1103 Chapter 22. The Respiratory System
22.6 Modifications in Respiratory Functions
By the end of this section, you will be able to:
- Define hypoxia
- Identify some causes of hypoxia, giving examples for each
- Specify some physiological consequences of hypoxia
- Define hyperventilation
- Identify some causes of hyperventilation
- Explain the physiological effects of hyperventilation
At rest, the respiratory system performs its functions at a constant, rhythmic pace, as regulated by the respiratory centers of the brain. At this pace, ventilation provides sufficient oxygen to all the tissues of the body. However, there are times that the respiratory system must alter the pace of its functions in order to accommodate the oxygen demands of the body.
Hyperpnea is an increased depth and rate of ventilation to meet an increase in oxygen demand as might be seen in exercise or disease, particularly diseases that target the respiratory or digestive tracts. This does not significantly alter blood oxygen or carbon dioxide levels, but merely increases the depth and rate of ventilation to meet the demand of the cells. In contrast, hyperventilation is an increased ventilation rate that is independent of the cellular oxygen needs and leads to abnormally low blood carbon dioxide levels and high (alkaline) blood pH.
Interestingly, exercise does not cause hyperpnea as one might think. Muscles that perform work during exercise do increase their demand for oxygen, stimulating an increase in ventilation. However, hyperpnea during exercise appears to occur before a drop in oxygen levels within the muscles can occur. Therefore, hyperpnea must be driven by other mechanisms, either instead of or in addition to a drop in oxygen levels. The exact mechanisms behind exercise hyperpnea are not well understood, and some hypotheses are somewhat controversial. However, in addition to low oxygen, high carbon dioxide, and low pH levels, there appears to be a complex interplay of factors related to the nervous system and the respiratory centers of the brain.
First, a conscious decision to partake in exercise, or another form of physical exertion, results in a psychological stimulus that may trigger the respiratory centers of the brain to increase ventilation. In addition, the respiratory centers of the brain may be stimulated through the activation of motor neurons that innervate muscle groups that are involved in the physical activity. Finally, physical exertion stimulates proprioceptors, which are receptors located within the muscles, joints, and tendons, which sense movement and stretching; proprioceptors thus create a stimulus that may also trigger the respiratory centers of the brain. These neural factors are consistent with the sudden increase in ventilation that is observed immediately as exercise begins. Because the respiratory centers are stimulated by psychological, motor neuron, and proprioceptor inputs throughout exercise, the fact that there is also a sudden decrease in ventilation immediately after the exercise ends when these neural stimuli cease, further supports the idea that they are involved in triggering the changes of ventilation.
In contrast to hyperpnea, hyperventilation is independent of physiological oxygen demands. Instead, it may be caused by abnormal functioning of the lungs as a result of conditions such as asthma or early emphysema). It may also be caused by increased metabolism as a result of such conditions as hyperthyroidism, infection, or fever. Although it has no effect on oxygen levels in the blood, hyperventilation significantly reduces the amount of carbon dioxide in the blood. This reduction in CO2 levels in turn leads to reduced carbonic acid levels in the blood, which results in alkalosis (blood plasma pH higher than normal). Decreased blood CO2 also decreases blood pressure, as the signals coming from peripheral CO2 receptors (normally stimulated by CO2) decrease in frequency and cause the vasomotor centre in the medulla oblongata to reduce constriction of the smooth muscle fibres in the walls of blood vessels and allow vasodilation. Finally, low CO2 and the associated high pH interfere with the ability of hemoglobin to release oxygen molecules to body tissues, including the brain, which can cause dizziness or unconsciousness.
High Altitude Effects
An increase in altitude results in a decrease in atmospheric pressure. Although the proportion of oxygen relative to gases in the atmosphere remains at 21 percent, its partial pressure decreases (Table 4). As a result, it is more difficult for a body to achieve the same level of oxygen saturation at high altitude than at low altitude, due to lower atmospheric pressure. In fact, hemoglobin saturation is lower at high altitudes compared to hemoglobin saturation at sea level. For example, hemoglobin saturation is about 67 percent at 19,000 feet above sea level, whereas it reaches about 98 percent at sea level.
|Partial Pressure of Oxygen at Different Altitudes (Table 4)|
|Example location||Altitude (feet above sea level)||Atmospheric pressure (mm Hg)||Partial pressure of oxygen (mm Hg)|
|New York City, New York||0||760||159|
|Pike’s Peak, Colorado||14,000||447||94|
|Denali (Mt. McKinley), Alaska||20,000||350||73|
|Mt. Everest, Tibet||29,000||260||54|
As you recall, partial pressure is extremely important in determining how much gas can cross the respiratory membrane and enter the blood of the pulmonary capillaries. A lower partial pressure of oxygen means that there is a smaller difference in partial pressures between the alveoli and the blood, so less oxygen crosses the respiratory membrane. As a result, fewer oxygen molecules are bound by hemoglobin. Despite this, the tissues of the body still receive a sufficient amount of oxygen during rest at high altitudes. This is due to two major mechanisms. First, the number of oxygen molecules that enter the tissue from the blood is nearly equal between sea level and high altitudes. At sea level, hemoglobin saturation is higher, but only a quarter of the oxygen molecules are actually released into the tissue. At high altitudes, a greater proportion of molecules of oxygen are released into the tissues. Secondly, at high altitudes, a greater amount of BPG is produced by erythrocytes, which enhances the dissociation of oxygen from hemoglobin. Physical exertion, such as skiing or hiking, can lead to altitude sickness due to the low amount of oxygen reserves in the blood at high altitudes. At sea level, there is a large amount of oxygen reserve in venous blood (even though venous blood is thought of as “deoxygenated”) from which the muscles can draw during physical exertion. Because the oxygen saturation is much lower at higher altitudes, this venous reserve is small, resulting in pathological symptoms of low blood oxygen levels. You may have heard that it is important to drink more water when traveling at higher altitudes than you are accustomed to. This is because your body will increase micturition (urination) at high altitudes to counteract the effects of lower oxygen levels. By removing fluids, blood plasma levels drop but not the total number of erythrocytes. In this way, the overall concentration of erythrocytes in the blood increases, which helps tissues obtain the oxygen they need.
Acute mountain sickness (AMS), or altitude sickness, is a condition that results from acute exposure to high altitudes due to a low partial pressure of oxygen at high altitudes. AMS typically can occur at 2400 meters (8000 feet) above sea level. AMS is a result of low blood oxygen levels, as the body has acute difficulty adjusting to the low partial pressure of oxygen. In serious cases, AMS can cause pulmonary or cerebral edema. Symptoms of AMS include nausea, vomiting, fatigue, lightheadedness, drowsiness, feeling disoriented, increased pulse, and nosebleeds. The only treatment for AMS is descending to a lower altitude; however, pharmacologic treatments and supplemental oxygen can improve symptoms. AMS can be prevented by slowly ascending to the desired altitude, allowing the body to acclimate, as well as maintaining proper hydration.
Especially in situations where the ascent occurs too quickly, traveling to areas of high altitude can cause AMS. Acclimatization is the process of adjustment that the respiratory system makes due to chronic exposure to a high altitude. Over a period of time, the body adjusts to accommodate the lower partial pressure of oxygen. The low partial pressure of oxygen at high altitudes results in a lower oxygen saturation level of hemoglobin in the blood. In turn, the tissue levels of oxygen are also lower. As a result, the kidneys are stimulated to produce the hormone erythropoietin (EPO), which stimulates the production of erythrocytes, resulting in a greater number of circulating erythrocytes in an individual at a high altitude over a long period. With more red blood cells, there is more hemoglobin to help transport the available oxygen. Even though there is low saturation of each hemoglobin molecule, there will be more hemoglobin present, and therefore more oxygen in the blood. Over time, this allows the person to partake in physical exertion without developing AMS.
The effects of high altitude discussed above are in part the result of hypoxia, a reduction in the amount of oxygen reaching body tissues. Hypoxia may be caused by a deficiency in atmospheric oxygen, whether due to high altitude or being in an enclosed space with limited airflow (e.g. a crowded room with poor ventilation).
Hypoxia may also be caused by physiological problems with the respiratory or cardiovascular system. In the case of the respiratory system, any interference in the process of breathing (e.g. abnormal muscle contractions) or obstruction in the air passages (e.g. excessive mucus) will cause hypoxia by ventilatory deficiency. Alternatively, hypoxia may be caused by a pulmonary diffusion defect in which the diffusion of oxygen gas across the respiratory membrane is impaired. Fluid in the pulmonary alveoli, for example, increases the distance across which oxygen must diffuse through liquid, effectively increasing the thickness of the respiratory membrane and therefore slowing the rate at which oxygen can move into the blood. In the cardiovascular system, hypoxia may be caused by a hemoglobin deficiency or a circulatory deficiency. A hemoglobin deficiency may be the result of anemia, where there is a shortage of functional red blood cells. It may also be the result of conditions such as carbon monoxide poisoning, where carbon monoxide displaces oxygen bound to hemoglobin molecules, rendering the hemoglobin incapable of carrying oxygen and thus effectively nonfunctional. Circulatory deficiencies may be the result of obstruction of a blood vessel (e.g. as a result of atherosclerosis), of low blood pressure (hypotension), or of structural problems that make the cardiovascular system less efficient than it should normally be (e.g. if the ductus arteriosus or foramen ovale fail to close after birth).
Finally, hypoxia may result from edema, where excessive fluid accumulates around cells, for example as a result of inflammation, renal failure, or congestive heart failure. This fluid buildup may occur in the lung tissue or alveoli (pulmonary edema), where it slows the diffusion of oxygen across respiratory membranes, or in other tissues where it can slow the diffusion of oxygen to body cells.
Hypoxia can result in cyanosis, where the skin and mucous membranes take on a bluish (or purplish) discoloration. It can also result in tachycardia, or increased heart rate, and dizziness as a result of insufficient oxygen reaching the brain.