the legs and
foots of the students. ECG measurement of heart in BPM was recorded on
each student for each experiment before (resting) and after exercise. The
BPM was measured in three different cardiac cycles times within each
situation. Mean of these hearts BPM was calculated on each. A biopac lab
manual procedure for ECG 1 was followed to measure the amplitude of the P
wave, QRS complex and T wave. This measurements were made in three
different cardiac cycles times within each experiment; before (resting) and
after exercise. Mean of these measurements were calculated on each as well.
The experiment procedure was repeated for the S-T segment, PR interval, QT
interval, T to R (end of T wave to the next R wave) and R to T (R wave peak
to end of T wave). All this information was then typed into a master excel
spreadsheet.

Results

An experiment was done to test whether stress which has been a factor for health risk like heart
disease can be detected through abnormalities of ECG in. A students t-test analysis was used.
The mean values and standard errors for P-R interval for high and low level stress group for
both exercises (Table 1) were [(0.13 (s), + 0.1 and 0.15 (s),+ 0.1) and (0.16 (s), + 0.04, and 0.13
(s), + 0.02)]. There is no significant difference between the two groups. The p-value before the
exercise (Table 1) is 0.39 whiles that of after the exercise is 0.68. Whiles S-T segment mean
values and standard errors for high and low level stress group for both exercises (Table 1) were
[(0.15 (s),+ 0.3 and 0.14 (s), + 0.02) and (0.13 (s), + 0.02 and 0.08 (s), + 0.01)]. There is no
significant difference between the groups for both exercises as well. The p-value before the
exercise (Table 1) is 0.86 and that of after the exercise is 0.08.
Also the data showed that the mean values and standard errors for P wave amplitude for high and
low level stress group for both exercises (Table 1) were [(0.12 (mV), + 0.01 and 0.16 (mV),+
0.03) and (0.18 (mV), + 0.02, and 0.22 (mV), + 0.02)]. There is no significant difference
between the two groups. The p-values before the exercise (Table 1) are 0.27 whiles that of after
the exercise is 0.13. Furthermore there is no significant difference between the two groups for
both exercises for T wave amplitude. The p-value before the exercise (Table 1) is 0.4 whiles that
of after the exercise is 0.09. The mean values and standard errors for T wave amplitude for high
and low level stress group for both exercises (Table 1) were [(0.23 (mV), + 0.02 and 0.26 (mV),+
0.03) and (0.29(mV), + 0.02, and 0.35 (mV), + 0.03)].
In addition, the mean values and standard errors for Q-T interval for high and low level stress
group for both exercises (Table 1) were [(0.34 (s),+ 0.02 and 0.35 (s), + 0.02) and (0.29 (s), +
0.02 and 0.29 (s), + 0.02)]. There is no significant difference between the groups for both
exercises as well. The p-value before the exercise (Table 1) is 0.6 whiles after the exercise is

0.95. Moreover, the mean values and standard errors for T to R duration for high and low level
stress group for both exercises (Table 1) were [(0.48 (s),+ 0.04 and 0.54 (s), + 0.04) and (0.33(s),
+ 0.05 and 0.31(s), + 0.03)]. There is no significant difference between the groups for both
exercises as well. The p-value before the exercise (Table 1) is 0.31 whiles after the exercise is
0.78. On top of that, there is no significant difference between the groups for both exercises as
well for R to T duration. The p-value before the exercise (Table 1) is 0.9 whiles after the exercise
is 0.26. The mean values and standard errors for R to T duration for high and low level stress
group for both exercises (Table 1) were [(0.33(s),+ 0.04 and 0.33 (s), + 0.02) and (0.24(s), +
0.02 and 0.27(s), + 0.02)].
The results indicated that there is a significant difference between the high and low level stress
groups during QRS amplitude ECG readings before and after performing the activity. The QRS
amplitude mean values and standard errors for high and low level stress group for before and
after exercises (Table 1) were [(1.11 (mV),+ 0.11 and 1.53 (mV), + 0.01) and (1.18 (mV), + 0.09
and 1.58 (mV), + 0.13)]. High level stress group and low level stress group showed significant
differences in QRS amplitude readings for both exercises. The p-value before the exercise (Table
1) is 0.01 whiles that of after the exercise is 0.02. Even though means of QRS amplitude showed
a significant difference for both groups, means of BPM (R to R) on the other hand did not. The
BPM (R to R) mean values and standard errors for high and low level stress group for both
exercises (Table 1) were [(86.97 (bpm),+ 5.94 and 72.58 (bpm), + 3.39) and (127.6 (bpm), + 7.4
and 118 (bpm), + 4.4)]. There is no significant difference between the two groups for both
exercises. The p-value before the exercise (Table 1) is 0.34 whiles that of after the exercise is
0.07. It can therefore be concluded that there was a significant difference between both groups
for QRS amplitude ECG readings for before and after performing the activity. However,

electrocardiogram (ECG) readings; P-R interval, S-T segment, BPM (R to R), P wave amplitude,
T wave amplitude, Q-T interval, T to R duration and R to T duration did not showed any
significant difference between both groups for before and after performing the activity.
Table 1: Effects of Stress on Electrocardiogram (ECG) Readings
BPM (R-R) BPM Before Exercise
BPM (R-R) BMP After Exercise
P wave amplitude (mV) Before Exercise
P wave amplitude (mV) After Exercise
QRS amplitude (mV) Before Exercise
QRS amplitude (mV) After Exercise
T wave (mV) Before Exercise
T wave (mV) After Exercise
S-T segment duration (s) Before Exercise
S-T segment duration (s) After Exercise
P-R interval duration (s) Before Exercise
P-R interval duration (s) After Exercise
Q-T interval duration (s) before Exercise
Q-T interval duration (s) After Exercise
T to R duration (s) Before Exercise
T to R duration (s) After Exercise
R to T duration (s) Before Exercise
R to T duration After Exercise

Mean + SEM
p-value
Mean + SEM
p-value
Mean + SEM
p-value
Mean + SEM
p-value
Mean + SEM
p-value
Mean + SEM
p-value
Mean + SEM
p-value
Mean + SEM
p-value
Mean + SEM
p-value
Mean + SEM
p-value
Mean + SEM
p-value
Mean + SEM
p-value
Mean + SEM
p-value
Mean + SEM
p-value
Mean + SEM
p-value
Mean + SEM
p-value
Mean + SEM
p-value
Mean + SEM

High
86.97 + 5.94
P = 0.07
127.60 + 7.4
P = 0.34
0.12 + 0.01
P = 0.27
0.18 + 0.02
P = 0.13
1.11 + 0.11
P = 0.02
1.18 + 0.09
P = 0.01
0.23 + 0.02
P = 0.4
0.29 + 0.02
0.09
0.15 + 0.03
P = 0.86
0.13 + 0.02
P = 0.08
0.13 + 0.01
P = 0.39
0.16 + 0.04
P = 0.68
0.34 + 0.02
P = 0.6
0.29 + 0.02
P = 0.95
0.48 + 0.04
P = 0.31
0.33 + 0.05
P = 0.78
0.33 + 0.04
P = 0.9
0.24 + 0.02

Low
72.58 + 3.39
118.4 + 4.4
0.16 + 0.03
0.22 + 0.02
1 .53 + 0.13
1.58 + 0.13
0.26 + 0.03
0.35 + 0.03
0.14 + 0.02
0.08 + 0.01
0.15 + 0.01
0.13 + 0.02
0.35 + 0.02
0.29 + 0.02
0.54 + 0.04
0.31 + 0.03
0.33 + 0.02
0.27 + 0.02

p-value
P = 0.26
The table above summarizes the data collected on the effects of stress level on electrocardiogram
(ECG) readings using a students t-test analysis. There were a total of twenty eight students;
sixteen were in high level group and the other twelve were in low level group.
0.18
0.16
0.14
0.12
0.1
P-R interval duration (s)

0.08
0.06
0.04
0.02
0

Before Exercise

After Exercise

Figure 1. The electrocardiogram (ECG) readings; P-R interval, taken on high and low level
stress groups for before and after exercises. There is a total sample of 28 students; 16 are in a
high level stress group and 12 in low level stress group. Of the two bar colors, the black color bar
represents high level stress group and the gray color bar represents low level stress group. There
is no significant difference between the mean P-R intervals of the two groups before the exercise.
The p-value before the exercise is 0.39. There is also no significant difference between the mean
P-R intervals of the two groups after the exercise. The p-value after the exercise is 0.68.

0.16
0.14
0.12
0.1
S-T segment duration (s)

0.08
0.06
0.04
0.02
0

Before Exercise

After Exercise

Figure 2. The electrocardiogram (ECG) readings; S-T segment, taken on high and low level
stress groups for before and after exercise. There is a total sample of 28 students; 16 are in a high
level stress group and 12 in low level stress group. Of the two bar colors, the black color bar
represents high level stress group and the gray color bar represents low level stress group. There
is no significant difference between the mean S-T segments of the two groups before the
exercise. The p-value before the exercise is 0.86. There is no significant difference between the
mean S-T segments of the two groups after the exercise. The p-value after the exercise is 0.08.

1.8
1.6
1.4
1.2
1
QRS amplitude (mV)

0.8
0.6
0.4
0.2
0

Before Exercise

After Exercise

Figure 3. The electrocardiogram (ECG) readings; QRS amplitude, taken on high and low level
stress groups for before and after exercises. There is a total sample of 28 students; 16 are in a
high level stress group and 12 in low level stress group. Of the two bar colors, the black color bar
represents high level stress group and the gray color bar represents low level stress group . There
is a significant difference between the mean QRS amplitude of the two groups before the
exercise. The p-value before the exercise is 0.02. Also there is a significant difference between
the mean QRS amplitude of the two groups after the exercise. The p-value after the exercise is
0.01.

140
120
100
80
BPM (R-R) (bpm)

60
40
20
0

Before Exercise

After Exercise

Figure 4. The electrocardiogram (ECG) readings; BPM (R to R), taken on high and low level
stress groups for before and after performing an activity. There is a total sample of 28 students;
16 are in a high level stress group and 12 in low level stress group. Of the two bar colors, the
black color bar represents high level stress group and the gray color bar represents low level
stress group. There is no significant difference between the mean BPM (R to R) of the two
groups before the exercise. The p-value before the exercise is 0.07. Also there is no significant
difference between the mean BPM (R to R) of the two groups after the exercise. The p-value
after the exercise is 0.34.

Discussion

The experiment showed a significant difference in ECG readings; QRS amplitude, proving that
high level of psychological stress can affects the heart rate as well as its ECG readings. The
outcome of the experiment showed that psychological stress irrespective of being high or low
level can have effects on the ventricles (QRS amplitude) of the heart. Overall, no significant
difference was demonstrated for all of the aspects, except the QRS amplitude. The hypothesis
predicted that not only QRS complex, but also P-R interval as well as BPM (R-R) would be
affected. However, the statistical tests demonstrated no significant difference for both high and
low groups for P-R interval and BPM (R-R).
Even though it was expected that during high level of psychological stress, the heart will beat
faster to respond to a stressful situation and activities as SA node occur faster, so do atrial
depolarization, contraction and relaxation (increase in P-R interval). In this case, ventricle
depolarization should occur faster as well (increase in QRS amplitude) which over all should
increase BPM (R-R) (Silverthorn 2013). This seemed not to be the case as atrial as well as the
BPM (R-R) which were not affected at all.
Basically, stress influenced a faster or rapid ventricular depolarization, which could possibly be a
result of narrowing of the QRS amplitude. This means that changes in ventricular depolarization
might come from above the ventricles (supraventricular tachycardia). This could be from the SA
node, atrial, AV node or His bundle. In this case, P-R interval appeared to be within the normal
limit (Table 1) so the changes seems not to be coming from either the SA node or the atria. (Not
1st degree heart block). Normal P-R interval means that depolarization was able to reach the
interventricular septum, which also suggests that the changes are not coming from the AV node
either (Not 2nd degree heart block). In this case the changes might be coming from the His
bundles or within the ventricles which might be a 3rd degree heart block (Ganz I L 2014).

Though it was expected, there was no effect of high psychological stress on overall heartbeat
BPM (R-R). There was no significant difference between both activates for both groups (Figure
4).This might be influenced by low in concentration of cytosolic calcium ion release which is
expected to increase during stress to induce increased in muscle contraction. Low in
concentration of cytosolic calcium ion released induces weaker contraction. Decreased in muscle
contractility cells will decrease stroke volume which leads to decrease in cardiac output and this
will affect the heart rate BPM (R-R) (Silverthorn 2013).
There was no relationship between psychological stress and the S-T segment. Even though the pvalue decreased from 0.86 for before exercise to 0.08 after exercise. This might have been
influenced by the narrowing of the QRS amplitude. There was no significant difference between
both groups and exercise.
Also T wave also showed no effect from psychological stress. The significant difference between
both groups stayed pretty much the same. Though the p-value for before exercise decreased from
0.4 to 0.09 after the exercise (Table 1) which was very interesting. Because since T to R
durations did not show any significant difference, T wave was not expected to show that
variations.
Though experiment demonstrated that the prediction for P-R interval BPM (R-R) were not
proved, the evidence from the experimental results still supported the hypothesis for QRS
amplitude readings (Figure 3). Other studies concluded that there were increase in QT dispersion
due to changes in JT dispersion (rather than QRS dispersion) when people with coronary disease
were subjected to acute psychological stress (James et al 2000). Though prior studies showed
changes in ECG readings related to QT dispersion, this experiment yielded that both high and

low level stress group differed in QRS amplitude for before and after exercises. It means that the
results of the experiment contradict to the conclusions of previous studies. One of the previous
studies stated that people with high level or chronic stress have abnormalities in ECG
measurements, but did not specify what aspects of ECG were affected. The studies showed how
people with high level or chronic stress like post traumatic stress disorder (PTSD) and depression
have changes in ECG readings due to cardiovascular disorder and dysfunction of autonomic
nervous system, which can lead to increase in heart rate and blood pressure. They also concluded
that people with PTSD and depression showed elevated rates of ECG abnormalities compared to
people who are not (Khazaie et al. 2013). Since their conclusion were general and was not
specific to any ECG readings, the hypothesis can be partially be supported by this studies.
The limitations of the experiment were that the sample size and the age were not not big enough
to reflect the true value of the findings (only 28 subjects), (ages were 20 to 27 years of age).
Another limitation was that when the subjects were divided into high and low stress level groups,
there were about 9 participants that were close to division value (medium).
There were some questions that needed to be answered but could not; how come ventricles
depolarized but it was not seems to be repolarized or systole. This experiment can be improved
or extended by increasing the population size and using people of different ages as well.

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