In respiratory physiology, ventilation (or ventilation rate) is the rate at which gas enters or leaves the lung. It is categorized under the following definitions:
|Minute ventilation||tidal volume * respiratory rate||the total volume of gas entering the lungs per minute.|
|Alveolar ventilation||(tidal volume – dead space) * respiratory rate||the volume of gas per unit time that reaches the alveoli, the respiratory portions of the lungs where gas exchange occurs.|
|Dead space ventilation||dead space * respiratory rate||the volume of gas per unit time that does not reach these respiratory portions, but instead remains in the airways (trachea, bronchi, etc.).|
Ventilation occurs under the control of the autonomic nervous system from parts of the brain stem, the medulla oblongata and the pons. This area of the brain forms the respiration regulatory center, a series of interconnected brain cells within the lower and middle brain stem which coordinate respiratory movements. The sections are the pneumotaxic center, the apneustic center, and the dorsal andventral respiratory groups. This section is especially sensitive during infancy, and the neurons can be destroyed if the infant is dropped and/or shaken violently. The result can be death due to “shaken baby syndrome”.
The breathing rate increases with the concentration of carbon dioxide in the blood, which is detected by peripheral chemoreceptors in the aorta and carotid artery and central chemoreceptors in the medulla. Exercise also increases respiratory rate, due to the action ofproprioceptors, the increase in body temperature, the release of epinephrine, and motor impulses originating from the brain. In addition, it can increase due to increased inflation in the lungs, which is detected by stretch receptors.
Inhalation is initiated by the diaphragm and supported by the external intercostal muscles. Normal resting respirations are 10 to 18 breaths per minute, with a time period of 2 seconds. During vigorous inhalation (at rates exceeding 35 breaths per minute), or in approaching respiratory failure, accessory muscles of respiration are recruited for support. These consist of sternocleidomastoid,platysma, and the scalene muscles of the neck. Pectoral muscles and latissimus dorsi are also accessory muscles.
Under normal conditions, the diaphragm is the primary driver of inhalation. When the diaphragm contracts, the ribcage expands and the contents of the abdomen are moved downward. This results in a larger thoracic volume and negative pressure (with respect to atmospheric pressure) inside the thorax. As the pressure in the chest falls, air moves into the conducting zone. Here, the air is filtered, warmed, and humidified as it flows to the lungs.
During forced inhalation, as when taking a deep breath, the external intercostal muscles and accessory muscles aid in further expanding the thoracic cavity. During inhalation the diaphragm contracts.
Exhalation is generally a passive process; however, active or forced exhalation is achieved by the abdominal and the internal intercostal muscles. During this process air is forced or exhaled out.
The lungs have a natural elasticity: as they recoil from the stretch of inhalation, air flows back out until the pressures in the chest and the atmosphere reach equilibrium.
During forced exhalation, as when blowing out a candle, expiratory muscles including the abdominal muscles and internal intercostal muscles, generate abdominal and thoracic pressure, which forces air out of the lungs.
The major function of the respiratory system is gas exchange between the external environment and an organism’s circulatory system. In humans and other mammals, this exchange facilitates oxygenation of the blood with a concomitant removal of carbon dioxide and other gaseous metabolic wastes from the circulation. As gas exchange occurs, the acid-base balance of the body is maintained as part of homeostasis. If proper ventilation is not maintained, two opposing conditions could occur: respiratory acidosis, a life threatening condition, and respiratory alkalosis.
Upon inhalation, gas exchange occurs at the alveoli, the tiny sacs which are the basic functional component of the lungs. The alveolar walls are extremely thin (approx. 0.2 micrometres). These walls are composed of a single layer of epithelial cells (type I and type II epithelial cells) close to the pulmonary capillaries which are composed of a single layer of endothelial cells. The close proximity of these two cell types allows permeability to gases and, hence, gas exchange. This whole mechanism of gas exchange is carried by the simple phenomenon of pressure difference. When the air pressure is high inside the lungs, the air from lungs flow out. When the air pressure is low inside, then air flows into the lungs.
Airway epithelial cells can secrete a variety of molecules that aid in the defense of lungs. Secretory immunoglobulins (IgA), collectins (including Surfactant A and D), defensins and other peptides and proteases, reactive oxygen species, and reactive nitrogen species are all generated by airway epithelial cells. These secretions can act directly as antimicrobials to help keep the airway free of infection. Airway epithelial cells also secrete a variety of chemokines and cytokines that recruit the traditional immune cells and others to site of infections.
Most of the respiratory system is lined with mucous membranes that contain mucosal-associated lymphoid tissue, which produceswhite blood cells such as lymphocytes.
Metabolic and endocrine functions of the lungs
In addition to their functions in gas exchange, the lungs have a number of metabolic functions. They manufacture surfactant for local use, as noted above. They also contain a fibrinolytic system that lyses clots in the pulmonary vessels. They release a variety of substances that enter the systemic arterial blood and they remove other substances from the systemic venous blood that reach them via the pulmonary artery. Prostaglandins are removed from the circulation, but they are also synthesized in the lungs and released into the blood when lung tissue is stretched. The lungs also activate one hormone; the physiologically inactive decapeptide angiotensin I is converted to the pressor, aldosterone-stimulating octapeptide angiotensin II in the pulmonary circulation. The reaction occurs in other tissues as well, but it is particularly prominent in the lungs. Large amounts of the angiotensin-converting enzyme responsible for this activation are located on the surface of the endothelial cells of the pulmonary capillaries. The converting enzyme also inactivates bradykinin. Circulation time through the pulmonary capillaries is less than one second, yet 70% of the angiotensin I reaching the lungs is converted to angiotensin II in a single trip through the capillaries. Four other peptidases have been identified on the surface of the pulmonary endothelial cells.
The movement of gas through the larynx, pharynx and mouth allows humans to speak, or phonate. Vocalization, or singing, in birds occurs via the syrinx, an organ located at the base of the trachea. The vibration of air flowing across the larynx (vocal cords), in humans results in sound. Because of this, gas movement is extremely vital for communication purposes.
Coughing and sneezing
Irritation of nerves within the nasal passages or airways, can induce coughing and sneezing. These responses cause air to be expelled forcefully from the trachea or nose, respectively. In this manner, irritants caught in the mucus which lines the respiratory tract are expelled or moved to the mouth where they can be swallowed. During coughing, contraction of the smooth muscle narrows the trachea by pulling the ends of the cartilage plates together and by pushing soft tissue out into the lumen. This increases the expired airflow rate to dislodge and remove any irritant particle or mucus.