Pulmonary System: Lung Anatomy and Function PDF

Part 1 Pulmonary 1) Students will identify the parts of the conducting and respiratory zones of the lungs and will interpret the functions of lung volumes and capacities. The respiratory system includes the lungs and a series of airways that connect the lungs to the external environment. The struc...

Part 1 Pulmonary 1) Students will identify the parts of the conducting and respiratory zones of the lungs and will interpret the functions of lung volumes and capacities. The respiratory system includes the lungs and a series of airways that connect the lungs to the external environment. The structures of the respiratory system are subdivided into a conducting zone (or conducting airways), which brings air into and out of the lungs, and a respiratory zone lined with alveoli where gas exchange occurs. The functions of the conducting and respiratory zones differ, and the structures lining them also differ. Conducting zone The conducting zone includes the nose, nasopharynx, larynx, trachea, bronchi, bronchioles, and terminal bronchioles. These structures function to bring air into and out of the respiratory zone for gas exchange and to warm, humidify, and filter the air before it reaches the critical gas exchange region. The progressively bifurcating airways are referred to by their generation number. The trachea, which is the zeroth generation, is the main conducting airway. The trachea divides into the right and left mainstem bronchi (the first generation), which divide into smaller bronchi, continuing this process through 23 generations, culminating in the airways of the 23rd generation. Cartilage is present in the walls of the zeroth to 10th generations of conducting airways; it functions structurally to keep those airways open. Starting with the 11th generation, cartilage disappears; to remain open, those airways with no cartilage depend on the presence of a favorable transmural pressure. The conducting airways are lined with mucus-secreting and ciliated cells that function to remove inhaled particles. Large particles are usually filtered out in the nose, while small particles are captured by mucus and swept upward by the rhythmic beating of cilia. The walls of the conducting airways contain smooth muscle, which is regulated by the autonomic nervous system: 1. Sympathetic adrenergic neurons activate β₂ receptors on bronchial smooth muscle, leading to relaxation and dilation of the airways. These β₂ receptors are also activated by epinephrine from the adrenal medulla and by β₂-adrenergic agonists such as isoproterenol. 2. Parasympathetic cholinergic neurons activate muscarinic receptors, leading to contraction and constriction of the airways. Changes in airway diameter affect airway resistance, altering air flow. β₂-adrenergic agonists (e.g., epinephrine, isoproterenol, albuterol) are used to dilate airways in the treatment of asthma. Part 1 Pulmonary Respiratory zone The respiratory zone includes structures lined with alveoli and thus involved in gas exchange: the respiratory bronchioles, alveolar ducts, and alveolar sacs. Respiratory bronchioles are transitional structures—they have cilia and smooth muscle, like the conducting airways, but also participate in gas exchange as alveoli occasionally bud off their walls. Alveolar ducts are completely lined with alveoli, but they contain no cilia and little smooth muscle. Alveolar sacs are the terminal structures of the respiratory zone, also lined with alveoli. Alveoli are pouchlike evaginations of the respiratory bronchioles, alveolar ducts, and alveolar sacs. Each lung contains approximately 300 million alveoli, with a diameter of ~200 micrometers (μm). The thin alveolar walls and large surface area allow rapid and efficient diffusion of oxygen (O₂) and carbon dioxide (CO₂) between alveolar gas and pulmonary capillary blood. The alveolar walls contain elastic fibers and epithelial cells called type I and type II pneumocytes (alveolar cells): Type II pneumocytes synthesize pulmonary surfactant, which reduces surface tension in the alveoli, and they have regenerative capacity for type I and type II pneumocytes. The alveoli also contain phagocytic cells called alveolar macrophages, which keep the alveoli free of dust and debris since alveoli have no cilia. Macrophages migrate to the bronchioles, where cilia transport debris to the pharynx for swallowing or expectoration. Part 1 Pulmonary 2) Students will calculate ventilation rates, dilution effect of dead space, alveolar ventilation, alveolar PO2 and FEV1 /FVC ratios. Static volumes of the lung are measured with a spirometer ( Table 5.1 ). Typically, the subject is sitting and breathes into and out of the spirometer, displacing a bell. The volume displaced is recorded on calibrated paper ( Fig. 5.2 ). First, the subject is asked to breathe quietly. Normal, quiet breathing involves inspiration and expiration of a tidal volume (V t ). Normal tidal volume is approximately 500 mL and includes the volume of air that fills the alveoli plus the volume of air that fills the airways. Next, the subject is asked to take a maximal inspiration, followed by a maximal expiration. With this maneuver, additional lung volumes are revealed. The additional volume that can be inspired above tidal volume is called the inspiratory reserve volume, which is approximately 3000 mL. The additional volume that can be expired below tidal volume is called the expiratory reserve volume, which is approximately 1200 mL. The volume of gas remaining in the lungs after a maximal forced expiration is the residual volume (RV), which is approximately 1200 mL and cannot be measured by spirometry. Lung capacities In addition to these lung volumes, there are several lung capacities; each lung capacity includes two or more lung volumes. The inspiratory capacity (IC) is composed of the tidal volume plus the inspiratory reserve volume and is approximately 3500 mL (500 mL + 3000 mL). The functional residual capacity (FRC) is composed of the expiratory reserve volume (ERV) plus the RV, or approximately 2400 mL (1200 mL + 1200 mL). FRC is the volume remaining in the lungs after a normal tidal volume is expired and can be thought of as the equilibrium volume of the lungs. The vital capacity (VC) is composed of the IC plus the expiratory reserve volume, or approximately 4700 mL (3500 mL + 1200 mL). Vital capacity is the volume that can be expired after maximal inspiration. Its value increases with body size, male gender, and physical conditioning and decreases with age. Finally, as the terminology suggests, the total lung capacity (TLC) includes all of the lung volumes: It is the vital capacity plus the RV, or 5900 mL (4700 mL + 1200 mL). Part 1 Pulmonary Because RV cannot be measured by spirometry, lung capacities that include the RV also cannot be measured by spirometry (i.e., FRC and TLC). Of the lung capacities not measurable by spirometry, the FRC (the volume remaining in the lungs after a normal expiration) is of greatest interest because it is the resting or equilibrium volume of the lungs. Two methods are used to measure FRC: helium dilution and the body plethysmograph. ♦ In the helium dilution method, the subject breathes a known amount of helium, which has been added to the spirometer. Because helium is insoluble in blood, after a few breaths the helium concentration in the lungs becomes equal to that in the spirometer, which can be measured. The amount of helium that was added to the spirometer and its concentration in the lungs are used to “back-calculate” the lung volume that the helium was distributed in. If this measurement is made after a normal tidal volume is expired, the lung volume being calculated is the FRC. ♦ The body plethysmograph employs a variant of Boyle’s law, which states that for gases, if the number of moles of gas and temperature are constant, gas pressure multiplied by gas volume is constant (P × V = constant). Therefore, if volume increases, pressure must decrease, and if volume decreases, pressure must increase. To measure FRC, the subject sits in a large airtight box called a plethysmograph. After expiring a normal tidal volume, the mouthpiece to the subject’s airway is closed. The subject then attempts to breathe. As the subject tries to inspire, the volume in the subject’s lungs increases and the pressure in his or her lungs decreases. Simultaneously, the volume in the box decreases, and the pressure in the box increases. The increase in pressure in the box can be measured and, from it, the perspiratory volume in the lungs can be calculated, which is the FRC. Dead space Dead space is the volume of the airways and lungs that does not participate in gas exchange. Dead space is a general term that refers to both the anatomic dead space of the conducting airways and a functional, or physiologic, dead space. Anatomic dead space The anatomic dead space is the volume of the conducting airways including the nose (and/or mouth), trachea, bronchi, and bronchioles. It does not include the respiratory bronchioles and alveoli. The volume of the conducting airways is approximately 150 mL. Thus for example, when a tidal volume of 500 mL is inspired, the entire volume does not reach the alveoli for gas exchange; 150 mL fills the conducting airways (the anatomic dead space, where no gas exchange occurs), and 350 mL fills the alveoli. Figure 5.3 shows that at the end of expiration the conducting airways are filled with alveolar air; that is, they are filled with air that has already been in the alveoli and exchanged gases with pulmonary capillary blood. With the inspiration of the next tidal volume, this alveolar air is first to enter the alveoli, although it will not undergo further gas exchange (“already been there, done that”). The next air to enter the alveoli is fresh air from the inspired tidal volume (350 mL), which will undergo gas exchange. The rest of the tidal volume (150 mL) does not make it to the alveoli but remains in the conducting airways; this air will not participate in gas exchange and will be the first air expired. (A related point arises from this discussion: The first air expired is dead space air that has not undergone gas exchange. To sample alveolar air, one must sample end -expiratory air.) Part 1 Pulmonary The concept of physiologic dead space is more abstract than the concept of anatomic dead space. By definition, the physiologic dead space is the total volume of the lungs that does not participate in gas exchange. Physiologic dead space includes the anatomic dead space of the conducting airways plus a functional dead space in the alveoli. The functional dead space can be thought of as ventilated alveoli that do not participate in gas exchange. The most important reason that alveoli do not participate in gas exchange is a mismatch of ventilation and perfusion, or so-called ventilation/perfusion defect, in which ventilated alveoli are not perfused by pulmonary capillary blood. In normal persons, the physiologic dead space is nearly equal to the anatomic dead space. In other words, alveolar ventilation and perfusion (blood flow) are normally well matched and functional dead space is small. In certain pathologic situations, however, the physiologic dead space can become larger than the anatomic dead space, suggesting a ventilation/perfusion defect. The ratio of physiologic dead space to tidal volume provides an estimate of how much ventilation is “wasted” (either in the conducting airways or in nonperfused alveoli). The volume of the physiologic dead space is estimated with the following method, which is based on the measurement of the partial pressure of CO2 (Pco2) of mixed expired air (PeCO2) and the following three assumptions: (1) All of the CO2 in expired air comes from exchange of CO2 in functioning (ventilated and perfused) alveoli; (2) there is essentially no CO2 in inspired air; and (3) the physiologic dead space (nonfunctioning alveoli and airways) neither exchanges nor contributes any CO2. If physiologic dead space is zero, then PeCO2 will be equal to alveolar Pco2 (PaCO2). However, if a physiologic dead space is present, then PeCO2 will be “diluted” by dead space air and PeCO2 will be less than PaCO2 by a dilution factor. Therefore, by comparing PeCO2 with PaCO2, the dilution factor (i.e., volume of the physiologic dead space) can be measured. A potential problem in measuring physiologic dead space is that alveolar air cannot be sampled directly. This problem can be overcome, however, because alveolar air normally equilibrates with pulmonary capillary blood (which becomes systemic arterial blood). Thus the Pco2 of systemic arterial blood (PaCO2) is equal to the Pco2 of alveolar air (PaCO2). Part 1 Pulmonary Using this assumption, the volume of physiologic dead space is calculated by the following equation: