Resting exhalation involves which of the following muscles

This produces a partial vacuum, which sucks air into the lungs by bulk flow. Air continues to move into the lungs until the intrapulmonary pressure is the same as atmospheric pressure. During forced inspiration, the accessory muscles in the neck may also be used to elevate the sternum and first two ribs Fig 1. This, combined with the maximal contraction of the inspiratory muscles, leads to the generation of a much more negative intrapleural pressure for example, cmH2O and more rapid airflow McGeown, Normally about ml 1 pint of air is moved in and out per breath - this is known as the tidal volume.

In healthy people quiet expiration or exhalation is passive and relies on elastic recoil of the stretched lungs as the inspiratory muscles relax, rather than on muscle contraction. The diaphragm and external intercostal muscles return to their resting position and the volume of the chest cavity and of the lungs decreases. Thus, air is driven out of the lungs by bulk flow, until the atmospheric pressure and pressure within the alveoli are equal.

Normally, expiration is effortless but if the respiratory passageways are narrowed by spasm of the bronchioles for example, in asthma or clogged with mucus or fluid for example, in chronic bronchitis or pneumonia , expiration becomes an active process Law and Watson, In forced expiration, when it is necessary to empty the lungs of more air than normal, the abdominal muscles contract and force the diaphragm upwards and contraction of the internal intercostal muscles actively pulls the ribs downwards.

This generates higher air pressures within the lungs and forces the air out more rapidly. Although breathing is simple mechanically, its control is complex. The respiratory control centre is situated in the medulla oblongata of the brain.

This sets the rhythm of breathing and contains neurons that are self-excitatory rather like the cells in the sino-atrial node in the heart and which fire off in a cycle. This maintains the normal respiratory rate of breaths a minute. When the inspiratory neurons in the medulla fire, they excite the muscles of inspiration - the phrenic nerve to the diaphragm and the intercostal nerves to the intercostal muscles - causing them to shorten and enlarge the volume of the chest cavity.

When the medullary neurons stop firing, the muscles recoil and the chest cavity returns to its resting size. During exercise we need to deliver more oxygen than normal to the tissues. The partial pressure, and thus concentration of carbon dioxide, is greater in the in the capillaries of the alveoli compared to the alveolar air, so carbon dioxide will passively diffuse from the bloodstream into the alveoli during gas exchange.

Additionally, because PaCO 2 is an indicator of the concentration of carbon dioxide in arterial blood, it can be used to measure blood pH and identify cases of respiratory acidosis and alkalkosis.

Inhalation is the flow of air into an organism that is due to a pressure difference between the atmosphere and alveolus. Inspiration refers to inhalation—it is the flow of the respiratory current into an organism.

In humans it is the movement of ambient air through the airways and into the alveoli of the lungs. Inspiration begins with the contraction of the diaphragm, which results in expansion of the thoracic cavity and the pleural cavity.

The pleural cavity normally has a lower pressure compared to ambient air —3 mmHg normally and typically —6 mmHg during inspiration , so when it expands, the pressure inside the lungs drops. Pressure and volume are inversely related to each other, so the drop in pressure inside the lung increases the volume of air inside the lung by drawing outside air into the lung. As the volume of air inside the lung increases, the lung pushes back against the expanded pleural cavity as a result of the drop in intrapleural pressure pressure inside the pleural cavity.

The force of the intrapleural pressure is even enough to hold the lungs open during inpiration despite the natural elastic recoil of the lung. The alveolar sacs also expand as a result of being filled with air during inspiration, which contributes to the expansion inside the lung. Eventually, the pressure inside the lung becomes less negative as the volume inside the lung increases and, when pressure and volume stabilize, air movement stops, inspiration ends, and expiration exhalation will begin.

Deeper breaths have higher tidal volumes and require a greater drop in intrapleural pressure compared to shallower breaths. Respiratory System: Resistance in any part of the respiratory tract can cause problems. The diaphragm is the primary muscle involved in breathing, however several other muscles play a role in certain circumstances.

These muscles are referred to as accessory muscles of inhalation. The accessory muscles assist breathing by expanding the thoracic cavity in a similar way to the diaphragm. However, they expand a much smaller part of the thoracic cavity compared to diaphragm. Therefore they should not be used as the primary mechanism of inhalation, because they take in much less air compared to the diaphragm resulting in a much lower tidal volume.

For example, singers need a lot of air to support the powerful voice production needed for singing. A common problem in novice singers is breathing with the accessory muscles of the neck, shoulder, and ribs instead of the diaphragm, which gives them a much smaller air supply than what is needed to sing properly. Expiration, also called exhalation, is the flow of the respiratory current out of the organism.

The purpose of exhalation is to remove metabolic waste, primarily carbon dioxide from the body from gas exchange.

The pathway for exhalation is the movement of air out of the conducting zone, to the external environment during breathing.

Respiratory System: As the diaphragm relaxes, the pleural cavity contracts, which exerts pressure on the lungs, which reduces the volume of the lungs as air is passively pushed out of the lungs. Expiration is typically a passive process that happens from the relaxation of the diaphragm muscle that contracted during inspiration. The primary reason that expiration is passive is due to the elastic recoil of the lungs.

The elasticity of the lungs is due to molecules called elastins in the extracellular matrix of lung tissues and is maintained by surfactant, a chemical that prevents the elasticity of the lungs from becoming too great by reducing surface tension from water.

Without surfactant the lungs would collapse at the end of expiration, making it much more difficult to inhale again. Because the lung is elastic, it will automatically return to its smaller size as air leaves the lung.

Exhalation begins when inhalation ends. An increase in pressure leads to a decrease in volume inside the lung, and air is pushed out into the airways as the lung returns to its smaller size.

While expiration is generally a passive process, it can also be an active and forced process. There are two groups of muscles that are involved in forced exhalation.

This happens due to elastic properties of the lungs, as well as the internal intercostal muscles that lower the rib cage and decrease thoracic volume. As the thoracic diaphragm relaxes during exhalation it causes the tissue it has depressed to rise superiorly and put pressure on the lungs to expel the air. Expiration can be either voluntary or involuntary in order to serve different purposes for the body. These two types of expiration are controlled by different centers within the body.

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.

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.