The goal of this system is to keep the pH of the blood stream within normal neutral ranges, around 7. A chemoreceptor, also known as chemosensor, is a sensory receptor that transduces a chemical signal into an action potential. The action potential is sent along nerve pathways to parts of the brain, which are the integrating centers for this type of feedback.
There are many types of chemoreceptors in the body, but only a few of them are involved in respiration. The respiratory chemoreceptors work by sensing the pH of their environment through the concentration of hydrogen ions.
Because most carbon dioxide is converted to carbonic acid and bicarbonate in the bloodstream, chemoreceptors are able to use blood pH as a way to measure the carbon dioxide levels of the bloodstream. Negative feedback responses have three main components: the sensor, the integrating sensor, and the effector.
For the respiratory rate, the chemoreceptors are the sensors for blood pH, the medulla and pons form the integrating center, and the respiratory muscles are the effector. Consider a case in which a person is hyperventilating from an anxiety attack. Their increased ventilation rate will remove too much carbon dioxide from their body.
Without that carbon dioxide, there will be less carbonic acid in blood, so the concentration of hydrogen ions decreases and the pH of the blood rises, causing alkalosis. In response, the chemoreceptors detect this change, and send a signal to the medulla, which signals the respiratory muscles to decrease the ventilation rate so carbon dioxide levels and pH can return to normal levels.
There are several other examples in which chemoreceptor feedback applies. A person with severe diarrhea loses a lot of bicarbonate in the intestinal tract, which decreases bicarbonate levels in the plasma. As bicarbonate levels decrease while hydrogen ion concentrations stays the same, blood pH will decrease as bicarbonate is a buffer and become more acidic.
In cases of acidosis, feedback will increase ventilation to remove more carbon dioxide to reduce the hydrogen ion concentration. Conversely, vomiting removes hydrogen ions from the body as the stomach contents are acidic , which will cause decreased ventilation to correct alkalosis.
Chemoreceptor feedback also adjusts for oxygen levels to prevent hypoxia, though only the peripheral chemoreceptors sense oxygen levels. In cases where oxygen intake is too low, feedback increases ventilation to increase oxygen intake. A more detailed example would be that if a person breathes through a long tube such as a snorkeling mask and has increased amounts of dead space, feedback will increase ventilation.
Respiratory feedback : The chemoreceptors are the sensors for blood pH, the medulla and pons form the integrating center, and the respiratory muscles are the effector. Evaluate the effect of proprioception the sense of the relative position of the body and effort being employed in movement on breathing. The lungs are a highly elastic organ capable of expanding to a much larger volume during inflation. While the volume of the lungs is proportional to the pressure of the pleural cavity as it expands and contracts during breathing, there is a risk of over-inflation of the lungs if inspiration becomes too deep for too long.
Physiological mechanisms exist to prevent over-inflation of the lungs. Cardiac and respiratory branches of the vagus nerve : The vagus nerve is the neural pathway for stretch receptor regulation of breathing. The Hering—Breuer reflex also called the inflation reflex is triggered to prevent over-inflation of the lungs.
There are many stretch receptors in the lungs, particularly within the pleura and the smooth muscles of the bronchi and bronchioles, that activate when the lungs have inflated to their ideal maximum point.
These stretch receptors are mechanoreceptors, which are a type of sensory receptor that specifically detects mechanical pressure, distortion, and stretch, and are found in many parts of the human body, especially the lungs, stomach, and skin. They do not detect fine-touch information like most sensory receptors in the human body, but they do create a feeling of tension or fullness when activated, especially in the lungs or stomach.
When the lungs are inflated to their maximum volume during inspiration, the pulmonary stretch receptors send an action potential signal to the medulla and pons in the brain through the vagus nerve.
This is called the inflation reflex. As inspiration stops, expiration begins and the lung begins to deflate. As the lungs deflate the stretch receptors are deactivated and compression receptors called proprioreceptors may be activated so the inhibitory signals stop and inhalation can begin again—this is called the deflation reflex.
Early physiologists believed this reflex played a major role in establishing the rate and depth of breathing in humans.
While this may be true for most animals, it is not the case for most adult humans at rest. However, the reflex may determine the breathing rate and depth in newborns and in adult humans when tidal volume is more than 1 L, such as when exercising.
Additionally, people with emphysema have an impaired Hering—Bauer reflex due to a loss of pulmonary stretch receptors from the destruction of lung tissue, so their lungs can over-inflate as well as collapse, which contributes to shortness of breath. As the Hering—Bauer reflex uses the vagus nerve as its neural pathway, it also has a few cardiovascular system effects because the vagus nerve also innervates the heart. During stretch receptor activation, the inhibitory signal that travels through the vagus nerve is also sent to the sinus-atrial node of the heart.
Its stimulation causes a short-term increase in resting heart rate, which is called tachycardia. The heart rate returns to normal during expiration when the stretch receptors are deactivated. When this process is cyclical it is called a sinus arrhythmia, which is a generally normal physiological phenomenon in which there is short-term tachycardia during inspiration. Sinus arryhthmias do not occur in everyone, and are more common in youth.
The sensitivity of the sinus-atrial node to the inflation reflex is lost over time, so sinus arryhthmias are less common in older people. 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 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 4. Figure 4. These two graphs show a respiratory volumes and b the combination of volumes that results in respiratory capacity. Tidal volume TV is the amount of air that normally enters the lungs during quiet breathing, which is about milliliters.
Expiratory reserve volume ERV is the amount of air you can forcefully exhale past a normal tidal expiration, up to 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 capacity is the combination of two or more selected volumes, which further describes the amount of air in the lungs during a given time.
TLC is about mL air for men, and about 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 and 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.
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.
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 By adolescence, the normal respiratory rate is similar to that of adults, 12 to 18 breaths per minute.
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 2.
The result is typically a rhythmic, consistent ventilation rate that provides the body with sufficient amounts of oxygen, while adequately removing carbon dioxide.
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 5. 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.
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, positive-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.
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. 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. This would not be a problem if people sat quietly every day but respiratory rates alter with activities such as running, climbing and singing, laughing or crying.
In order to help us to tailor our breathing to meet the needs of everyday life, a number of physiological mechanisms influence this basic breathing pattern.
Centres in the pons close to the medulla in the brain stem influence the respiratory neurones in the medulla Fig 1. It achieves this by sending constant inhibitory impulses to the inspiratory centre in the medulla to limit the period of inspiration. The lungs contain stretch receptors or baroreceptors which also appear to influence respiration.
When the lungs expand during inspiration, stretch receptors in the lung walls are activated and act via the vagus nerve to inhibit the inspiratory centre in the medulla oblongata and allow reflex expiration to occur Bourke, These receptors are particularly important in animals and in young babies who have a poorly organised brainstem Stocks, but their role in adults remains uncertain, especially during quiet respiration.
Marieb suggests that this mechanism is probably protective rather than regulatory. Other receptors in the lungs are sensitive to irritants such as gases, debris, inhaled foreign bodies and excess mucus. When they are activated, these receptors influence the respiratory centre via the vagus nerve so that coughing can occur to clear the irritant.
The higher centres of the brain are the areas where we understand and manipulate information and experience thoughts, feelings and emotions.
These centres can also influence respiration. Respiratory rate and depth alter when the centres of the limbic system involved with emotions such as pain, anger or excitement are activated, though this effect is involuntary and outside our control.
Centres in the hypothalamus are activated and influence both the rate and the depth of respiration via the pons Martini and Bartholomew, and the medullary inspiration centre. Respiration can be increased or decreased via this pathway.
Examples of this mechanism in action include gasping with fear or cold, a rise in respiratory rate when the body temperature is high, and breath-holding during times of anger.
From the cerebral cortex we can also voluntarily change our respiratory pattern by sending signals direct to the muscles of inspiration and bypassing the medullary centres Marieb, The cortex is the area of the brain where we interpret and manipulate information and when we need, for example, to swim a length under water, sing or simply chat to friends, we can consciously control our breathing pattern.
Many of us, in our younger days, tried to hold our breath until we collapsed, but it is impossible to alter our breathing beyond certain limits because the other respiratory control mechanisms ultimately override the influence of the higher centres.
Perhaps the most important influence on respiratory rate and depth are chemicals. Specialised receptors chemoreceptors respond to chemical changes in the blood and cerebrospinal fluid CSF. Peripheral chemoreceptors in the aortic arch and the carotid bodies respond to changes in the oxygen O2 , carbon dioxide CO2 and acidity pH levels in arterial blood.
It is these chemoreceptors that are ultimately responsible for the homeostasis of O2 and CO2 levels in the blood. They ensure that there is adequate oxygen circulating for the needs of cells throughout the body and that the waste products of cellular metabolism, carried as CO2, can be deposited in the lungs.
Arterial pressures of O2 and, especially, CO2 are maintained within narrow limits despite large changes in consumption and production. Normally it is a small rise in arterial CO2 that triggers these chemoreceptors and results in a negative feedback homoeostatic response to reduce these levels. As a result, the CSF rapidly becomes more acidic and its pH falls.
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