Rebreathing air reabsorbs CO2 that was exhaled, and recycling unused O2, this causes CO2 levels to be higher than normal and for blood to have a lower pH. The oxygen content decrease slowly because there is a reservoir of oxygen attached to hemoglobin (Fox 556). An increase of H+ cannot influence the medullary receptors, but carbon dioxide in the arterial blood can cross the blood-brain barrier and lower the pH of cerebrospinal fluid and brain interstitial fluid (Fox 557). Lower in pH on the medulla oblongata stimulates the central chemoreceptors, either directly or via glia cells to release ATP as a transmitter in response to lowered pH (Fox 557). This will then increase ventilation but in several minutes. Aortic and carotid bodies sense the
The decrease in her PCO2 and pH will cause her central nervous system to slow down causing her breathing to slow down to try to give her body more carbon dioxide to level out the amount of oxygen/carbon dioxide ratio.
At higher altitudes respiration rate is increased which leads to increases in ventilation (possibly a five-fold increase from sea level). Chemoreceptors in the arterial blood vessels are stimulated to signal the brain to increase ventilation. The increase in ventilation is associated with increased breathing frequency and tidal volume.
PCO2 decreased during rapid breathing because more CO2 was removed from the blood than normal. Each breath expels a certain amount of CO2. If the breathing rate increases, then more CO2 is expelled.
The same happens with Carbon Dioxide (CO2). The blood in the surrounding capillaries has a higher concentration of CO2 than the inspired air due to it being a waste product of energy production. This is when O2 and CO2 pass each other going back around the body systems to the heart. Once this is done the flow goes from Deoxygenated blood to Oxygenated blood.
The diffusion of oxygen across the lungs and into the blood is decreased. The oxygen levels will be lowered, triggering chemoreceptors to send an afferent message to the brain, creating the sensation of dyspnea.
The complexity of the respiratory system and the physiology behind pulmonary respiration can be considered extraordinary high. Within the single system, individual organs, actions and co-ordinations are culminated to equate in the survival of humans. The respiratory system carries out many roles within the body; control of bodily pH, aid in speech production and olfaction, regulation of blood pressure and promotion of venous and lymphatic flow. Although these function are necessary to optimally function, the exchange of gases from the internal bodily environment to the external bodily environment is the most important function and role of the respiratory system (Martini, Ober, Nath 2011).
THE CONTROL SYSTEM FOR RESPIRATION The control unit of ventilation consists of a processor or breathing centre in the brain which integrates emotional, chemical and physical stimuli inputs and controls an effector - in this case the lungs via motor nerves from the spinal cord. Ventilation is normally autonomic with a limited voluntary override. Ondine's curse is the exception to this where the autonomic control is lost. The mechanism of generation is not completely understood but involves the integration of neural signals by respiratory control centres in the medulla and pons. In the medulla we have the ventral respiratory group i.e. nucleus retroambigualis, nucleus ambiguus, nucleus parambigualis and the pre-Botzinger complex. This group controls voluntary forced exhalation and also works to increase the force of inspiration. The medulla also contains the dorsal respiratory group consisting mainly of the nucleus tractus solitarius and this controls mostly inspiratory movements and their timing. The pons contains the pneumotaxic centre which is involved with the fine tuning of the respiration rate and the apneustic centre. In addition there is further integration in the anterior horn cells of the spinal cord. The actual breathing rate of a human is controlled in the following way. Chemoreceptors detect the levels of carbon dioxide in the blood by monitoring
High alveolar ventilation brings more O2 into the alveoli, increasing O2 , and rapidly eliminating CO2 from the lungs (for chemical abbreviations see Table 2).
Gas exchange occurs between the air and blood in the lungs. Since the oxygen saturation of air is higher in the lungs than in the blood, oxygen diffuses from air to blood. Carbon dioxide moves from the blood to the air within the lungs by diffusing down its concentration gradient. As a result of this exchange, the inspired air contains more oxygen and less carbon dioxide than the expired air. The lungs provide necessary oxygen to the body, in addition to removing carbon dioxide. More importantly, blood leaving the lungs has a higher oxygen and lower carbon dioxide concentration than the blood delivered to the lungs in the pulmonary arteries. This is because the lungs function to bring the blood into gaseous equilibrium in the air. Gas exchange between the air and blood occurs entirely by diffusion through the lung tissue
These results are due to metabolic rates and the need for homeostasis which is driven by the production of CO2 (Mason, 2015). The results suggest that the values obtained in the normal ventilation condition for PO2, PCO2 and %O2 are consistent with the proposed values 100 mmHg, 40 mmHg and around 98% (Silverthorn, Johnson & Ober, 2013, p. 590). This is due to arterial gas composition being approximately equal to alveolar gas composition (Silverthorn, Johnson & Ober, 2013, p. 590). The breath-hold after hypoventilation condition resulted in an increased CO2 intake into the lungs due to breathing deeply. There was a decrease in PO2 and %O2 and increase in PCO2 as arterial PCO2 rose because metabolic processes continued without a new intake of air into the lungs. This disturbance of respiratory homeostasis hinders the ability to hold one’s breath (Mason, 2015). CO2 decreases pH of extracellular brain fluid, which stimulates central chemoreceptors, causing a break-point in breath-hold (Moreira, Takakura, Colombari & Guyenet, 2006). CO2 is detected very quickly in the blood (respiratory acidosis) by peripheral chemoreceptors (carotid and aortic bodies) (Miller, Cunningham, Lloyd & Young, 1974). The respiratory centre is controlled by chemoreceptor response, which then re-establishes respiratory homeostasis, by inducing a change in ventilation (Haldane & Priestley, 1905). However, the hyperventilation pattern, which involved shallow breathing, caused an increase in PO2 due to greater accumulation rate of O2 and larger O2 store in the lungs. A reduction in arterial PCO2 and increased expiration of CO2, increased %O2, which explains why there was a reduction in PCO2 (Lindholm &
Control centers: the medulla oblongata and neural circuits establish a person’s breathing rhythm that gathers information from the internal environment to coordinate breathing based on the body’s need for oxygen. To accomplish this, the sensors in the medulla monitor the pH of the cerebrospinal fluid to indicate the concentration of carbon dioxide in the body. A normal pH is about ~7.4. When the blood pH falls below this range, the medulla’s sensors detect a low pH in the cerebrospinal fluid and blood. This cause the ribs and diaphragm to increase their rate of rate of ventilation, causing the carbon dioxide level in the blood to fall and raising the blood and cerebrospinal fluid pH once again. The higher the carbon dioxide level, the more hydrogens that are present in a substance, causing its pH to
Chyle is a fatty fluid absorbed into the lymphatics from the digestive system. It’s accumulation in the pleural cavity leads to a chylous pleural effusion. The pleural effusion reduces the ability of the lungs to expand and therefore reduce the amount of oxygen than can be taken in. This leads us to the tachypnea. Tachypnea is an abnormal increase in respiratory rate. Low arterial oxygen concentration can lead to increased respiratory rate by stimulation of chemoreceptors. The mechanism not definite, but it’s believed that low oxygen is detected by glomus cells with in the carotid or aortic bodies and causes stimulation of the nerve endings because these so called glomus cells of oxygen sensitive potassium channels that become inactivated the blood oxygen levels decrease. There is a strong stimulation of the chemoreceptors which in turn increase respiratory rate.
This results in the person having repetitive periods of insufficient ventilation and jeopardized gas exchange. This occurs when the inhibitory input to the brain exceeds excitatory output; or in simpler terms the brain fails to signal the muscles to breathe.
When the contraction of the diaphragm has stopped the vacuum, the lungs with their bronchial apparatus, return to their normal relaxed state. This relaxation expels the remaining air. The expelled air carries away the carbon dioxide that was exchanged in the alveoli and continues on the reverse course of our journey up the trachea through the glottis, the oral and nasopharynx, and out the nostrils or mouth.
pressure increases within the lungs and the thoracic cavity causing the air to move out (Borden,