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ЗмістVoluntary control of respiration
The reflex control of respiration
Other reflex modulations of respiration
The role of blood gases level in breathing regulation
The effects of breathing different gas mixtures
Regulation of respiration
Breathing is an automatic, rhythmical process that is constantly adjusted to meet the everyday requirements of life such as exercise and speech. To account for this remarkable fact it is necessary to consider three important questions.
3- How is the rate and depth of respiration controlled?
The respiratory rhythm is established by specific groups of neurons that lie within the lower part of the brainstem
How we can prove, that it is correctly?
If the brainstem of an anaesthetized animal is completely cut through above the pons, the basic rhythm of respiration continues. Section of the spinal cord below the outflow of the phrenic nerve (C3—C5) leads to paralysis of the intercostal muscles but not of the diaphragm (which is innervated by the phrenic nerve). Section of the lower region of the medulla, however, will block all respiratory movements. The basic rhythm is maintained even if all the afferent nerves are sectioned. From these observations two things are clear:
1. The respiratory muscles themselves have no intrinsic rhythmic activity. The caudal part of the brainstem has all of the neuronal mechanisms required to generate and maintain a basic respiratory rhythm.
2. If the vagus nerves are cut, respiration becomes slower and deeper. If the brainstem is subsequently cut across between the medulla and pons, there is little change in the respiratory pattern. Sections through the pons, however, alter the pattern of respiration, so that inspiration becomes relatively prolonged with brief episodes of expiration. Stimulation of specific groups of nerve cells in the pons synchronizes the discharge of the phrenic nerves with the stimulus. From these and other experimental observations, the pons has been shown to have an important role in regulating the respiratory rhythm. It is here that afferent information concerning the state of the lungs is believed to act to modulate the rate and depth of respiration.
How is the respiratory rhythm generated?
There are two groups of neurons in the medulla that discharge action potentials with an intrinsic rhythm that corresponds to that of the respiratory cycle.
These are known as the
dorsal respiratory group
ventral respiratory group
The dorsal respiratory group mainly discharge action potentials just prior to and during inspiration and are Therefore mainly inspiratory neurons. They are upper motoneurons which project to the lower respiratory motoneurons of the contralateral phrenic nerve. The ventral respiratory group consists of both inspiratory and expiratory neurons and receives inputs from the dorsal respiratory group. They are the upper respiratory motoneurons for both the contralateral phrenic and intercostal nerves.
The dorsal and ventral respiratory groups receive a variety of inputs from higher centers in the brain, including the cerebral cortex and pons. They also receive inputs from the carotid and aortic bodies and the vagus nerve.
It appears that the dorsal respiratory group initiates the activity that leads to inspiration and that intrinsic activity within the dorsal respiratory neurons sums with afferent activity coming from lung stretch receptors to switch off inspiration and commence expiration. A simple diagram of the arrangement of the respiratory control pathway is shown in Fig. 16.20.
The activity of the expiratory respiratory motoneurons in the spinal cord (the lower respiratory motoneurons) is inhibited during inspiration while that of the inspiratory motoneurons is inhibited during expiration. This pattern of reciprocal inhibition has its origin in the dorsal and ventral respiratory groups and is not a local spinal reflex.
The efferent activity of the thoracic respiratory neurons can be monitored by recording the electrical activity of intercostal muscles and diaphragm (Fig. 16.21). Throughout the respiratory cycle the motor units of the respiratory muscles are active. During inspiration, the activity of the inspiratory muscles (the diaphragm and external intercostal muscles) progressively
Fig. 16.20 A flow diagram showing the interrelations between the main neural elements that regulate the rate and depth of respiration.
increases, additional motor units are recruited, and the muscles shorten progressively, so expanding the volume of the chest. During expiration their activity gradually declines and the muscles relax, allowing the chest to return to its resting volume (FRC).
Hering—Breuer lung inflation reflex
The lung has slowly adapting stretch receptors in the smooth muscle of the upper airways (trachea, bronchi, and bronchioles). When the lung is inflated, these receptors are activated and send impulses to the dorsal respiratory group via the vagus nerves. This afferent information tends to inhibit respiratory activity and so acts to limit inspiration. This is known as the Hering—Breuer lung inflation reflex. If the lungs are inflated by positive pressure, the frequency of respiratory movements falls and may cease altogether (apnea).
In animals such as the cat and rabbit, the Hering—Breuer reflex appears to play a significant part in the control of the respiratory rhythm. In humans, this reflex is not activated at normal tidal volumes. It is, however, activated when tidal volumes exceed about 0.8—1 liter. For this reason it is thought that the Hering—Breuer reflex may play a role in regulating inspiration during exercise.
Normal regular breathing (or eupnea) is an automatic process although the rate and depth of breathing can be readily adjusted by voluntary means. For example, it is possible to suspendbreathing for a short period. This breath-holding is known as voluntary apnea and its duration is normally limited by the rise in arterial Pco2. Equally, it is possible to increase the rate and depth of breathing deliberately (сознательно) during voluntary hyperventilation (also known as voluntary hyperpnea). The pathways involved in voluntary regulation are not known with any certainty but presumably have their origin in the motor cortex. This is important during speech, singing, or the playing of a wind instrument.
Cough and sneeze
In addition to their stretch receptors, the airways possess receptors that respond to irritants. When they are stimulated, these receptors elicit a cough or, in the case of irritants on the nasal mucosa, a sneeze. The initial phase of either response is a deep inspiration followed by a forced expiration against a closed glottis. As the pressure in the airways rises, the glottis suddenly opens and the trapped air is expelled at high speed. This dislodges some of the mucus covering the epithelium of the airways and helps to carry the irritant away with it via the mouth or nose. If the lungs become congested, breathing becomes shallow and rapid (called pulmonary tachypnea). The receptors that mediate this response are C-fiber endings located in the interstitial space of the alveolar walls, previously known as J-receptors (for juxtapulmonary capillary receptors). The role these receptors play in normal breathing is not known. Stimulation of lung irritant receptors and pulmonary C-fiber endings is associated with bronchoconstriction.
During swallowing respiration is inhibited. This is part of a complex reflex pattern: as food or drink passes into the oropharynx, the nasopharynx is closed by the upward movement of the soft palate and the contraction of the upper pharyngeal muscles. Respiration is inhibited at the same time and the laryngeal muscles contract, closing the glottis. The result is that aspiration of food into the airways is avoided. The act of swallowing is followed by an expiration which serves to dislodge any food particles lying near the glottis. These actions are coordinated by neural networks in the medulla. If particles of food are accidentally inhaled, they stimulate irritant receptors in the upper airways and elicit a cough reflex.
The normal pattern of breathing is modified by many other factors. For example, passive movement of the limbs results in an increase in ventilation which is believed to occur as a result of stimulation of proprioceptors in the muscles and joints. This reflex may play an important role in the increase in ventilation during exercise (Chapter 25). Pain results in alterations to the normal pattern of respiration. Prolonged severe pain is associated with fast shallow breathing. Immersion of the face in cold water elicits the diving response in which there is apnea, bradycardia, and peripheral vasoconstriction (Chapter 30).
The blood gases are of major importance in the control of ventilation and are sensed by peripheral and central chemoreceptors.
The purpose of respiration is to provide the tissues with oxygen and to remove the carbon dioxide derived from oxidative metabolism. This is achieved by close regulation of the Pco2 and Po2 of the arterial blood (i.e. the PaCO2 and PaO2), which are maintained within very close limits throughout life. Indeed, the PaCO2 and PaO2 vary little between deep sleep and severe exercise when the oxygen consumption and carbon dioxide output of the body may increase more than tenfold -десятикратный. Clearly, to achieve such remarkable stability the body needs some means of sensing the PaCO2 and PaO2 and relaying that information to the neurons that determine the rate and depth of ventilation. This role is performed by the peripheral and central chemoreceptors.
The peripheral arterial chemoreceptors—the carotid and aortic bodies—are located just above the carotid bifurcation and scattered around the arch of the aorta. The carotid body is a small organ, about 7X5 mm in size, that is innervated by the carotid sinus nerve, which is a branch of the glossopharyngeal (IX cranial) nerve. It receives its blood supply from the external carotid artery and has a very high blood flow relative to its mass (about 20 1 kg-1 min"1). The function of the carotid body on each side of the body is the same, both respond to changes in the PaO2, PaCO2, and pH of the arterial blood.
The carotid bodies are anatomically and functionally separate from the baroreceptors that are located in the wall of the carotid sinus (Fig. 16.22). Nevertheless, afferent fibers from the carotid body and from the carotid sinus run in the same nerve—the carotid sinus nerve. Afferents from the carotid body increase their rate of discharge very significantly as the PaO2 falls below about 8 kPa (60mmHg), as shown in Fig. 16.25. The aortic bodies are diffuse islets of tissue which have a similar microscopic structure to the carotid bodies. There is, however, no evidence to suggest that they play a significant role in humans although they may do so in other species.
The carotid bodies respond to changes in PaO2, PaCO,, and pH of the arterial blood. They are the only receptors that are able to elicit a ventilatory response to hypoxia. Thus, after the carotid body has been surgically removed for therapeutic reasons, the ventilatory response to hypoxia is lost—even though the aortic bodies remain intact. When breathing normal room air, the influence of the carotid bodies on the rate of ventilation is small. For example, if a subject suddenly switches from breathing room air to breathing 100 per cent oxygen, the minute volume falls by about 10 per cent for a brief period before returning to its previous level. The transient nature of this response can be explained as follows: breathing pure oxygen reduces the respiratory drive from the peripheral chemoreceptors and this has the effect of reducing the minute volume. During this period the PaCO2 rises slightly and this acts on the central chemoreceptors to cause the minute volume to return to its original value.
During hypoxia, however, the carotid bodies play an important role in stimulating ventilation. This can be shown in anesthetized, spontaneously breathing animals. If the arterial Po2 is lowered by giving the animal a gas mixture of 8 per cent O2 and 92 per cent N2, the minute volume increases by about 50 per cent. This is a reflex response which can be blocked by cutting the aortic and carotid sinus nerves. The increase in minute volume seen following administration of a gas mixture containing 5 per cent CO2 (in 21 per cent O2 and 74 per cent N2) is unaffected by section of these nerves, showing that the response to hypercapnia is mediated by the central chemoreceptors.
The central chemoreceptors respond to changes in the pH of the c.s.f. resulting from alterations in PaCO2. They are located on or close to the ventral surface of the medulla, near to the origin of the glossopharyngeal and vagus nerves, and provide most of the chemical stimulus to respiration under normal resting conditions. The mechanism by which they sense the PaCO2 is illustrated in Fig. 16.23. Increased PaCO2 results in an increase in the Pco2 of the c.s.f. and the hydration reaction for carbon dioxide is driven to the right, leading to the increased liberation of hydrogen ions:
Unlike the blood, the c.s.f. has little protein so the hydrogen ions produced by this reaction are not buffered to any great extent. As a result, the pH falls in proportion to the rise in Pco2 and stimulates the chemoreceptors. Conversely, during hyperventilation, CO2 is lost from the blood and this causes a reduction in the Pco2 of the c.s.f. The hydration reaction is driven to the left, and the pH of the c.s.f. rises and ventilation decreases.
If the PaCO2 were to be persistently above or below its normal value of 5.3 kPa (40 mmHg), the central chemoreceptors would be less sensitive to changes in PaCO2 than normal. In these situations the bicarbonate concentration of the c.s.f. is regulated by exchange with chloride ions derived from the plasma. This compensation is important during chronic changes in PaCO7 arising from residence at high altitude (where the Paco2 falls—see Chapter 30) or from chronic respiratory disease (where the PaCO2 rises).
The relative importance of CO2 and O2 in determining the ventilatory volume is readily investigated by asking subjects to breathe different gas mixtures.
When air containing a significant amount of CO2 is inhaled, its partial pressure in the alveoli and arterial blood rises. This is known as hypercapnia. If a subject deliberately hyperventilates for a brief period, the partial pressure of carbon dioxide in the alveoli and arterial blood falls as it is lost from the lungs faster than it is being generated in the tissues. This fall in the partial pressure of CO2 is known as hypocapnia.
If subjects are asked to breathe a gas mixture in which the Po2 is lower than the normal 21.2 kPa (159 mmHg) its partial pressure in the arterial blood will fall. This is known as hypoxemia. If the oxygen content is insufficient for the needs of the body, the subject is said to be hypoxic. The total absence of oxygen is anoxia.
If a normal healthy subject breathes a gas mixture containing 21 per cent oxygen, 5 per cent carbon dioxide, and 74 per cent nitrogen for a few minutes, their ventilation increases about threefold. A higher fraction of carbon dioxide in the inhaled gas mixture will stimulate breathing even more. Even a single breath of air containing an elevated concentration of carbon dioxide is sufficient to increase ventilation for a short time. Conversely, if a subject hyperventilates for a brief period, the subsequent ventilation is temporarily decreased. Thus any maneuver that alters the partial pressure of CO2 in the alveolar air (PAco2) results in a change in ventilation that tends to restore the PACO2 to its normal value (5.3 kPa or 40 mmHg). The relationship between the partial pressure of CO2 in the alveolar air and total ventilation is shown in Fig. 16.24.
From these observations, it appears that the principal chemical stimulus to respiration is the Pco2 of the alveolar air rather than the Po2. At first this may appear strange, as the main purpose of gas exchange is to maintain the oxygenation of the tissues. The reason for the relatively small ventilatory effect of mild hypoxia can be understood by looking at the oxyhemoglobin dissociation curve (which is also plotted in Fig. 16.25) which shows that at a Po7 of 8 kPa (60 mmHg) the hemoglobin is still about 90 per cent saturated. It is below this value that the percentage saturation rapidly falls. Consequently, at normal atmospheric pressure (101 kPa or 760 mmHg), hypoxia would be a relatively insensitive stimulus to ventilation.
As Fig. 16.26 shows, the increase in ventilation with increasing alveolar Pco2 becomes steeper as the Po2 falls. This shows that the sensitivity of the respiratory drive to carbon dioxide is greater during hypoxia than it is when the Po2 is normal. The effects of hypoxia and hypercapnia are not simply additive, they have a strong synergistic interaction. This is of some importance during breath holding and asphyxia where hypoxia and hypercapnia occur together. In this context is should be noted that breathing air containing more than 5 per cent carbon dioxide is unpleasant and causes mental confusion. Prolonged breathing of air containing a high concentration of carbon dioxide or breathing air with a very low Po2 may lead to loss of consciousness.
While the emphasis in this section has been on the role of Paco2 as a ventilatory stimulus, it is important to realize that changes in PaCO2 cause very significant changes to blood pH. Indeed one important consequence of the changes in ventilation in response to altered Paco2 is to limit the magnitude of the pH change in the blood. The pulmonary control of blood pH and its role in acid-base balance is discussed in greater detail in Chapter 29.
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