Respiration: Pulmonary Ventilation PDF

23.5 Respiration: Pulmonary Ventilation Respiration is a general term for the exchange of respiratory gases (oxygen and carbon dioxide) between the atmosphere and the systemic cells of the body—it is organized into four continuous and simultaneously occurring processes: Pulmonary ventilation—movemen...

23.5 Respiration: Pulmonary Ventilation Respiration is a general term for the exchange of respiratory gases (oxygen and carbon dioxide) between the atmosphere and the systemic cells of the body—it is organized into four continuous and simultaneously occurring processes: Pulmonary ventilation—movement of respiratory gases between the atmosphere and the alveoli of the lungs Pulmonary gas exchange—exchange of respiratory gases between the air in the alveoli and the blood in the pulmonary capillaries Gas transport—transport of respiratory gases within the blood between the lungs and systemic cells of the body Tissue gas exchange—exchange of respiratory gases between the blood in the systemic capillaries and systemic cells of the body Please see figure 23.18, which illustrates and summarizes the movement of respiratory gases involving these four processes. Notice that the net movement of oxygen (O2) is from the atmosphere to the systemic cells, and the net movement of carbon dioxide (CO2) is from the systemic cells to the atmosphere. We begin by discussing pulmonary ventilation in this section. The other three processes of respiration are covered in 23.7. sections 23.6 and Figure 23.18 Overview of Respiration. Respiration involves four processes: pulmonary ventilation, pulmonary gas exchange, gas transport, and tissue gas exchange. Respiration supports cellular respiration, which is a metabolic process that provides ATP in cells. 23.5a Introduction to Pulmonary Ventilation LEARNING OBJECTIVE 22. Define the general concept of ventilation and the specific physiologic process of pulmonary ventilation. Ventilation is the replacement of air in a space with fresh air. Pulmonary ventilation, or simply breathing, is specifically the replacement of air within the alveoli of the lungs by the movement of air between the atmosphere and the alveoli. It consists of two cyclic phases: inspiration (also called inhalation), which brings air into the alveoli, and expiration (also called exhalation), which moves air out of the alveoli. Breathing may be either quiet or forced. Quiet breathing (or eupnea [yūp-nē-ă]) is the rhythmic breathing that occurs at rest; forced breathing is vigorous breathing that accompanies exercise or hard exertion. The principles involved in breathing, whether quiet or forced, use the same physiologic processes. Autonomic nuclei in the brainstem (see sections 13.5b and 13.5c) initiate nerve signals to be sent along somatic motor neurons to cause the skeletal muscles of breathing (e.g., the diaphragm) to rhythmically contract and relax, resulting in thoracic cavity volume changes. Dimensional changes within the thoracic cavity during breathing result in pressure changes, establishing a changing pressure gradient between the atmosphere and the alveoli. Air moves down the pressure gradient either from the atmosphere into the alveoli during inspiration or from the alveoli into the atmosphere during expiration. Three major topics are addressed in this section: (a) how pressure gradients are established between the atmosphere and the alveoli during breathing (mechanics of breathing), (b) how breathing is rhythmically controlled by nuclei within the brainstem and altered by other regions of the brain, and (c) the various means of clinically evaluating pulmonary ventilation by measuring respiratory function. Page 914 WHAT DID YOU LEARN? 20 What are the general steps of pulmonary ventilation, beginning with the autonomic nuclei? INTEGRATE LEARNING STRATEGY 23.2 Pulmonary ventilation (or breathing) involves the replacement of air within the alveoli with fresh air. This requires (a) a pump (i.e., the respiratory pump; see figure 20.12b), which “expands and releases” the thoracic cavity by contraction and relaxation of skeletal muscles of breathing, and (b) electrical signals to control the pump, which are initiated in the brain and relayed by somatic motor nerves to the skeletal muscles of breathing. 23.5b Mechanics of Breathing LEARNING OBJECTIVES 23. Explain how pressure gradients are established by skeletal muscles of breathing and result in pulmonary ventilation. 24. Explain the relationship between pressure and volume as described by Boyle’s law. 25. Compare and contrast quiet and forced breathing. The mechanics of breathing involve several integrated aspects: (a) the specific actions of the skeletal muscles of breathing; (b) dimensional (volume) changes within the thoracic cavity; (c) pressure changes resulting from volume changes (based on Boyle’s gas law); (d) pressure gradients; and (e) volumes and pressures associated with breathing. Each of these aspects of breathing is discussed, and then this information is integrated to describe how breathing occurs. Skeletal Muscles of Breathing The skeletal muscles of breathing (see section 11.5) are classified into the following three categories: muscles of quiet breathing, muscles of forced inspiration, and muscles of forced expiration ( figure 23.19): Page 915 Figure 23.19 Skeletal Muscles of Breathing. Each listed action occurs when the given muscle is contracting. (The opposite occurs when the muscle is relaxing.) Muscles of quiet breathing are the skeletal muscles involved in normal rhythmic breathing that occurs at rest. They are the diaphragm and external intercostals. These muscles alternately contract and relax, resulting in movement of air into and out of the lungs. The diaphragm forms the rounded “floor” of the thoracic cavity and is dome-shaped when relaxed. When it contracts, its central portion flattens and moves inferiorly to press against the abdominal viscera. The external intercostals extend from a superior rib inferomedially to the adjacent inferior rib; contraction of these muscles elevates the ribs. Contraction of both the diaphragm and external intercostals increase the volume of the thoracic cavity (described shortly). Muscles of forced inspiration are used during a deep inspiration, as occurs during heavy exercise or prior to “holding a long note” while singing. These muscles include the sternocleidomastoid, scalenes, pectoralis minor, serratus posterior superior, and erector spinae. These muscles, except for the erector spinae, are located in a more superior location relative to the thoracic cavity and can effectively move the rib cage superiorly, laterally, and anteriorly, resulting in a greater increase in the volume within the thoracic cavity than occurs during quiet inspiration. Located along the length of the vertebral column, the erector spinae muscles also aid in lifting the rib cage, but do so by extending the vertebral column, as occurs when you “sit up straight.” Page 916 Muscles of forced expiration contract during a hard expiration—for example, when one blows up a balloon or coughs. The muscles of forced expiration include the internal intercostals, abdominal muscles, transversus thoracis, and serratus posterior inferior. In general, these muscles either pull the rib cage inferiorly, medially, and posteriorly or compress the abdominal contents to move the diaphragm superiorly into the thoracic cavity, resulting in a greater decrease in volume within the thoracic cavity than occurs during quiet expiration. The muscles of forced inspiration and forced expiration are collectively referred to as the accessory muscles of breathing. Volume Changes in the Thoracic Cavity The contraction of breathing muscles causes thoracic cavity volume changes, as just described. These volume changes occur in three dimensions: vertically, laterally, and in an anterior-posterior direction ( figure 23.20). Figure 23.20 Thoracic Cavity Dimensional Changes Associated with Breathing. The boxlike thoracic cavity changes size during inspiration and expiration. The box increases in vertical, lateral, and anterior-posterior dimensions during inspiration due to movement of the diaphragm, ribs, and sternum. These dimensions decrease during expiration. APR Module 11: Respiratory: Animations: Thoracic Cavity Dimensional Changes Vertical dimension changes of the thoracic cavity result from the movement of the diaphragm. When it contracts, its central portion flattens and moves inferiorly, which increases the vertical dimensions of the thoracic cavity. When the diaphragm relaxes and returns to its original position, the vertical dimensions decrease. Only small movements of the diaphragm are required for breathing, and usually the changes in vertical dimension measure only a few millimeters during quiet breathing. Greater changes in the superior movement of the diaphragm occur during forced expiration because of contraction of the abdominal muscles. Lateral dimension changes occur either as the rib cage is elevated and the thoracic cavity widens or as the rib cage depresses and thoracic cavity narrows. This action can be mimicked by placing your hands at the sides of your ribs and then abducting and adducting your hands relative to your ribs. Anterior-posterior dimension changes occur as the inferior portion of the sternum moves anteriorly and then posteriorly. This action can be visualized by placing one hand on the front of your lower chest and lifting it outwardly away from the chest and then back. In general, lateral and anterior-posterior dimensional changes both occur as a result of the contraction and relaxation of all the muscles of breathing shown in for the diaphragm. figure 23.19, except Boyle’s Law: Relationship of Volume and Pressure Volume changes in the thoracic cavity cause gas pressure changes in the thoracic cavity. Boyle’s law states that at a constant temperature, the pressure (P) of a gas decreases if the volume (V) of the container increases, and vice versa. The law may be expressed by the following formula: where P1 and V1 represent the initial conditions, and P2 and V2 represent the changed conditions for pressure and volume, respectively. This formula expresses an inverse relationship that exists between gas pressure and volume. Table 23.1 illustrates this relationship for Boyle’s law (as well as the two other gas laws, which are discussed in section 23.6a). Page 917 Table 23.1 Gas Laws Boyle’s Law In a closed system at a constant temperature, the volume and pressure of a gas are inversely related: As volume of the container increases, the pressure decreases. As volume of the container decreases, the pressure increases. Dalton’s law The total pressure in a mixture of gases is equal to the sum of all of the individual partial pressures. Henry’s law At a given temperature, the solubility of a gas in a liquid (i.e., how much gas can either enter or leave the liquid) is dependent upon the: (a) Partial pressure of the gas (total pressure × % of the gas) For a given gas, the greater the partial pressure, the greater the amount of gas that enters the liquid. The lower the partial pressure, the lower the amount of gas that enters the liquid. (b) Solubility coefficient of a gas (reflects how chemically compatible the gas and liquid are, or in other word how well does the gas “play” in the liquid) Comparison of two gases at the same partial pressure: The greater the solubility coefficient of a gas, the greater the amount of gas that enters the liquid. The lower the solubility coefficient of a gas, the lower the amount of gas that enters the liquid. Pressure Gradients An air pressure gradient occurs when the force per unit area is greater in one area than in another. If a pressure gradient exists between two regions, and they are interconnected, then air moves from the region of higher pressure to the region of lower pressure until the pressure in the two regions becomes equal. Figure 23.21a shows this relationship. Figure 23.21 Pressure Gradients and the Respiratory System. (a) The figure shows that air does not move if the pressure is equal between two areas. It also shows how air moves from an area of high pressure to an area of low pressure when pressure gradients are established by changes in volume. (b) Three significant pressures are associated with breathing. Atmospheric pressure is 760 mm Hg at sea level. The other two pressures are the intrapulmonary pressure and the intrapleural pressure, which both change during breathing as a result of changing volumes. Volumes and Pressures Associated with Breathing A similar relationship exists with respect to the atmosphere and the lungs, which are interconnected by the respiratory passageway ( figure 23.21b). The atmosphere is the air in the environment that surrounds us. Atmospheric pressure is the pressure (weight) gases in the air exert in the environment. Its value changes with altitude. The standard value is given at sea level because air becomes less dense, or “thins,” with increased altitude. The “thinner air” exerts a correspondingly lower atmospheric pressure. The value for atmospheric pressure at sea level can be expressed in several ways: 14.7 pounds per square inch = 1 atmosphere (atm) = 760 mm Hg. The value used in this text is 760 mm Hg. Atmospheric pressure does not change in the context of breathing. Page 918 The thoracic cavity contains the lungs. The collective volume of the alveoli within the lungs is called the alveolar volume, and its associated pressure is the intrapulmonary pressure (first described in section 23.4d). This pressure fluctuates with breathing and may be higher, lower, or the same as atmospheric pressure. Intrapulmonary pressure is equal to atmospheric pressure (at sea level = 760 mm Hg) at the end of both inspiration and expiration. Recall from section 23.4c that the lungs are separated from the wall of the thoracic cavity by the pleural cavity. The pressure exerted within the pleural cavity is called the intrapleural pressure. Intrapleural pressure also fluctuates with breathing and is always lower than intrapulmonary pressure so that the lungs remain inflated (see section 23.4d). At the end of an expiration, it (intrapleural pressure) is generally about 4 mm Hg lower than intrapulmonary pressure (756 mm Hg). Note that a volume change in the thoracic cavity alters pressure within the thoracic cavity, which establishes a pressure gradient between the atmosphere and the thoracic cavity. This pressure gradient determines the direction of airflow. Thus, an increase in volume of the thoracic cavity, with an accompanying decrease in pressure, results in air moving into the lungs during inspiration. In contrast, a decrease in volume of the thoracic cavity, with an accompanying increase in pressure, results in air moving out of the lungs during expiration. Integration of Concepts: Quiet Breathing Quiet breathing was described as the normal breathing that occurs when you are relaxed (see section 23.5a). Refer to figure 23.22 as you read through this description of the stepwise sequence of events that alter volume and pressure during quiet breathing: Figure 23.22 Mechanics of Quiet Breathing. Concept Overview Physiology Interactives APR Module 11: Respiratory: Animations: Alveolar Pressure Changes Quiet Inspiration 1 The diaphragm contracts and changes from its domed position to a flattened position, and the external intercostals contract, elevating the ribs. 2 The vertical, lateral, and anterior-posterior dimensions of the thoracic cavity increase, which collectively increases the thoracic cavity volume. Specifically, the pleural cavity volume increases and the lungs expand increasing alveolar volume. During quiet breathing, diaphragmatic movement may account for about two-thirds of the thoracic cavity volume change, and external intercostal movement for about one-third. 3 The intrapleural pressure decreases (with the increase in pleural cavity volume), and the intrapulmonary pressure decreases (with the increase in alveolar volume) from 760 mm Hg to 759 mm Hg. 4 When the intrapulmonary pressure decreases below atmospheric pressure, a pressure gradient is established and air moves down the pressure gradient from the environment into the alveoli, until the intrapulmonary pressure is once again equal to atmospheric pressure (760 mm Hg). The volume of air that moves from the atmosphere into the lungs during a single breath in quiet breathing is approximately 500 milliliters (mL), or 0.5 liter (L). ThiThe diaphragm relaxess volume of air is called the tidal volume. Note that during quiet inspiration the respiratory muscles—the diaphragm and external intercostals—and the outward recoil of the chest wall work to stretch the elastic tissue of the lungs. Quiet Expiration 1 The diaphragm relaxes, changing from the flattened position to the domed position, and external intercostals relax and the ribs fall. The lung tissue that was stretched during inspiration passively recoils. (No muscle contraction is required during quiet expiration.) 2 The vertical, lateral, and anterior-posterior dimensions decrease, which collectively decreases the thoracic cavity volume. Specifically, the pleural cavity volume decreases and the lungs recoil decreasing alveolar volume. 3 The intrapleural pressure increases (with the decrease in pleural cavity volume), and the intrapulmonary pressure increases (with the decrease in alveolar volume) from 760 mm Hg to 761 mm Hg. 4 When intrapulmonary pressure exceeds atmospheric pressure, a pressure gradient is established, and air moves down the pressure gradient from the alveoli into the atmosphere. This continues until the intrapulmonary pressure is once again equal to atmospheric pressure (760 mm Hg). Approximately 500 mL of air moves out of the lungs. Page 919 Note that whereas quiet inspiration requires muscle contraction, quiet expiration does not. Instead, the driving force for quiet expiration is dependent upon the recoil of the elastic tissue of the lungs. Each expiration ends when the pull of the recoil of the elastic tissue of the lungs is equal to the outward pull of the chest wall. (The loss of the elastic tissue of the lungs occurs in some respiratory diseases, such as emphysema; see “Emphysema.”) Clinical View 23.15: Integration of Concepts: Forced Breathing Forced breathing involves steps similar to quiet breathing. However, both forced inspiration and expiration are active processes, requiring contraction of accessory muscles of breathing (see figure 23.19). Their activity causes greater changes in both the thoracic cavity volume and the intrapulmonary pressure. Consequently, a steeper air pressure gradient is established and more air moves into and out of the lungs. Significant chest volume changes are apparent that accompany forced breathing, unlike the barely perceptible changes in the chest cavity volume that occur during quiet breathing. WHAT DID YOU LEARN? 21 Describe the sequence of events of quiet inspiration. 22 How are larger amounts of air moved between the lungs and atmosphere during forced inspiration and forced expiration? Is more energy expended during forced breathing? Why? Page 920 23.5c Nervous Control of Breathing LEARNING OBJECTIVES 26. Describe the anatomic structures involved in regulating breathing. 27. Explain the physiologic events associated with controlling quiet breathing. 28. Explain the different reflexes that alter breathing rate and depth. 29. Compare and contrast autonomic nervous system innervation of structures of the respiratory system and the somatic nervous system innervation of the skeletal muscles involved in breathing. The skeletal muscles of breathing are innervated by somatic motor neurons and are rhythmically coordinated by nuclei within the brainstem. The rate and depth of breathing are either altered through reflexes involving the brainstem ( section 13.5) or consciously controlled by the cerebrum (see section 13.3). Here we first describe the anatomic components of the (a) respiratory center within the brainstem, which regulates breathing; (b) skeletal muscles of breathing and their innervation; and (c) receptors that detect stimuli and relay sensory input to the respiratory center to alter breathing rate and depth. We then integrate these structures to discuss how the nervous system controls breathing. Please refer to figure 23.23 as you read through this section. Page 921 Figure 23.23 Respiratory Center. (a) The respiratory center rhythmically initiates nerve signals that ultimately reach the somatic motor neurons to the diaphragm and external intercostals to regulate quiet breathing. The respiratory center is stimulated to alter the breathing rate and depth primarily by (b) sensory input from central chemoreceptors in the brain and peripheral chemoreceptors within the carotid and aortic bodies. Based on this sensory input, nerve signals are then relayed to somatic motor neurons to (c) the skeletal muscles of breathing to alter the breathing rate or depth. Sensory input is also relayed to the respiratory center from (d) other sensory receptors, including irritant receptors of the mucosal lining of the respiratory tract, baroreceptors (stretch receptors) of the lungs and visceral pleura, and proprioceptors of muscles, tendons, and joints. Note that breathing can be consciously controlled by the cerebral cortex; its motor output bypasses the respiratory center to directly stimulate lower motor neurons innervating skeletal muscles of breathing. Anatomic Structures The autonomic nuclei within the brainstem that control breathing are collectively called the respiratory center ( figure 23.23a). One portion of this center, which is located within the medulla oblongata, is called the medullary respiratory center. Two groups of nuclei compose the medullary respiratory center. These are the ventral respiratory group (VRG), located within the anterior region of the medulla (which contains both inspiratory neurons and expiratory neurons), and the dorsal respiratory group (DRG), located posterior to the VRG. The other portion of the respiratory center is within the pons and is called the pontine respiratory center (or pneumotaxic center). Skeletal muscles of breathing include the diaphragm, the external intercostal muscles, and the accessory muscles of breathing, as previously described (see figure 23.19). Lower motor neurons that innervate the skeletal muscles of quiet breathing are within either the phrenic nerves that innervate the diaphragm (see section 14.5d) or the intercostal nerves that innervate the intercostal muscles (see section 14.5c). Accessory muscles of respiration are innervated by other individually named somatic nerves (not individually named in figure 23.23). Chemoreceptors are the primary sensory receptors involved in altering breathing ( figure 23.23b). Chemoreceptors can potentially monitor fluctuations in concentration of both hydrogen ions (H+) and respiratory gases (Pco2 and Po2) within both the cerebrospinal fluid (CSF) and the blood, depending upon the location of the chemoreceptors. Note that the concentrations of respiratory gases are expressed as the partial pressure of carbon dioxide (Pco2) and the partial pressure of oxygen (Po2). Partial pressures are discussed in section 23.6a. For now, just remember that the higher the partial pressure for a gas, the greater its concentration. Chemoreceptors are housed both within the brain (central chemoreceptors) and within specific blood vessels (peripheral chemoreceptors): Central chemoreceptors are within the medulla oblongata in close proximity to the medullary respiratory center. Central chemoreceptors monitor only H+ changes of CSF induced by changes in blood Pco2. Carbon dioxide (CO2) diffuses from the blood into the CSF. In the CSF, carbonic anhydrase catalyzes CO2 and water (H2O) to carbonic acid (H2CO3). The carbonic acid then dissociates into bicarbonate ( ) and hydrogen + + ions (H ). Thus, central chemoreceptors are monitoring H concentration within the CSF, which is formed from CO2 that diffuses there from the blood. (Other acids in the blood, such as lactic acid or ketoacids, are not able to cross the blood-brain barrier to exit the blood and enter the CSF. For this reason acid [H+] in the blood is not monitored by central chemoreceptors.) It is important to note that the CSF (unlike the blood) lacks proteins to buffer the gain or loss of H+. (See the discussion of chemical buffers in section 25.5d.) Consequently, H+ changes within the CSF most accurately reflect the changes in blood Pco2. Peripheral chemoreceptors are located both within the aortic arch (called the aortic bodies) and at the split of each common carotid artery into the external and internal carotid arteries (called carotid bodies). Peripheral chemoreceptors normally detect changes in the concentration of both H+ and Pco2 within arterial blood. The peripheral chemoreceptors differ from central chemoreceptors because they are stimulated by changes in H+ produced independently of Pco2. This may, for example, occur due to kidney failure (kidneys normally eliminate H+; see section 24.6d) or as result of uncontrolled diabetes mellitus (ketoacids are a by-product from metabolism of fatty acids; see section 25.6c). Peripheral chemoreceptors can also be stimulated by relatively large changes in blood Po2. When stimulated by changes in either blood H+ or blood respiratory gases, the carotid bodies alter nerve signals relayed along the glossopharyngeal nerves, and the aortic bodies alter nerve signals relayed along the vagus nerves to the respiratory center. INTEGRATE LEARNING STRATEGY 23.3 This summary can help you remember what is monitored by the two different types of chemoreceptors. Central chemoreceptors monitor cerebrospinal fluid H+ levels in CSF (which is produced from CO2 that has diffused there from the blood). Peripheral chemoreceptors monitor blood: (a) CO2 levels, (b) H+ levels that are produced through metabolic processes (e.g., lactic acid, ketoacids), and (c) relatively large changes in O2. INTEGRATE CLINICAL VIEW 23.12 Apnea Apnea (ap΄nē-ă; a = absence, pnea = breathing) is the absence of breathing. It can occur voluntarily (during swallowing or holding your breath), be druginduced (e.g., anesthesia), or result from neurologic disease or trauma. Sleep apnea is the temporary cessation of breathing during sleep. Individuals diagnosed with sleep apnea may be prescribed a CPAP (continuous positive airway pressure) machine to be worn during sleep. This machine consists of a fan, a tube, and a mask that is worn over the nose (and sometimes also over the mouth). The machine pressurizes the air and pushes the air through the mask, which forces the airway to remain open during sleep. Amy Walters/Shutterstock Page 922 Other receptors include irritant receptors (a type of nociceptor; see section 16.1d) located within the respiratory passageways that are stimulated by dust and other particulate matter, baroreceptors (see section 16.1d) located within both the visceral pleura and the bronchiole smooth muscle that are stretch receptors, and proprioceptors (see section 16.2b) located within muscles, tendons, and joints that are stimulated by body movement ( figure 23.23d). Physiology of Breathing There is much still unknown about how breathing is completely controlled, and research continues into the details of the specific mechanisms. The following description provides some insight into what is generally accepted. Quiet Breathing Quiet inspiration is initiated when nuclei within the medullary respiratory center initiate nerve signals that are sent through the nerve pathways to the skeletal muscles of quiet breathing. These signals lasts for approximately 2 seconds, and intensity of the nerve signals increases over these 2 seconds. This stimulates both the diaphragm and external intercostal muscles to contract, resulting in an increase in volume and a decrease in pressure in the thoracic cavity. Thus, a pressure gradient is established, and air moves from the atmosphere into the alveoli (as described in section 23.5b). Quiet expiration occurs with cessation of nerve signals that are relayed along nerve pathways to the skeletal muscles of quiet breathing; this lasts typically for approximately 3 seconds. Lack of stimulation causes both the diaphragm and external intercostal muscles to relax. The elastic tissue of the lungs recoils, and the thoracic cavity volume decreases and its pressure increases. Thus, a pressure gradient is established and air moves from the alveoli into the atmosphere (as described in section 23.5b). A breathing rhythm that involves 2 seconds of inspiration followed by 3 seconds of expiration results in an average respiratory rate of 12 times per minute. The average range for the rate of quiet breathing is generally between 12 and 15 times per minute—a rate referred to as eupnea. The specific role of the pontine respiratory center in breathing is to relay nerve signals to the medullary respiratory center to facilitate a smooth transition between inspiration and expiration. Individuals who have experienced damage to this center are able to still breathe. However, the breathing is erratic and involves long, gasping inspirations followed by occasional expirations. INTEGRATE LEARNING STRATEGY 23.4 The functions of the autonomic nuclei within the brainstem that control breathing can be compared to positions in a business: (a) The medullary respiratory center is the boss that controls the output (thus, controls breathing), and (b) the pontine respiratory center is an external regulatory group that makes sure everything runs smoothly. WHAT DO YOU THINK? 3 The phrenic nerves extend from the cervical plexus formed by the rami of spinal nerves C3–C5 (see section 14.5d), whereas the intercostal nerves are the anterior rami of spinal nerves T1–T11 (see section 14.5c). Predict the consequences to breathing for each condition if a spinal cord injury is (a) at C2 or above, (b) between C6 and T11, and (c) T12 or below. Reflexes That Can Alter Breathing Rate and Depth Reflexes that can alter our breathing are primarily initiated by chemoreceptors. However, our breathing patterns can also be changed by sensory input from other receptors, including proprioceptors, baroreceptors, and irritant receptors. Altering Breathing Rate and Depth Through Reflexes Involving Chemoreceptors Breathing rate and depth are primarily altered by reflexes that respond to sensory input from chemoreceptors. Nerve signals from these receptors are sent along sensory neurons to the medullary respiratory center, which ultimately results in a change in the rate and depth of breathing. Change in the rate of breathing is accomplished by altering the amount of time spent in both inspiration and expiration, whereas altering the depth of breathing is accomplished through stimulation of accessory muscles, which results in greater thoracic volume changes. Breathing rate and depth can be reflexively increased if either (a) the central chemoreceptors detect an increase in H+ concentration in the CSF (which is produced from CO2 that diffused into the CSF from the blood) or (b) the peripheral chemoreceptors detect an increase in blood H+ concentration, an increase in blood Pco2, or both. Central chemoreceptors relay additional nerve signals directly to the closely located medullary respiratory center, and peripheral chemoreceptors relay additional nerve signals along sensory neurons within either the glossopharyngeal nerves from the carotid bodies or the vagus nerves from the aortic bodies to the medullary respiratory center. Respiration rate and depth are increased and additional CO2 is expelled, ultimately returning blood Pco2 and CSF H+ levels to normal levels. Conversely, a decrease in either H+ or Pco2 initiates fewer nerve signals relayed to the medullary respiratory center, and respiration rate and depth are decreased. The most important stimulus affecting breathing rate and depth is blood Pco2. The chemoreceptors are very sensitive to changes in blood Pco2 levels; increases in Pco2 levels as small as 5 mm Hg will double the breathing rate. The changes in blood Pco2 can stimulate respiratory rate changes most powerfully when the carbon dioxide is joined to water, forming carbonic acid in the CSF. This is because, as described earlier in this section, changes in H+ within the CSF most accurately reflect the changes in blood Pco2 because the CSF (unlike the blood) lacks proteins to buffer H+. Generally, changes in blood Po2 are not an independent means of regulating breathing. Note that the arterial oxygen level in the blood must decrease substantially from its normal Po2 level of 100 mm Hg to an abnormally low level of 60 mm Hg before it can stimulate the chemoreceptors independently of Pco2. This relationship can have deadly consequences to swimmers who hyperventilate before swimming under water. This hyperventilation causes the blood Pco2 levels to decrease to the point where chemoreceptors are not stimulated. The swimmer’s blood Po2 level is decreased at the same time by exertion, but not enough to stimulate chemoreceptors. A swimmer may lose consciousness and drown as a result. Po2 levels normally influence breathing rate by causing the chemoreceptors to be more sensitive to changes in blood Pco2. This relationship has a synergistic effect: The combination of decreased Po2 and increased Pco2, along with the subsequent production of H+, causes greater stimulation of the chemoreceptors. Page 923 INTEGRATE CLINICAL VIEW 23.13 Hypoxic Drive Certain respiratory disorders (such as emphysema) result in decreased ability to expire carbon dioxide, and the decreased blood Po2 levels can become the stimulus for breathing. The decreased blood Po2 as the stimulus for breathing is called the hypoxic (hĪ-pok΄sik) drive. It occurs as carbon dioxide levels in the blood become elevated and remain elevated over a long period of time. Chemoreceptors become less sensitive to Pco2 and, by default, decreased Po2 levels stimulate them. Since a low Po2 is the stimulus for breathing, administering oxygen would elevate Po2 and thus interfere with the person’s ability to breathe on his or her own. Altering Breathing Patterns Through Reflexes Involving Other Receptors Receptors other than chemoreceptors alter breathing patterns; these include proprioceptors, baroreceptors, and irritant receptors. Proprioceptors within muscles, tendons, and joints, when stimulated by body movement, increase nerve signals to the respiratory center with a subsequent increase in breathing depth. Baroreceptors within both the visceral pleura and bronchiole smooth muscle are stimulated by stretch. These sensory receptors initiate a reflex to prevent overstretching of the lungs by inhibiting inspiration activities. This reflex is referred to as the inhalation reflex, or Hering-Breuer reflex. It effectively protects the lungs from damage due to overinflation. When overstretched, these baroreceptors send nerve signals through the vagus nerves to the respiratory center to shut off inspiration activity, thus resulting in expiration. This may be a normal means of controlling respiration in infants, but it is thought to serve only as a protective reflex after infancy. Irritant receptors, when stimulated, initiate either a sneezing or coughing reflex. A sneeze reflex is initiated by irritants within the nasal cavity and a cough reflex by irritants within the trachea and bronchi. Nerve signals are relayed by sensory neurons to the medulla oblongata (sneezing or coughing nuclei, respectively; see section 13.5c). These nuclei initiate nerve signals along motor neurons, which cause the vocal cords to close and the abdominal muscles to contract forcefully. The vocal cords, which are initially closed, then open abruptly as the pressure increases in the thoracic cavity. Both reflexes result in an explosive blast of exhaled air that potentially removes the irritant. Action of Higher Brain Centers Higher brain centers, including the hypothalamus, limbic system, and cerebral cortex, can influence breathing rate (see figure 13.1). The hypothalamus increases the breathing rate if the body is warm and decreases it if the body is cold. The limbic system alters the breathing rate in response to emotions and emotional memories. The frontal lobe of the cerebral cortex controls voluntary changes in our breathing pattern for various activities, such as talking, singing, breath-holding, performing the Valsalva maneuver (see section 23.2d), and other actions. Unlike the other higher areas of the brain that relay impulses to the respiratory center, nerve signals from the cerebral cortex bypass the respiratory center to directly stimulate lower motor neurons in the spinal cord ( figure 23.23). Nervous Control of Anatomic Structures of the Respiratory System and Anatomic Structures of Breathing We distinguish between the innervation to the anatomic structures of the respiratory system and the anatomic structures that function in breathing. Anatomic structures of the respiratory system, which are composed of both smooth muscle and glands, are innervated by the axons of lower motor neurons of the sympathetic and parasympathetic divisions of the autonomic nervous system and controlled by autonomic nuclei within the brainstem (see section 23.4b). In contrast, breathing muscles, which are skeletal muscles, are innervated by axons of the lower motor neurons of the somatic nervous system (see section 12.1b). However, the control of the breathing muscles comes from both autonomic nuclei in the brainstem and somatic nuclei in the cerebral cortex. The autonomic nuclei forming the respiratory center within the brainstem regulate normal breathing with their rhythmic output along the lower motor neurons of the phrenic and intercostal nerves, and, via reflexes, this center alters breathing rate and depth in response to various sensory input, as described. The cerebral cortex consciously regulates breathing by directly stimulating lower motor neurons that extend to the skeletal muscles of breathing. This diverse motor output from the nervous system allows breathing to be controlled both reflexively and consciously. WHAT DID YOU LEARN? 23 What are the functions of the (a) medullary respiratory center and (b) the pontine respiratory center? What analogous positions in a business would these two areas in the brain perform? 24 Which of the following stimuli will cause an increase in the respiratory rate: (a) increase in blood Pco2, (b) increase in blood H+, (c) increase in H+ within the CSF, and (d) increase in blood Po2? 25 Are the skeletal muscles of breathing innervated by somatic nerves or autonomic nerves? Explain. 23.5d Airflow, Pressure Gradients, and Resistance LEARNING OBJECTIVES 30. Define airflow. 31. Explain how pressure gradients and resistance determine airflow. Airflow Airflow is the amount of air that moves into and out of the respiratory tract with each breath. Sufficient exchange of air must be maintained for normal body functions; this exchange is in part determined by airflow and variables that affect it. Airflow is a function of two factors: (a) the pressure gradient established between atmospheric pressure and intrapulmonary pressure and (b) the resistance that occurs due to conditions within the respiratory tract, lungs, and chest wall ( figure 23.24). The formula for airflow is expressed here: The parameters are F = airflow, ΔP = difference in pressure between atmosphere (atm) and the intrapulmonary pressure within the alveoli (alv), and R = resistance. Pressure Gradient This mathematical expression demonstrates that airflow is directly related to the pressure gradient between the atmosphere and lungs. The pressure gradient (ΔP) in the air passageway is the difference between atmospheric pressure and intrapulmonary pressure (Patm – Palv). Most importantly, the air pressure gradient is the driving force for airflow into and out of the lungs. The pressure gradient can be changed by altering the volume of the thoracic cavity through the skeletal muscles of breathing ( figure 23.24a). Generally, the more forceful their contractions, the greater the pressure gradient, and the greater the airflow. During normal quiet breathing, contraction of both the diaphragm and the external intercostals establish a relatively small pressure gradient that allows approximately 500 mL of air to enter the lungs. The thoracic cavity volume is further increased and a steeper pressure gradient is established if accessory muscles of forced inspiration are stimulated. The steeper pressure air gradient increases airflow. However, it is a change exhibited only with greater effort exerted by the skeletal muscles of breathing. Page 924 Figure 23.24 Factors That Influence Airflow. Airflow is directly related to the pressure gradient and inversely related to resistance. (a) Air pressure gradients are established by the skeletal muscles of breathing. The stronger the muscular force generated, the steeper the pressure gradient, the greater the airflow; the weaker the muscular force generated, the less steep the pressure gradient and the smaller the airflow. (b) Resistance always opposes airflow, and it is influenced by bronchiole diameter, and compliance, which is a function of both the ease with which the chest wall and lungs inflate and the surface tension within the alveoli. INTEGRATE CONCEPT CONNECTION A similar mathematical relationship expresses blood flow in the cardiovascular system as a function of a pressure gradient and resistance (see section 20.5c). Similar to how the skeletal muscles of breathing establish air pressure gradients to move air into and out of the lungs, the heart establishes the blood pressure gradient to drive blood through the cardiovascular system. And just as air experiences resistance in the respiratory tract and opposes airflow, blood experiences resistance within the blood vessels and opposes blood flow. In comparison, smaller pressure gradients may be established from weakness of muscles of breathing (e.g., as may be caused by muscular dystrophy or myasthenia gravis). This results in smaller increases in thoracic cavity volume and smaller pressure gradients. As a result, airflow into the lungs decreases. Thus, it is the skeletal muscles of breathing that “power breathing” to establish the pressure gradient to move air through the respiratory passageway. Resistance This mathematical expression also demonstrates that airflow is inversely related to resistance. Airflow is always opposed by resistance. Resistance includes all the factors that make it more difficult to move air from the atmosphere through the respiratory passageway into the alveoli. Resistance may be altered through the following ( figure 23.24b): a change in the bronchiole diameter or the size of the passageway through which air moves, and a change in compliance. Bronchiole diameter influences airway resistance, because of the friction the air experiences as it moves through the air passageway. Airway resistance increases with bronchoconstriction, which is caused by parasympathetic division stimulation, histamine release, or exposure to cold. Abnormal changes within the bronchioles (e.g., accumulation of mucus, inflammation) decrease the diameter of each bronchiole lumen, which also increases resistance. In contrast, resistance decreases with bronchodilation, which is caused by sympathetic division stimulation and the subsequent release of epinephrine and norepinephrine from the adrenal medulla, or with external administration of epinephrine. Page 925 In addition to bronchiole diameter, resistance is influenced by compliance. Compliance is the ease with which the chest wall and lungs expand, and it is dependent upon the distensibility (ability to stretch) of the chest wall and lungs ( figure 23.24b). Young, healthy chest walls and lung tissue are naturally distensible. The more stretchy the chest wall and lungs, the greater the compliance. However, as we age, elastic connective tissue decreases in both the chest wall and the lungs, making them less distensible. A decrease in the distensibility of the chest wall and lungs is also observed, for example, in an individual with a vertebral column malformation, such as scoliosis; arthritis within the thoracic cage; or if elastic connective tissue in the lungs has been replaced with inflexible scar tissue, which occurs with pulmonary fibrosis. Because these changes decrease distensibility, they also decrease compliance (the ease with which the lungs expand). INTEGRATE LEARNING STRATEGY 23.5 The experience of blowing up balloons might help in understanding compliance. Some balloons are easier to inflate because their walls are more stretchable (i.e., they are more compliant), whereas other balloons take greater effort to inflate because they are less stretchable (i.e., they are less compliant). Compliance is also influenced by surface tension within the alveoli. The amount of surface tension is primarily a function of surfactant (see section 23.3c). High surface tension occurs if alveolar type II cells are not producing sufficient pulmonary surfactant because this condition increases resistance. This variable is generally important only with premature infants who are unable to produce sufficient pulmonary surfactant (healthy lungs continue to produce pulmonary surfactant beginning approximately 2 months prior to full-term birth). Without pulmonary surfactant, the alveoli in the lungs of these premature infants collapse with each expiration (see figure 23.12b). With each inspiration, the high surface tension caused by the wet inner surface of the alveoli must be overcome for air to enter and reinflate the alveoli for gas exchange. These infants, therefore, experience greater resistance to airflow. This condition is referred to as respiratory distress syndrome (RDS). Given that airflow and resistance are inversely related, if resistance increases with either bronchiole constriction (e.g., bronchitis) or decreased compliance (e.g., pulmonary fibrosis), airflow decreases. In comparison, if resistance decreases with either bronchiole dilation (e.g., epinephrine) or increased compliance (with healthy elastic chest wall and lungs), airflow increases. WHAT DO YOU THINK? 4 Epinephrine is administered in the treatment of asthma. Does epinephrine increase or decrease airway resistance? Does epinephrine increase or decrease airflow? Respiratory diseases and anatomic abnormalities that increase resistance to airflow are associated with either a decrease in the size of the lumen of bronchioles (e.g., asthma) or a decrease in compliance (e.g., pulmonary fibrosis), or both. These changes produce an increase in resistance. If adequate airflow is to be maintained, the increased resistance must be met with more forceful inspirations to establish a steeper pressure gradient. The muscles of inspiration must work harder, and a greater amount of the body’s metabolic energy must be spent on breathing, for more forceful inspirations to occur. Approximately 5% of the total energy expenditure of the body normally is spent for quiet breathing. This value increases as airway resistance increases, and it can reach 20% to 30% of energy expenditure. This four-fold to six-fold increase in energy is so demanding that individuals with these disorders can become exhausted simply from breathing. WHAT DID YOU LEARN? 26 The two factors that determine airflow are the pressure gradient and resistance. What are the major factors that increase resistance to airflow? What changes to breathing must occur to maintain adequate airflow if resistance is increased? 23.5e Minute Ventilation and Alveolar Ventilation LEARNING OBJECTIVES 32. Compare and contrast minute ventilation and alveolar ventilation, and explain the significance of each. 33. Describe the relationship between anatomic dead space and physiologic dead space. How much air do you normally breathe in a minute? This volume of air is called, appropriately, minute ventilation (or minute volume or total pulmonary ventilation). The normal adult breathes approximately 500 mL per breath (tidal volume), and this occurs about 12 times per minute. The amount of air taken in during 1 minute is calculated using the following formula: WHAT DO YOU THINK? 5 Is all of the air taken in during minute ventilation available for gas exchange? Why or why not? Note that only the air reaching the alveoli is available for gas exchange with the blood. When air is moved from the atmosphere into the respiratory tract, a portion of it remains in the conducting zone. This collective space, where there is no exchange of respiratory gases, is referred to as the anatomic dead space, and it has an average volume of approximately 150 mL. (However, a general rule is that the volume of the anatomic dead space in milliliters is approximately equal to an individual’s body weight in pounds.) The amount of air that reaches the alveoli and is available for gas exchange per minute is termed alveolar ventilation. This volume is less than minute ventilation because the volume of air in the anatomic dead space must be subtracted from the volume of air inhaled with each breath. Thus, alveolar ventilation is calculated using the following mathematical formula: Deeper breathing is more effective for maximizing alveolar ventilation than faster, shallower breathing. Assuming you take one deep breath, you have to overcome the dead air space only one time. All the additional air inhaled in that breath is available for gas exchange. If you take two quick breaths, you have to fill the dead air space twice. Page 926 Some respiratory disorders result in a decreased number of alveoli participating in gas exchange. This decrease can be due either to damage to the alveoli or to a change in the respiratory membrane, such as when fluid accumulates in the lungs with pneumonia (see Clinical View 23.8: “Pneumonia”). The difference in volume of air available for gas exchange is accounted for by the more inclusive term physiologic dead space, which is the normal anatomic dead space plus any loss of alveoli. The anatomic dead space is equivalent to the physiologic dead space in a healthy individual, because the loss of alveoli should be minimal. WHAT DID YOU LEARN? 27 A person in yoga class is encouraged to take long, slow, deep breaths. Would this person have greater or lesser alveolar ventilation than an individual with more shallow breathing? Explain. 23.5f Measuring Respiratory Function LEARNING OBJECTIVES 34. Define the four different respiratory volume measurements and explain how the four respiratory capacities are calculated from the volume measurements. 35. Define and explain the significance of forced vital capacity, forced expiratory volume (FEV), and maximum voluntary ventilation (MVV). Respiratory volumes vary throughout a 24-hour period and during different stages of your life. They also vary from individual to individual. The variation is significant enough to be used as a diagnostic tool for determining the health of an individual’s respiratory system. Values for an individual are compared to standard values of a reference population. Respiratory measurements are often used to diagnose respiratory disease, monitor changes in respiratory impairment over time, and assess effectiveness of treatment (e.g., allergies, asthma, emphysema, cystic fibrosis). These tests may also be part of routine physicals for healthy individual, and to monitor employee health in certain industries (e.g., coal mines). For individuals who have impaired lung or heart function, or who are smokers, respiratory tests may be used to determine if the individual is sufficiently healthy for surgery or other medical procedures. One way to measure respiratory volumes is with a spirometer, which is a device composed of inverted hollow container that is immersed in water, which moves when an individual blows into a connecting tube. The more modern technique involves electronic measurements that record results when an individual blows into a tube. Four major respiratory volumes are typically measured ( figure 23.25). Tidal volume (TV) is the amount of air inhaled or exhaled per breath during quiet breathing, which typically averages 500 mL (see section 23.5b). Inspiratory reserve volume (IRV) is the amount of air that can be forcibly inhaled beyond the tidal volume (after a normal inspiration). IRV is a measure of lung compliance. Expiratory reserve volume (ERV) is the amount that can be forcibly exhaled beyond the tidal volume (after a normal expiration). ERV is a measure of lung and chest wall elasticity. Finally, residual volume (RV) is the amount of air left in the lungs even after the most forceful expiration. Figure 23.25 Respiratory Volumes and Capacities. Pulmonary volumes include tidal volume, inspiratory reserve volume, expiratory reserve volume, and residual volume. Capacities are the sum of two or more volumes. Inspiratory capacity includes tidal volume and inspiratory reserve volume. Functional residual capacity includes expiratory reserve volume and residual volume. Vital capacity includes tidal volume, inspiratory reserve volume, and expiratory reserve volume. Total lung capacity is the sum of all four volumes. (Notice that inspiratory capacity and functional residual capacity when added together equal the total lung capacity.) There are four major respiratory capacities that can be calculated from the summation of two or more of these respiratory volumes. Inspiratory capacity (IC) is the sum of the tidal volume plus the inspiratory reserve volume. Functional residual capacity (FRC) is the sum of the expiratory reserve volume plus the residual volume. It is the volume of air that is normally left in the lungs after a quiet expiration. Vital capacity (VC) is the sum of the tidal volume plus both the inspiratory reserve volume and expiratory reserve volume. (The residual volume is not part of the vital capacity.) VC is significant because it is a measure of the maximum amount of air that can be forcefully expired after a forced inspiration. Finally, total lung capacity (TLC) is the sum of all the volumes, including the residual volume, and is the maximum volume of air that the lungs can hold. Certain pulmonary function tests involve measuring the rate of airflow. These tests include forced expiratory volume and maximum voluntary ventilation. Forced expiratory volume (FEV) is the percentage of the vital capacity that can be forcefully expelled in a specific period of time. For example, FEV1 is the vital capacity percentage that is expired in 1 second. This value is obtained by inspiring as much air as possible and then expelling the air from the lungs as quickly as possible. A healthy person should be able to expel 75% to 85% of the vital capacity in 1 second. These pulmonary function tests that measure FEV provide a means of distinguishing a chronic obstructive pulmonary disorder (COPD) such as emphysema, where individuals have trouble expiring, from a chronic restrictive pulmonary disease (CRPD), such as pulmonary fibrosis, where an individual has trouble inspiring. Individuals with a COPD have trouble expiring air, which results in a lower than normal value for FEV1 (see Clinical View 23.15: “Emphysema”). Maximum voluntary ventilation (MVV) is the greatest amount of air that can be taken into, and then expelled from, the lungs in 1 minute. MVV levels are obtained by breathing as quickly and as deeply as possible for 1 minute. Maximum voluntary ventilation can be as high 30 L/min (compared to the minute ventilation at rest of 6 L/min). All individuals with respiratory disorders have an impaired ability to inspire, expire, or both—thus, they will exhibit lower than normal MVV values. WHAT DID YOU LEARN? 28 How are the respiratory capacities calculated?