Respiratory System Physiology-Virtual Experiments
Online Virtual Experiments:
For Virtual Experiment Visit this link. Click on "Exercise 7: Respiratory System Mechanics".
Click on one of the following titles:
- Respiratory Volumes,
- Factors Affecting Respirations,
- Variations in Breathing,
- Comparative Spirometry.
A. Examining the Effect of Surfactant: At any gas-liquid boundary, the molecules of the liquid are attracted more strongly to each other than they are to the air molecules. This unequal attraction produces tension at the liquid surface called surface tension. Because surface tension resists any force that tends to increase surface area, it acts to decrease the size of hollow spaces, such as the alveoli or microscopic air spaces within the lungs. If the film lining the air spaces in the lung were pure water, it would be very difficult, if not impossible, to inflate the lungs. However, the aqueous film covering the alveolar surfaces contains surfactant, a detergent-like lipoprotein that decreases surface tension by reducing the attraction of water molecules for each other. You will explore the action of surfactant in this experiment (see the video and the results table).
B. Investigating Intrapleural Pressure: The pressure within the pleural cavity, intrapleural pressure, is less than the pressure within the alveoli. This negative pressure condition is caused by two forces, the tendency of the lung to recoil due to its elastic properties and the surface tension of the alveolar fluid. These two forces act to pull the lungs away from the thoracic wall, creating a partial vacuum in the pleural cavity. Because the pressure in the intrapleural space is lower than atmospheric pressure, any opening created in the thoracic wall equalizes the intrapleural pressure with the atmospheric pressure by allowing air to enter the pleural cavity, a condition called pneumothorax. Pneumothorax allows lung collapse, a condition called atelectasis. In the simulated respiratory system on the computer screen (video), the intrapleural space is the space between the wall of the bell jar and the outer wall of the lung it contains. The pressure difference between inspiration and expiration for the left lung is displayed in the Pressure Left window below the oscilloscope; the Pressure Right window gives the data for the right lung. The results of this virtual experiment is shown in table.
C. The
effect of changing the pump rate (see video) on various measured parameters is shown in table. Questions: 1. What happened to the FEV1 (%) as
the radius of the airways was decreased? How has the airflow changed compared
to the baseline run? 2. Premature infants often have
difficulty breathing. Explain why this might be so? 3. What effect does the addition of surfactant have
on the airflow? How well did the results compare with your prediction? 4. What emergency medical condition
does opening the left valve simulate? 5. What effect did opening the
valve on the left lung? Why does this happen? 6. How did the pressure in the collapsed lung differ from that in
the expanded lung? Explain your reasoning. 7. How did the total air flow in this trial compare with that in
the previous trial in which the pleural cavities were intact? What do you think
would happen if the two lungs were in a single large cavity instead of separate
cavities?
3. Comparative
Spirometry: In
this activity, you will explore what happens to these values when pathophysiology develops or during episodes
of aerobic exercise. Using a water-filled spirometer and knowledge of
respiratory mechanics, changes to these values in each condition can be predicted, documented, and explained. The setup of
this virtual experiment is shown in figure and in video. The results of this experiment in shown in Table. In a person with emphysema,
there is a significant loss of intrinsic elastic recoil in the lung tissue.
This loss of elastic recoil occurs as the disease destroys the walls of the
alveoli. Airway resistance is also increased as the lung tissue in general
becomes more flimsy and exerts less mechanical tethering on the surrounding
airways. Thus the lung becomes overly compliant and expands easily. Conversely,
a great effort is required to exhale as the lungs can no longer passively
recoil and deflate. A noticeable and exhausting muscular effort is required for
each exhalation. Thus a person with emphysema exhales slowly. During an acute
asthma attack, bronchiole smooth muscle will spasm and thus the airways become
constricted (that is, they have a reduced diameter). They also become clogged
with thick mucus secretions. These two facts lead to significantly increased
airway resistance. Underlying these symptoms is an airway inflammatory response
brought on by triggers such as allergens (e.g., dust and pollen), extreme
temperature changes, and even exercise. Similar to emphysema, the airways
collapse and pinch closed before a forced expiration is completed. Thus the
volumes and peak flow rates are significantly reduced during an asthma attack.
However, the elastic recoil is not diminished in an acute asthma attack. Questions: 1. What do you think is the clinical importance of the FVC and FEV1
values? Why do you think the ratio of these two values is important to the
clinician when diagnosing respiratory diseases? 2. In a person with emphysema, is the FVC reduced or increased? Is the FEV1
reduced or increased? Which of these two changed more? Explain the
physiological reasons for the lung volumes and capacities that changed in the
spirogram for this condition. 3. During an acute asthma attack, is the FVC reduced or increased?
Is the FEV1 reduced or increased? Which of these two changed more? Explain the
physiological reasons for the lung volumes and capacities that changed in the
spirogram for this condition. How is this condition similar to having
emphysema? How is it different? 4. Emphysema and asthma are called obstructive
lung diseases as they limit expiratory flow and volume. How would
a spirogram look for someone with a restrictive lung
disease, such as pulmonary fibrosis? What volumes and capacities would change in
this case, and would these values be increased or decreased? In an acute asthma attack, the compliance of the lung is
decreased, not increased as it was for emphysema, and air flows freely through
the bronchioles. Therefore, will the FEV1/ FVC percentage be less than normal,
equal to normal, or higher. Acute
Asthma Attack Breathing with Inhaler Medication Applied: When an acute asthma
attack occurs, many people seek relief from the symptoms by using an inhaler.
This device atomizes the medication and allows for direct application onto the
afflicted airways. Usually the medication includes a smooth muscle relaxant
(e.g., a beta-2 agonist or an acetylcholine antagonist) that relieves the
bronchospasms and induces bronchiole dilation. The medication may also contain
an anti-inflammatory agent such as a corticosteroid that suppresses the
inflammatory response. Airway resistance is reduced by the use of the inhaler. 5. Has the FVC reduced or
increased? Is it “normal”? Has the FEV1 reduced or increased? Is it “normal”? Which
of these two changed more? Explain the physiological reasons for the lung
volumes and capacities that changed in the spirogram with the application of
the medication. 6. How much of an increase in
FEV1 do you think is required for it to be considered significantly improved by
the medication? Breathing
during exercise: During moderate aerobic exercise, the human body has an
increased metabolic demand, which is met in part by changes in respiration.
During heavy exercise, further changes in respiration are required to meet the
extreme metabolic demands of the body. 7. In moderate aerobic exercise,
which do you predict will change more, the ERV or the IRV? 8. Do you predict that the
respiratory rate will change significantly in moderate exercise? 9. Comparing heavy exercise to
moderate exercise, what values do you predict will change when the body’s
significantly increased metabolic demands are being met by the respiratory
system? 10. During heavy exercise, what
will happen to the lung volumes and capacities that have been considered thus
far? e. Will the respiratory rate change? If so, how?
Virtual Experiment on pH and Hb-Oxygen binding:
Download this folder. Open the folder and double click on "index". Click on "OBJECTIVES & INTRODUCTION" and read it. Read the file "Steps" in the main "pH and Hb-Oxygen binding" folder and follow the steps. You start your virtual experiment by clicking on "LABORATORY EXERCISE" and follow the steps in "Steps" file. You can also browse through the following titles "PRE-LAB QUIZ, WET LAB, LABORATORY EXERCISE, POST-LAB QUIZ & LAB REPORT".
Virtual Experiment on 2,3 DPG and Hb-Oxygen binding:
Download this folder. Open the folder and double click on "index". Click on "OBJECTIVES & INTRODUCTION" and read it. Read the file "Steps" in the main "2,3 DPG and Hb-Oxygen binding" folder and follow the steps. You start your virtual experiment by clicking on "LABORATORY EXERCISE" and follow the steps in "Steps" file. You can also browse through the following titles "PRE-LAB QUIZ, WET LAB, LABORATORY EXERCISE, POST-LAB QUIZ & LAB REPORT".
Virtual Experiment on Lung and Body Position:
Download this folder. Open the folder and double click on "index". Click on "OBJECTIVES &
INTRODUCTION" and read it. Read the file "Steps" in the main "Lung and Body Position" folder and follow the steps. You start your virtual experiment by clicking on "LABORATORY EXERCISE" and follow the steps in "Steps" file.
You can also browse through the following titles "PRE-LAB QUIZ, WET LAB, LABORATORY EXERCISE, POST-LAB QUIZ
& LAB REPORT".
In the human lung, air travels through the airways (trachea, bronchi and bronchioles) to the alveoli, where gas exchange takes place between the blood and the air. The barrier for exchange is about one micron thick, and consists of a thin layer of fluid, a basement membrane, and the endothelial cell of the capillary. The efficient diffusion of gases between the air and the blood is facilitated by the thin exchange barrier, the large surface area provided by the alveoli, and the low oxygen and high carbon dioxide levels of the (deoxygenated) blood in the pulmonary artery. The flow of blood to the alveoli can be influenced by several parameters, including the level of oxygen in the alveoli and the blood pressure. Even if adequate ventilation keeps oxygen levels high in the alveoli, the pulmonary capillaries will collapse if the arterial blood pressure is not high enough to force them open. Thus, any area in the lung that experiences a decreased blood pressure will be more likely to experience capillary collapse and little or no gas exchange. One factor that can influence blood pressure is gravity, because a fluid flowing against gravity experiences a decline in pressure. This laboratory will test the idea that the gravitational effects on blood pressure will be greater when a volunteer is standing, rather than lying, and that this will change the tidal volume, that is, the amount of air traveling in and out of the lungs in a resting person. The breathing apparatus, or spirometer, is connected to the Data Acquisition Unit. The volunteer breathes into the disposable mouthpiece, and the pressure sensors detect the air currents. The signal is integrated and displayed on a computer screen, so that inhalation produces an upward deflection of the trace and exhalation produces a downward deflection (see video). The result is shown in table. Question: Why the tidal volume in standing position is larger than in supine position?
Virtual Experiment on Altering Air Volume:
Download this folder. Open the folder and double click on "index". Click on "OBJECTIVES & INTRODUCTION" and read it. Read the file "Steps" in the main "Altering Air Volume" folder and follow the steps. You start your virtual experiment by clicking on "LABORATORY EXERCISE" and follow the steps in "Steps" file. You can also browse through the following titles "PRE-LAB QUIZ, WET LAB, LABORATORY EXERCISE, POST-LAB QUIZ & LAB REPORT".
In the lung, air travels through the airways (trachea, bronchi and bronchioles) to the alveoli. The efficient diffusion of gases between the air in the alveoli and the blood is facilitated by the thin exchange barrier, the large surface area provided by the alveoli, and the low oxygen and high carbon dioxide levels of the (deoxygenated) blood in the pulmonary artery. Air moves in and out of the lungs through the airways. When you inhale, the last 150 mL of the fresh air that enters your lungs stays in the airways and does not reach the alveoli. This fresh air that is trapped in the airways, or ‘anatomical dead space’, is not available for gas exchange with the blood and when you exhale this volume of fresh air is the first to leave the lungs. Furthermore, stale air from the alveoli remains in the airways when you exhale, and returns to the alveoli when you inhale. As a result, the tidal flow of air in and out of the human lung creates a mixing of fresh air and stale air in the alveoli, so that the air presented to the blood has a lower oxygen level and high carbon dioxide level than fresh air. The ‘tidal volume’ is the amount of air that goes in or out of the lungs during any one breathing cycle, but not all of the air that enters the lung reaches the alveoli. The difference between the tidal volume and the anatomical dead space, the alveolar ventilation, represents the amount of air that enters the alveoli. Under normal conditions, the anatomical dead space remains constant, because the volume of airways does change. Therefore, a change in the tidal volume will produce a similar change in the amount of air that enters the alveoli. For example, if you take a deep breath and inhale 100 mL of extra air, all of the extra 100 mL of fresh air will enter the alveoli and be available for exchange with the blood. However, what would happen if you artificially increased the anatomical dead space? What compensatory changes would have to be made to the tidal volume to maintain a constant amount of air entering the alveoli? This lab will address these questions by using a spirometer to measure the tidal volume from a student volunteer who will breathe normally and then through a plastic tube, which will increase his anatomical dead space. The breathing apparatus, or spirometer, is connected to the Data Acquisition Unit. The volunteer breathes into the disposable mouthpiece, and the pressure sensors detect the air currents. The signal is integrated and displayed on a computer screen, so that inhalation produces an upward deflection of the trace and exhalation produces a downward deflection (see video). The results are shown in Table. Question: Why is the volume of air (tidal volume) with plastic tube inserted in the mouth piece larger than without it?
Virtual Experiment on Exercise-Induced Respiratory Changes:
Download this folder. Open the folder and double click on "index". Click on "OBJECTIVES & INTRODUCTION" and read it. Read the file "Steps" in the main "Exercise-Induced Respiratory Changes" folder and follow the steps. You start your virtual experiment by clicking on "LABORATORY EXERCISE" and follow the steps in "Steps" file. You can also browse through the following titles "PRE-LAB QUIZ, WET LAB, LABORATORY EXERCISE, POST-LAB QUIZ & LAB REPORT".
In the human lung, air travels through a system of tubes or airways (trachea, bronchi, and bronchioles) to the alveoli, where gas exchange takes place between the blood and the air. Not all of the air that is inspired reaches the alveoli--some air remains in the tubes, in what is termed the 'anatomical dead space'. The volume of the anatomical dead space remains constant at about 150 mL, and this air is not available for gas exchange with the blood. Alveolar ventilation (AV), which is the total amount of fresh air that enters the alveoli per minute, is calculated using the tidal volume (TV) - the air that moves in or out of the lungs during any one breathing cycle - the volume of the anatomical dead space (ADS), and the breathing rate, as follows: AV = (TV - ADS.) x Breathing rate. One function of the respiratory system is to match the body's oxygen requirements with the amount of oxygen it makes available at the alveoli. Because the anatomical dead space volume remains constant, the respiratory system must accommodate an increase in metabolism by adjusting the remaining variables in the above equation. Alveolar ventilation (AV), therefore, can be increased by increasing the tidal volume (TV) (i.e., the depth of breathing) or by increasing the breathing rate, to make more oxygen available to the body. The ‘tidal volume’ is the amount of air that moves in and out of the lungs during one breathing cycle. After you have exhaled normally, more air can be force from the lungs; this is the ‘expiratory reserve volume’. Similarly, after a normal breath, more air can be taken into the lungs; this is the ‘inspiratory reserve volume’. These three volumes, the inspiratory reserve volume, the tidal volume, and the expiratory reserve volume, represent the maximum amount of air that can pass through the lungs in one breath, and is called the ‘vital capacity’. During exercise the body uses more oxygen, and these demands must be met by changing breathing patterns. In this lab you will use a virtual spirometer to monitor air flow through the mouth of a healthy student volunteer. The student will breathe normally for three breathing cycles, and then inhale and exhale as much as possible; the spirometer signal will be displayed as a line tracing on the screen of a virtual monitor. You will measure the breathing rate, the expiratory and inspiratory reserve volumes, and the tidal volume. You will make observations from the volunteer at rest and immediately after exercise to determine the effect of exercise on breathing. The breathing apparatus, or spirometer, is connected to the Data Acquisition Unit. The volunteer breathes into the disposable mouthpiece, and the pressure sensors detect the air currents. The signal is integrated and displayed on a computer screen, so that inhalation produces an upward deflection of the trace and exhalation produces a downward deflection (see video). The results are shown in Table. Questions: 1. Explain why there are increases in respiratory rate, and tidal volume upon exercise? 2. Explain why there are decreases in IRV and ERV upon exercise?
Virtual Experiment on Deep breathing and Cardiac function:
Download this folder. Open the folder and double click on "index". Click on "OBJECTIVES & INTRODUCTION" and read it. Read the file "Steps" in the main "Deep breathing and Cardiac function" folder and follow the steps. You start your virtual experiment by clicking on "LABORATORY EXERCISE" and follow the steps in "Steps" file. You can also browse through the following titles "PRE-LAB QUIZ, WET LAB, LABORATORY EXERCISE, POST-LAB QUIZ & LAB REPORT".
During a normal breathing cycle, a contraction of the inspiratory muscles (the diaphragm and the external intercostals muscles) increases the volume of the thoracic cavity. This creates a negative pressure inside the fluid-filled pleural sac, a structure that connects the lungs to the thorax, and increases the volume of the lungs. As the lungs expand, the pressure inside decreases and, as long as the airways are open, fresh air is drawn in and the person is said to inhale. The muscles then relax and decrease the volume of, and increase the pressure inside, the thoracic cavity. The volume of the lungs decreases, the pressure increases, and the person exhales as air passes out of the lungs through the open airways. Under normal conditions, the heart provides sufficient pressure to push blood through the arteries and capillaries to the veins. However, friction between the blood and the vessel walls produces a gradual decline in pressure as blood travels through the circulatory system, and results in a low blood pressure in the veins. In a standing individual, blood in veins located in the head and chest simply flows back to the heart, but venous blood in the lower extremities has insufficient pressure to return against the force of gravity. This problem is alleviated by contractions of the leg muscles, which squeeze the veins and push blood up to the hips, but further movement of the venous blood against gravity must utilize other mechanisms. One such mechanism involves the negative pressures produced by the inspiratory muscles inside the thoracic cavity. Because the heart is located in the thoracic cavity, the negative pressure that produces lung expansion and the entry of air into the lungs also draws venous blood into the heart to increase the venous return from the lower extremities. In contrast, during exhalation, the positive pressure inside the thorax will slow venous return from the lower extremities.
In this lab, you will examine changes in cardiac function during slow, deep breathing in a volunteer. The thoracic pressure changes during slow breathing are exaggerated and maintained for a longer time period than during normal breathing. These pressure changes can be contrasted against stroke volume and heart rate to reveal the relationships between changes in the breathing cycle and cardiac function. The Velcro strap on the finger pulse unit is used to attach the unit to a finger. The cable is connected to an input on the Data Acquisition Unit, and blood flow is seen as a tracing on the computer screen. The breathing apparatus, or spirometer, is connected to a second input on the Data Acquisition Unit. The volunteer breathes slowly and deeply into the disposable mouthpiece. The pressure sensors in the breathing apparatus detect the air currents. The signal is integrated and displayed as a second tracing on a computer screen, so that inhalation produces an upward deflection of the trace and exhalation produces a downward deflection (see video). Question: Explain the causes of respiratory Sinus Arrhythmia.