Chapter 12. The Respiratory System
12.6 Ventilatory Patterns and Control of Ventilation
Learning Objectives
By the end of this section, you will be able to:
- define respiratory rate;
- define eupnea, hyperpnea, hyperventilation, and apnea;
- explain in general the roles of the medullary respiratory centers and the pontine respiratory centers in controlling ventilation;
- discuss factors that can influence the respiratory rate;
- describe the effect of exercise on the respiratory system; and
- describe the effects of high altitude on the respiratory system.
Respiratory Rate and Control of Ventilation
The respiratory rate is the total number of breaths, or respiratory cycles, that occur each minute. Respiratory rate can be an important indicator of health, as the rate may increase or decrease during illness or in a disease condition.
The normal respiratory rate 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 30. By adolescence, the normal respiratory rate is similar to that of adults, 12 to 18 breaths per minute. A normal, unlabored respiratory rate and rhythm is called eupnea.
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 lower blood carbon dioxide levels and higher blood pH. Hypoventilation is decreased ventilation rate that is independent of cellular oxygen needs and leads to higher blood carbon dioxide levels and lower blood pH.
Recall that the diaphragm, external intercostals, and accessory muscles of ventilation are skeletal muscles. The regular contraction of these muscles that results in eupnea is due to the rhythmic firing of the somatic motor neurons innervating the muscles. What, in turn, causes the regular firing of these neurons? The answer lies in the brain stem: the brain stem contains critical centers for the control of breathing. These regions produce what is often referred to as the reflex drive to breathe, or brain stem drive to breathe.
Ventilatory Control: The Role of the Brain Stem
The medullary respiratory centers in the medulla oblongata consists of the dorsal respiratory group (DRG) and the ventral respiratory group (VRG):
- The VRG maintains a constant breathing rhythm by stimulating the diaphragm and external intercostal muscles to contract, resulting in inspiration. The VRG also contains neurons that fire during expiration, inhibiting the activity of the inspiratory neurons. When activity in the VRG ceases, it no longer stimulates the diaphragm and intercostals to contract, allowing them to relax, resulting in expiration.
- The DRG receives input from sensors such as lung stretch receptors and peripheral chemoreceptors. The DRG integrates this information, then communicates with the VRG to modify respiratory rhythm.
The pontine respiratory center of the pons consists of the apneustic and pneumotaxic centers, seen in Figure 12.6.1 but not discussed in detail here. The pontine respiratory center modifies the activities of the medullary respiratory centers, including smoothing out the transition between inspiration and expiration and vice versa. Similar to the DRG, the pontine respiratory center receives input from peripheral sensory receptors and from higher brain areas.
| System Component | Function |
|---|---|
| Medullary respiratory center: ventral respiratory group (VRG) | Generates the breathing rhythm; stimulates diaphragm and external intercostals to contract, causing inspiration |
| Medullary respiratory center: dorsal respiratory group: (DRG) | receives input from the stretch receptors and the chemoreceptors in the periphery and communicates to VRG to modify respiratory rate |
| Pontine respiratory center | modifies the activities of the medullary respiratory centers (e.g., smooths out transition between inspiration and expiration) |
| Sensory Receptor Type | Factor Detected |
|---|---|
| Central chemoreceptors | changes in H+ in the CSF |
| Peripheral chemoreceptors | changes in blood PCO2, PO2, and pH |
| Proprioceptors | Send impulses regarding joint and muscle movements |
| Airway irritant receptors | irritants in airways |
| Stretch receptors in pleurae | stretch of lungs |
Ventilatory Control: Extrinsic Factors Affecting the Rate and Depth of Respiration
- blood PCO2, blood pH, and blood PO2 detected by chemoreceptors throughout the body;
- proprioceptors in joints and muscles;
- stretch receptors in the lungs;
- irritant receptors in the airways;
- cerebral cortex input; and
- hypothalamic input.
Chemical Factors
Concentrations of chemicals in the blood and cerebrospinal fluid (CSF) are sensed by chemoreceptors. When stimulated, the chemoreceptors in turn signal the brain stem respiratory centers. A central chemoreceptor is one of the specialized receptors that are located in throughout the brain stem, whereas a peripheral chemoreceptor is one of the specialized receptors located in the walls of the carotid arteries and aortic arch.
PCO2 and H+ (pH)
The major chemical factor that influences ventilation is surprisingly not oxygen, but carbon dioxide. As mentioned previously, arterial blood PCO2 is normally about 40 mmHg. This level is tightly regulated in homeostatic fashion which primarily by sensing rising levels of CO2 in the plasma and in the brain stem. As PCO2 increases, ventilation rate an depth increase. Elevated PCO2 in the blood is called hypercapnea. (Low PCO2 is termed hypocapnea.)
As PCO2 in the blood increases, more CO2 readily diffuses across the blood-brain barrier, where it collects in the CSF. The increased CO2 levels lead to increased levels of H+ ions, decreasing pH. The increase in H+ in the brain is sensed by central chemoreceptors and respiratory rate and depth increase. As a result of this hyperventilation, more CO2 is expelled.
In contrast, decreased blood PCO2 blood results in lower levels of CO2 in the brain CSF and consequently lower H+ ion levels. This leads to a decrease in the rate and depth of pulmonary ventilation (hypoventilation). If PCO2 becomes abnormally low, periods of apnea (breathing cessation) may occur until PCO2 rises enough to stimulate ventilation.
pH
Another chemical factor that influences the respiratory centers of the brain is systemic arterial concentrations of H+ ions. Increasing carbon dioxide levels can lead to increased H+ levels, as mentioned above, as well as other metabolic activities, such as lactic acid accumulation after strenuous exercise. 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 H+ ions, thus increasing systemic pH.
PO2
The peripheral chemoreceptors are responsible for sensing large changes in blood oxygen levels. If blood oxygen levels become quite low—about 60 mmHg or less—then peripheral chemoreceptors stimulate an increase in ventilation. 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.
Airway Irritant Receptors
Receptors in the airways detect inhaled debris, dust, and noxious fumes for example. They also are stimulated by accumulated mucus. When stimulated, these receptors send signals to the brain that cause a variety of effects, depending on the irritant and the location of stimulation. Examples of responses are constriction of the bronchioles, coughing, and sneezing.
Cortical and Hypothalamic Controls
The hypothalamus and other regions associated with the limbic system are involved in regulating ventilation 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 ventilation rate.
Conscious, voluntary control over breathing occurs via activities originating in the cerebral cortex. Signals from the cerebral motor cortex stimulate the motor neurons innervating the respiratory muscles, bypassing the brain stem.
Inflation Reflex
The pleurae and certain conducting passages in the lungs contain stretch receptors, the main function of which is to prevent overinflation of the lungs during inspiration. As the lungs are stretched. the receptors fire impulses that travels to the brain stem and inspiration ceases. This reflex is thought to be more of a protective mechanism than a usual regulatory mechanism.
Exercise and Hyperpnea
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.
Recall that 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.
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.
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%, its partial pressure decreases (Table 12.4). 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% at 19,000 feet above sea level, whereas it reaches about 98% at sea level.
| 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 |
| Boulder, Colorado | 5,000 | 632 | 133 |
| Aspen, Colorado | 8,000 | 565 | 118 |
| 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, PO2 gradients are extremely important in determining how much gas can cross the respiratory membrane and enter the blood of the pulmonary capillaries. A lower PO2 in the alveoli 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 2,3 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 venous reserve in the blood at high altitudes. At sea level, there is a larger venous reserve 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 2,400 meters (8,000 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.
Acclimatization
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.
Disorders of the Respiratory System – Sleep Apnea
The term apnea means a cessation of breathing. 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.
In central sleep apnea, the respiratory centers of the brain do not respond properly to rising carbon dioxide levels and therefore do not stimulate the contraction of the diaphragm and intercostal muscles regularly. As a result, inspiration does not occur and breathing stops for a short period. In some cases, the cause of central sleep apnea is unknown. However, some medical conditions, such as stroke and congestive heart failure, may cause damage to the pons or medulla oblongata. In addition, some pharmacologic agents, such as morphine, can affect the respiratory centers, causing a decrease in the respiratory rate. The symptoms of central sleep apnea are similar to those of obstructive sleep apnea.
A diagnosis of sleep apnea is usually done during a sleep study, where the patient is monitored in a sleep laboratory for several nights. The patient’s blood oxygen levels, heart rate, respiratory rate, and blood pressure are monitored, as are brain activity and the volume of air that is inhaled and exhaled. Treatment of sleep apnea commonly includes the use of a device called a continuous positive airway pressure (CPAP) machine during sleep. The CPAP machine has a mask that covers the nose, or the nose and mouth, and forces air into the airway at regular intervals. This pressurized air can help to gently force the airway to remain open, allowing more normal ventilation to occur. Other treatments include lifestyle changes to decrease weight, eliminate alcohol and other sleep apnea–promoting drugs, and changes in sleep position. In addition to these treatments, patients with central sleep apnea may need supplemental oxygen during sleep.
Section Review
The respiratory centers of the brain stem maintain a consistent, rhythmic breathing rate called eupnea. Hyperpnea is an increase in breathing rate and depth that does not change levels of oxygen or carbon dioxide in the blood. Hyperventilation and hypoventilation, by contrast, are changes in ventilation rate that do change the levels of oxygen and carbon dioxide in the blood.
The activities of the respiratory centers are influenced by several systemic (extrinsic) factors including arterial PCO2, pH, and PO2.
Exercise results in hyperpnea, and this hyperpnea appears to be a function of three neural mechanisms that include a psychological stimulus, motor neuron activation of skeletal muscles, and the activation of proprioceptors in the muscles, joints, and tendons. As a result, hyperpnea related to exercise is initiated when exercise begins, as opposed to when tissue oxygen demand actually increases.
Acute exposure to a high altitude, particularly during times of physical exertion, results in low blood and tissue levels of oxygen. This change is caused by a low partial pressure of oxygen in the air, because the atmospheric pressure at high altitudes is lower than the atmospheric pressure at sea level. This can lead to a condition called acute mountain sickness (AMS) with symptoms that include headaches, disorientation, fatigue, nausea, and lightheadedness. Over a long period of time, a person’s body will adjust to the high altitude, a process called acclimatization. During acclimatization, the low tissue levels of oxygen will cause the kidneys to produce greater amounts of the hormone erythropoietin, which stimulates the production of erythrocytes. Increased levels of circulating erythrocytes provide an increased amount of hemoglobin that helps supply an individual with more oxygen, preventing the symptoms of AMS.
Review Questions
Critical Thinking Questions
Glossary
- acclimatization
- process of adjustment that the respiratory system makes due to chronic exposure to high altitudes
- apnea
- cessation of breathing
- eupnea
- normal, unlabored breathing
- central chemoreceptors
- chemoreceptors located in the brain stem; sense increased H+ levels resulting from increased carbon dioxide in the plasma and provide input to the respiratory centers
- hypercapnea
- elevated plasma PCO2
- hyperpnea
- increased rate and depth of ventilation due to an increase in oxygen demand that does not significantly alter blood oxygen or carbon dioxide levels
- hyperventilation
- increased ventilation rate that leads to low blood carbon dioxide levels and higher blood pH
- hypocapnea
- low plasma PCO2
- hypoventilation
- decreased ventilation rate that leads to higher blood carbon dioxide levels and lower blood pH
- peripheral chemoreceptors
- chemoreceptors located in the carotid arteries and aortic arch
- pontine respiratory group
- respiratory center that smooths out the transition between inspiration and expiration
- proprioceptors
- receptors in the muscles, joints, and tendons that sense stretching and movement
- respiratory rate
- total number of breaths, or respiratory cycles, per minute
- ventral respiratory group
- the medullary respiratory group that generates the breathing rate and rhythm
Glossary Flashcards
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