Respiratory System Function PDF

Automatic ZoomActual SizePage Width100%50%75%100%125%150%200%300%400% Chapter 14: Respiration 494 Lesson 14.2 **Respiratory System Function** Introduction The respiratory system functions to bring oxygen (O2) into the body for distribution to cells and to remove carbon dioxide (CO2) waste gene...

Automatic ZoomActual SizePage Width100%50%75%100%125%150%200%300%400% Chapter 14: Respiration 494 Lesson 14.2 **Respiratory System Function** Introduction The respiratory system functions to bring oxygen (O2) into the body for distribution to cells and to remove carbon dioxide (CO2) waste generated by cellular metabolism from the body. In addition, the respiratory system participates in regulation of body pH and body temperature, produces sounds used for vocal communication, and protects the body from inhaled pathogens and other harmful inhaled substances. This lesson describes mechanisms by which the respiratory system carries out its primary functions. 14.2.01 Mechanism of Respiration Functions of the respiratory system entail movement of air into and out of the lungs via a process called **ventilation**, which consists of alternating phases of **inspiration** and **expiration**. Air movement to and from the lungs occurs due to differences in pressure between air in the lungs and air outside the body. Within the lungs, changes in pressure that result in inspiration or expiration occur via activity of [skeletal](javascript:void(0)) [muscles](javascript:void(0)) coupled with the lungs\' natural resiliency (ie, elasticity). Skeletal muscles that function primarily in ventilation include the dome-shaped **diaphragm** and the **intercostal muscles**, which are attached to the ribs (Figure 14.5). Chapter 14: Respiration 495 **Figure 14.5** Muscles primarily involved in ventilation. Inspiration occurs when pressure within the lungs\' alveoli drops below atmospheric pressure. This decrease in alveolar pressure occurs when the volume of the thoracic cavity increases due to contraction (ie, flattening) of the diaphragm and, to a lesser extent, rib cage expansion via contraction of the external intercostal muscles. Because pleural membranes connect the lungs to the thoracic cavity wall, thoracic cavity expansion causes lung expansion, resulting in decreased lung pressure in accordance with [Boyle\'s law](javascript:void(0)). Consequently, air moves from an area of higher pressure in the atmosphere to an area of lower pressure in the lungs. Expiration occurs when the volume of the thoracic cavity decreases, which causes air pressure within the lungs to exceed atmospheric pressure, driving air from the respiratory system out of the body. Passive (ie, unforced) expiration takes place as the diaphragm relaxes and resumes a dome shape, whereas forced expiration is an active process that involves contraction of the internal intercostal muscles and abdominal muscles. The recoil of elastic fibers that stretch during inspiration facilitates expiration by generating a force that constricts alveoli. Figure 14.6 summarizes factors responsible for inspiration and expiration. A diagram of the human body Description automatically generated Chapter 14: Respiration 496 **Figure 14.6** Factors responsible for inspiration and expiration. Proper lung function is dependent on the maintenance of a thin layer of watery fluid called **alveolar lining fluid (ALF)**, which is found on the interior surface of alveoli. This fluid protects alveoli from desiccation (ie, drying out), provides immune defense of the lungs via alveolar macrophages and antimicrobial proteins, and mediates respiratory gas exchange. The interface between ALF and alveolar air results in the development of **surface tension**, which, along with the behavior of elastic fibers around alveoli, creates lung resiliency. **Pulmonary surfactant**, a lipid-protein mixture secreted into ALF by type II alveolar cells, reduces surface tension, thereby lowering the amount of work needed to expand alveoli during inspiration (see Figure 14.7). A potentially fatal condition called neonatal respiratory distress syndrome can occur in premature infants who do not produce sufficient surfactant. This condition greatly increases the amount of energy these infants expend during inspiration.  Chapter 14: Respiration 497 **Figure 14.7** Effect of pulmonary surfactant on lung resiliency. Some aspects of lung function can be evaluated via [spirometry](javascript:void(0)), a diagnostic test used to determine various [lung volumes and capacities](javascript:void(0)) (see Figure 14.8). The following parameters can be directly measured via spirometry or indirectly calculated from other test results: **Tidal volume (TV)** is the amount of air that moves into or out of the lungs during one respiratory cycle while at rest (ie, during a single unforced inspiration and expiration cycle). **Inspiratory reserve volume (IRV)** is the amount of additional air that can be forcefully breathed in following a normal, quiet inspiration. **Expiratory reserve volume (ERV)** is the amount of additional air that can be forcefully breathed out following a normal, passive expiration. **Inspiratory capacity (IC)** is the total amount of air that can be forcefully breathed in following a normal, passive expiration (ie, IC = TV + IRV). A diagram of a structure Description automatically generated Chapter 14: Respiration 498 **Vital capacity (VC)** is the maximum amount of air that can be forcefully breathed out following a forceful, maximal inspiration (ie, VC = TV + IRV + ERV). **Residual volume (RV)** is the amount of air present in the lungs following a forceful, maximal expiration (ie, RV = FRC − ERV). **Functional residual capacity (FRC)** is the amount of air present in the lungs following a normal, passive expiration (ie, FRC = ERV + RV). **Total lung capacity (TLC)** is the maximum amount of air that can be contained within the lungs (ie, TLC = TV + IRV + ERV + RV). **Anatomical dead space** is the total volume of the structures that constitute the respiratory system\'s conducting zone (which extends from the nose to the terminal bronchioles and contains inspired air that does not participate in alveolar gas exchange). **Figure 14.8** Lung volumes and capacities. Respiratory system function can be adversely affected by various diseases that impact ventilation and/or lung volumes and capacities. For example, **asthma**, which involves airway inflammation and bronchoconstriction (ie, narrowing of bronchi and bronchioles via contraction of smooth muscle), results in increased resistance to airflow. Asthma can also involve an overproduction of mucus, which can further impede airflow. Acute asthma attacks can be life-threatening due to greatly reduced gas exchange resulting from a lack of lung ventilation. **Chronic obstructive pulmonary disease (COPD)** also causes reduced airflow and makes ventilation difficult. The main types of COPD are [emphysema and chronic bronchitis](javascript:void(0)). Emphysema, which is typically associated with cigarette smoking, results in damage to the lungs\' alveoli. Emphysema leads to the enlargement of alveoli due to destruction of alveolar walls and also results in a loss of alveolar elasticity. These changes cause reduced alveolar surface area available for gas exchange and [increased](javascript:void(0)) [residual volume](javascript:void(0)), which reduces ventilation efficiency. Figure 14.9 illustrates the effects of asthma and emphysema.  Chapter 14: Respiration 499 **Figure 14.9** Effects of asthma and emphysema. The structures through which air passes to reach the lungs (Figure 14.10) condition the air. The changes made to inhaled air help facilitate gas exchange and protect the lungs\' delicate alveoli from damage due to desiccation or cold temperatures. As air passes through the nasal cavity, pharynx, and trachea, A diagram of human organs Description automatically generated Chapter 14: Respiration 500 mucous membranes lining these structures transfer heat and moisture to the air. In addition, as discussed in Concept 14.1.02, the mucociliary escalator operates within the nasal cavity, larynx, trachea, bronchi, and bronchioles to remove particulates (eg, dust, pathogens) from the air before it reaches the alveoli. The larynx, the opening to which is covered during swallowing by the **epiglottis** to prevent food or liquid from entering the airway, contains **vocal folds** (ie, true vocal cords). These folds of tissue can produce sounds via vibration as air passes between them during expiration. The length and tension of the vocal folds can be changed by contraction of muscles within the larynx to regulate the sound\'s [pitch](javascript:void(0)). The loudness of the sound is a function of airflow force between the vocal folds, with stronger airflow producing louder sounds. Airflow force is dependent on the activity level of the muscles responsible for forced expiration. Forced expiration also enables the respiratory system to expel potentially harmful materials via coughing or sneezing. Coughing can be performed voluntarily and is also triggered reflexively by substances that irritate the airways (eg, larynx, bronchioles) in some manner. Sneezing functions to reflexively expel irritating substances from the nasal cavity. **Figure 14.10** Components and functions of the upper respiratory tract.  Chapter 14: Respiration 501 14.2.02 Gas Exchange [Gas exchange](javascript:void(0)) between air within the lungs\' alveoli and blood within pulmonary capillaries around the alveoli is driven by differences in [partial pressures](javascript:void(0)) of respiratory gases (ie, O2 and CO2). Like other gases, O2 and CO2 move from regions of higher partial pressure to regions of lower partial pressure. As described by [Henry\'s law](javascript:void(0)), the amount of a gas that becomes dissolved in a solution with which the gas is in contact is directly proportional to the gas\'s partial pressure. Therefore, the dissolved gas content of blood moving through pulmonary capillaries varies based on partial pressures of the gases in alveolar air. [Blood is carried](javascript:void(0)) from the heart to the gas exchange sites (ie, alveoli) of the lungs via pulmonary arteries. Blood returns to the heart from the lungs via pulmonary veins and is pumped to the rest of the body (see Concept 13.1.07). As shown in Figure 14.11, the partial pressure of O2 (ie, PO2) in alveolar air is initially greater than the PO2 of blood plasma carried past the alveoli within pulmonary capillaries. Consequently, O2 diffuses from the alveolar air into the blood within the pulmonary capillaries until the blood\'s PO2 matches the PO2 of the alveolar air (ie, [reaches dynamic equilibrium](javascript:void(0))). The partial pressure of CO2 (PCO2) in blood plasma within pulmonary capillaries is initially greater than the PCO2 of alveolar air (see Figure 14.11), causing CO2 to diffuse out of the blood into the air within the alveoli. The air within the alveoli is then removed from the body via expiration. **Figure 14.11** Gas exchange in the lung. A diagram of blood flow Description automatically generated Chapter 14: Respiration 502 Gas exchange also occurs between blood in systemic capillaries and tissues in the body. Because metabolically active body tissues consume O2 and produce CO2 via [cellular respiration](javascript:void(0)), the PO2 in tissues is typically lower than the PO2 of blood in systemic capillaries. Furthermore, the PCO2 in tissues is typically higher than the PCO2 in systemic capillaries. As a result, O2 diffuses from the blood into metabolically active tissues and CO2 diffuses from metabolically active tissues into the blood, as shown in Figure 14.12. **Figure 14.12** Gas exchange in a body tissue. 14.2.03 Respiration and Thermoregulation The respiratory system contributes to **thermoregulation**, the overall process by which the body maintains an internal temperature within the normal physiological range. As discussed in Concept 19.2.03, the skin plays a primary role in thermoregulation via regulation of blood flow through capillaries near the skin\'s surface as well as via sweat production, which allows for body cooling through evaporation. The respiratory system similarly participates in thermoregulation by regulating blood flow through capillary beds located near the air-exposed internal surfaces of the nasal cavity and trachea. The nasal cavity contains structures (ie, nasal conchae) that increase the surface area of the nasal mucosa (ie, [respiratory epithelium](javascript:void(0))), to which air entering and leaving the respiratory system via the nose is exposed. This extensive mucosa transfers heat and moisture (ie, water vapor) to inspired air, and [vasodilation](javascript:void(0)) of [arterioles](javascript:void(0)) supplying blood to capillary beds in the nasal cavity facilitates this air-warming and humidification process. When expiration occurs through the nose, some of the heat and water that were added to the inspired air are reclaimed as the warmer air exits the cooler nose, causing condensation of water back onto the nasal mucosa. Not all of the water vapor that evaporates into inspired air can be reclaimed via condensation in the nose during expiration; therefore, ventilation results in a net loss of water from the body. Because evaporation is an [endothermic](javascript:void(0)) (ie, heat-absorbing) process, a net loss of water via evaporation results in a net loss of heat from the body (ie, ventilation typically *cools* the body). Figure 14.13 illustrates the effects of inspiration and expiration through the nose on thermoregulation.  Chapter 14: Respiration 503 **Figure 14.13** Effects of inspiration and expiration through the nose on thermoregulation. Increased ventilation accompanied by decreased tidal volume (ie, **panting**) results in increased water evaporation from the respiratory system, thereby [increasing heat dissipation](javascript:void(0)) (Table 14.1). Inspiration during panting occurs through the nose but may also occur through the mouth to facilitate cooling by allowing additional water to evaporate (ie, from the oral mucosa and tongue). Body cooling via panting is maximized when inspiration occurs through the nose and expiration occurs through the mouth. This pattern of air flow prevents condensation (which causes heat to *return* to the body) from occurring in the nasal cavity. A diagram of the nose and nose expirating Description automatically generated Chapter 14: Respiration 504 **Table 14.1** Mechanisms by which the respiratory system participates in thermoregulation. 14.2.04 Control of Respiration As discussed in Concept 14.2.01, ventilation occurs due to the activity of skeletal muscles (eg, diaphragm, intercostal muscles), which contract upon receipt of signals from the [central nervous system](javascript:void(0)) (ie, brain, spinal cord) via somatic [motor neurons](javascript:void(0)). As shown in Figure 14.14, the brain contains **respiratory centers**, which govern involuntary ventilation. These respiratory centers are located within the **pons** and **medulla** of the [brainstem](javascript:void(0)). The brain\'s **cerebral cortex** controls voluntary ventilation. The respiratory center in the medulla is composed of a network of neurons that establishes the basic rhythm of involuntary respiration, which is characterized by a resting ventilation rate of approximately 12--16 breaths per minute. Neurons in the pons participate in respiratory control by communicating with and affecting the activity of the medullary respiratory center. The respiratory centers receive input from a variety of sensory receptors, including **central chemoreceptors** located in the brainstem and **peripheral chemoreceptors** located in blood vessels that carry blood to the brain (ie, aortic arch and carotid arteries, see Figure 14.14). Integration of this sensory input allows the respiratory centers to adjust the rate and depth of ventilation to meet changing demands, which are typically brought about by changes in the body\'s activity level. In addition, input from higher brain centers (eg, cerebral cortex, [hypothalamus](javascript:void(0))) regulates respiratory center output and influences involuntary ventilation.  Chapter 14: Respiration 505 **Figure 14.14** Structures involved in respiration control. The body is able to meet changing demands for ventilation by monitoring the concentrations of CO2, hydrogen ions (H+), and O2 in body fluids. Peripheral chemoreceptors monitor all three of these factors in arterial blood, and central chemoreceptors detect CO2 levels in the brain\'s cerebrospinal fluid (CSF). More specifically, the central chemoreceptors monitor [pH](javascript:void(0)) (ie, H+ concentration) of the CSF, which becomes more acidic (ie, pH decreases) as CO2 moves from the blood into the CSF by readily diffusing across the [blood-brain barrier](javascript:void(0)). The effect of CO2 concentration on body fluid pH is discussed in greater detail in Concept 14.2.05. Under normal conditions, arterial blood CO2 concentration is the most important determinant of ventilatory rate and depth, primarily via the effect of blood CO2 concentration on CSF pH. The partial pressure of CO2 (PCO2) in arterial blood is tightly regulated, typically being held at approximately 40 mm Hg due to A diagram of a human body Description automatically generated Chapter 14: Respiration 506 [negative feedback](javascript:void(0)). When arterial blood PCO2 rises, excess CO2 is eliminated via increased ventilation resulting from increased stimulatory input from chemoreceptors. Conversely, if arterial blood PCO2 is too low, CO2 is allowed to accumulate in the blood through decreased ventilation resulting from decreased chemoreceptor stimulation. The level of O2 in arterial blood typically does not play a major role in regulating ventilation. Blood O2 content becomes a primary factor in determining ventilatory rate only if the partial pressure of O2 (PO2) in arterial blood drops below approximately 60 mm Hg (ie, 20--40% lower than typical arterial blood PO2). If arterial blood PO2 drops below this point, decreased PO2 stimulates increased ventilation by triggering increased stimulatory input to the respiratory centers by the peripheral chemoreceptors. Table 14.2 summarizes the effects of activated peripheral and central chemoreceptors on ventilation control. **Table 14.2** Effects of sensory inputs sent from activated chemoreceptors to respiratory centers. Activity of the respiratory centers is also affected by other inputs. For example, pain and strong emotions, such as fear and excitement, affect ventilation (typically by increasing ventilation rate) via inputs from the [amygdala](javascript:void(0)) and hypothalamus. In addition, the lungs contain **mechanoreceptors** (ie, stretch receptors) that are stimulated by lung inflation and send inhibitory signals to the respiratory centers. This inhibitory input from mechanoreceptors likely prevents lung overinflation. The cerebral cortex controls voluntary respiration via motor neurons that bypass the brainstem\'s respiratory centers and directly stimulate inspiratory muscles. However, voluntary control of ventilation (eg, breath-holding) is limited because involuntary signals from the respiratory centers eventually override voluntary signals from the cerebral cortex as the PCO2 in the blood and CSF rises.  Chapter 14: Respiration 507 **Concept Check 14.2** The table shows blood test results obtained from a human subject with no underlying health problems who provided blood samples for analysis on three separate occasions. Complete the table by ranking the subject\'s likely ventilation rate at the time of sample collection as highest, intermediate, or lowest. [**Solution**](javascript:void(0)) 14.2.05 Role in Regulating pH The respiratory system (along with the excretory system, as described in Concept 16.2.01) plays a major role in regulating the pH of body fluids. Specifically, ventilation provides a mechanism by which minute-to-minute changes in body fluid pH can be responded to and corrected, thereby maintaining acid-base balance (ie, pH [homeostasis](javascript:void(0))). The respiratory system can regulate pH in the body because carbon dioxide (CO2), which is eliminated from the body via ventilation, has a significant impact on body fluid pH by reacting with water (H2O) in body fluids to produce carbonic acid (H2CO3) as follows: CO 2 \+ H 2 O⇋ H 2 CO 3 ⇋ HCO ― 3 \+ H \+ This equation shows that CO2 and H2O are in [equilibrium](javascript:void(0)) with H2CO3, which in turn is in equilibrium with bicarbonate ions (HCO3−) and hydrogen ions (H+). Consequently, in accordance with [Le Châtelier\'s](javascript:void(0)) [principle](javascript:void(0)), if the CO2 concentration in a body fluid increases, the concentrations of H2CO3 and H+ in this fluid will also increase, resulting in decreased pH (because [pH decreases](javascript:void(0)) as H+ concentration increases). Likewise, if the CO2 concentration in a body fluid decreases, less H2CO3 will be produced, resulting in lower H+ concentration and higher pH. The body regulates blood pH via the respiratory system by adjusting ventilation rate. Changes in ventilation rate cause changes in blood pH by affecting the extent to which CO2 is removed from the blood via expiration. As shown in Figure 14.15, an increased ventilation rate raises blood pH (ie, makes the blood more alkaline) by transferring more CO2 from the blood into the alveoli and eliminating that CO2 from the body via expiration. Likewise, a decreased ventilation rate lowers blood pH (ie, makes the blood more acidic) by allowing more CO2 to remain in the blood rather than being transferred to the alveoli and expired. A blue check mark in a square Description automatically generated  Chapter 14: Respiration 508 **Figure 14.15** Effect of ventilation rate on blood pH. Various factors (eg, diseases, medications, emotional state) that affect ventilation rate can lead to altered blood pH. Factors that result in **hyperventilation** (ie, rapid, deep breathing) typically produce respiratory alkalosis (abnormalllly high blood pH). Conversely, factors that result in **hypoventilation** (ie, slow, shallow breathing) typically produce respiratory acidosis (abnormally low blood pH). Figure 14.16 illustrates the effects of hyperventilation and hypoventilation on blood pH. A diagram of a blood ph and a diagram of a blood ph Description automatically generated Chemical buffer system within the body provide an important means by which the body resists changes in pH. Buffer systems help maintain pH homeostasis by releasing H+ in response to increased pH and binding H+ in response to decreased pH. The **bicarbonate buffer system**, which consists of the [reversible reactions](javascript:void(0))involving carbonic acid and bicarbonate ions previously described in this concept, is the primary buffer system that stabilizes pH in the body\'s extracellular fluids (including blood plasma). As described in Concept 13.1.04, the enzyme **carbonic anhydrase** is present within red blood cells to catalyze the formation of carbonic acid, which dissociates to produce bicarbonate ions and hydrogen ions. The protein hemoglobin, which is present in abundance within red blood cells, functions as a buffer by binding these hydrogen ions, thereby preventing a significant decrease in pH. Hemoglobin molecules, along with other intracellular proteins and blood plasma proteins (eg, albumin), make up the **protein buffer system**, which helps stabilize the pH of both intracellular and extracellular fluids. The **phosphate buffer system** is similar to the bicarbonate buffer system but uses hydrogen phosphate ions (HPO42−) rather than bicarbonate ions. The concentration of phosphate in blood plasma is relatively low; therefore, the phosphate buffer system functions primarily within cells and in urine, locations in which phosphate concentration is higher