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 student’s 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 heart’s 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 student’s 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 student’s 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 student’s 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 student’s 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

High LowBPM (R-R) BPM Before Exercise Mean + SEM 86.97 + 5.94 72.58 + 3.39

p-value P = 0.07BPM (R-R) BMP After Exercise Mean + SEM 127.60 + 7.4 118.4 + 4.4

p-value P = 0.34P wave amplitude (mV) Before Exercise Mean + SEM 0.12 + 0.01 0.16 + 0.03

p-value P = 0.27P wave amplitude (mV) After Exercise Mean + SEM 0.18 + 0.02 0.22 + 0.02

p-value P = 0.13QRS amplitude (mV) Before Exercise Mean + SEM 1.11 + 0.11 1 .53 + 0.13

p-value P = 0.02QRS amplitude (mV) After Exercise Mean + SEM 1.18 + 0.09 1.58 + 0.13

p-value P = 0.01T wave (mV) Before Exercise Mean + SEM 0.23 + 0.02 0.26 + 0.03

p-value P = 0.4T wave (mV) After Exercise Mean + SEM 0.29 + 0.02 0.35 + 0.03

p-value 0.09S-T segment duration (s) Before Exercise Mean + SEM 0.15 + 0.03 0.14 + 0.02

p-value P = 0.86S-T segment duration (s) After Exercise Mean + SEM 0.13 + 0.02 0.08 + 0.01

p-value P = 0.08P-R interval duration (s) Before Exercise Mean + SEM 0.13 + 0.01 0.15 + 0.01

p-value P = 0.39P-R interval duration (s) After Exercise Mean + SEM 0.16 + 0.04 0.13 + 0.02

p-value P = 0.68Q-T interval duration (s) before Exercise Mean + SEM 0.34 + 0.02 0.35 + 0.02

p-value P = 0.6Q-T interval duration (s) After Exercise Mean + SEM 0.29 + 0.02 0.29 + 0.02

p-value P = 0.95T to R duration (s) Before Exercise Mean + SEM 0.48 + 0.04 0.54 + 0.04

p-value P = 0.31T to R duration (s) After Exercise Mean + SEM 0.33 + 0.05 0.31 + 0.03

p-value P = 0.78R to T duration (s) Before Exercise Mean + SEM 0.33 + 0.04 0.33 + 0.02

p-value P = 0.9R to T duration After Exercise Mean + SEM 0.24 + 0.02 0.27 + 0.02

p-value P = 0.26The table above summarizes the data collected on the effects of stress level on electrocardiogram

(ECG) readings using a student’s 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.

Before Exercise After Exercise0

0.02

0.04

0.06

0.08

0.1

0.12

0.14

0.16

0.18 P

-R in

terv

al d

urati

on (s

)

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.

Before Exercise After Exercise0

0.02

0.04

0.06

0.08

0.1

0.12

0.14

0.16

S-T

segm

ent d

urati

on (s

)

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.

Before Exercise After Exercise0

0.2

0.4

0.6

0.8

1

1.2

1.4

1.6

1.8Q

RS a

mpl

itude

(mV)

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.

Before Exercise After Exercise0

20

40

60

80

100

120

140 B

PM (R

-R) (

bpm

)

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 p-

value 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.

References

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