20.4: Respiratory Zone

By the end of this section, you will be able to:

• Name the structures of the respiratory zone and give the structure of each
• Explain how the structure of the respiratory membrane maximizes gas exchange
• Describe how the muscular system, nervous system, and respiratory system interact in ventilation

Respiratory Zone

In contrast to the conducting zone, the respiratory zone includes structures that are directly involved in gas exchange. The respiratory zone begins where a terminal bronchiole becomes respiratory bronchioles, the smallest type of bronchiole (Figure \(\PageIndex{1}\)). These respiratory bronchioles branch into alveolar ducts which terminate in alveolar sacs, the site of gas exchange. The structure of respiratory bronchioles is very similar to that of terminal bronchioles; however, the lumen of respiratory bronchioles is lined with cuboidal epithelial tissue instead of while terminal bronchioles have columnar epithelial cells. 

Figure \(\PageIndex{1}\): Respiratory Zone. Each respiratory bronchiole branches to a few alveolar ducts that connect to alveoli in the respiratory zone.  (Image credit: "Respiratory Zone Structures" by Jennifer Lange is licensed under CC BY-NC-SA 4.0, modification of The Respiratory Zone by OpenStax.  "Respiratory Zone Histology" by Jennifer Lange is licensed under CC BY-NC-SA 4.0, slide provided by the Regents of the University of Michigan Medical School © 2022 under CC BY-NC-SA 3.0.)

Alveolar Ducts and Alveoli

Respiratory bronchioles divide distally to form alveolar ducts. An alveolar duct does not have its own walls, but are channels created by the walls of the alveoli that line it.  Each alveolar duct opens into a cluster of alveoli. An alveolar duct and all of the alveoli connected to it form a cluster called an alveolar sac. There are an average of 480 million alveoli in the lungs, yielding an incredibly large surface area for gas exchange.  Alveoli are connected to their neighbors by alveolar pores, which help maintain equal air pressure throughout the alveoli and lung.

Each alveolar sac is surrounded by a capillary bed with a network of capillaries that distribute several capillaries to route along the outside of each alveolus in the alveolar sac (Figure \(\PageIndex{2}\)). Deoxygenated blood is delivered to the capillary bed via an arteriole branching from the pulmonary artery and oxygenated blood is collected by a venule that drains to the pulmonary vein. An alveolus is approximately 200 μm in diameter with elastic walls that allow the alveolus to stretch during air intake like a balloon inflating, which greatly increases the surface area available for gas exchange, and then return to a smaller size to assist with expiration.

Figure \(\PageIndex{2}\): Respiratory Membrane. The alveolus is responsible for gas exchange with the blood in capillaries.  Their areas of closest contact are is called the respiratory membrane, which is made of two layers of simple squamous epithelium with a shared basement membrane.  (Image credit: "Respiratory Membrane" by Jennifer Lange is licensed under CC BY-NC-SA 4.0, modification of The Respiratory Zone by OpenStax; includes Red blood cells by Jessica Polka.) 

The simple squamous epithelium of the alveolar wall consists of three major cell types: type I alveolar cells, type II alveolar cells, and alveolar macrophages (see Figure \(\PageIndex{2}\)). Type I alveolar cells (aka type I pneumocytes or squamous alveolar cells) are squamous epithelial cells of the alveoli, which constitute up to 97 percent of the alveolar surface area. These cells are about 25 nm (there are a thousand nanometers in a millimeter!) thick and are highly permeable to gases. Type II alveolar cells (aka type II pneumocytes or great alveolar cells) are interspersed among the type I cells and secrete pulmonary surfactant, a substance  that reduces the surface tension of the alveoli. Type II alveolar cells also play an important role in initiating repair of an alveolus is damaged. Roaming around the alveolar wall is the alveolar macrophage, a phagocytic cell of the immune system that removes debris and pathogens that have reached the alveoli.

The simple squamous epithelium formed by type I alveolar cells is attached to a thin, elastic basement membrane. Attaching to the opposite side of the same basement membrane is the endothelium of the capillaries, which is also simple squamous epithelium. Taken together, the alveoli and capillary walls form a respiratory membrane that is approximately 0.5 micrometers thick. The respiratory membrane allows gases to cross by simple diffusion, allowing oxygen to be picked up by the blood for transport and CO₂ to be released into the air of the alveoli to be excreted during the exhale.

Pulmonary Ventilation

Pulmonary ventilation is the act of breathing, which can be described as the movement of air into and out of the lungs. When you take a deep breath, notice the expansion of your rib cage. Contraction of the diaphragm and external intercostal muscles increases the volume in the chest cavity, which in turn lowers the pressure and draws air into the lungs for inspiration. The process for expiration (or exhalation) is similar. Elastic recoil plus an increase in inter pleural pressure cause the lungs to become smaller. This increases the pressure within the thoracic cavity and are leaves the lungs. (Figure \(\PageIndex{3}\)). During exercise, additional muscles aid with inspiration. The process for expiration. Forced inspiratory muscles such as the sternocleidomastoid and the pectoralis minor help to raise the ribs even more; this causes a greater area within the thoracic and the resulting lower pressure draws even more air in. Conversely, the internal intercostals can pull the ribs further in than their "resting" position forcing air out. Therefore, the internal intercostal would be considered a forced expiratory muscle. 

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, partly due to lung elasticity, during expiration causes compression of the lungs. While typical expiration is a passive process caused by relaxation of muscles and elasticity of tissues, a forced or maximal expiration can involve contraction of the internal intercostals and other muscles that compress the rib cage.

Figure \(\PageIndex{3}\): Inspiration and Expiration. During inspiration, the diaphragm and external intercostal muscles contract, expanding the volume in the thoracic cavity, creating a pressure gradient with lower air pressure in the lungs that draws air in. During expiration, the diaphragm and external intercostal muscles relax, reducing the volume in the thoracic cavity and reversing the pressure gradient with higher air pressure in the lungs that forces air out. (Image credit: "Inspiration and Expiration" by OpenStax is licensed under CC BY 3.0)

DISORDERS OF THE...

Respiratory System: Chronic Obstructive Pulmonary Disorder (COPD)

Chronic Obstructive Pulmonary Disorder (COPD) is used to describe a number of closely related respiratory conditions including chronic bronchitis and emphysema. COPD is often associated with heavy smokers, although it can affect individuals that never smoked. In chronic bronchitis, the walls of the bronchioles are chronically inflamed, reducing the volume of the lumen and marked by an over-production of mucus that can obstruct the movement of air during ventilation. In emphysema, the alveolar walls lose their elasticity and are destroyed, often by a build-up of damage and debris being cleaned up by alveolar macrophages (Figure \(\PageIndex{4}\)). The damage leads to fibrosis in which normal tissue is replaced by scar tissue, further reducing the elasticity of the alveolar walls and perpetuating the progression fo the disease.

Patients with COPD can have shortness of breath and can have difficulty in particular with expiration, which affects the efficiency of ventilation. Coupled with alveolar damage, the result is reduced oxygen levels in the blood, which can affect the function of many systems of the body. Bronchodilators and anti-inflammatory medications are typically used to treat COPD. Eventually, in those with severe COPD, even treatment with supplemental oxygen will not be sufficient to prevent respiratory failure.

Figure \(\PageIndex{4}\): Chronic Obstructive Pulmonary Disorder. Lungs with COPD contain fewer alveoli after the walls between adjacent alveoli are destroyed, forming fewer, larger alveoli and reducing the surface area for gas exchange. Bronchioles lose their shape and are clogged with excessive mucus. (Image credit: "COPD_2010Side" by National Heart Lung and Blood Institute is in the Public Domain)

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 (Figure \(\PageIndex{4}\)) in the brain, which responds primarily to input received from central and peripheral chemoreceptors that sense carbon dioxide and blood pH.  While blood oxygen levels are not the primary drive of respiratory rate, the respiratory center will receive input if they get dangerously low. The respiratory control centers of the medulla oblongata are further influenced by a rate control center in the pons. 

Figure \(\PageIndex{5}\): Inspiration and Expiration. During inspiration, the diaphragm and external intercostal muscles contract, expanding the volume in the thoracic cavity, creating a pressure gradient with lower air pressure in the lungs that draws air in. During expiration, the diaphragm and external intercostal muscles relax, reducing the volume in the thoracic cavity and reversing the pressure gradient with higher air pressure in the lungs that forces air out. (Image credit: "Midsagittal Brain" by Justin Greene is licensed under CC BY-NC-SA 4.0.)

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.

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 (Figure \(\PageIndex{6}\)). 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.

Figure \(\PageIndex{6}\): Chronic Obstructive Pulmonary Disorder. Lungs with COPD contain fewer alveoli after the walls between adjacent alveoli are destroyed, forming fewer, larger alveoli and reducing the surface area for gas exchange. Bronchioles lose their shape and are clogged with excessive mucus. (Image credit: "COPD_2010Side" by National Heart Lung and Blood Institute is in the Public Domain.)

Concept Review

Pulmonary ventilation is the process of breathing, which is driven by pressure differences between the lungs and the atmosphere. Pulmonary ventilation consists of the process of inspiration (or inhalation), where air enters the lungs, and expiration (or exhalation), where air leaves the lungs. During inspiration, the diaphragm and external intercostal muscles contract, causing the rib cage to expand and move outward, and expanding the thoracic cavity and lung volume. This creates a lower pressure within the lung than that of the atmosphere, causing air to be drawn into the lungs. During expiration, the diaphragm and intercostals relax, causing the thorax and lungs to recoil. The air pressure within the lungs increases to above the pressure of the atmosphere, causing air to be forced out of the lungs. However, during forced exhalation, the internal intercostals and abdominal muscles may be involved in forcing air out of the lungs.

Both respiratory rate and depth are controlled by the respiratory centers of the brain, which are stimulated by factors such as chemical and pH changes in the blood. A rise in carbon dioxide or a decline in oxygen levels in the blood stimulates an increase in respiratory rate and depth.

External respiration is the process of gas exchange that occurs between the alveoli and the bloodstream. Transport of gases describes the movement of oxygen and carbon dioxide through the bloodstream from where each gas originates to its destination in the body. Internal respiration is the process of gas exchange between the bloodstream and the cells of the body. Cellular respiration is the metabolic process of consuming oxygen to convert glucose into ATP energy.

Review Questions

Query \(\PageIndex{1}\)

 

Critical Thinking Questions

Query \(\PageIndex{2}\)

 

Glossary

Query \(\PageIndex{3}\)

Contributors and Attributions

 

 

OpenStax Anatomy & Physiology (CC BY 4.0). Access for free at https://openstax.org/books/anatomy-and-physiology