Control of Breathing

Control of Breathing

Respiratory control has both involuntary and voluntary components. The involuntary centers of the brain regulate the respiratory muscles. They control respiratory minute volume by adjusting the depth and frequency of pulmonary ventilation. This occurs in response to sensory information that arrives from the lungs, various portions of the respiratory tract, and a variety of other sites.

The respiratory areas of the brain control inspi-ration as well as exhalation. The voluntary control of respiration reflects activity in the cerebral cortex that affects either the output of the respiratory center in the medulla oblongata and pons or the output of motor neurons in the spinal cord that control respira-tory muscles. The most important parts comprise the medullary respiratory center, which consists of the dorsal and ventral respiratory groups and the respira-tory group of the pons (FIGURE 21-17).

The dorsal respiratory group is located near the root of cranial nerve IX. It is important in stimulating the muscles of inspiration but is still not fully under-stood. Increased impulses result in more forceful muscle contractions and deeper breathing. Decreased impulses result in passive expiration. It is known that the dorsal respiratory group integrates input from chemoreceptors and peripheral stretch ­receptors. It communicates this information to the ventral respiratory group.

The ventral respiratory group controls other respiratory muscles, mostly the intercostals and abdominals, to increase the force of expiration and sometimes to increase inspiratory efforts. It is believed to be a center of integration and generation of rhythm. It is a network of neurons extending from the spinal cord, through the ventral brain stem, to the pons–medulla junction. Some neurons fire during inspiration, whereas others fire during expiration. The inspiratory neurons send impulses along the phrenic and intercostal nerves, exciting the diaphragm and external intercostal muscles, respectively. Therefore, damage to the phrenic nerves can increase respira-tory rate. The expiratory neurons cause the output to stop and passive expiration to occur, as the inspiratory muscles relax and the lungs then recoil.

This inspiratory and expiratory cycling is contin-uous, producing the normal respiratory rate of 12 to 15 breaths per minute. Inspiratory phases last about two seconds, whereas expiratory phases last about three seconds. Eupnea is the term describing this nor-mal respiratory rate and rhythm. In severe hypoxia, the ventral respiratory group causes the individual to gasp for air. This may be a final effort to restore oxygen to the brain. When certain clustered neurons are completely suppressed, respiration stops. Causes of this include overdoses of alcohol or drugs such as morphine.

The basic rhythm of breathing may also be con-trolled by the pontine respiratory group in the pons. This consists of several centers influencing and modi-fying medullary neuron activities. The pontine group is believed to make the transitions between inspiration and expiration and the reverse, smoother processes. Lesions to the superior region of the pontine respi-ratory group cause prolonged inspirations to occur, which is called apneustic breathing.

However, the rhythmic quality of breathing is not fully understood. The most accepted theory is that normal respiratory rhythm is based on reciprocal inhi-bition of interconnected networks of neurons in the medulla. Instead of one set of “pacemaker neurons,” two sets of neurons inhibit each other. Their activity occurs in cycles, and this generates respiratory rhythm.

Factors of Respiratory Rate and Depth

The depth of inspiration during breathing is based on the level of activity of the respiratory center and its stimulation of motor neurons that serve the respira-tory muscles. With more stimulation, increased num-bers of motor units are excited. Therefore, respiratory muscles contract with greater force. Respiratory rate is established by the length of time the inspiratory center is active or how fast it is turned off. Deep breathing is referred to as diaphragmatic breathing, while shallow breathing is known as costal breathing.

Certain chemicals also affect respiratory rate and depth. Important substances include CO₂, hydrogen, and oxygen ions in the arterial blood. Other factors include emotional states, lung stretching capability, and levels of physical activity. Chemosensitive areas known as central chemoreceptors, located in the medulla oblongata, sense CO₂ and hydrogen ion changes in the cerebrospinal fluid. When these levels change, respira-tory rate and TV are signaled to increase. More CO₂ is exhaled, and both blood and cerebrospinal fluid levels of these chemicals fall, decreasing breathing rate.

CO₂ is the most important chemical regulator of respiration. Arterial partial pressure of CO₂ is usually 40 mm Hg, maintained within 3 mm Hg of this level, mostly by how rising CO₂ levels affect the central che-moreceptors. Hypercapnia is a condition in which CO₂ accumulates in the brain. The accumulating CO₂ is hydrated and H₂CO₃ is formed. When the acid is dissociated, hydrogen ions are freed and pH drops. This also happens when CO₂ enters red blood cells.

Increased hydrogen ions excite the central chemore-ceptors, which extensively synapse with the respiratory­ regulatory centers. Breathing depth and rate, ­therefore, increase. Because alveolar ventilation is enhanced, CO₂ is quickly flushed out of the blood and pH rises. ­Alveolar ventilation is doubled with an elevation of only 5 mm Hg in arterial partial pressure of CO₂. This is true even when there is no change in arterial oxygen levels or pH. The response to elevated partial pressure of CO₂ is even more extensive when partial pressure of oxygen and pH are lower than normal. Increased ventilation is usually self-limited. It stops when there is restoration of homeostatic blood partial pressure of CO₂.

The rising levels of hydrogen ions within the brain increase the activity of the central chemoreceptors, even though rising blood CO₂ is the first stimulus. Although hydrogen does not easily diffuse across the blood–brain barrier, CO₂ accomplishes this with no problem. Therefore, control of breathing while resting mostly is based on regulation of hydrogen ion concen-tration in the brain.

However, peripheral chemoreceptors in the carotid and aortic bodies also help and are able to sense changes in blood oxygen levels (FIGURE 21-18). Then, they increase the breathing rate, but this action requires extremely low levels of blood oxygen to occur.

The depth of breathing is regulated by the ­inflation reflex, which occurs when stretched lung tissues stimu-late stretch receptors in the visceral pleura, bronchioles, and alveoli. The duration of inspiratory ­movements is shortened, preventing overinflation of the lungs during forceful breathing. Emotional upset such as that caused by fear and pain usually increase breathing rate. If breathing stops, even for a short time, blood levels of CO₂ and hydrogen ions rise and oxygen levels fall. Chemoreceptors are stimulated and the urge to inhale increases, overcoming the lack of oxygen. The deflation reflex usually only functions during forced exhalation and inhibits the expiratory centers while stimulating the inspiratory centers when the lungs are deflating.

How Partial Pressure of Oxygen Influences Breathing

The peripheral chemoreceptors contain cells that are sensitive to arterial levels of oxygen. These chemo-receptors lie in the aortic bodies of the aortic arch and the carotid bodies at the bifurcation of the com-mon carotid arteries. Those in the carotid bodies are the main oxygen sensors. Normally, reducing par-tial pressure of oxygen only affects ventilation­ mini-mally. This primarily involves enhanced sensitivity of peripheral receptors to increased partial pressure of CO₂. For oxygen levels to become a strong stimulus for increased ventilation, arterial partial pressure of oxygen must drop greatly, to at least 60 mm Hg.

How Arterial pH Influences Breathing

Even during normal levels of oxygen and CO₂, changes to arterial pH can modify the rate and rhythm of breathing. Increased ventilation occurring because of reduced arterial pH is controlled via the peripheral chemoreceptors. This is in part because hydrogen ions do not cross the blood–brain barrier. Changes in par-tial pressure of CO₂ and hydrogen ion concentration are related, yet different.

Reduced blood pH may be related to retention of CO₂. However, it may also occur because of meta-bolic reasons. These include lactic acid accumulation because of exercise or fatty acid metabolite or ketone body accumulation because of uncontrolled diabetes mellitus. No matter what the reason, as arterial pH declines, the respiratory system will attempt to com-pensate and raise the pH. This occurs by the increase of respiratory rate and depth in an attempt to elimi-nate CO₂ and H₂CO₃ from the blood.

How Higher Brain Centers Influence Breathing

Respiratory rate and depth are modified when pain or strong emotions send signals to the respiratory centers. This occurs via the limbic system, including the hypothalamus. Changes in body temperature also affect respiration, with hotter temperatures increasing it and colder temperatures decreasing it.

Conscious control of breathing can also occur. The cerebral motor cortex sends impulses to the motor neurons, causing stimulation of respiratory muscles. This bypasses the medullary centers. Holding the breath is a limited function because the brain stem respiratory centers automatically reinitiate breathing once CO₂ levels in the blood become critical.

1. Describe the medullary respiratory center.

2. Are peripheral chemoreceptors as sensitive to levels of CO2 as they are to levels of oxygen?

3. Differentiate between the central and peripheral chemoreceptors and their actions.