The body maintains a stable internal environment through a process called homeostasis, and the respiratory system plays a major role in this regulation. Respiratory homeostasis is the precise mechanism by which the body keeps the concentrations of gases in the blood within a narrow range. This constant fine-tuning of breathing ensures that cells receive the oxygen they require while simultaneously disposing of metabolic waste. Maintaining this delicate balance is fundamental for the proper functioning of all physiological processes.
The Principal Regulated Parameters
The respiratory system primarily regulates three interconnected parameters in the arterial blood: the partial pressure of oxygen (\(\text{PO}_2\)), the partial pressure of carbon dioxide (\(\text{PCO}_2\)), and the blood’s acidity, or \(\text{pH}\). Although oxygen is consumed by cells for energy, the control system is far more sensitive to changes in \(\text{PCO}_2\) and \(\text{pH}\). The normal \(\text{pH}\) range for arterial blood is tightly guarded between 7.35 and 7.45.
The partial pressure of carbon dioxide is the most potent driver of respiratory adjustments because it directly links to \(\text{pH}\) via the bicarbonate buffer system. Carbon dioxide combines with water to form carbonic acid, which dissociates into bicarbonate and hydrogen ions. An increase in \(\text{CO}_2\) drives this reaction to produce more hydrogen ions, thereby lowering the \(\text{pH}\) and making the blood more acidic. Conversely, removing \(\text{CO}_2\) shifts the reaction in the opposite direction, consuming hydrogen ions and raising the \(\text{pH}\).
The body’s regulatory mechanisms focus on maintaining a stable \(\text{PCO}_2\) because it rapidly influences blood acidity. While a low \(\text{PO}_2\) is a serious threat, the body tolerates a modest drop in oxygen more easily than a significant shift in \(\text{pH}\). The respiratory system acts almost instantaneously to adjust ventilation depth and rate to keep \(\text{PCO}_2\) within its normal range of 35 to 45 mmHg.
The Detection and Processing System
The continuous monitoring required for respiratory homeostasis is performed by specialized sensory structures known as chemoreceptors. These sensors are divided into two main categories based on their location and the primary chemical signals they detect. Central chemoreceptors are situated in the medulla oblongata of the brainstem, near the primary respiratory control centers.
These central sensors respond not to blood \(\text{CO}_2\) directly, but to the resulting change in the \(\text{pH}\) of the cerebrospinal fluid (CSF). Carbon dioxide is highly lipid-soluble and easily diffuses from the blood into the CSF, where it forms carbonic acid and releases hydrogen ions. Even a small increase in blood \(\text{PCO}_2\) triggers a strong signal, causing a reflex increase in breathing to expel the excess \(\text{CO}_2\).
Peripheral chemoreceptors are located outside the central nervous system, in the carotid and aortic bodies. These peripheral sensors primarily monitor arterial \(\text{PO}_2\) and serve as the main sensors for oxygen deprivation. They become significantly active only when the arterial \(\text{PO}_2\) drops dramatically, typically below 60 mmHg. They also respond to increases in \(\text{PCO}_2\) and decreases in blood \(\text{pH}\), but their response is much less pronounced than that of the central chemoreceptors.
The signals from both sets of chemoreceptors are relayed to the respiratory centers housed within the brainstem: the medulla and the pons. The medulla contains the dorsal respiratory group, controlling the basic rhythm of inspiration, and the ventral respiratory group, involved in forced breathing. The pons contains the pneumotaxic and apneustic centers that fine-tune the rate and depth of breathing. These centers integrate all incoming information to send signals down to the effector muscles, primarily the diaphragm and the intercostal muscles, to adjust the ventilation pattern.
Dynamic Responses to Environmental Changes
The homeostatic system is challenged by changes in metabolic rate and the external environment. During physical exercise, the body’s metabolic rate increases substantially, leading to a rapid rise in \(\text{CO}_2\) production and oxygen consumption. Despite the massive increase in gas exchange, the respiratory system maintains a remarkably stable arterial \(\text{PCO}_2\) and \(\text{pH}\).
The increase in ventilation during exercise is initially triggered not only by rising \(\text{CO}_2\) levels but also by signals from moving joints and muscles. This anticipatory response quickly increases the rate and depth of breathing to meet the rising demands. The increased rate of breathing, or hyperpnea, ensures that the extra \(\text{CO}_2\) produced by the working muscles is efficiently expelled, preventing the blood from becoming too acidic.
Exposure to high altitude presents a challenge because lower ambient air pressure results in a reduced partial pressure of oxygen. This low ambient \(\text{O}_2\) immediately lowers the arterial \(\text{PO}_2\), which strongly stimulates the peripheral chemoreceptors. The resulting signal causes hyperventilation, the body’s first line of defense against altitude hypoxia.
This initial hyperventilation, while increasing oxygen intake, causes excessive blowing off of \(\text{CO}_2\). The reduced \(\text{PCO}_2\) causes the blood \(\text{pH}\) to rise, leading to respiratory alkalosis. Over a few days, acclimatization occurs, involving the kidneys adjusting the excretion of bicarbonate ions to help normalize the blood \(\text{pH}\) despite the persistent hyperventilation. The sustained hyperventilation then allows for a higher-than-normal alveolar \(\text{PO}_2\), which partially compensates for the low oxygen in the environment.
When Homeostasis Fails
When the respiratory control system is overwhelmed or impaired, it cannot maintain the balance of \(\text{PCO}_2\) and \(\text{pH}\), leading to serious acid-base disturbances. The failure to adequately remove \(\text{CO}_2\) results in respiratory acidosis. This occurs when hypoventilation causes \(\text{CO}_2\) to accumulate, driving the bicarbonate buffer reaction to the right and increasing the concentration of acid-forming hydrogen ions.
Respiratory acidosis lowers the blood \(\text{pH}\) below 7.35 and can be caused by conditions that depress the central respiratory drive, such as an opioid overdose or severe brain injury. It can also be caused by diseases that physically impair the lungs’ ability to exchange gases, such as severe chronic obstructive pulmonary disease (COPD). The body’s inability to ventilate adequately means the blood retains too much acid, which can be life-threatening if not corrected rapidly.
Conversely, respiratory alkalosis occurs when the respiratory system eliminates \(\text{CO}_2\) too rapidly, a state caused by hyperventilation. This excessive expulsion of \(\text{CO}_2\) causes the blood \(\text{pH}\) to rise above 7.45. A common non-pathological example is hyperventilation triggered by anxiety or a panic attack. Exposure to high altitude also initially causes respiratory alkalosis as the body attempts to maximize oxygen intake. The primary disturbance is an imbalance between the rate of \(\text{CO}_2\) production and the rate of its removal by the lungs.