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22.19: Gas Exchange across the Alveoli - Biology

22.19: Gas Exchange across the Alveoli - Biology


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In the body, oxygen is used by cells of the body’s tissues and carbon dioxide is produced as a waste product. The ratio of carbon dioxide production to oxygen consumption is the respiratory quotient (RQ). Because of this, less carbon dioxide is produced than oxygen is consumed and the RQ is, on average, about 0.7 for fat and about 0.8 for protein.

The RQ is used to calculate the partial pressure of oxygen in the alveolar spaces within the lung, the alveolar . Above, the partial pressure of oxygen in the lungs was calculated to be 150 mm Hg. However, lungs never fully deflate with an exhalation; therefore, the inspired air mixes with this residual air and lowers the partial pressure of oxygen within the alveoli. This means that there is a lower concentration of oxygen in the lungs than is found in the air outside the body. Knowing the RQ, the partial pressure of oxygen in the alveoli can be calculated:

With an RQ of 0.8 and a in the alveoli of 40 mm Hg, the alveolar is equal to:

Notice that this pressure is less than the external air. Therefore, the oxygen will flow from the inspired air in the lung into the bloodstream .

In the lungs, oxygen diffuses out of the alveoli and into the capillaries surrounding the alveoli. Oxygen (about 98 percent) binds reversibly to the respiratory pigment hemoglobin found in red blood cells (RBCs). RBCs carry oxygen to the tissues where oxygen dissociates from the hemoglobin and diffuses into the cells of the tissues. More specifically, alveolar is higher in the alveoli than blood in the capillaries. Because this pressure gradient exists, oxygen diffuses down its pressure gradient, moving out of the alveoli and entering the blood of the capillaries where O2 binds to hemoglobin. At the same time, alveolar is lower than blood . CO2 diffuses down its pressure gradient, moving out of the capillaries and entering the alveoli.

Oxygen and carbon dioxide move independently of each other; they diffuse down their own pressure gradients.

As blood leaves the lungs through the pulmonary veins, the venous = 100 mm Hg, whereas the venous = 40 mm Hg. As blood enters the systemic capillaries, the blood will lose oxygen and gain carbon dioxide because of the pressure difference of the tissues and blood. In systemic capillaries, , but in the tissue cells, . This pressure gradient drives the diffusion of oxygen out of the capillaries and into the tissue cells. At the same time, blood and systemic tissue . The pressure gradient drives CO2 out of tissue cells and into the capillaries. The blood returning to the lungs through the pulmonary arteries has a venous and a . The blood enters the lung capillaries where the process of exchanging gases between the capillaries and alveoli begins again (Figure 1).

Practice Question

Which of the following statements is false?

  1. In the tissues, drops as blood passes from the arteries to the veins, while increases.
  2. Blood travels from the lungs to the heart to body tissues, then back to the heart, then the lungs.
  3. Blood travels from the lungs to the heart to body tissues, then back to the lungs, then the heart.
  4. is higher in air than in the lungs.

[reveal-answer q=”660519″]Show Answer[/reveal-answer]
[hidden-answer a=”660519″]Statement c is false.[/hidden-answer]

In short, the change in partial pressure from the alveoli to the capillaries drives the oxygen into the tissues and the carbon dioxide into the blood from the tissues. The blood is then transported to the lungs where differences in pressure in the alveoli result in the movement of carbon dioxide out of the blood into the lungs, and oxygen into the blood.

Watch this video to learn how to carry out spirometry.

A link to an interactive elements can be found at the bottom of this page.


NCLEX : Gas Exchange

Which of the following structures is the site of gas exchange in the lung?

Gas exchange in the lung occurs exclusively in the alveoli, the tiny grape-like clusters of sacks at the terminus of the bronchioles of the lung. The gas contained in the larger structures of the lung - the trachea, bronchi, and bronchioles, is termed "dead space" as it does not participate in gas exchange.

Example Question #1 : Gas Exchange

Which of the following is the main trigger for the impulse to breathe?

Dilation of the bronchioles

High blood carbon dioxide

Constriction of the bronchioles

High blood carbon dioxide

The main trigger for the impulse to breathe is high carbon dioxide (decreased blood pH). In response to a decrease in blood pH, the medullary respiratory center triggers the diaphragm and the external intercostal muscles to increase breathing rate.

Example Question #1 : Gas Exchange

Myoglobin can bind with __________ molecule(s) of oxygen, while hemoglobin can bind with __________ molecule(s) of oxygen.

Myoglobin, an oxygen-binding protein in the muscle tissue, can bind with one molecule of oxygen. Hemoglobin, the main oxygen-binding metalloprotein in red blood cells, can bind four molecules of oxygen.

Example Question #1 : Gas Exchange

Hyperventilation results in which of the following?

While hyperventilation or tachypnea may be triggered by various forms of acidosis, they will not cause a decrease in blood pH, but rather push the blood into a more alkaline state. This occurs due to loss of carbon dioxide during respiration, followed by a compensatory decrease in bicarbonate ions. The result is in an elevation in the pH of the blood. This condition is known as respiratory alkalosis.

Example Question #1 : Gas Exchange

What does the term "partial pressure" describe?

The difference between the gas pressure at a particular altitude and sea level

The pressure of a gas at above sea level

The pressure contributed by a single gas in a gas mixture

The pressure of an overall gas mixture during transition (adding a new gas)

The pressure contributed by a single gas in a gas mixture

Many gases, such as room air, are composed of several gasses (in the case of room air, primarily nitrogen, oxygen, and several trace gasses). Partial pressure is the amount of pressure that each gas contributes. To find the total pressure of a gas mixture, one would find the sum of all partial pressures of each individual gas.

Example Question #1 : Gas Exchange

How do oxygen and carbon dioxide cross the capillary epithelium and alveolar cell membranes during gas exchange?

Gas exchange in the alveoli occurs by the process of simple diffusion. The blood that enters the lung capillaries is relatively low in oxygen and high in , in comparison to the room air that is drawn into the alveoli during respiration. The separation between the capillaries and the alveolar epithelium is thin enough that these gasses can exchange across their pressure gradients by the process of simple diffusion.

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Gas exchange

Air enters the body through the mouth or nose and quickly moves to the pharynx, or throat. From there, it passes through the larynx, or voice box, and enters the trachea.

The trachea is a strong tube that contains rings of cartilage that prevent it from collapsing.

Within the lungs, the trachea branches into a left and right bronchus. These further divide into smaller and smaller branches called bronchioles.

The smallest bronchioles end in tiny air sacs. These are called alveoli. They inflate when a person inhales and deflate when a person exhales.

During gas exchange oxygen moves from the lungs to the bloodstream. At the same time carbon dioxide passes from the blood to the lungs. This happens in the lungs between the alveoli and a network of tiny blood vessels called capillaries, which are located in the walls of the alveoli.

Here you see red blood cells traveling through the capillaries. The walls of the alveoli share a membrane with the capillaries. That's how close they are.

This lets oxygen and carbon dioxide diffuse, or move freely, between the respiratory system and the bloodstream.

Oxygen molecules attach to red blood cells, which travel back to the heart. At the same time, the carbon dioxide molecules in the alveoli are blown out of the body the next time a person exhales.

Gas exchange allows the body to replenish the oxygen and eliminate the carbon dioxide. Doing both is necessary for survival.


Final Thoughts

So there you have it. That wraps up our study guide on Gas Exchange and Transport. I hope that this information was helpful.

If you don’t feel comfortable with this information yet — that’s okay. Just be sure to go through these practice questions until the information sticks.

Thank you so much for reading and as always, breathe easy my friend.

References

  • Faarc, Kacmarek Robert PhD Rrt, et al. Egan’s Fundamentals of Respiratory Care. 12th ed., Mosby, 2020. [Link]
  • Jardins, Des Terry. Cardiopulmonary Anatomy & Physiology: Essentials of Respiratory Care. 7th ed., Cengage Learning, 2019. [Link]
  • “Transport of Gases between the Environment and Alveoli – Theoretical Foundations.” National Center for Biotechnology Information, U.S. National Library of Medicine, 2 Apr. 2015, www.ncbi.nlm.nih.gov/pmc/articles/PMC4382809.
  • Wagner, Peter. “The Physiological Basis of Pulmonary Gas Exchange: Implications for Clinical Interpretation of Arterial Blood Gases.” European Respiratory Society, 1 Jan. 2015, erj.ersjournals.com/content/45/1/227.

Disclosure: The links to the textbooks are affiliate links which means, at no additional cost to you, we will earn a commission if you click through and make a purchase.


The Process of Breathing

  • Describe the mechanisms that drive breathing
  • Discuss how pressure, volume, and resistance are related
  • List the steps involved in pulmonary ventilation
  • Discuss the physical factors related to breathing
  • Discuss the meaning of respiratory volume and capacities
  • Define respiratory rate
  • Outline the mechanisms behind the control of breathing
  • Describe the respiratory centers of the medulla oblongata
  • Describe the respiratory centers of the pons
  • Discuss factors that can influence the respiratory rate

Pulmonary ventilation is the act of breathing, which can be described as the movement of air into and out of the lungs. The major mechanisms that drive pulmonary ventilation are atmospheric pressure (Patm) the air pressure within the alveoli, called intra-alveolar pressure (Palv) and the pressure within the pleural cavity, called intrapleural pressure (Pip).

Mechanisms of Breathing

The intra-alveolar and intrapleural pressures are dependent on certain physical features of the lung. However, the ability to breathe&mdashto have air enter the lungs during inspiration and air leave the lungs during expiration&mdashis dependent on the air pressure of the atmosphere and the air pressure within the lungs.

Pressure Relationships

Inspiration (or inhalation) and expiration (or exhalation) are dependent on the differences in pressure between the atmosphere and the lungs. In a gas, pressure is a force created by the movement of gas molecules that are confined. For example, a certain number of gas molecules in a two-liter container has more room than the same number of gas molecules in a one-liter container (Figure 22.15). In this case, the force exerted by the movement of the gas molecules against the walls of the two-liter container is lower than the force exerted by the gas molecules in the one-liter container. Therefore, the pressure is lower in the two-liter container and higher in the one-liter container. At a constant temperature, changing the volume occupied by the gas changes the pressure, as does changing the number of gas molecules. Boyle&rsquos law describes the relationship between volume and pressure in a gas at a constant temperature. Boyle discovered that the pressure of a gas is inversely proportional to its volume: If volume increases, pressure decreases. Likewise, if volume decreases, pressure increases. Pressure and volume are inversely related (P = k/V). Therefore, the pressure in the one-liter container (one-half the volume of the two-liter container) would be twice the pressure in the two-liter container. Boyle&rsquos law is expressed by the following formula:

In this formula, P1 represents the initial pressure and V1 represents the initial volume, whereas the final pressure and volume are represented by P2 and V2, respectively. If the two- and one-liter containers were connected by a tube and the volume of one of the containers were changed, then the gases would move from higher pressure (lower volume) to lower pressure (higher volume).

Figure 22.15 Boyle's Law In a gas, pressure increases as volume decreases.

Pulmonary ventilation is dependent on three types of pressure: atmospheric, intra-alveolar, and intrapleural. Atmospheric pressureis the amount of force that is exerted by gases in the air surrounding any given surface, such as the body. Atmospheric pressure can be expressed in terms of the unit atmosphere, abbreviated atm, or in millimeters of mercury (mm Hg). One atm is equal to 760 mm Hg, which is the atmospheric pressure at sea level. Typically, for respiration, other pressure values are discussed in relation to atmospheric pressure. Therefore, negative pressure is pressure lower than the atmospheric pressure, whereas positive pressure is pressure that it is greater than the atmospheric pressure. A pressure that is equal to the atmospheric pressure is expressed as zero.

Intra-alveolar pressure (intrapulmonary pressure) is the pressure of the air within the alveoli, which changes during the different phases of breathing (Figure 22.16). Because the alveoli are connected to the atmosphere via the tubing of the airways (similar to the two- and one-liter containers in the example above), the intrapulmonary pressure of the alveoli always equalizes with the atmospheric pressure.

Figure 22.16 Intrapulmonary and Intrapleural Pressure Relationships Intra-alveolar pressure changes during the different phases of the cycle. It equalizes at 760 mm Hg but does not remain at 760 mm Hg.

Intrapleural pressure is the pressure of the air within the pleural cavity, between the visceral and parietal pleurae. Similar to intra-alveolar pressure, intrapleural pressure also changes during the different phases of breathing. However, due to certain characteristics of the lungs, the intrapleural pressure is always lower than, or negative to, the intra-alveolar pressure (and therefore also to atmospheric pressure). Although it fluctuates during inspiration and expiration, intrapleural pressure remains approximately &ndash4 mm Hg throughout the breathing cycle.

Competing forces within the thorax cause the formation of the negative intrapleural pressure. One of these forces relates to the elasticity of the lungs themselves&mdashelastic tissue pulls the lungs inward, away from the thoracic wall. Surface tension of alveolar fluid, which is mostly water, also creates an inward pull of the lung tissue. This inward tension from the lungs is countered by opposing forces from the pleural fluid and thoracic wall. Surface tension within the pleural cavity pulls the lungs outward. Too much or too little pleural fluid would hinder the creation of the negative intrapleural pressure therefore, the level must be closely monitored by the mesothelial cells and drained by the lymphatic system. Since the parietal pleura is attached to the thoracic wall, the natural elasticity of the chest wall opposes the inward pull of the lungs. Ultimately, the outward pull is slightly greater than the inward pull, creating the &ndash4 mm Hg intrapleural pressure relative to the intra-alveolar pressure. Transpulmonary pressure is the difference between the intrapleural and intra-alveolar pressures, and it determines the size of the lungs. A higher transpulmonary pressure corresponds to a larger lung.

Physical Factors Affecting Ventilation

In addition to the differences in pressures, breathing is also dependent upon the contraction and relaxation of muscle fibers of both the diaphragm and thorax. The lungs themselves are passive during breathing, meaning they are not involved in creating the movement that helps inspiration and expiration. This is because of the adhesive nature of the pleural fluid, which allows the lungs to be pulled outward when the thoracic wall moves during inspiration. The recoil of the thoracic wall during expiration causes compression of the lungs. Contraction and relaxation of the diaphragm and intercostals muscles (found between the ribs) cause most of the pressure changes that result in inspiration and expiration. These muscle movements and subsequent pressure changes cause air to either rush in or be forced out of the lungs.

Other characteristics of the lungs influence the effort that must be expended to ventilate. Resistance is a force that slows motion, in this case, the flow of gases. The size of the airway is the primary factor affecting resistance. A small tubular diameter forces air through a smaller space, causing more collisions of air molecules with the walls of the airways. The following formula helps to describe the relationship between airway resistance and pressure changes:

As noted earlier, there is surface tension within the alveoli caused by water present in the lining of the alveoli. This surface tension tends to inhibit expansion of the alveoli. However, pulmonary surfactant secreted by type II alveolar cells mixes with that water and helps reduce this surface tension. Without pulmonary surfactant, the alveoli would collapse during expiration.

Thoracic wall compliance is the ability of the thoracic wall to stretch while under pressure. This can also affect the effort expended in the process of breathing. In order for inspiration to occur, the thoracic cavity must expand. The expansion of the thoracic cavity directly influences the capacity of the lungs to expand. If the tissues of the thoracic wall are not very compliant, it will be difficult to expand the thorax to increase the size of the lungs.

Pulmonary Ventilation

The difference in pressures drives pulmonary ventilation because air flows down a pressure gradient, that is, air flows from an area of higher pressure to an area of lower pressure. Air flows into the lungs largely due to a difference in pressure atmospheric pressure is greater than intra-alveolar pressure, and intra-alveolar pressure is greater than intrapleural pressure. Air flows out of the lungs during expiration based on the same principle pressure within the lungs becomes greater than the atmospheric pressure.

Pulmonary ventilation comprises two major steps: inspiration and expiration. Inspiration is the process that causes air to enter the lungs, and expiration is the process that causes air to leave the lungs (Figure 22.17). A respiratory cycle is one sequence of inspiration and expiration. In general, two muscle groups are used during normal inspiration: the diaphragm and the external intercostal muscles. Additional muscles can be used if a bigger breath is required. When the diaphragm contracts, it moves inferiorly toward the abdominal cavity, creating a larger thoracic cavity and more space for the lungs. Contraction of the external intercostal muscles moves the ribs upward and outward, causing the rib cage to expand, which increases the volume of the thoracic cavity. Due to the adhesive force of the pleural fluid, the expansion of the thoracic cavity forces the lungs to stretch and expand as well. This increase in volume leads to a decrease in intra-alveolar pressure, creating a pressure lower than atmospheric pressure. As a result, a pressure gradient is created that drives air into the lungs.

Figure 22.17 Inspiration and Expiration Inspiration and expiration occur due to the expansion and contraction of the thoracic cavity, respectively.

The process of normal expiration is passive, meaning that energy is not required to push air out of the lungs. Instead, the elasticity of the lung tissue causes the lung to recoil, as the diaphragm and intercostal muscles relax following inspiration. In turn, the thoracic cavity and lungs decrease in volume, causing an increase in intrapulmonary pressure. The intrapulmonary pressure rises above atmospheric pressure, creating a pressure gradient that causes air to leave the lungs.

There are different types, or modes, of breathing that require a slightly different process to allow inspiration and expiration. Quiet breathing, also known as eupnea, is a mode of breathing that occurs at rest and does not require the cognitive thought of the individual. During quiet breathing, the diaphragm and external intercostals must contract.

A deep breath, called diaphragmatic breathing, requires the diaphragm to contract. As the diaphragm relaxes, air passively leaves the lungs. A shallow breath, called costal breathing, requires contraction of the intercostal muscles. As the intercostal muscles relax, air passively leaves the lungs.

In contrast, forced breathing, also known as hyperpnea, is a mode of breathing that can occur during exercise or actions that require the active manipulation of breathing, such as singing. During forced breathing, inspiration and expiration both occur due to muscle contractions. In addition to the contraction of the diaphragm and intercostal muscles, other accessory muscles must also contract. During forced inspiration, muscles of the neck, including the scalenes, contract and lift the thoracic wall, increasing lung volume. During forced expiration, accessory muscles of the abdomen, including the obliques, contract, forcing abdominal organs upward against the diaphragm. This helps to push the diaphragm further into the thorax, pushing more air out. In addition, accessory muscles (primarily the internal intercostals) help to compress the rib cage, which also reduces the volume of the thoracic cavity.

Respiratory Volumes and Capacities

Respiratory volume is the term used for various volumes of air moved by or associated with the lungs at a given point in the respiratory cycle. There are four major types of respiratory volumes: tidal, residual, inspiratory reserve, and expiratory reserve (Figure 22.18). Tidal volume (TV) is the amount of air that normally enters the lungs during quiet breathing, which is about 500 milliliters. Expiratory reserve volume (ERV) is the amount of air you can forcefully exhale past a normal tidal expiration, up to 1200 milliliters for men. Inspiratory reserve volume (IRV) is produced by a deep inhalation, past a tidal inspiration. This is the extra volume that can be brought into the lungs during a forced inspiration. Residual volume (RV) is the air left in the lungs if you exhale as much air as possible. The residual volume makes breathing easier by preventing the alveoli from collapsing. Respiratory volume is dependent on a variety of factors, and measuring the different types of respiratory volumes can provide important clues about a person&rsquos respiratory health (Figure 22.19).

Figure 22.18 Respiratory Volumes and Capacities These two graphs show (a) respiratory volumes and (b) the combination of volumes that results in respiratory capacity.

Figure 22.19 Pulmonary Function Testing

Respiratory capacity is the combination of two or more selected volumes, which further describes the amount of air in the lungs during a given time. For example, total lung capacity (TLC) is the sum of all of the lung volumes (TV, ERV, IRV, and RV), which represents the total amount of air a person can hold in the lungs after a forceful inhalation. TLC is about 6000 mL air for men, and about 4200 mL for women. Vital capacity (VC) is the amount of air a person can move into or out of his or her lungs, and is the sum of all of the volumes except residual volume (TV, ERV, and IRV), which is between 4000 and 5000 milliliters. Inspiratory capacity (IC) is the maximum amount of air that can be inhaled past a normal tidal expiration, is the sum of the tidal volume and inspiratory reserve volume. On the other hand, the functional residual capacity (FRC) is the amount of air that remains in the lung after a normal tidal expiration it is the sum of expiratory reserve volume and residual volume (see Figure 22.18).

INTERACTIVE LINK

Watch this video to learn more about lung volumes and spirometers. Explain how spirometry test results can be used to diagnose respiratory diseases or determine the effectiveness of disease treatment.

In addition to the air that creates respiratory volumes, the respiratory system also contains anatomical dead space, which is air that is present in the airway that never reaches the alveoli and therefore never participates in gas exchange. Alveolar dead spaceinvolves air found within alveoli that are unable to function, such as those affected by disease or abnormal blood flow. Total dead space is the anatomical dead space and alveolar dead space together, and represents all of the air in the respiratory system that is not being used in the gas exchange process.

Respiratory Rate and Control of Ventilation

Breathing usually occurs without thought, although at times you can consciously control it, such as when you swim under water, sing a song, or blow bubbles. The respiratory rate is the total number of breaths, or respiratory cycles, that occur each minute. Respiratory rate can be an important indicator of disease, as the rate may increase or decrease during an illness or in a disease condition. The respiratory rate is controlled by the respiratory center located within the medulla oblongata in the brain, which responds primarily to changes in carbon dioxide, oxygen, and pH levels in the blood.

The normal respiratory rate of a child decreases from birth to adolescence. A child under 1 year of age has a normal respiratory rate between 30 and 60 breaths per minute, but by the time a child is about 10 years old, the normal rate is closer to 18 to 30. By adolescence, the normal respiratory rate is similar to that of adults, 12 to 18 breaths per minute.

Ventilation Control Centers

The control of ventilation is a complex interplay of multiple regions in the brain that signal the muscles used in pulmonary ventilation to contract (Table 22.1). The result is typically a rhythmic, consistent ventilation rate that provides the body with sufficient amounts of oxygen, while adequately removing carbon dioxide.

Summary of Ventilation Regulation

System componentFunction
Medullary respiratory renterSets the basic rhythm of breathing
Ventral respiratory group (VRG)Generates the breathing rhythm and integrates data coming into the medulla
Dorsal respiratory group (DRG)Integrates input from the stretch receptors and the chemoreceptors in the periphery
Pontine respiratory group (PRG)Influences and modifies the medulla oblongata&rsquos functions
Aortic bodyMonitors blood PCO2, PO2, and pH
Carotid bodyMonitors blood PCO2, PO2, and pH
HypothalamusMonitors emotional state and body temperature
Cortical areas of the brainControl voluntary breathing
ProprioceptorsSend impulses regarding joint and muscle movements
Pulmonary irritant reflexesProtect the respiratory zones of the system from foreign material
Inflation reflexProtects the lungs from over-inflating

Neurons that innervate the muscles of the respiratory system are responsible for controlling and regulating pulmonary ventilation. The major brain centers involved in pulmonary ventilation are the medulla oblongata and the pontine respiratory group (Figure 22.20).

Figure 22.20 Respiratory Centers of the Brain

The medulla oblongata contains the dorsal respiratory group (DRG) and the ventral respiratory group (VRG). The DRG is involved in maintaining a constant breathing rhythm by stimulating the diaphragm and intercostal muscles to contract, resulting in inspiration. When activity in the DRG ceases, it no longer stimulates the diaphragm and intercostals to contract, allowing them to relax, resulting in expiration. The VRG is involved in forced breathing, as the neurons in the VRG stimulate the accessory muscles involved in forced breathing to contract, resulting in forced inspiration. The VRG also stimulates the accessory muscles involved in forced expiration to contract.

The second respiratory center of the brain is located within the pons, called the pontine respiratory group, and consists of the apneustic and pneumotaxic centers. The apneustic center is a double cluster of neuronal cell bodies that stimulate neurons in the DRG, controlling the depth of inspiration, particularly for deep breathing. The pneumotaxic center is a network of neurons that inhibits the activity of neurons in the DRG, allowing relaxation after inspiration, and thus controlling the overall rate.

Factors That Affect the Rate and Depth of Respiration

The respiratory rate and the depth of inspiration are regulated by the medulla oblongata and pons however, these regions of the brain do so in response to systemic stimuli. It is a dose-response, negative-feedback relationship in which the greater the stimulus, the greater the response. Thus, increasing stimuli results in forced breathing. Multiple systemic factors are involved in stimulating the brain to produce pulmonary ventilation.

The major factor that stimulates the medulla oblongata and pons to produce respiration is surprisingly not oxygen concentration, but rather the concentration of carbon dioxide in the blood. As you recall, carbon dioxide is a waste product of cellular respiration and can be toxic. Concentrations of chemicals are sensed by chemoreceptors. A central chemoreceptor is one of the specialized receptors that are located in the brain and brainstem, whereas a peripheral chemoreceptor is one of the specialized receptors located in the carotid arteries and aortic arch. Concentration changes in certain substances, such as carbon dioxide or hydrogen ions, stimulate these receptors, which in turn signal the respiration centers of the brain. In the case of carbon dioxide, as the concentration of CO2 in the blood increases, it readily diffuses across the blood-brain barrier, where it collects in the extracellular fluid. As will be explained in more detail later, increased carbon dioxide levels lead to increased levels of hydrogen ions, decreasing pH. The increase in hydrogen ions in the brain triggers the central chemoreceptors to stimulate the respiratory centers to initiate contraction of the diaphragm and intercostal muscles. As a result, the rate and depth of respiration increase, allowing more carbon dioxide to be expelled, which brings more air into and out of the lungs promoting a reduction in the blood levels of carbon dioxide, and therefore hydrogen ions, in the blood. In contrast, low levels of carbon dioxide in the blood cause low levels of hydrogen ions in the brain, leading to a decrease in the rate and depth of pulmonary ventilation, producing shallow, slow breathing.

Another factor involved in influencing the respiratory activity of the brain is systemic arterial concentrations of hydrogen ions. Increasing carbon dioxide levels can lead to increased H + levels, as mentioned above, as well as other metabolic activities, such as lactic acid accumulation after strenuous exercise. Peripheral chemoreceptors of the aortic arch and carotid arteries sense arterial levels of hydrogen ions. When peripheral chemoreceptors sense decreasing, or more acidic, pH levels, they stimulate an increase in ventilation to remove carbon dioxide from the blood at a quicker rate. Removal of carbon dioxide from the blood helps to reduce hydrogen ions, thus increasing systemic pH.

Blood levels of oxygen are also important in influencing respiratory rate. The peripheral chemoreceptors are responsible for sensing large changes in blood oxygen levels. If blood oxygen levels become quite low&mdashabout 60 mm Hg or less&mdashthen peripheral chemoreceptors stimulate an increase in respiratory activity. The chemoreceptors are only able to sense dissolved oxygen molecules, not the oxygen that is bound to hemoglobin. As you recall, the majority of oxygen is bound by hemoglobin when dissolved levels of oxygen drop, hemoglobin releases oxygen. Therefore, a large drop in oxygen levels is required to stimulate the chemoreceptors of the aortic arch and carotid arteries.

The hypothalamus and other brain regions associated with the limbic system also play roles in influencing the regulation of breathing by interacting with the respiratory centers. The hypothalamus and other regions associated with the limbic system are involved in regulating respiration in response to emotions, pain, and temperature. For example, an increase in body temperature causes an increase in respiratory rate. Feeling excited or the fight-or-flight response will also result in an increase in respiratory rate.

DISORDERS OF THE.

Respiratory System: Sleep Apnea

Sleep apnea is a chronic disorder that can occur in children or adults, and is characterized by the cessation of breathing during sleep. These episodes may last for several seconds or several minutes, and may differ in the frequency with which they are experienced. Sleep apnea leads to poor sleep, which is reflected in the symptoms of fatigue, evening napping, irritability, memory problems, and morning headaches. In addition, many individuals with sleep apnea experience a dry throat in the morning after waking from sleep, which may be due to excessive snoring.

There are two types of sleep apnea: obstructive sleep apnea and central sleep apnea. Obstructive sleep apnea is caused by an obstruction of the airway during sleep, which can occur at different points in the airway, depending on the underlying cause of the obstruction. For example, the tongue and throat muscles of some individuals with obstructive sleep apnea may relax excessively, causing the muscles to push into the airway. Another example is obesity, which is a known risk factor for sleep apnea, as excess adipose tissue in the neck region can push the soft tissues towards the lumen of the airway, causing the trachea to narrow.

In central sleep apnea, the respiratory centers of the brain do not respond properly to rising carbon dioxide levels and therefore do not stimulate the contraction of the diaphragm and intercostal muscles regularly. As a result, inspiration does not occur and breathing stops for a short period. In some cases, the cause of central sleep apnea is unknown. However, some medical conditions, such as stroke and congestive heart failure, may cause damage to the pons or medulla oblongata. In addition, some pharmacologic agents, such as morphine, can affect the respiratory centers, causing a decrease in the respiratory rate. The symptoms of central sleep apnea are similar to those of obstructive sleep apnea.

A diagnosis of sleep apnea is usually done during a sleep study, where the patient is monitored in a sleep laboratory for several nights. The patient&rsquos blood oxygen levels, heart rate, respiratory rate, and blood pressure are monitored, as are brain activity and the volume of air that is inhaled and exhaled. Treatment of sleep apnea commonly includes the use of a device called a continuous positive airway pressure (CPAP) machine during sleep. The CPAP machine has a mask that covers the nose, or the nose and mouth, and forces air into the airway at regular intervals. This pressurized air can help to gently force the airway to remain open, allowing more normal ventilation to occur. Other treatments include lifestyle changes to decrease weight, eliminate alcohol and other sleep apnea&ndashpromoting drugs, and changes in sleep position. In addition to these treatments, patients with central sleep apnea may need supplemental oxygen during sleep.


Abstract

The discovery that the gas nitric oxide (NO) is an important signaling molecule in the cardiovascular system earned its Nobel prize in 1998. NO has since been found to play important roles in a variety of physiologic and pathophysiologic processes in the body including vasoregulation, hemostasis, neurotransmission, immune defense, and respiration. The surprisingly high concentrations of NO in the nasal airway and paranasal sinuses has important implications for the field of otorhinolaryngology. NO provides a first-line defense against micro-organisms through its antiviral and antimicrobial activity and by its upregulation of ciliary motility. Nasal treatments such as polypectomy, sinus surgery, removal of hypertrophic adenoids and tonsils, and treatment of allergic rhinitis may alter NO output and, therefore, the microbial colonization of the upper airways. Nasal surgery aimed at relieving nasal obstruction may do the same but would also be expected to improve pulmonary function in patients with asthma and upper airway obstruction. NO output rises in a number of conditions associated with chronic airway inflammation, but not all of them. Concentrations are increased in asthma, allergic rhinitis, and viral respiratory infections, but reduced in sinusitis, cystic fibrosis, primary ciliary dysfunction, chronic cough, and after exposure to tobacco and alcohol. Therefore, NO, similar to several other inflammatory mediators, probably subserves different functions as local conditions dictate. At present, it seems that the measurement of NO in the upper airway may prove valuable as a simple, noninvasive diagnostic marker of airway pathologies. The objective of this review is to highlight some aspects of the origin, physiology, and functions of upper airway NO, and to discuss the particular methodological problems that result from the complex anatomy. (Am J Otolaryngol 200122:19-32. Copyright © 2001 by W.B. Saunders Company)

the Catholic University of Rio Grande do Sul, Porto Alegre, Brazil

Zhenjiang First People's Hospital, Jiangsu, People's Republic of China and

§the Department of Otolaryngology, St. Michael's Hospital, University of Toronto, Canada.


Crossword – Gas Exchange in Fish, Insects & Plants (Answers Provided)

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22.3 The Process of Breathing

Pulmonary ventilation is the act of breathing, which can be described as the movement of air into and out of the lungs. The major mechanisms that drive pulmonary ventilation are atmospheric pressure (Patm) the air pressure within the alveoli, called intra-alveolar pressure (Palv) and the pressure within the pleural cavity, called intrapleural pressure (Pip).

Mechanisms of Breathing

The intra-alveolar and intrapleural pressures are dependent on certain physical features of the lung. However, the ability to breathe—to have air enter the lungs during inspiration and air leave the lungs during expiration—is dependent on the air pressure of the atmosphere and the air pressure within the lungs.

Pressure Relationships

Inspiration (or inhalation) and expiration (or exhalation) are dependent on the differences in pressure between the atmosphere and the lungs. In a gas, pressure is a force created by the movement of gas molecules that are confined. For example, a certain number of gas molecules in a two-liter container has more room than the same number of gas molecules in a one-liter container (Figure 22.15). In this case, the force exerted by the movement of the gas molecules against the walls of the two-liter container is lower than the force exerted by the gas molecules in the one-liter container. Therefore, the pressure is lower in the two-liter container and higher in the one-liter container. At a constant temperature, changing the volume occupied by the gas changes the pressure, as does changing the number of gas molecules. Boyle’s law describes the relationship between volume and pressure in a gas at a constant temperature. Boyle discovered that the pressure of a gas is inversely proportional to its volume: If volume increases, pressure decreases. Likewise, if volume decreases, pressure increases. Pressure and volume are inversely related (P = k/V). Therefore, the pressure in the one-liter container (one-half the volume of the two-liter container) would be twice the pressure in the two-liter container. Boyle’s law is expressed by the following formula:

In this formula, P1 represents the initial pressure and V1 represents the initial volume, whereas the final pressure and volume are represented by P2 and V2, respectively. If the two- and one-liter containers were connected by a tube and the volume of one of the containers were changed, then the gases would move from higher pressure (lower volume) to lower pressure (higher volume).

Pulmonary ventilation is dependent on three types of pressure: atmospheric, intra-alveolar, and intrapleural. Atmospheric pressure is the amount of force that is exerted by gases in the air surrounding any given surface, such as the body. Atmospheric pressure can be expressed in terms of the unit atmosphere, abbreviated atm, or in millimeters of mercury (mm Hg). One atm is equal to 760 mm Hg, which is the atmospheric pressure at sea level. Typically, for respiration, other pressure values are discussed in relation to atmospheric pressure. Therefore, negative pressure is pressure lower than the atmospheric pressure, whereas positive pressure is pressure that it is greater than the atmospheric pressure. A pressure that is equal to the atmospheric pressure is expressed as zero.

Intra-alveolar pressure (intrapulmonary pressure) is the pressure of the air within the alveoli, which changes during the different phases of breathing (Figure 22.16). Because the alveoli are connected to the atmosphere via the tubing of the airways (similar to the two- and one-liter containers in the example above), the intrapulmonary pressure of the alveoli always equalizes with the atmospheric pressure.

Intrapleural pressure is the pressure of the air within the pleural cavity, between the visceral and parietal pleurae. Similar to intra-alveolar pressure, intrapleural pressure also changes during the different phases of breathing. However, due to certain characteristics of the lungs, the intrapleural pressure is always lower than, or negative to, the intra-alveolar pressure (and therefore also to atmospheric pressure). Although it fluctuates during inspiration and expiration, intrapleural pressure remains approximately –4 mm Hg throughout the breathing cycle.

Competing forces within the thorax cause the formation of the negative intrapleural pressure. One of these forces relates to the elasticity of the lungs themselves—elastic tissue pulls the lungs inward, away from the thoracic wall. Surface tension of alveolar fluid, which is mostly water, also creates an inward pull of the lung tissue. This inward tension from the lungs is countered by opposing forces from the pleural fluid and thoracic wall. Surface tension within the pleural cavity pulls the lungs outward. Too much or too little pleural fluid would hinder the creation of the negative intrapleural pressure therefore, the level must be closely monitored by the mesothelial cells and drained by the lymphatic system. Since the parietal pleura is attached to the thoracic wall, the natural elasticity of the chest wall opposes the inward pull of the lungs. Ultimately, the outward pull is slightly greater than the inward pull, creating the –4 mm Hg intrapleural pressure relative to the intra-alveolar pressure. Transpulmonary pressure is the difference between the intrapleural and intra-alveolar pressures, and it determines the size of the lungs. A higher transpulmonary pressure corresponds to a larger lung.

Physical Factors Affecting Ventilation

In addition to the differences in pressures, breathing is also dependent upon the contraction and relaxation of muscle fibers of both the diaphragm and thorax. The lungs themselves are passive during breathing, meaning they are not involved in creating the movement that helps inspiration and expiration. This is because of the adhesive nature of the pleural fluid, which allows the lungs to be pulled outward when the thoracic wall moves during inspiration. The recoil of the thoracic wall during expiration causes compression of the lungs. Contraction and relaxation of the diaphragm and intercostals muscles (found between the ribs) cause most of the pressure changes that result in inspiration and expiration. These muscle movements and subsequent pressure changes cause air to either rush in or be forced out of the lungs.

Other characteristics of the lungs influence the effort that must be expended to ventilate. Resistance is a force that slows motion, in this case, the flow of gases. The size of the airway is the primary factor affecting resistance. A small tubular diameter forces air through a smaller space, causing more collisions of air molecules with the walls of the airways. The following formula helps to describe the relationship between airway resistance and pressure changes:

As noted earlier, there is surface tension within the alveoli caused by water present in the lining of the alveoli. This surface tension tends to inhibit expansion of the alveoli. However, pulmonary surfactant secreted by type II alveolar cells mixes with that water and helps reduce this surface tension. Without pulmonary surfactant, the alveoli would collapse during expiration.

Thoracic wall compliance is the ability of the thoracic wall to stretch while under pressure. This can also affect the effort expended in the process of breathing. In order for inspiration to occur, the thoracic cavity must expand. The expansion of the thoracic cavity directly influences the capacity of the lungs to expand. If the tissues of the thoracic wall are not very compliant, it will be difficult to expand the thorax to increase the size of the lungs.

Pulmonary Ventilation

The difference in pressures drives pulmonary ventilation because air flows down a pressure gradient, that is, air flows from an area of higher pressure to an area of lower pressure. Air flows into the lungs largely due to a difference in pressure atmospheric pressure is greater than intra-alveolar pressure, and intra-alveolar pressure is greater than intrapleural pressure. Air flows out of the lungs during expiration based on the same principle pressure within the lungs becomes greater than the atmospheric pressure.

Pulmonary ventilation comprises two major steps: inspiration and expiration. Inspiration is the process that causes air to enter the lungs, and expiration is the process that causes air to leave the lungs (Figure 22.17). A respiratory cycle is one sequence of inspiration and expiration. In general, two muscle groups are used during normal inspiration: the diaphragm and the external intercostal muscles. Additional muscles can be used if a bigger breath is required. When the diaphragm contracts, it moves inferiorly toward the abdominal cavity, creating a larger thoracic cavity and more space for the lungs. Contraction of the external intercostal muscles moves the ribs upward and outward, causing the rib cage to expand, which increases the volume of the thoracic cavity. Due to the adhesive force of the pleural fluid, the expansion of the thoracic cavity forces the lungs to stretch and expand as well. This increase in volume leads to a decrease in intra-alveolar pressure, creating a pressure lower than atmospheric pressure. As a result, a pressure gradient is created that drives air into the lungs.

The process of normal expiration is passive, meaning that energy is not required to push air out of the lungs. Instead, the elasticity of the lung tissue causes the lung to recoil, as the diaphragm and intercostal muscles relax following inspiration. In turn, the thoracic cavity and lungs decrease in volume, causing an increase in intrapulmonary pressure. The intrapulmonary pressure rises above atmospheric pressure, creating a pressure gradient that causes air to leave the lungs.

There are different types, or modes, of breathing that require a slightly different process to allow inspiration and expiration. Quiet breathing , also known as eupnea, is a mode of breathing that occurs at rest and does not require the cognitive thought of the individual. During quiet breathing, the diaphragm and external intercostals must contract.

A deep breath, called diaphragmatic breathing, requires the diaphragm to contract. As the diaphragm relaxes, air passively leaves the lungs. A shallow breath, called costal breathing, requires contraction of the intercostal muscles. As the intercostal muscles relax, air passively leaves the lungs.

In contrast, forced breathing , also known as hyperpnea, is a mode of breathing that can occur during exercise or actions that require the active manipulation of breathing, such as singing. During forced breathing, inspiration and expiration both occur due to muscle contractions. In addition to the contraction of the diaphragm and intercostal muscles, other accessory muscles must also contract. During forced inspiration, muscles of the neck, including the scalenes, contract and lift the thoracic wall, increasing lung volume. During forced expiration, accessory muscles of the abdomen, including the obliques, contract, forcing abdominal organs upward against the diaphragm. This helps to push the diaphragm further into the thorax, pushing more air out. In addition, accessory muscles (primarily the internal intercostals) help to compress the rib cage, which also reduces the volume of the thoracic cavity.

Respiratory Volumes and Capacities

Respiratory volume is the term used for various volumes of air moved by or associated with the lungs at a given point in the respiratory cycle. There are four major types of respiratory volumes: tidal, residual, inspiratory reserve, and expiratory reserve (Figure 22.18). Tidal volume (TV) is the amount of air that normally enters the lungs during quiet breathing, which is about 500 milliliters. Expiratory reserve volume (ERV) is the amount of air you can forcefully exhale past a normal tidal expiration, up to 1200 milliliters for men. Inspiratory reserve volume (IRV) is produced by a deep inhalation, past a tidal inspiration. This is the extra volume that can be brought into the lungs during a forced inspiration. Residual volume (RV) is the air left in the lungs if you exhale as much air as possible. The residual volume makes breathing easier by preventing the alveoli from collapsing. Respiratory volume is dependent on a variety of factors, and measuring the different types of respiratory volumes can provide important clues about a person’s respiratory health (Figure 22.19).

Respiratory capacity is the combination of two or more selected volumes, which further describes the amount of air in the lungs during a given time. For example, total lung capacity (TLC) is the sum of all of the lung volumes (TV, ERV, IRV, and RV), which represents the total amount of air a person can hold in the lungs after a forceful inhalation. TLC is about 6000 mL air for men, and about 4200 mL for women. Vital capacity (VC) is the amount of air a person can move into or out of his or her lungs, and is the sum of all of the volumes except residual volume (TV, ERV, and IRV), which is between 4000 and 5000 milliliters. Inspiratory capacity (IC) is the maximum amount of air that can be inhaled past a normal tidal expiration, is the sum of the tidal volume and inspiratory reserve volume. On the other hand, the functional residual capacity (FRC) is the amount of air that remains in the lung after a normal tidal expiration it is the sum of expiratory reserve volume and residual volume (see Figure 22.18).

Interactive Link

Watch this video to learn more about lung volumes and spirometers. Explain how spirometry test results can be used to diagnose respiratory diseases or determine the effectiveness of disease treatment.

In addition to the air that creates respiratory volumes, the respiratory system also contains anatomical dead space , which is air that is present in the airway that never reaches the alveoli and therefore never participates in gas exchange. Alveolar dead space involves air found within alveoli that are unable to function, such as those affected by disease or abnormal blood flow. Total dead space is the anatomical dead space and alveolar dead space together, and represents all of the air in the respiratory system that is not being used in the gas exchange process.

Respiratory Rate and Control of Ventilation

Breathing usually occurs without thought, although at times you can consciously control it, such as when you swim under water, sing a song, or blow bubbles. The respiratory rate is the total number of breaths, or respiratory cycles, that occur each minute. Respiratory rate can be an important indicator of disease, as the rate may increase or decrease during an illness or in a disease condition. The respiratory rate is controlled by the respiratory center located within the medulla oblongata in the brain, which responds primarily to changes in carbon dioxide, oxygen, and pH levels in the blood.

The normal respiratory rate of a child decreases from birth to adolescence. A child under 1 year of age has a normal respiratory rate between 30 and 60 breaths per minute, but by the time a child is about 10 years old, the normal rate is closer to 18 to 30. By adolescence, the normal respiratory rate is similar to that of adults, 12 to 18 breaths per minute.

Ventilation Control Centers

The control of ventilation is a complex interplay of multiple regions in the brain that signal the muscles used in pulmonary ventilation to contract (Table 22.1). The result is typically a rhythmic, consistent ventilation rate that provides the body with sufficient amounts of oxygen, while adequately removing carbon dioxide.

System component Function
Medullary respiratory center Sets the basic rhythm of breathing
Ventral respiratory group (VRG) Generates the breathing rhythm and integrates data coming into the medulla
Dorsal respiratory group (DRG) Integrates input from the stretch receptors and the chemoreceptors in the periphery
Pontine respiratory group (PRG) Influences and modifies the medulla oblongata’s functions
Aortic body Monitors blood PCO2, PO2, and pH
Carotid body Monitors blood PCO2, PO2, and pH
Hypothalamus Monitors emotional state and body temperature
Cortical areas of the brain Control voluntary breathing
Proprioceptors Send impulses regarding joint and muscle movements
Pulmonary irritant reflexes Protect the respiratory zones of the system from foreign material
Inflation reflex Protects the lungs from over-inflating

Neurons that innervate the muscles of the respiratory system are responsible for controlling and regulating pulmonary ventilation. The major brain centers involved in pulmonary ventilation are the medulla oblongata and the pontine respiratory group (Figure 22.20).

The medulla oblongata contains the dorsal respiratory group (DRG) and the ventral respiratory group (VRG) . The DRG is involved in maintaining a constant breathing rhythm by stimulating the diaphragm and intercostal muscles to contract, resulting in inspiration. When activity in the DRG ceases, it no longer stimulates the diaphragm and intercostals to contract, allowing them to relax, resulting in expiration. The VRG is involved in forced breathing, as the neurons in the VRG stimulate the accessory muscles involved in forced breathing to contract, resulting in forced inspiration. The VRG also stimulates the accessory muscles involved in forced expiration to contract.

The second respiratory center of the brain is located within the pons, called the pontine respiratory group, and consists of the apneustic and pneumotaxic centers. The apneustic center is a double cluster of neuronal cell bodies that stimulate neurons in the DRG, controlling the depth of inspiration, particularly for deep breathing. The pneumotaxic center is a network of neurons that inhibits the activity of neurons in the DRG, allowing relaxation after inspiration, and thus controlling the overall rate.

Factors That Affect the Rate and Depth of Respiration

The respiratory rate and the depth of inspiration are regulated by the medulla oblongata and pons however, these regions of the brain do so in response to systemic stimuli. It is a dose-response, negative-feedback relationship in which the greater the stimulus, the greater the response. Thus, increasing stimuli results in forced breathing. Multiple systemic factors are involved in stimulating the brain to produce pulmonary ventilation.

The major factor that stimulates the medulla oblongata and pons to produce respiration is surprisingly not oxygen concentration, but rather the concentration of carbon dioxide in the blood. As you recall, carbon dioxide is a waste product of cellular respiration and can be toxic. Concentrations of chemicals are sensed by chemoreceptors. A central chemoreceptor is one of the specialized receptors that are located in the brain and brainstem, whereas a peripheral chemoreceptor is one of the specialized receptors located in the carotid arteries and aortic arch. Concentration changes in certain substances, such as carbon dioxide or hydrogen ions, stimulate these receptors, which in turn signal the respiration centers of the brain. In the case of carbon dioxide, as the concentration of CO2 in the blood increases, it readily diffuses across the blood-brain barrier, where it collects in the extracellular fluid. As will be explained in more detail later, increased carbon dioxide levels lead to increased levels of hydrogen ions, decreasing pH. The increase in hydrogen ions in the brain triggers the central chemoreceptors to stimulate the respiratory centers to initiate contraction of the diaphragm and intercostal muscles. As a result, the rate and depth of respiration increase, allowing more carbon dioxide to be expelled, which brings more air into and out of the lungs promoting a reduction in the blood levels of carbon dioxide, and therefore hydrogen ions, in the blood. In contrast, low levels of carbon dioxide in the blood cause low levels of hydrogen ions in the brain, leading to a decrease in the rate and depth of pulmonary ventilation, producing shallow, slow breathing.

Another factor involved in influencing the respiratory activity of the brain is systemic arterial concentrations of hydrogen ions. Increasing carbon dioxide levels can lead to increased H + levels, as mentioned above, as well as other metabolic activities, such as lactic acid accumulation after strenuous exercise. Peripheral chemoreceptors of the aortic arch and carotid arteries sense arterial levels of hydrogen ions. When peripheral chemoreceptors sense decreasing, or more acidic, pH levels, they stimulate an increase in ventilation to remove carbon dioxide from the blood at a quicker rate. Removal of carbon dioxide from the blood helps to reduce hydrogen ions, thus increasing systemic pH.

Blood levels of oxygen are also important in influencing respiratory rate. The peripheral chemoreceptors are responsible for sensing large changes in blood oxygen levels. If blood oxygen levels become quite low—about 60 mm Hg or less—then peripheral chemoreceptors stimulate an increase in respiratory activity. The chemoreceptors are only able to sense dissolved oxygen molecules, not the oxygen that is bound to hemoglobin. As you recall, the majority of oxygen is bound by hemoglobin when dissolved levels of oxygen drop, hemoglobin releases oxygen. Therefore, a large drop in oxygen levels is required to stimulate the chemoreceptors of the aortic arch and carotid arteries.

The hypothalamus and other brain regions associated with the limbic system also play roles in influencing the regulation of breathing by interacting with the respiratory centers. The hypothalamus and other regions associated with the limbic system are involved in regulating respiration in response to emotions, pain, and temperature. For example, an increase in body temperature causes an increase in respiratory rate. Feeling excited or the fight-or-flight response will also result in an increase in respiratory rate.

Disorders of the.

Respiratory System: Sleep Apnea

Sleep apnea is a chronic disorder that can occur in children or adults, and is characterized by the cessation of breathing during sleep. These episodes may last for several seconds or several minutes, and may differ in the frequency with which they are experienced. Sleep apnea leads to poor sleep, which is reflected in the symptoms of fatigue, evening napping, irritability, memory problems, and morning headaches. In addition, many individuals with sleep apnea experience a dry throat in the morning after waking from sleep, which may be due to excessive snoring.

There are two types of sleep apnea: obstructive sleep apnea and central sleep apnea. Obstructive sleep apnea is caused by an obstruction of the airway during sleep, which can occur at different points in the airway, depending on the underlying cause of the obstruction. For example, the tongue and throat muscles of some individuals with obstructive sleep apnea may relax excessively, causing the muscles to push into the airway. Another example is obesity, which is a known risk factor for sleep apnea, as excess adipose tissue in the neck region can push the soft tissues towards the lumen of the airway, causing the trachea to narrow.

In central sleep apnea, the respiratory centers of the brain do not respond properly to rising carbon dioxide levels and therefore do not stimulate the contraction of the diaphragm and intercostal muscles regularly. As a result, inspiration does not occur and breathing stops for a short period. In some cases, the cause of central sleep apnea is unknown. However, some medical conditions, such as stroke and congestive heart failure, may cause damage to the pons or medulla oblongata. In addition, some pharmacologic agents, such as morphine, can affect the respiratory centers, causing a decrease in the respiratory rate. The symptoms of central sleep apnea are similar to those of obstructive sleep apnea.

A diagnosis of sleep apnea is usually done during a sleep study, where the patient is monitored in a sleep laboratory for several nights. The patient’s blood oxygen levels, heart rate, respiratory rate, and blood pressure are monitored, as are brain activity and the volume of air that is inhaled and exhaled. Treatment of sleep apnea commonly includes the use of a device called a continuous positive airway pressure (CPAP) machine during sleep. The CPAP machine has a mask that covers the nose, or the nose and mouth, and forces air into the airway at regular intervals. This pressurized air can help to gently force the airway to remain open, allowing more normal ventilation to occur. Other treatments include lifestyle changes to decrease weight, eliminate alcohol and other sleep apnea–promoting drugs, and changes in sleep position. In addition to these treatments, patients with central sleep apnea may need supplemental oxygen during sleep.


22.19: Gas Exchange across the Alveoli - Biology

What is the most significant modifiable risk factor for the development of impaired gas exchange?

When evaluating the concept of gas exchange, how would the nurse best describe the movement of oxygen and carbon dioxide?

  1. Oxygen and carbon dioxide are exchanged across the capillary membrane to provide oxygen to hemoglobin.
  2. Gas moves from an area of high pressure to an area of low pressure across the alveolar membrane.
  3. The level of inspired oxygen must be sufficient to displace the carbon dioxide molecules in the alveoli.
  4. Gases are exchanged between the atmosphere and the blood based on the oxygen-carrying capacity of the hemoglobin.

B. Gas moves from an area of high pressure to an area of low pressure across the alveolar membrane.

A patient is having the arterial blood gas (ABG) measured. What would the nurse identify as the parameters to be evaluated by this test?

  1. Ratio of hemoglobin and hematocrit
  2. Status of acid–base balance in arterial blood
  3. Adequacy of oxygen transport
  4. Presence of a pulmonary embolus

B. Status of acid–base balance in arterial blood

The nurse would anticipate that which of the following patients will need to be treated with insertion of a chest tube?

  1. A patient with asthma and severe shortness of breath
  2. A patient undergoing a bronchoscopy for a biopsy
  3. A patient with a pleural effusion requiring fluid removal
  4. A patient experiencing a problem with a pneumothorax

D. A patient experiencing a problem with a pneumothorax

The nurse is administering oral glucocorticoids to a patient with asthma. What assessment finding would the nurse identify as a therapeutic response to this medication?

  1. No observable respiratory difficulty or shortness of breath over the last 24 hours
  2. A decrease in the amount of nasal drainage and sneezing
  3. No sputum production, and a decrease in coughing episodes
  4. Relief of an acute asthmatic attack

A. No observable respiratory difficulty or shortness of breath over the last 24 hours

The nurse is caring for a patient with chronic obstructive pulmonary disease (COPD). The patient tells the nurse he is having a “hard time breathing.” His respiratory rate is 32 breaths per minute, his pulse is 120 beats per minute, and the oxygen saturation is 90%. What would be the best nursing intervention for this patient?

  1. Begin oxygen via a face mask at 60% FiO2 (fraction of inspired oxygen).
  2. Administer a PRN (as necessary) dose of an intranasal glucocorticoid.
  3. Encourage coughing and deep breathing to clear the airway.
  4. Initiate oxygen via a nasal cannula, and begin at a flow rate of 3 L/min.

D. Initiate oxygen via a nasal cannula, and begin at a flow rate of 3 L/min.


MATERIALS AND METHODS

According to the Chinese Clinical Guidance for COVID-19 Pneumonia Diagnosis and Treatment (seventh edition) issued by the National Health Commission of China (29), clinical classifications are divided into mild, moderate, severe, and critically severe symptoms. According to the guide’s discharge standard, patients that meet the following conditions can be discharged: (i) The body temperature returns to normal for more than three consecutive days (ii) significant improvement of the respiratory symptoms (iii) pulmonary CT images showing significant improvement of the acute exudative lesions (iv) and negative nucleic acid test results of sputum, nasopharynx swab, and other respiratory samples for two consecutive tests (with sampling time at least 1 day apart). A total of 13 COVID-19 pneumonia discharged patients (4 men and 9 women, average age is 35.8 years) with moderate symptoms were recruited for our study. All patients had been laboratory confirmed for COVID-19 when first admitted to the hospital and subsequently verified by the Wuhan CDC. They have no history of lung disease and smoking, and lung health was also confirmed by chest x-ray examination, which was performed in the annual physical examination (year 2019). Clinical records, laboratory results, and chest CT scans were retrospectively reviewed for these discharged patients, who were admitted to Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. We also recruited 12 healthy volunteers with an average age of 32.5 years (range, 24 to 40 years) as the control group. Our study was approved by the Ethics Commission of Tongji Medical College, Huazhong University of Science and Technology, and all subjects signed the informed consent forms.

Final CT scans were obtained with patients in the supine position (11 patients underwent scanning after discharge, and two patients underwent scanning shortly before discharge) using one of the three CT systems: LightSpeed 16 or volume CT, GE Healthcare, Wisconsin, USA (9/13) Somatom Definition AS+, Siemens, Germany (2/13) and uCT 780, United Imaging, China (2/13). The following parameters were used: tube voltage = 100 to 120 kilovolt peak, matrix = 512 × 512, slice thickness = 1.00 to 1.25 mm, and field of view (FOV) = 350 mm × 350 mm. The tube current was regulated through an automatic exposure modulation system, and the single collimation width of reconstructed images was 0.50 to 1.25 mm.

All MRI scans were performed using a 3.0-T multinuclear whole-body MRI Scanner [uMR780(Xe), Wuhan, China] with a horizontal magnet using a transmit-receive vest RF coil (35.45 MHz for 129 Xe). HP 129 Xe was produced with the spin-exchange optical pumping technique using a commercial polarizer system (verImagin Healthcare, Wuhan, China), with a freeze-out accumulation procedure in a cold finger. A gas mixture of 2% enriched xenon (86% 129 Xe isotope), 88% 4 He, and 10% N2 was used in this study (36). After the xenon accumulation process, HP gas was thawed using hot water and extracted into a 1-liter Tedlar bag, which was purged to approximately 9 Pa with a vacuum pump. The available spin polarization of 129 Xe gas in the Tedlar bag was approximately 25%. Before the magnetic resonance (MR) experiments, the subject inhaled 1 liter of gas mixture (5% xenon + 95% N2) from the functional residual capacity (FRC) to calibrate the flip angle. Afterward, the subject inhaled 1 liter of gas mixture (40% xenon + 60% N2) from the FRC for measuring pulmonary ventilation function, gas exchange function, and microstructure parameters, respectively. For each patient, a total of four bags of xenon gas were used. The patients were kept in the MRI scanner for less than 15 min for each xenon MRI scan, the duration was less than 15 s.

Pulmonary ventilation function was assessed using HP 129 Xe gas MRI. The MRI scans were performed on each subject using a three-dimensional balanced steady-state free precession sequence with FOV = (38 cm) 2 , matrix = 96 × 84, slice number = 20, slice thickness = 9 mm, bandwidth = 800 Hz per pixel, flip angle = 12° to 14°, and repetition time/echo time = 5.6/2.65 ms. Proton images of the thoracic cavity for matching were also acquired using the 1 H body coil after the 129 Xe MRI scan during the same breath-hold. Proton MRI scans were acquired using a fast-spoiled gradient-echo sequence with FOV = (38 cm) 2 , matrix = 96 × 48 (partial echo = 82%), number of slices = 20, slice thickness = 9 mm, bandwidth = 800 Hz per pixel, flip angle = 20°, and repetition time/echo time = 4.5/2.2 ms. All 129 Xe gas and proton images were reconstructed to a 96 × 96 matrix for purposes of calculating the ventilation defects. In this study, we did not perform a retrospective bias field correction, which has been used by other groups for correcting B1 inhomogeneity (3335), because these corrections often inadvertently remove intensity nonuniformity caused by physiological changes. The technique of HP 129 Xe chemical shift saturation recovery (CSSR) was used to obtain the gas-blood exchange functional parameters of the lung by the model of xenon exchange (MOXE) using a dissolved-phase 129 Xe diffusion coefficient of 3.3 × 10 −6 cm 2 s −1 (16). For the CSSR data collection, 21 exchange time points ranging from 10 to 700 ms were used, and the spectra were acquired using a 90° RF pulse with a bandwidth of 50 Hz per points and 1024 sampling points. The bottom part of Fig. 4 shows the physiological parameters, including T, d, and blood hematocrit (Hct). The ratio of xenon signal from RBCs and xenon signal from interstitial TP at an exchange time of 100 ms was calculated (RBC/TP) (17, 25). HP 129 Xe DW-MRI images were used to derive the pulmonary microstructure parameters. DW-MRI scans were acquired for four b values (0, 10, 20, and 30 s/cm 2 ) using interleaved sampling and acquisition parameters: FOV = (38 cm) 2 , matrix = 64 × 32, slice number = 4, slice thickness = 30 mm, bandwidth = 600 Hz per pixel, flip angle = 8° to 11°, and repetition time/echo time = 15.5/12.5 ms. As shown in the top part of Fig. 4, the pulmonary morphometric parameters, including R, Lm, and SVR, were extracted by fitting the DW-MRI data to the anisotropic diffusion model (37) of the 129 Xe diffusion pixel by pixel using a nonlinear least squares algorithm after reconstructing the images to 64 × 64 matrix (18). PFTs were performed on the same day as the MRI scans using a handheld spirometer (sp-1, Schiller AG, Switzerland). MRI-derived microstructural parameters R, Lm, SVR, and ADC were computed as maps (i.e., on a pixel-by-pixel basis) however, the values reported in this article are volume averaged over the patient’s lungs, and the error bars cited are SDs over the same region.

The top schematic shows the two generations of lung respiratory airways of the Weibel lung model: The main morphometric parameters include external radius (R), internal radius (r), and depth of alveolar sleeve (h). The bottom illustration shows the diagram of the gas-blood exchange region of the alveoli. The total septal thickness is assumed to be d. T is the xenon gas exchange time constant in the lung. Hct is the hematocrit of the lung.



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