BSN 1-1
ANATOMY AND PHYSIOLOGY
CHAPTER 15: RESPIRATORY SYSTEM ( REVIEWER )
ANATOMY OF THE RESPIRATORY SYSTEM
The respiratory system consists of the structures used to acquire oxygen (O2) and remove carbon dioxide
(CO2) from the blood. Oxygen is required for the body’s cells to synthesize the chemical energy molecule, ATP. Carbon
dioxide is a by-product of ATP production and must be removed from the blood. Otherwise, increased levels of CO2 will
lower the pH of the blood. The blood pH must be maintained within relatively narrow limits to maintain homeostasis.
Structures that compose the respiratory system:
1. External Nose - encloses the chamber for air inspiration. Although air can be inspired through the mouth, the
mouth is part of the digestive system rather than the respiratory system.
2. Nasal Cavity - a cleaning, warming, and humidifying chamber for inspired air.
3. Pharynx - commonly called the throat, serves as a shared passageway for food and air.
4. Larynx - frequently called the voice box, has a rigid structure that helps keep the airway constantly open (patent).
5. Trachea - commonly known as the windpipe, serves as an air-cleaning tube to funnel inspired air to each lung.
6. Bronchi - tubes that direct air into the lungs.
7. Lungs - each lung is a labyrinth of air tubes and a complex network of air sacs, called alveoli, and capillaries. The
air sacs are separated by walls of connective tissue containing both collagenous and elastic fibers. Each air sac is
the site of gas exchange between the air and the blood.
FUNCTIONS OF THE RESPIRATORY SYSTEM
Respiration includes the following processes:
1. ventilation, or breathing – movement of air into and out of the lungs
2. the exchange of oxygen and carbon dioxide between the air in the lungs and blood
3. transport of oxygen and carbon dioxide in the blood
4. the exchange of oxygen and carbon dioxide between the blood and the tissues
Other functions of the respiratory system:
1. Regulation of blood PH - the respiratory system can alter blood pH by changing blood carbon dioxide levels
2. Voice production - air movement past the vocal cords makes sound and speech possible
3. Olfaction - the sensation of smell occurs when airborne molecules are drawn into the nasal cavity
4. Innate immunity - the respiratory system protects against some microorganisms and other pathogens, such as
viruses, by preventing them from entering the body and by removing them from respiratory surfaces
STRUCTURES AND HISTOLOGY OF THE RESPIRATORY TRACT
THE UPPER RESPIRATORY TRACT
● The upper respiratory tract includes the nasal cavity, pharynx, and larynx, which function primarily in filtering,
warming, and moistening incoming air while also facilitating voice production.
STRUCTURES OF THE UPPER RESPIRATORY TRACT
NASAL CAVITY
1. External Nose - supported by cartilage and bone; contains nostrils for air entry.
2. Nasal Septum - divides the cavity into two halves.
3. Conchae (Turbinates) - bony projections that increase surface area and create turbulence for better filtration.
4. Paranasal Sinuses - air-filled spaces within the bones of the skull that lighten the head and contribute to voice
resonance.
5. Olfactory Region - contains olfactory receptors for the sense of smell.
PHARYNX
Divided into three regions:
1. Nasopharynx - located posterior to the nasal cavity, connected to the Eustachian tubes.
2. Oropharynx - lies posterior to the oral cavity and serves as a passage for both air and food.
3. Laryngopharynx - continues as the esophagus or larynx.
LARYNX
1. Cartilages - includes the thyroid cartilage (Adam's apple), cricoid cartilage, and epiglottis (prevents food entry into
the respiratory tract).
2. Vocal Cords - produce sound through vibration as air passes through.
3. Glottis - the opening between the vocal cords.
THE LOWER RESPIRATORY TRACT
TRACHEA
● is commonly known as the windpipe.
● It allows air to flow into the lungs.
● The trachea is a membranous tube attached to the larynx and consists of dense regular connective tissue and
smooth muscle.
● The trachea is reinforced with 15–20 C- shaped pieces of hyaline cartilage called tracheal rings.
● supported by incomplete cartilaginous rings that prevent collapse and maintain an open airway.
● These rings primarily reinforce the anterior and lateral sides, while the posterior wall lacks cartilage and consists
of an elastic ligamentous membrane and smooth muscle.
● The smooth muscle can contract to narrow the trachea, increasing airflow force during coughing to expel mucus
or foreign objects.
● lined with a mucous membrane, where goblet cells produce mucus that traps dust, bacteria, and other foreign
particles.
● Chronic irritation, such as from smoking, can cause the tracheal epithelium to transform into moist stratified
squamous epithelium, which lacks cilia and goblet cells.
● This change impairs the normal function of the tracheal epithelium, hindering the clearance of foreign matter.
BRONCHI
● The trachea divides to form two smaller tubes called main bronchi, or primary bronchi, each of which extends
to a lung.
At the location where the trachea divides into the two main bronchi is a ridge of cartilage called the CARINA
● an important landmark for reading x-rays. In addition, the mucous membrane of the carina is very sensitive to
mechanical stimulation.
● If foreign matter is inspired to the level of the carina, it stimulates a powerful cough reflex.
TRACHEOBRONCHIAL TREE
● consists of the trachea and the network of air tubes in the lungs,
● The trachea splits into the left and right main bronchi, which further divide into smaller bronchi, eventually
leading to microscopic tubes and sacs.
● The right main bronchus is larger and more aligned with the trachea, making it more prone to lodging foreign
objects.
● The air passageways are supported by cartilage and smooth muscle, with ciliated epithelium that moves
mucus and trapped debris toward the larynx.
● There are four main classes of air passageways, from largest to smallest, with around 16 levels of branching.
These are the:
1. Lobar Bronchi
● These branch from the main bronchi, with cartilage plates and ciliated epithelium. The left lung has two,
and the right lung has three, each supplying a lung lobe.
2. Segmental Bronchi
● These supply bronchopulmonary segments within each lobe, with decreasing cartilage and increasing
smooth muscle.
3. Bronchioles
● Smaller than 1 mm, with less cartilage and more smooth muscle, lined with ciliated columnar epithelium.
4. Terminal Bronchioles
● The smallest bronchioles, with no cartilage but prominent smooth muscle, lined with ciliated cuboidal
epithelium.
CHANGES IN AIR PASSAGEWAY DIAMETER
● The bronchi and bronchioles are capable of changing their diameter.
● The smooth muscle layer in them can relax and contract.
BRONCHODILATION occurs when the smooth muscle relaxes, making the bronchiole diameter larger.
BRONCHOCONSTRICTION occurs when the smooth muscle contracts, making the bronchiole diameter smaller.
This works in the same way as vasoconstriction and vasodilation. The flow of air decreases when the resistance to
airflow is increased by conditions that reduce the diameter of the respiratory passageways.
However, during an asthma attack, there is severe bronchoconstriction. The bronchoconstriction decreases the
diameter of the airways, which increases resistance to airflow and greatly reduces air movement. In severe cases, air
movement can be so restricted that the patient dies.
Medications, such as albuterol, help counteract the effects of an asthma attack by promoting smooth muscle relaxation
in the walls of terminal bronchioles so that air can flow more freely.
ALVEOLI
● are small, air-filled chambers where the air and the blood come into close contact with each other.
● From the terminal bronchioles to the alveoli, there are multiple levels of branching.
All of the lower respiratory tract structures we’ve discussed have functioned only for ventilation, or within the conducting
zone.
RESPIRATION can occur only where gas exchange between inspired air and the blood is possible. The sites of external
respiration are the alveoli.
The branching of the respiratory system continues from the smallest bronchioles to the sites of gas exchange:
1. Respiratory Bronchioles
● These are the first structures with a few attached alveoli.
● As they divide, the number of alveoli increases.
2. Alveolar Ducts
● These arise from respiratory bronchioles and have many openings (alveolar "doorways") leading to
alveoli.
● The wall of the duct eventually becomes composed mostly of alveoli.
3. Alveolar Sacs
● These are chambers at the end of alveolar ducts, connected to two or more alveoli, where gas exchange
occurs.
The tissue surrounding the alveoli contains elastic fibers, enabling the alveoli to expand during inspiration and recoil
during expiration.
Both alveolar ducts and alveoli are made of simple squamous epithelium. Although the epithelium is not ciliated,
macrophages help remove debris by moving over the cell surf
ALVEOLAR STRUCTURE
The two lungs contain approximately 300 million alveoli, each with an average diameter of 250 μm and an extremely thin
wall.
The alveolar wall consists of TWO TYPES OF CELLS:
1. Squamous Epithelial Cells
● These cells make up 90% of the alveolar surface and are primarily involved in gas exchange between the
alveolar air and the blood.
2. Surfactant-Secreting Cells
● These round or cube-shaped cells produce surfactant, which reduces surface tension and helps the
alveoli expand more easily during inspiration.
THE RESPIRATORY MEMBRANE
● is formed by the alveolar walls and surrounding pulmonary capillaries and is the site of external respiration (where
O₂ enters the blood and CO₂ exits).
● To facilitate gas diffusion, the respiratory membrane is extremely thin, and thinner than tissue paper.
The components of the respiratory membrane include:
1. Alveolar Cell Layer - A thin layer of alveolar fluid and simple squamous epithelium.
2. Interstitial Space - The thin gap between the alveolar and capillary layers.
3. Capillary Endothelial Layer - A single layer of simple squamous cells.
The layers involved in the respiratory membrane include:
➢ A thin layer of alveolar fluid
➢ Alveolar epithelium (single layer of squamous cells)
➢ Basement membrane of the alveolar epithelium
➢ A thin interstitial space
➢ Basement membrane of the capillary endothelium
➢ Capillary endothelium (single layer of squamous cells)
THORACIC WALL AND MUSCLES OF RESPIRATION
THORACIC CAVITY
● the space enclosed by the thoracic wall and the diaphragm, which acts as a partition between the thoracic and
abdominal cavities.
DIAPHRAGM
● a sheet of skeletal muscle that plays a crucial role in changing the volume of the thoracic cavity during ventilation
(breathing).
Other skeletal muscles associated with the thoracic wall also contribute to this process.
The thoracic wall consists of the following components:
1. Thoracic vertebrae
2. Ribs
3. Costal cartilages
4. Sternum
5. Associated muscles
LUNGS
● The lungs are the primary organs of respiration, with the right lung having three lobes and the left lung two.
● They extend from the diaphragm to just above the clavicle.
HILUM
● the indentation on the medial side of the lungs where structures like the bronchus, blood vessels, and nerves
enter or exit.
➢ Each lung lobe is supplied by a lobar bronchus, and the lobes are further subdivided into
bronchopulmonary segments (9 in the left lung, 10 in the right).
➢ These segments are separated by connective tissue, allowing for surgical removal of diseased segments
without damaging the rest of the lung. Each segment is further divided into lobules, supplied by
bronchioles.
BLOOD SUPPLY TO THE LUNGS
● Blood that has passed through the lungs and picked up O2 is called oxygenated blood, and blood that has
passed through the tissues and released some of its O2 is called deoxygenated blood.
● There are two blood flow routes to the lungs:
1. Blood flow to the alveoli
2. Blood flow to the tissues of the bronchial tree
The major route takes deoxygenated blood to the alveoli in the lungs, where it is oxygenated.
To get to the alveoli, the deoxygenated blood flows through pulmonary arteries to pulmonary capillaries. In the
capillaries, the blood becomes oxygenated and returns to the heart through pulmonary veins.
The second route takes oxygenated blood to the tissues of the bronchi down to the respiratory bronchioles.
LYMPHATIC SUPPLY TO THE LUNGS
● The lungs have two types of lymphatic vessels: superficial and deep. The superficial lymphatic vessels are
located beneath the visceral pleura and drain lymph from the superficial lung tissue and the pleura.
● The deep lymphatic vessels follow the bronchi and drain lymph from the bronchi and surrounding connective
tissues.
● Both types of lymphatic vessels converge and exit the lung at the hilum.
● Lymphatic vessels help remove debris and foreign materials inhaled into the lungs by transporting them via
phagocytic cells.
● Over time, in individuals exposed to pollutants or smoking, particles can accumulate in the lungs, giving them a
gray or black appearance.
● While the lymphatic vessels aid in clearing harmful substances, they can also serve as pathways for cancer cells
to spread from the lungs to other parts of the body.
PLEURA
● The lungs are located within the thoracic cavity, which contains two pleural cavities, each housing one lung.
● These pleural cavities are lined by a serous membrane.
● The membrane covering the inner thoracic wall, the superior diaphragm surface, and the mediastinum is called
the PARIETAL PLEURA.
● At the hilum of each lung, the parietal pleura transitions into the VISCERAL PLEURA, which covers the surface
of the lung itself.
BEHAVIOR OF GASES
BEHAVIOR OF GASES AND VENTILATION
VENTILATION
● the movement of air into the lungs.
➢ Primary Aspects of Ventilation
➔ Actions of the Muscles of Respiration
➔ Air Pressure Gradients
MUSCLES OF RESPIRATION
● changes the volume of the thoracic cavity, which allows for air to flow into and out of the lungs.
MUSCLES OF INSPIRATION
● acts to increase the volume of the thoracic cavity
➔ Diaphragm
➔ External Intercostals
➔ Pectoralis Minor
➔ Scalene Muscles
MUSCLES OF EXPIRATION
● muscles that decrease the volume by depressing the ribs and sternum.
➔ Internal Intercostals
➔ Transverse Thoracis, with assistance from the abdominal muscles
MUSCLES OF RESPIRATION IN QUIET BREATHING COMPARED WITH LABORED BREATHING:
● Several differences can be recognized between normal, quiet breathing and labored breathing.
● During labored inspiration, more air moves into the lungs because all of the inspiratory muscles are active.
● They contract more forcefully than during quiet breathing, which causes a greater increase in thoracic volume.
● During labored expiration, more air moves out of the lungs due to the forceful contraction of the internal
intercostals and the abdominal muscles.
● This produces a more rapid and greater decrease in thoracic volume than would be produced by the passive
recoil of the thorax and lungs.
THE RELATIONSHIP BETWEEN PRESSURE GRADIENTS AND VENTILATION:
● In order to fully understand why increasing thoracic cavity volume allows inspiration to occur, it is necessary to
recognize the relationship between pressure and volume.
PRESSURE AND VOLUME:
● The relationship between pressure and volume is an inverse one.
● That is to say that as the volume of a container increases, the pressure in that container decreases.
● Thus, upon inspiration, the air pressure within the thoracic cavity decreases.
● Conversely, upon expiration, the air pressure within the thoracic cavity increases because the volume of the
thoracic cavity decreases.
PRESSURE GRADIENTS AND AIRFLOW:
● During inspiration, air flows into the lungs down its pressure gradient.
● During expiration, air flows out of the lungs down its pressure gradient.
● This pressure gradient is provided, in part, by atmospheric pressure - the combined force of all the gases that
make up the air we breathe.
MEASUREMENT OF LUNG FUNCTION
PULMONARY VOLUMES AND CAPACITIES
1. Spirometry
● process of measuring volumes of air that move into and out of the respiratory system
2. Spirometer
● device used to measure these pulmonary volumes
FOUR PULMONARY VOLUMES EXIST
1. TIDAL VOLUME
● normal volume of air inspired and expired with each breath.
● At rest, quiet breathing results in a tidal volume of approximately 500 mL
2. INSPIRATORY RESERVE VOLUME
● amount of air that can be inspired forcefully after a normal inspiration (approximately 3000 mL at rest).
3. EXPIRATORY RESERVE VOLUME
● amount of air that can be forcefully expired after a normal expiration (approximately 1100 mL at rest)
4. RESIDUAL VOLUME
● volume of air still remaining in the respiratory passages and lungs after the most forceful expiration
(approximately 1200 mL)
PULMONARY CAPACITIES
● the sum of two or more pulmonary volumes and include inspiratory capacity, functional residual capacity, vital
capacity, and total lung capacity.
1. INSPIRATORY CAPACITY
● tidal volume plus the inspiratory reserve volume. It is the amount of air a person can inspire
maximally after a normal expiration (approximately 3500 mL at rest).
2. VITAL CAPACITY
● the sum of the inspiratory reserve volume, the tidal volume, and the expiratory reserve volume. It
is the maximum volume of air a person can expel from the respiratory tract after a maximum
inspiration (approximately 4600 mL).
3. FUNCTIONAL RESIDUAL CAPACITY
● expiratory reserve volume plus the residual volume. It is the amount of air remaining in the lungs
at the end of a normal expiration (approximately 2300 mL at rest).
4. TOTAL LUNG CAPACITY
● the sum of the inspiratory and expiratory reserve volumes plus the tidal volume and the residual
volume (approximately 5800 mL).
FORCED VITAL CAPACITY
● A functional measure of lung performance
ALVEOLAR VENTILATION
● is the measure of the volume of air available for gas exchange per minute.
● Only a portion of each breath reaches the alveoli for gas exchange.
● The remaining areas where no gas exchange occurs is called the dead space.
● There are two types of dead space within the respiratory system:
1. ANATOMICAL DEAD SPACE
● includes all structures of the upper respiratory tract and the conducting zone of the lower
respiratory tract up to the terminal bronchioles. It typically holds about 1 mL of air per pound of an
individual's ideal body weight.
2. PHYSIOLOGICAL DEAD SPACE
● combines the anatomical dead space with the volume of alveoli that have reduced gas exchange.
FACTORS AFFECTING VENTILATION
GENDER, AGE, BODY SIZE, AND PHYSICAL FITNESS
● Factors such as gender, age, body size, and physical conditioning cause variations in respiratory volumes and
capacities from one individual to another. For example, the vital capacity of adult females is usually 20–25% less
than that of adult males.
● The vital capacity reaches its maximum amount in young adults and gradually decreases in the elderly. Taller
people usually have a greater vital capacity than people with a shorter stature, and slender people have a greater
vital capacity than obese individuals.
● Well-trained athletes can have a vital capacity 30–40% above that of people with a sedentary lifestyle. In patients
whose respiratory muscles are paralyzed by spinal cord injury or diseases such as poliomyelitis or muscular
dystrophy, vital capacity can be reduced to values not consistent with survival (less than 500–1000 mL).
Disease States
● In a healthy person, anatomical and physiological dead spaces are nearly the same, meaning that most alveoli
are functional. However, in patients with emphysema, alveolar walls degenerate, and small alveoli combine to
form larger alveoli. The result is not only fewer alveoli but also alveoli with an increased volume and decreased
surface area. Although the enlarged alveoli are still ventilated, their surface area is inadequate for complete gas
exchange, and the physiological dead space increases.
BEHAVIOR OF GASES AND RESPIRATION
VENTILATION
● supplies atmospheric air to the alveoli.
EXTERNAL RESPIRATION
● the next step in the process of respiration.
● the diffusion of gases between the alveoli and the blood in the pulmonary capillaries.
● gases move from the air into the blood for O2 and from the blood to air for Co2.
PARTIAL PRESSURE
● the individual pressure of each gas.
● PRESSURE
➔ used to express the amount of each gas in a mixture.
● At sea level, the pressure of all the gases in the air or atmospheric pressure, is approximately 760 mm Hg.
DETERMINING THE PARTIAL PRESSURE OF EACH GAS
● its percentage is multiplied times the total pressure.
➢ Nitrogen: (79%) PN2 = 0.79 x 760 mm Hg = 600 mm Hg
➢ Oxygen: (21%) Po2 = 0.21 x 760 mm Hg = 160 mm Hg
➢ Carbon Dioxide: (0.04%) Pco2 = 0.04 x 760 mm Hg = 0.3 mm Hg
➢ Water Vapor: (0.0%) PH20 = 0.0 x 760 mm Hg = 0.0 mm Hg
● Atmospheric Pressure of dry air at sea level is calculated using the following:
ATMOSPHERIC AIR: PN + Po2 + Pco2 + PH20 + 760.3 mm Hg
PN2 = 600 mm Hg
Po2 = 160 mm Hg
Pco2 = 0.3 mm Hg
PH20 = 0.0 mm Hg
760.3 mm Hg
● Total atmospheric pressure that is lower at higher altitudes than at sea level. An example is the atmospheric
pressure at an elevation of 14,000 ft above sea level, the elevation of Pike’s Peak in Colorado, is about 430 mm
Hg. The percentage of the air that is O2 remains at 21%. Thus, 0.21 x 430 mm Hg = 90 mm Hg
● Factors that cause differences in the composition among alveolar air, expired air, and atmospheric air:
➢ Air entering the respiratory system is humidified
➢ O2 diffuses from the alveoli into the blood, while Co2 diffuses from the blood into the alveoli
➢ The alveolar air is only partially replaced with atmospheric air during each inspiration.
DIFFUSION OF GASES INTO AND OUT OF LIQUIDS
● Gas moves from air into a liquid or liquid to air
● Gases move from a higher partial pressure to a lower partial pressure
● Equal partial pressures between air and liquid means they are in equilibrium.
PHYSIOLOGY OF THE RESPIRATORY SYSTEM
MECHANISMS OF ALVEOLAR VENTILATION
● When a person inspires, the pressure in the alveoli decreases because the alveolar volume has increased.
Conversely, when a person expires, the pressure in the alveoli increases because the alveolar volume has
decreased. It is the pressure difference between atmospheric pressure and pressure in the alveoli that results in
air movement during one respiratory cycle.
1. Alveolar pressure equals atmospheric pressure.
● At the end of expiration, before the next respiratory cycle starts, atmospheric pressure and
pressure in the alveoli are equal and no air moves into or out of the lungs.
2. Alveolar pressure is less than atmospheric pressure.
● As inspiration begins, contraction of inspiratory muscles increases thoracic volume, which
results in expansion of the lungs and an increase in alveolar volume.
● The increased alveolar volume causes a decrease in intra-alveolar pressure below atmospheric
pressure.
● Air flows into the lungs because barometric air pressure is greater than pressure in the alveoli.
3. Alveolar pressure again equals atmospheric pressure.
● At the end of inspiration, the thorax stops expanding, the alveoli stops expanding, and pressure
inside the alveoli becomes equal to barometric air pressure because of airflow into the lungs.
● No movement of air occurs after pressure in the alveoli becomes equal to atmospheric pressure,
but the volume of the lungs is larger than it was at the end of expiration.
4. Alveolar pressure is greater than atmospheric pressure.
● During expiration, the volume of the thorax decreases as the diaphragm relaxes, and the thorax
and lungs recoil.
● Because thoracic volume determines alveolar volume, the smaller thoracic volume results in a
corresponding decrease in alveolar volume.
● Thus, pressure inside the alveoli rises above atmospheric air pressure.
● Because pressure inside the alveoli is greater than atmospheric air pressure, air flows out of the
lungs.
● As expiration ends, the decrease in thoracic volume stops, and the alveoli stop changing size.
● The process repeats, beginning at step 1.
FACTORS AFFECTING ALVEOLAR VENTILATION
● While changes in pressure differences are the principal factors in driving alveolar ventilation, there are two other
factors that influence the ability of alveoli to increase and decrease in volume.
● These two factors are:
1. Lung Recoil
2. Pleural Pressure
LUNG RECOIL
● the tendency for the lungs to decrease in size after they are stretched
➔ Imagine a stretched rubber band snapping back to its original size when released.
➔ Similarly, upon expiration, the tension on the lungs is released and they return to their original, smaller
size, which compresses the alveoli.
LUNG RECOIL OCCURS FOR TWO REASONS:
1. Elastic recoil
2. Surface tension
ELASTIC RECOIL
● occurs because elastic fibers within the lungs and thoracic wall return to their original shape and size once the
tension on them is released, just like the rubber band.
● Lung recoil due to surface tension is because of hydrogen bonding within the alveoli.
● ALVEOLI
➔ lined with an aqueous alveolar fluid, which adheres to the wall of the alveoli.
● However, the water molecules in the alveolar fluid are also attracted to each other toward the center of each
alveolus.
● As hydrogen bonds form, the walls of each alveolus are pulled inward, which causes it to collapse.
● Collapse of the alveoli due to surface tension is prevented by the molecule surfactant (ser-FAK- tant; surface
acting agent).
SURFACTANT
● a mixture of lipoprotein molecules produced by the surfactant-secreting cells of the alveolar epithelium
● it forms a one-molecule-thick layer over the alveolar fluid, which reduces the surface tension in the alveoli
➢ Premature infants do not produce enough surfactant. This is what is meant by the common statement
that “their lungs are immature.”
➢ Too little surfactant production results in infant respiratory distress syndrome (IRDS). Surfactant is not
produced in adequate quantities until about the seventh month of gestation. Thereafter, the amount
produced increases as the fetus matures.
➢ Pregnant women who are likely to deliver prematurely can be given cortisol, which crosses the placenta
into the fetus and stimulates surfactant synthesis.
PLEURAL PRESSURE
● the pressure within the pleural cavity between the parietal pleura and the visceral pleura.
PLEURAL FLUID
● analogous to a thin film of water between two sheets of glass (the visceral and parietal pleurae); the glass sheets
can easily slide over each other, but it is difficult to separate them.
➢ When the thoracic wall expands during inspiration, the parietal pleura exerts an outward force on the
visceral pleura covering the lungs and the lungs expand.
➢ Pleural pressure pulls the lungs outward and is lower than pressure inside the alveoli.
➢ This aids in alveolar expansion.
If the visceral and parietal pleurae become separated, such as if the thoracic wall or lung is pierced, the lungs
collapse. Because the two pleural cavities are independent, it is possible to have only one lung collapse. The separation
of the visceral and parietal pleurae increases pleural pressure.
PNEUMOTHORAX
● increase in pleural pressure
● may be treated by inserting a chest tube that aspirates the pleural cavity and restores a negative pressure, which
can cause reexpansion of the lung
IT HAS TWO MAJOR POSSIBLE CAUSES:
1. PENETRATING TRAUMA
● include being stabbed, getting shot by a gun, and breaking a rib
2. NONPENETRATING TRAUMA
● include a blow to the chest; a medical procedure, such as insertion of a catheter to withdraw pleural fluid;
disease, such as an infection or emphysema; and severe, spastic coughing
TENSION PNEUMOTHORAX
● the pressure within the pleural cavity is always higher than barometric air pressure
➢ Any situation where a pneumothorax occurred can lead to a tension pneumothorax.
➢ If a tear in the pleural cavity forms a tissue flap that acts as a flutter valve, it will allow air to enter the
pleural cavity during inspiration but will not allow it to exit during expiration. The result is an increase in air
and, as a result, pressure within the pleural cavity, which could lead to inadequate delivery of O2 to
tissues.
➢ The insertion of a large-bore needle into the pleural cavity allows air to escape and releases the pressure.
FACTORS AFFECTING DIFFUSION THROUGH THE RESPIRATORY MEMBRANE
● In order for humans to utilize O2 in the air we breathe, O2 must be able to diffuse across the respiratory
membrane into the blood.
Three major factors influence the rate of gas diffusion through the respiratory membrane:
1. PARTIAL PRESSURE GRADIENTS:
● Gas moves from areas of higher partial pressure to areas of lower partial pressure.
● For O₂, it diffuses from the alveoli (high O₂ pressure) into the blood (low O₂ pressure).
● For CO₂, it diffuses in the opposite direction, from the blood (high CO₂ pressure) to the alveoli (low CO₂
pressure).
● A steeper partial pressure gradient increases diffusion efficiency.
2. Thickness of the Respiratory Membrane:
● The thicker the respiratory membrane, the slower the rate of gas diffusion.
● Conditions like pulmonary edema, pneumonia, or inflammation can increase the membrane thickness,
impeding gas exchange.
● Diseases that cause fluid accumulation or lung tissue damage hinder the membrane's function, reducing
O₂ and CO₂ exchange.
3. Surface Area of the Respiratory Membrane:
● A larger surface area provides more space for gas exchange.
● A healthy adult has about 70 m² of respiratory membrane surface area.
● However, diseases like emphysema, lung cancer, or surgeries removing lung tissue can decrease surface
area, limiting gas diffusion and reducing overall respiratory efficiency.
OXYGEN AND CARBON DIOXIDE TRANSPORT IN THE BLOOD
Once O2 and CO2 enter the blood, they each interact with components there that aid in their solubility and reduce
the potentially dangerous impact CO2 could have on blood pH. Both O2 and CO2 are transported by the protein,
hemoglobin; however, CO2 is also transported in other ways.
HEMOGLOBIN
● a complex protein synthesized by immature red blood cells
● remains within the cytoplasm of red blood cells and occupies about one-third of their total volume.
● consists of four subunits, each containing one iron-based heme group
1. It is the heme group to which O2 binds, so one hemoglobin can carry up to four O2 molecules.
2. An altered form of hemoglobin can be found in individuals with sickle-cell disease. Under low O2 conditions, this
type of hemoglobin molecule binds to other sickle-cell hemoglobin molecules inside red blood cells.
3. The binding together of the sickle-cell hemoglobin molecules causes the red blood cells to become sickle-shaped.
4. The sickle-shaped red blood cells become lodged inside small capillaries and block blood flow.
TRANSPORT OF O2
● Once O2 diffuses through the respiratory membrane into the blood, it is transported to all the cells
of the body.
● Approximately 98.5% of O2 is transported reversibly bound to hemoglobin within red blood cells, and the
remaining 1.5% is dissolved in the plasma.
● Cells use O2 in aerobic respiration to synthesize ATP.
TRANSPORT OF CO2
● Carbon dioxide is formed as a by-product of the breakdown of glucose when cells use O2 to
● produce ATP.
● The CO2 diffuses out of individual cells into the blood.
● The blood concentration of CO2 needs to be very tightly regulated because too much CO2 in the blood causes
the blood to become acidic.
THERE ARE THREE WAYS CO2 IS TRANSPORTED IN THE BLOOD
1. dissolved in the plasma
2. bound to hemoglobin
3. converted to bicarbonate ion (HCO3−)
TRANSPORT OF CO2 IN THE PLASMA
● About 7% of CO2 dissolves directly in the plasma as it diffuses out of the cells and into the blood.
● The remaining CO2 diffuses into the red blood cells where it either binds to hemoglobin or is converted to HCO3−.
TRANSPORT OF CO2 BY HEMOGLOBIN
● Approximately 23% of CO2 is transported bound to hemoglobin.
● Many CO2 molecules bind in a reversible fashion to the protein chains of hemoglobin molecules.
● Carbon dioxide’s ability to bind to hemoglobin is affected by the amount of O2 bound to hemoglobin.
● The smaller the amount of O2 bound to hemoglobin, the greater the amount of CO2 able to bind to it,
and vice versa.
● In tissues, as hemoglobin binds CO2, the affinity of hemoglobin for O2 is reduced.
● This is beneficial because tissues with higher levels of CO2 demand more O2 in order to continue
aerobic respiration, our cells’ most efficient means of producing ATP.
TRANSPORT OF CO2 AS BICARBONATE IONS
About 70% of blood CO2 is transported in the form of HCO3−, dissolved in either the cytoplasm of red blood cells
or the plasma of the blood. Within red blood cells, an enzyme called CARBONIC ANHYDRASE catalyzes a reversible
reaction. CARBONIC ANHYDRASE catalyzes the production of carbonic acid (H2CO3) from CO2 and H2O. The H2CO3
then dissociates into H+
As CO2 levels increase, more H+ is produced. Recall from chapter 2 that higher concentrations of H+ cause the
pH to decrease and the solution becomes acidic. However, because this is a reversible reaction, if CO2 levels decrease,
carbonic anhydrase creates H2CO3 upon the combining of H+ and HCO3−. The H2CO3 then dissociates to form CO2
and H2O, which lowers H+ concentration and pH increases into a more basic (alkaline) range.
At the tissues, where CO2 levels are higher, HCO3− is removed from the red blood cell by an HCO3−/Cl−
antiporter. In the tissues, HCO3− diffuses out of the red blood cell while Cl− diffuses in through the antiporter. This
exchange maintains electrical neutrality in the red blood cells and plasma.
PHYSIOLOGICAL FACTORS AFFECTING GAS TRANSPORT
● Respiratory system maintains blood O2 and CO2 concentrations and blood pH within normal values.
● Changes in these levels out of their normal range have a noticeable influence on the relationship between
hemoglobin, O2, and CO2.
● CHEMORECEPTORS
➔ specialized neurons that detect changes in the concentration of specific chemicals. These involved in
regulating respiration respond to changes in pH, changes in Po2, Pco2, or all three.
EFFECT OF PO2 ON O2 TRANSPORT
● Hemoglobin binds oxygen (O₂) at specific heme group sites, similar to a ligand-receptor interaction.
● Each hemoglobin molecule can bind up to four O₂ molecules, achieving 100% saturation when fully loaded.
● When an average of two O₂ molecules are bound per hemoglobin molecule, it is 50% saturated.
EFFECT OF PO2 ON CO2 TRANSPORT
● At low Po₂ levels, hemoglobin binds more CO₂, reducing its affinity for O₂.
● This effect facilitates CO₂ transport and promotes O₂ release where it is needed most.
EFFECT OF PH AND PCO2 ON O2 TRANSPORT
● Blood pH and Pco₂ significantly affect hemoglobin saturation.
● A decrease in pH (from higher H⁺ levels) lowers hemoglobin's affinity for O₂ by altering its shape.
● Conversely, an increase in pH enhances O₂ binding.
● Elevated Pco₂ further reduces hemoglobin's O₂ affinity by lowering pH and directly binding to hemoglobin.
● These changes help tissues with high O₂ demand receive more oxygen.
EFFECT OF PH AND PCO2 ON CO2 TRANSPORT
● The main effect of pH and Pco₂ is on hemoglobin's ability to bind O₂.
● Higher Pco₂ lowers pH, which can stimulate an increase in respiratory rate to help regulate blood pH.
● This CO₂ sensitivity is essential for maintaining acid-base balance.
● In a breath-holding experiment, hyperventilating beforehand reduces CO₂ levels in the blood.
● This delays the buildup of CO₂ and the urge to breathe, theoretically allowing you to hold your breath longer the
second time.
EFFECT OF TEMPERATURE ON O2 TRANSPORT
● Higher temperatures reduce hemoglobin's affinity for O₂, promoting its release to tissues.
● This ensures that metabolically active tissues, which generate more heat, receive more O₂.
● In contrast, cooler, less active tissues retain more O₂ bound to hemoglobin.
EFFECT OF TEMPERATURE ON CO2 TRANSPORT
● An increase in body temperature typically raises ATP production, resulting in more CO₂ entering the blood.
● This CO₂ is converted into H⁺ and HCO₃⁻, lowering blood pH. To compensate, the respiratory rate increases,
helping to expel excess CO₂ and restore pH balance.
EFFECT OF GLUCOSE METABOLISM ON O2 TRANSPORT
● Red blood cells metabolize glucose, producing a by-product that lowers hemoglobin's affinity for O₂, facilitating
oxygen release to tissues.
● In stored blood, this by-product diminishes over time, reducing the blood's effectiveness.
● As a result, blood stored in blood banks is typically discarded after about six weeks.
REGULATION OF VENTILATION
RESPIRATORY AREAS IN THE BRAINSTEM
The respiratory centers in the brainstem are located in the medulla oblongata and pons, and are responsible for
generating and maintaining the rhythm of breathing:
MEDULLA OBLONGATA
● The main respiratory control center in the brainstem.
● It controls the basic rhythm of breathing, and sends signals to the muscles that control respiration.
● The medulla also controls other involuntary activities, such as swallowing and heart rate.
PONS
● Located underneath the medulla, the pons controls the rate of involuntary respiration.
➔ The pons contains two main functional regions:
1. APNEUSTIC CENTER
● Sends signals for long and deep breaths.
2. PNEUMOTAXIC CENTER
● Sends signals to inhibit inspiration, allowing it to finely control the respiratory rate.
GENERATION OF RHYTHMIC VENTILATION
● The central nervous system's brainstem generates the automatic, rhythmic breathing process, also known as
VENTILATION
1. STARTING INSPIRATION
● Neurons in the medullary respiratory center spontaneously establish the basic rhythm of ventilation.
● The medullary respiratory center constantly receives stimulation from receptors that monitor blood gas levels,
blood temperature, and the movements of muscles and joints.
2. INCREASING INSPIRATION
● Once inspiration begins, more and more neurons are gradually activated.
● The result is progressively stronger stimulation of the respiratory muscles, which lasts for approximately 2
seconds.
3. STOPPING INSPIRATION
● The neurons stimulating the muscles of respiration also stimulate the neurons in the medullary respiratory center
that are responsible for stopping inspiration.
● The neurons responsible for stopping inspiration also receive input from the pontine respiratory group, stretch
receptors in the lungs, and probably other sources.
● When these inhibitory neurons are activated, they inhibit the neurons that stimulate respiratory muscles.
NEURONS
● A network of neurons in the medulla oblongata and pons generate the respiratory rhythm.
➔ These neurons are organized into three groups:
1. DORSOMEDIAL MEDULLA
● Mainly inspiratory neurons
2. VENTROLATERAL MEDULLA
● Inspiratory and expiratory neurons
3. ROSTRAL PONS
● Neurons that discharge during both inspiration and expiration
EFFECT OF PO2 ON RESPIRATORY RATE
● Oxygen levels in the blood affect ventilation when a 50% or greater decrease from normal exists.
● Decreased O2 is detected by receptors in the carotid and aortic bodies, which then stimulate the respiratory
center.
● A decrease in O2 below its normal values is called hypoxia.
● If Po2 levels in the arterial blood are markedly reduced while the pH and Pco2 are held constant, an increase in
ventilation rate occurs.
● However, within a normal range of Po2 levels, the effect of O2 on the regulation of respiration is small.
EFFECT OF PCO2 ON RESPIRATORY RATE
● Carbon dioxide is the major regulator of ventilation.
● An increase in CO2 or a decrease in pH can stimulate the chemosensitive area, causing a greater rate and depth
of ventilation.
1. HYPERCAPNIA
● A greater-than-normal amount of CO2 in the blood
2. HYPOCAPNIA
● lower than normal CO2 level. Results in periods when the breathing rate is reduced or does not
occur at all.
EFFECT OF PH ON RESPIRATORY RATE
● Central Chemoreceptors in the medulla oblongata detect changes in blood pH due to changes in Co2
● Carotid and Aortic Bodies detect changes in pH due to changes in H+ concentrations.
● Carbon dioxide easily diffuses across the blood-brain barrier and the blood-cerebrospinal fluid barrier.
● Lower pH stimulates the respiratory center, resulting in a greater rate and depth of breathing reducing Co2 levels,
and blood pH increases to normal levels.
THE HERING-BREUER REFLEX AND RESPIRATORY RATE
● HERING - BREUER REFLEX
➔ limits the depth of inspiration and prevents overinflation of the lungs
● Reflex depends on stretch receptors in the walls of the bronchi and bronchioles of the lungs.
● In infants, the Hering-Breuer reflex plays a role in regulating the basic rhythm of breathing and in
preventing overinflation of the lungs.
● In adults, reflex is important only when the tidal volume is large, such as during exercise.
CEREBRAL AND LIMBIC SYSTEM CONTROL OF RESPIRATORY RATE
● The rate and depth of breathing is controlled both voluntarily and involuntarily by the cerebral cortex. For example,
during talking or singing, air movement is controlled to produce sounds, as well as to facilitate gas exchange.
➢ During exercise, respiratory rate changes are controlled through various inputs to the respiratory center.
Initially, there is a very rapid increase that occurs too quickly to be accounted for by changes in
metabolism. For example, movement of the limbs has a strong stimulatory influence on the respiratory
center.
➢ After the initial immediate increase in respiratory rate, there is a gradual increase that levels off within 4-6
minutes.
➢ ANAEROBIC THRESHOLD
➔ The highest level of exercise that can be performed without causing a significant change in blood
pH. If the exercise intensity is high enough to exceed the anaerobic threshold, blood pH drops.
The drop in pH stimulates the carotid bodies, which increases ventilation.
➢ In fact, ventilation can increase so much that arterial Pco decreases below resting levels and arterial Po
increases above resting levels. In response to training, athletic performance increases because the
cardiovascular and respiratory systems become more efficient at delivering O, and picking up CO,
Ventilation does not limit performance in most individuals because ventilation can increase to a greater
extent than does cardiovascular function. In conditioned athletes, the respiratory rate at rest or during
submaximal exercise is slightly lower than in a non-athlete.
➢ However, athletes have higher respiratory rates at maximal exercise. Emotions acting through the limbic
system of the brain can also affect the respiratory center. For example, strong emotions can cause
hyperventilation or produce the sobs and gasps of crying.
OTHER MODIFICATIONS OF VENTILATION
● Higher brain centers control the respiratory system when touch, thermal, or pain receptors are activated (see
figure 15.18/). For example, irritants in the nasal cavity can initiate a sneeze reflex, and irritants in the lungs can
stimulate a cough reflex. An increase in body temperature can stimulate increased ventilation because
metabolism is elevated and more CO2 is produced, which then needs to be expelled from the body.
SYSTEMS PATHOLOGY
ASTHMA
● this is characterized by abnormally increased constriction of the trachea and bronchi in response to various
stimuli, which decreases ventilation efficiency.
● SYMPTOMS
➢ rapid and shallow breathing, wheezing, coughing, and shortness of breath
➢ typically reverse either spontaneously or with therapy
● there is no definitive pathological feature or diagnostic test for asthma
3 IMPORTANT CHARACTERISTICS OF ASTHMA
1. CHRONIC AIRWAY INFLAMMATION
● can block airflow through the bronchi
2. AIRWAY HYPERREACTIVITY
● the smooth muscle in the trachea and bronchi contracts greatly in response to a stimulus, thus decreasing
the airway's diameter and increasing airflow resistance.
3. AIRFLOW OBSTRUCTION
● the combination of the effects of inflammation and airway hyperreactivity
EFFECTS OF ASTHMA ON OTHER BODY ORGAN SYSTEMS
EFFECT OF ASTHMA ON EASE OF BREATHING AND AIR PASSAGES
ASTHMA
● many cases appear to be associated with a chronic inflammatory response by the immune system
● INFLAMMATION
➔ linked to airway hyperreactivity by some chemical mediators released by immune cells
● STIMULI THAT PROMPT AIRFLOW OBSTRUCTION
➔ vary from one individual to another
● ALLERGENS
➔ some asthmatics react particularly to it
➔ foreign substances that evoke an inappropriate immune system response
➔ EXAMPLES: inhaled pollen, animal dander, dust mites, and droppings and carcasses of cockroaches
➔ OTHER INHALED SUBSTANCES: chemicals in the workplace or cigarette smoke, can provoke an
asthma attack without stimulating an allergic reaction
● ASTHMA ATTACK
➔ also stimulated by ingested substances such as some medicines
● STRENUOUS EXERCISE
➔ can precipitate an asthma attack, especially in cold weather
➔ these episodes can often be avoided by using a bronchodilator prior to exercise
● ELICIT ASTHMA ATTACKS
➔ viral infections, emotional upset, stress, air pollution, and even reflux of stomach acid into the esophagus
● TREATMENT
➢ avoiding the causative stimulus
➢ taking medications
● STEROIDS AND MAST CELL
➔ stabilizing agents
➔ prevent the release of chemical mediators from mast cells
➔ can reduce airway inflammation
● BRONCHODILATORS
➔ used to increase airflow
REPRESENTATIVE DISEASES AND DISORDERS: RESPIRATORY SYSTEM