Factors Effecting Cardiac Output Physical Education Essay

Inotropy can have positive or negative effect on the heart, especially the ventricles. There are few factors that can influence inotropy; this can either be neuronal, hormonal. The neuronal influence is predominately from the autonomic nerves, either the parasympathetic or the sympathetic nerves and these have both negative and positive effect on inotropy. However, other influences come from some drugs which have positive or negative effect on inotropy. This will consequently affect the cardio output by changing the state of for example ESV, preload, stroke volume and heart rate. All of these factors are related and depend on each other.
Section A:
The autonomic nerves are divided into two, parasympathetic and sympathetic nerves. The sympathetic nerves cause a positive inotropy. It does this by releasing norpinephrine by the postganlionic fibers and the secretion of epinephrine from adrenal medulla. These hormones, norpinephrine and epinephrine, causes the cardiac muscle cell metabolism. Hence, the contraction and the force of contraction in the cardiac muscle increase. This increases because of special types of receptors called adrenergic receptors found on the plasma membrane of the cardiac muscle cells. There are two types; one is called the alpha receptors and the other type is called the beta receptors. These receptors bind to and recognise both norepinephrine and epinephrine. Because of the cardiac muscle cells contraction increases this will cause the ventricles to contract harder. This will decrease the end systolic volume, because the amount of blood ejected from the ventricles increases.

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The other types of nerves that influence the inotropy are called parasympathetic nerves. The parasympathetic stimulation from the vagus causes the release of acetylcholine (ACh), which is a neurotransmitter. The ACh binds to two types of receptors; they are known as the muscarinic and nicotinic cholinergic receptors. There are different types of mascarinic receptors; and the M2 muscarinic receptors are specific for the heart. These receptors work by maintaining the heart to stay at its constant state. When the ACh is released it binds to M2 mascurinic receptors. Therefore, after the reactions occur between the M2 mascurinic receptors and the ACh, the effect it has on the heart is that it reduces the heart rate; it also reduces the action potential produced by the SA node and the AV node. However, it also affects the heart’s ability to contract. Both the arterial and ventricular muscle cells are innervated by the sympathetic and parasympathetic nerves. However, in the ventricular muscle cells, the parasympathetic nerves have more compact than the sympathetic nerves. For these reasons the parasympathetic stimulation has a negative effect on the inotropy.
Beside the parasympathetic and sympathetic stimulations having influence on the inotropic state; there are few hormones, described above, and drugs that can also influence the inotropic state of the heart. As mentioned above, epinephrine, which is released from the adrenal gland, and norepinephrine, which is released from the sympathetic nerves, increases the heart rate. This has a positive effect on the inotropic state of the heart. However, there are few drugs that have the opposite effect of the norepinephrine and epinephrine; these drugs are known as antagonist, because they block the action of the hormones. Some examples of such drugs are propanolol and digoxin. Propranolol works by blocking the beta adrenergic receptors that binds with epinephrine. This means that epinephrine cannot longer bind to these receptors, so therefore its effects are no longer seen and blocked. This is why propranolol and drugs similar to it are called beta-blockers. The actions seen by these drugs on the heart is that it slows down the heart rate.
When the ventricles contract with great deal of force, the ventricles have to overcome some sort of tension; this tension is known as afterload and comes from the aorta pressure. Therefore, if the afterload is increased, this will mean the ventricular muscle cells will contract for longer period. Hence, the greater the end systolic volume will be; this is because the blood ejected is less and this will reduce the stroke volume, which means cardiac output will decrease as well. This mechanism only happens when the inotropy is increased and this can be done by hormonal or anatomic stimulation influence. On the other hand, a reduced inotropic sate, in this case the afterload is increased as well, will have the opposite effect on the end systolic volume.
Section B:
The preload is directly proportional to the end diastolic volume; therefore if there is an increase in the preload, there is an increase in the end diastolic volume. Basically what preload does is that it affects the cardiac muscle cell’s ability of creating tension. So this means during systole, during the contraction of the ventricular muscle cells, the force produced increases and is forceful. Therefore increasing inotropy, by hormones such as epinephrine or stimulation from the autonomic nervous system, will increase in the force of contraction of the ventricles. Another way the inotropy can be increased depends on the amount of blood that is returned to the heart, which is known as the venous return. This can for example be caused by excise; this will increase the venous return and which will increase the end diastolic volume. Hence the increase of end diastolic volume will cause the increase of both stroke volume and cardiac output. What the venous return does is that it stretches the ventricular muscle cells because of the more blood. So this means the sacromere length will increase so does the tension. This results in the contraction of the ventricular muscle cells with greater force and the ejection of more blood. Thus, an increase in the preload will cause an increase in end diastolic volume; so therefore stroke volume is increased and cardiac output. This mechanism is known as the Frank-Starling law; this law basically states that the more the heart is stretched, the harder the heart contracts to eject more blood.
When the ventricles contract with great deal of force, the ventricles have to overcome some sort of tension; this tension is known as afterload and comes from the aorta pressure. Therefore, if the afterload is increased, this will mean the ventricular muscle cells will contract for longer period. Hence, the greater the end systolic volume will be; this is because the blood ejected is less and this will reduce the stroke volume, which means cardiac output will decrease as well. This mechanism only happens when the inotropy is increased and this can be done by hormonal or anatomic stimulation influence. On the other hand, a reduced inotropic sate, in this case the afterload is increased as well, will have the opposite effect on the end systolic volume.
The contractility of the heart can, especially the ventricles, can have a great deal on the pressure and the development tension on the ventricles. This has an effect on the ejection fraction, because the inotropy changes the amount of blood ejected from the ventricles. There are two types of factors that increase the inotropic state. The types are either said to have positive inotropic or negative inotropic.
In order for the cardiac muscles cells to contract, the sarcoplasmic reticulum has to release Ca2+ .What causes the contraction of the cardiac cells are the entry of Ca2+ into the cells. Therefore what the positive inotropic does is that it increases the amount of Ca2+ that enter into the cardiac muscle cells. This increases the stroke volume and lowers the ESV which in return increases the cardiac output. An example of this is the sympathetic stimulation on the heart. However, the negative inotropic has the opposite effect. This can for example be the parasympathetic stimulation; basically this will block the entry of the Ca2+ into the cardiac muscle cells. Thus the ejection fraction is reduced which leads to an increase on the ESV; hence the stroke volume decrease and cardiac output as well.
The heart rate is defined as the number of times the heart beats in one minutes. In a normal person at rest beats as 70 beats per minutes. The body controls the heart rate different ways that might increase or decrease heart rate. Activities from the parasympathetic nerves decreases the heart rate, basically what happens is that stimulations sent from the parasympathetic nerves to the heart decreases heart rate; whereas the sympathetic nerves have the opposite effect. The effect seen from this is that the pacemaker potential decreases due to a decrease in the F-type sodium ions. This means the threshold is reached more slowly than it is normally, thus heart rate decreases and consequently the cardiac out decreases as well.
Heart rate can also be affected by hormonal influence. One primarily example is the release of epinephrine which is released from adrenal medulla. This hormone basically acts on the receptors found on beta-adrenergic receptors in the SA node. These receptors normally accept norepinephrine, which is released from the neurons. The effect of these hormones is that it increases the heart rate, hence the cardiac output.
 

Variables Effecting Vital Capacities Among Undergraduate Biology Students

Abstract

Vital capacity’s importance is to determine an individual’s lung function, or how what volume of air can be expelled from a person’s lungs. In this study, we investigated the relationships between vital capacity and heart rate, chest circumference, height, gender, and stature in undergraduate Biology students. This was measured via a spirometer. We found that the average vital capacity in males while standing was 4.25 L while females was 3.22 L. Comparing stature, the average standing vital capacity for all students was 3.53 L and seated was 3.40 L, showing that there is no discernible difference in the two. Heart rate held no correlation to vital capacity. On the other hand, chest circumference and height had a positive correlation with vital capacity. In summary, the majority of these variables produced anticipated data, while heart rate did not.

Introduction

Vital capacity (VC) is defined as the maximum volume of air that an individual can exhale after a maximum inhalation (Hoffman, et al. 2018). This is important to study to understand one’s respiratory health. We know that having healthy lungs can minimize respiratory problems because it enables us to consume the necessary amount of oxygen for daily metabolic functions. A healthy individual will have a vital capacity between 2 and 5 liters. Keeping our lungs well inflated will maintain our oxygen levels to ensure we are getting enough in our bodies where it is needed. The normal breathing we do on a day to day basis is called tidal volume (TV). Inhaling beyond the normal tidal volume is considered the inspiratory reserve volume (IRV), and the opposite, breathing outward is called expiratory reserve volume (ERV). The sum of inspiratory reserve volume, expiratory reserve volume, and tidal volume equals vital capacity. A spirometer is a tool used to measure vital capacity, which was invented in 1842 by Dr. John Hutchinson (Geddes, 2016). His studies, conducted by a calibrated bell inverted in water, concluded that vital capacity was directly related to height and inversely related to a person’s age (Petty, 2002). Many studies have shown that vital capacity can be affected by other numerous factors.

Some factors have a positive correlation with vital capacity, gender being one of them.

A spirometry test was done between triathletes from Malaysia to test the forced vital capacity (FVC) and forced expiratory volume in one second (FEV1). After taking body composition measurements, the results showed that the male’s vital capacity was more statistically significant than the female triathletes (Johari, 2017). Another factor that has shown a positive effect on vital capacity is chest circumference and height. A study conducted by measuring the height and chest circumference of 1276 men weighing between 100 lbs and 200 lbs showed that the taller men and the individuals with larger chest circumference exhibited greater total exhalation (Hutchinson, 1846).

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This knowledge led to other researchers testing new variables, some of which have a negative effect on vital capacity. Expiratory volumes of a person in the seated position, when compared to standing, was found to have a statistically significant value of p=0.001 in a study conducted with 90 middle-aged male subjects alternating between the two positions (Townsend, 1983). Little research has been studied on whether heart rate plays a role in vital capacity. Although there is not a lot of research on the effects of pulse, exploration in the relationship between the heart rates of moderate to severe COPD patients and lung function were shown to hold a negative correlation in lung function, specifically FEV (forced expiratory volume) (Mazzuco, 2015). Smoking, which serves as a key player in inhibiting the lungs has shown to also have a negative effect on the respiratory system. Vital capacity and other lung functions were tested in 34 smokers and 34 nonsmokers between the ages of 15 and 18. There was a significant decrease in VC in the group who smoked compared to the youth who did not (Tantisuwat, 2014). Lung disease also appears to show a negative effect on vital capacity. A study done between normal and asthmatic children revealed that children with asthma indicted lower vital capacities when compared to children without it (Kattan, et al. 1978).

In this study, the relationships were investigated between vital capacity and variables of height, chest circumference, resting pulse rate, gender, and stature. Based on previous research, we expect to see the male students to have a larger vital capacity than females. We also believe that the subjects in standing position will exhibit a larger vital capacity compared to the sitting trials. It is anticipated that there will be a negative relationship between heart rate, but a positive correlation with height and chest circumference and vital capacity.

Materials and Methods

In this study, a variety of factors were measured that affect vital capacity. It was conducted by a group of 67 (20 male and 47 female) undergraduate Slippery Rock University Principles of Biology students. Height was measured in centimeters. Chest circumferences were measured by wrapping a tape measure (cm) around the individual’s chest, just below the sternum, or under the bra level. Resting pulse (bpm) was recorded by placing two fingers on the radial artery and counting the number of pulses in a 15-second interval and multiplying that number by 4. This was done in three trials to get an average reading of resting heart rate. A spirometer was used to measure vital capacity (L). Each student measured their vital capacity by inhaling maximally, placed their mouth on the tube and exhaled maximally. All experiments were measured in triplicate, as was for the seated and standing positions. Along with recording the number of males and females, lifestyle factors were also noted, such as if the student was an athlete, has been diagnosed with asthma, or was considered a smoker.

Results

Upon completion of the experiment, spirometry data for the 67 Principles of Biology students showed an average standing vital capacity of 3.53 L, while the seated vital capacity was 3.40 L (Table 1). This suggests that there is no difference between the two statures. For the 20 males, the average standing vital capacity was 4.25 L and seated was 3.23 L. For the 47 females, the average standing VC was 3.22 L, while the seated VC was 3.04 L (Table 1). This shows males had a higher vital capacity than females. Height and vital capacity exhibited a positive correlation in our study (Figure 1). This advocates as the height of the individual increased so did vital capacity. The results showed a positive correlation found between chest circumference and standing vital capacity (Figure 2). This evidence suggests that larger chest circumference and/or height, the more oxygen one can respire. On the other hand, there was no correlation found between pulse and vital capacity in our study (Figure 3).

 

Discussion:

The collected data found was mainly as expected, apart from heart rate. As discussed, we believed to see positive correlations between height/chest circumference and vital capacity, and a negative correlation with pulse. Out of these trends, the data supported the claims of chest circumference and height. This was exhibited similarly in the study showing the men who are taller/larger chest circumferences produced a higher average vital capacity (Hutchinson, 1846). Although our results were not conclusive with having a negative correlation between heart rate and vital capacity in a previous study, other research found that heart rate variability (HRV) correlated moderately, but not significantly (Biachim, et al. 2017). This research supports the results found in this study since there was no correlation in pulse and VC. We also expected to see a higher standing vital capacity than seated, which was not supported by our results. In a study done in brass players, researchers asked the participants to produce a note of maximum duration while seated and while they stood. There was a significant reduction in vital capacity in the seated positions compared to the standing position (Price, et al. 2014). Since there were no discernable differences in this study, our findings did not support this research. We did not conduct this study in musicians who are trained to produce a maximal musical note, therefore this might explain the differences in our results. Looking at the differences between males and females, in both variables of seated or standing, the average vital capacity in males was higher than those of females. In additional research, the volume of adult female lungs is typically 10-12% smaller than male lungs even if they are the same height and age (Bellemare, et al. 2003). Having a smaller lung volume capacity would not allow you inhale or exhale as much oxygen compared to someone with larger lungs. This research and the results of our study support our expectancies that males have a greater vital capacity on average than females. In summary, we anticipated the results of chest circumference, height and gender on VC. Additional research helped explain why our results showed no correlation/significance in heart rate and stature on VC.

References

Bianchim, MS., Sperandio, EF., Martinhão, GS., Matheus, AC., Lauria, VT., Da Silva, RP., Spadari, RC., Gagliardi, AR., Arantes, RL., Romiti, M. and Dourado, VZ. 2016. Correlation Between Heart Rate Variability and Pulmonary Function Adjusted by Cofounding Factors in Healthy Adults. Brazilian Journal of Medical and Biological Research 49(3). https://doi.org/10.1590/1414-431X20154435

Geddes, D. 2016. The History of Respiratory Disease Management. Medicine 44(6): 393-397.

Hoffman, F., Pugliese, F., Strain, S., Beeching, S., Chmielewski, J., DeNicola, D., Falso, P., Forbes, WM., Hrizo, S., Krayeski, D., Layne, JR., Rohorek, S., and Strain, S. 2018. Spirometry. Principles of Biology Laboratory Manual. Exercise 18.

Hutchinson, J. 1846. On the Capacity of Lungs, and on Respiratory Functions, with a View of Establishing a Precise and Easy Method of Detecting Disease by the Spirometer. Medico-Chirurgical Transactions 29: 137-252.

Kattan, CM., Keens, TG., Mellis, CM., and Levison, H. 1978. The Response to Exercise in Normal and Asthmatic Children. The Journal of Pediatrics 92(5): 718-721.

Lutfi, MF. 2017. The Physiological Basis and Clinical Significance of Lung Volume Measurements. Multidisciplinary Respiratory Medicine 12(3): https://doi.org/10.1186/s40248-017-0084-5.

Mazzuco, A., Medeiros, WM., Rizk-Sperling, MP., De Souza, AS., Noman-Alencar, MC., Arbex, FF., Neder, JA., Arena, R., and Borghi-Silva A. 2015. Relationship Between Linear and Nonlinear Dynamics of Heart Rate and Impairment of Lung Function in COPD patients. International Journal of Chronis Obstructive Pulmonary Disease 10 (1651-61): https://doi.org/10.2147/COPD.S81736.

Petty, TL. 2002. Josh Hutchinson’s Mysterious Machine Revisited. Chest 121(5): https://doi.org/10.1378/chest.121.5_suppl.219S.

Price, K., Schartz, P., and Watson, AH. 2014. The Effect of Standing and Sitting Postures on Breathing in Brass Players. Springerplus 3(210): https://doi.org/10.1186/2193-1801-3-210.

Tantisuwat, A. and Thaveeratitham, P. 2014. Effects of Smoking on Chest Expansion, Lung Function, and Respiratory Muscle Strength of Youths. Journal of Physical Therapy Science 26(2): 167-170.

Townsend, MC. 1983. Spirometric Forced Expiratory Volumes Measured in the Standing Versus the Sitting Posture. American Review of Respiratory Disease 130(1): https://doi.org/10.1164/arrd.1984.130.1.123.

 

Table 1: Average Vital Capacities between males and females while sitting and standing

Standing Average Vital Capacity (L)

Seated Average Vital Capacity (L)

Whole Class

3.53

3.40

Males

4.25

4.23

Females

3.22

3.04

Figure 1: The relationship between height and vital capacity in undergraduate students while standing, as measured using a spirometer. There is a positive correlation in the data.

Figure 2: The relationship between chest circumference and vital capacity in undergraduate students while standing, as measured using a spirometer. A positive correlation was found in the data.

Figure 3: The relationship between pulse and vital capacity in undergraduate students while standing, as measured using a spirometer. No correlation was found in the data.
 

Factors Effecting Voltage of Electrochemical Cells

Introduction
Electrochemistry is the science that studies this union of chemistry and electricity. Batteries and fuel cells utilize spontaneous redox processes to convert chemical energy into electrical energy.
Oxidation reactions (or redox reactions) are an important part of chemical reactions. They involve the transfer of electrons from one source to the other via oxidation and reduction. When this process occurs spontaneously, forming products that are in a lower energy state than the reactants, the excess energy is released to the surroundings, frequently in the form of heat. Combustion in your car’s engine, “burning” calories in the gym and the rusting of iron are some examples of exothermic reactions. When the oxidation and reduction processes are physically separated in an electrochemical cell, the electrons are transferred through a wire connecting the cells and an electrical current can either be generated or used to drive the reaction. Add conclusion?
Electrochemistry is the science that studies this union of chemistry and electricity. Batteries and fuel cells utilize spontaneous redox processes to convert chemical energy into electrical energy. On the other hand, electrical energy can be used to drive non-spontaneous processes, converting the electrical energy into chemical energy that is stored in the reaction products.
Electrochemical Cells
Electrochemical cells fall into two broad categories. Voltaic (or galvanic) cells produce electricity from spontaneous redox processes. Batteries are a common example of this type of cell. Cells that use electricity to drive non-spontaneous reactions are called electrolytic cells. The basic components of an electrochemical cell are:

Two compartments separated by a “salt bridge” through which ions can flow. Oxidation occurs in the anode compartment and reduction occurs in the cathode compartment.
Two solid electrodes that are connected by a wire. The electrodes themselves don’t necessarily participate in the reaction.
Two solutions of electrolytes into which the electrodes are immersed. The ions of the electrolytes may participate in the reaction or they may be inert electrolytes that are present to carry charge.

Different metals have different tendencies to undergo oxidation, or lose electrons. Likewise, their cations have different tendencies to undergo reduction. This tendency is measured in terms of the metal cation’s reduction potential. The cell potential for a given electrochemical cell is the difference between the tendencies of the metal cations in their respective half-cells to undergo reduction. In a voltaic cell, the substance with the highest (most positive, or least negative) reduction potential will undergo reduction and the metal in the other compartment will be oxidized. The cell potential, Ecell, represents the difference between the tendencies of the metal ions to undergo reduction. For the reaction to be spontaneous, the overall cell potential must be positive.
Aim
The aim of the experiment was to see which of the three factors affects electrochemical cells. The three factors, Surface area, Concentration and Temperature. Each of these factors will be explored to see how they affect the current generated by the cell.
Hypothesis
Electrochemical cells are different from normal reactions; however the amount of volts produced by the cell will be effected by the factors that affect chemical reaction rates. The main factors that affect chemical reactions are Temperature, Surface area and Concentration. By increasing the amount of collisions per second the amount of volts should also be affected by the increased collision rates too.
Planning and Preliminary trials

A panel volt meter was given, however it was quite hard to read so it was swapped with an electronic volt meter that would give a much more accurate reading.
Since the beakers lips where curved the electrode would be at an angle, to fix this, the electrodes where dangled from a utility stand.
When the concentrations were tested it was noticed strange results, like how 0.5M KNO3 would be better than 1M, and it was found that the surface area of the salt bridge was different, therefore surface area tests had to be conducted and then be cut out the same sizes for every experiment after.
The surface area of the anodes and cathodes did not make any difference in the test, however they should make a difference if the battery is of a larger capacity (See figure 2.1 for example)

Figure 2.1

The heat capacity of the solutions where different, so only a rough estimate could be taken (eg. CuSO4 is at 59.4°C while ZnSO4 is at 62.4°C)

Theory: CuSO4 98.53 J/(mol–1 K)
ZnSO4 116.0 J/(mol–1 K)
The copper sulphate will heat up faster than the zinc sulphate, which means that the copper sulphate needs to be taken off the hot plate before the Zinc or otherwise the copper has a much higher temperature compared to zinc.
Materials
100mL beakers
Strips of copper, zinc, magnesium and iron (different sizes)
200mL x 0.5 mol zinc sulfate solution
400mL x 1 mol zinc sulfate solution
200mL x 2 mol zinc sulfate solution
200mL x 0.5 mol copper sulfate solution
400mL x 1 mol copper sulfate solution
200mL x 2 mol copper sulfate solution
200mL x 0.5 mol magnesium sulfate solution
400mL x 1 mol magnesium sulfate solution
200mL x 2 mol magnesium sulfate solution
200mL x 0.5 mol iron sulfate solution
400mL x 1 mol iron sulfate solution
200mL x 2 mol iron sulfate solution
100mL x 1 mol potassium nitrate solution
100mL x 2 mol potassium nitrate solution
100mL x 1 mol potassium sulfate solution
100mL x 2 mol potassium sulfate solution
200mL x 1 mol aluminum sulfate solution
Aluminum
Filter paper
Measuring cylinders
Volt Meters
Alligator clips
Conductivity Meter
Electric Thermometer
Large container (Enough to hold 2 x 250ml beakers)
Goggles
Ice
Steel wool
Method
Salt bridge solution test

Use steel wool or sandpaper to polish the metal strips, wash with distilled water after and wipe dry with a towel.
Place 60 mL of the 1 M ZnSO4solution in a 50-mL beaker. Place a strip of polished zinc in the beaker.
Place 60 mL of the 1 M CuSO4solution in a 50-mL beaker. Place a strip of polished copper in the beaker.
Connect alligator clip probes to a DC voltmeter. Connect the clips to the metal strips.
Cut a strip of filter paper and soak it in 1 M KNO3 solution and slowly lower it so both sides of the filter paper touches the contents of both beakers. Measure the reading on the volt meter.
Repeat the step 5 but use different concentrations of KNO3 and K2SO4
Repeat steps 1-6 except use Fe(II)SO4 and MgSO4 instead of ZnSO4 and CuSO4
The following experiments will be done with the salt bridge that gave the best result during the above experiment.

Concentration of solution test

Place 60 mL of the 1 M ZnSO4solution in a 50-mL beaker. Place a strip of polished zinc in the beaker (take down the temperature of both the ZnSO4 and CuSO4 solution for the next part of the experiment).
Place 60 mL of the 1 M CuSO4solution in a 50-mL beaker. Place a strip of polished copper in the beaker.
Connect alligator clip probes to a DC voltmeter. Connect the clips to the metal strips.
Cut a strip of filter paper and soak it in KNO3 solution and slowly lower it so both sides of the filter paper touches the contents of both beakers. Measure the reading on the volt meter.
Repeat the following steps with 0.25 and 0.5 M concentrations of CuSO4and ZnSO4.
Polish the iron and magnesium strips with steel wool.
Place 60 mL of the 1 M Fe(II)SO4solution in a 50-mL beaker. Place a strip of polished iron in the beaker.
Place 60 mL of the 1 M MgSO4solution in a 50-mL beaker. Place a strip of polished magnesium in the beaker.
Connect alligator clip probes to a DC voltmeter. Connect the clips to the metal strips.
Cut a strip of filter paper and soak it in KNO3 solution and slowly lower it so both sides of the filter paper touches the contents of both beakers. Measure the reading on the volt meter.
Repeat the following steps with 0.25 and 0.5 M concentrations.

Temperature of solution test

Place two 50mL beakers into an ice-cream container
Pour 60 mL of the 1 M ZnSO4solution into one 50-mL beaker. Place a strip of polished zinc in the beaker.
Pour 60 mL of the 1 M CuSO4solution into the other 50-mL beaker. Place a strip of polished copper in the beaker.
Fill the ice-cream container with ice and then fill it up with water, wait till the temperature of both solutions becomes steady then continue with the following steps.
Connect alligator clip probes to a DC voltmeter. Connect the clips to the metal strips.
Cut a strip of filter paper and soak it in KNO3 solution and slowly lower it so both sides of the filter paper touch the contents of both beakers equally. Measure the reading on the volt meter.
Repeat except place the beakers on a hot plate instead of an ice cream container.

Surface area of salt bridge test

Cut strips of filter paper at different sizes (1cm x 6.25cm, 2cm x 6.25cm and 3cmx6.25cm)
Pour 60 mL of the 1 M ZnSO4solution into one 50-mL beaker. Place a strip of polished zinc in the beaker.
Pour 60 mL of the 1 M CuSO4solution into the other 50-mL beaker. Place a strip of polished copper in the beaker.
Connect alligator clip probes to a DC voltmeter. Connect the clips to the metal strips.
Carefully lower the salt bridge between the beakers making sure it is evenly placed in the middle.
Measure the voltage produced and repeat with the different salt bridges.

Experimental Results
Table 1. Salt Bridge Solutions

Solution

Redox Reaction

Voltage

1M K2SO4

Zn(s) + Cu2+Zn2+ + Cu(s)

1.06V

0.5M K2SO4

1.03V

1M KNO3

1.03V

0.5M KNO3

1.01V

1M K2SO4

Mg(s) + Fe2+Mg2+ + Fe(s)

2.06V

0.5M K2SO4

2.04V

1M KNO3

2.08V

0.5M KNO3

2.05V

Table 2. Surface Area of Salt Bridge

Surface Area

Redox Reaction

Average Voltage

6.25cm2

Zn(s) + Cu2+Zn2+ + Cu(s)

1.06V

12.5cm2

1.11V

18.75cm2

1.12V

6.25cm2

Mg(s) + Fe2+Mg2+ + Fe(s)

2.07V

12.5cm2

2.13V

18.75cm2

2.16V

Table 3. Concentration

Concentration

Redox Reaction

Average Voltage

1M

Zn(s) + Cu2+Zn2+ + Cu(s)

1.09V

.5M

1.07V

.25M

1.06V

1M

Mg(s) + Fe2+Mg2+ + Fe(s)

2.10V

.5M

2.08V

.25M

2.06V

0.5M

2Al + 3Cu2+2Al3+ + 3Cu(s)

1.95V

0.25M

1.93V

0.125M

1.92V

Table 4. Temperature

Temperature

Redox Reaction

Average Voltage

16°C

Zn(s) + Cu2+Zn2+ + Cu(s)

 

24°C

 

60°C

 

16°C

Mg(s) + Fe2+Mg2+ + Fe(s)

 

24°C

 

60°C

 

16.7°C and 18.3°C

2Al + 3Cu2+2Al3+ + 3Cu(s)

0.39V

24°C both

0.5V

51.3°C and 48.6°C

0.57V

Table 5. Conductivity of Salt Bridge

Solution

Seimens (µs/m)
Higher is better

1M K2SO4

3839

0.5M K2SO4

3831

1M KNO3

3865

0.5M KNO3

3861

Discussion
To theoretically calculate the amount of voltage produced by each cell, the theoretical standard potential of the half cells need to be found.
The standard potential for the chemicals used in this experiment are:

Oxidants ⇌ Reductants

E°(V)

Cu2+ + 2e– ⇌Cu(s)

0.34

Fe2+ + 2e– ⇌Fe(s)

-0.41

Zn2+ + 2e– ⇌Zn(s)

-0.76

Al3+ + 3e– ⇌Al(s)

-1.71

Mg2+ + 2e– ⇌Mg(s)

-2.38

These values are when the cell is at STP. Source: Text book
To get the cell potential at STP:
 
Zn(s) + Cu2+Zn2+ + Cu(s)
Cu2+ + 2e– ⇌Cu(s) = 0.34V
Zn2+ + 2e– ⇌Zn(s) = -0.76
E°oxidation of Zn= – (-0.76 V) = + 0.76 V
E°cell= E°reduction+ E°oxidation
E°cell= 0.34 + 0.76
E°cell= +1.10 V
For all standard cell potential calculations refer to appendix 1.1
When the cell isn’t at STP the Nernst Equation has to be used.
Ecellis the cell potential E°cellrefers to standard cell potential R is thegas constant (8.3145 J/mol·K) T is theabsolute temperature n is the number of moles of electrons transferred by the cell’s reaction F is Faraday’s constant (96485.337 C/mol)
The Nernst equation was designed to be used when the values or environment was not at STP. The Nernst equation however does not support what happens if temperature changes but the concentration values are both equal. See example below.

Even though the temperature is at 350K the voltage will not change since log of 1 will be 0 and it cancels out RT/nF.
0.5M Aluminum Sulfate + 1M Copper Sulphate cell at 24.8°C

For all calculations containing the Nernst equation refer to appendix 1.2
The evidence backs up the hypothesis that states “the factors that affect reaction rate will also affect electrochemical cells” The voltages does increase and decrease in all 4 test:

As surface area increases so does the voltage for both cells.
As concentration increases so does the voltage for all 3 types of cells.
As temperature increases so does the voltage for all 3 types of cells.

The only downside is how the change in tests 2 and 3 are very small and almost negligible.
However the experimental results obtained did not match up to the theoretical results; but they are very similar and there might be a few reasons on why:

The resistance of the copper wire
The alligator clips don’t provide a lot of contact (decrease in possible surface area)
The temperature of the substances could be different since only room temperature was taken not the temperature of the actual solution.
The salt bridge could’ve been too small and stemmed the flow of electrons that could flow through it.

In the “Salt Bridge Solutions” experiment the results proved inconclusive so a conductivity meter was used to test the conductivity of each substance.
KNO3 will make a better salt bridge due to its higher conductivity rate; this is because of its solubility level which is at 316 g/Lat 20°C compared to K2SO4 solubility which is only 111g/L at 20°C.
Surface area test:
The tests were successful and backed up the hypothesis, however further tests were not taken since the beakers were too small and it would be a waste of material when the desired voltage has already been achieved.
It can be seen how the change in voltage is decreasing as the surface area increases which means that it will probably flatten out soon and there will not be a change at all. (See graph 1 and 2 in results)
Concentration:
For all the experiments on the 3 electrochemical cells the result backs up the hypothesis however concentration does not provide as much impact on voltage (See table 3 for results). The electrons are already there and making contact with the plate since it doesn’t really matter about which angle it hits the electrode nor how much power it hits with. It is hypothesized that by increasing concentration you increase the amount of electrons and that should be directly proportional to how long the cell would last; if you have double the amount of electrons but you are using them at the same rate that means that it should last twice as long since you have twice as many electrons.

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Temperature
There are no big changes in voltage when temperature is changed, like stated before “it doesn’t really matter about which angle it hits the electrode nor how much power it hits with”. Changing the temperature does two things, increases the rate at which the atom hits per second and changes how much force it hits with by providing it kinetic energy. However if a copper atom hits an electrode stronger, the KE doesn’t transfer over to the electron due to its size, also the electron will be transferred at the same rate since it has to go through a copper wire before it can get over to the cathode. Secondly if you hit an object more even though it can’t carry any more electrons won’t do anything, just like how a reaction is limited by its limiting reagent.
Percentage Error
P.E of 1M Copper and Zinc Cell
P.E =
P.E =
P.E = 0.00909%
See all Percentage Error calculations in Appendix 1.3
Conclusion
By conducting various experiments to see which of the three factors affects electrochemical cells. The three factors being Surface area, Concentration and Temperature. The results obtained were very close to the accepted value and the average percentage error was only XXX%.
The results obtained demonstrates that the hypothesis was indeed correct in stating that the factors that effect rate of reaction will also effect electrochemical cells, as stated by the hypothesis “by increasing the amount of collisions per second the amount of volts should also be affected by the increased collision rates too.” It should also be possible to gather further data to back up the hypothesis however the timeframe did not allow it.
Nevertheless even in ideal situation and also the simplicity of the experiment, the results should not have changed. In the 1M Copper and Zinc cell the voltage should’ve been 1.10V however 1.09V was the output which leads to further questions as to why it wasn’t exact. The reaction remains the same and energy was not lost since neither heat nor sound was produced during the experiment. It is assumed that unless at STP then the voltage can only be determined to ±0.02V (based on other experiments) For a more precise measurement a larger experiment needs to be conducted to a higher level where the experiment cannot be subjected to human error.
Appendix
Zn(s) + Cu2+Zn2+ + Cu(s)
Cu2+ + 2e– ⇌Cu(s) = 0.34V
Zn2+ + 2e– ⇌Zn(s) = -0.76
E°oxidation of Zn= – (-0.76 V) = + 0.76 V
E°cell= E°reduction+ E°oxidation
E°cell= 0.34 + 0.76
E°cell= +1.10 V
_____________________________________
2Al(s) + 3Cu2+2Al3+ + 3Cu(s)
Cu2+ + 2e– ⇌Cu(s) = 0.34V
Al3+ + 3e– ⇌Zn(s) = -1.71
E°oxidation of Al= – (-1.71 V) = + 1.71 V
E°cell= E°reduction+ E°oxidation
E°cell= 0.34 + 1.71
E°cell= +2.05 V
______________________________________
Mg(s) + Fe2+Mg2+ + Fe(s)
Fe2+ + 2e– ⇌Fe(s) = -0.41V
Mg2+ + 2e– ⇌Mg(s) = -2.38
E°oxidation of Zn= – (-0.76 V) = + 0.76 V
E°cell= E°reduction+ E°oxidation
E°cell= 0.34 + 0.76
E°cell= +1.10 V
References